A M EDICAL D ICTIONARY , B IBLIOGRAPHY , AND A NNOTATED R ESEARCH G UIDE TO I NTERNET R EFERENCES
J AMES N. P ARKER , M.D. AND P HILIP M. P ARKER , P H .D., E DITORS
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ICON Health Publications ICON Group International, Inc. 4370 La Jolla Village Drive, 4th Floor San Diego, CA 92122 USA Copyright Ó2003 by ICON Group International, Inc. Copyright Ó2003 by ICON Group International, Inc. All rights reserved. This book is protected by copyright. No part of it may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without written permission from the publisher. Printed in the United States of America. Last digit indicates print number: 10 9 8 7 6 4 5 3 2 1
Publisher, Health Care: Philip Parker, Ph.D. Editor(s): James Parker, M.D., Philip Parker, Ph.D. Publisher's note: The ideas, procedures, and suggestions contained in this book are not intended for the diagnosis or treatment of a health problem. As new medical or scientific information becomes available from academic and clinical research, recommended treatments and drug therapies may undergo changes. The authors, editors, and publisher have attempted to make the information in this book up to date and accurate in accord with accepted standards at the time of publication. The authors, editors, and publisher are not responsible for errors or omissions or for consequences from application of the book, and make no warranty, expressed or implied, in regard to the contents of this book. Any practice described in this book should be applied by the reader in accordance with professional standards of care used in regard to the unique circumstances that may apply in each situation. The reader is advised to always check product information (package inserts) for changes and new information regarding dosage and contraindications before prescribing any drug or pharmacological product. Caution is especially urged when using new or infrequently ordered drugs, herbal remedies, vitamins and supplements, alternative therapies, complementary therapies and medicines, and integrative medical treatments. Cataloging-in-Publication Data Parker, James N., 1961Parker, Philip M., 1960Arthritis: A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References / James N. Parker and Philip M. Parker, editors p. cm. Includes bibliographical references, glossary, and index. ISBN: 0-597-83554-3 1. Arthritis-Popular works. I. Title.
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Disclaimer This publication is not intended to be used for the diagnosis or treatment of a health problem. It is sold with the understanding that the publisher, editors, and authors are not engaging in the rendering of medical, psychological, financial, legal, or other professional services. References to any entity, product, service, or source of information that may be contained in this publication should not be considered an endorsement, either direct or implied, by the publisher, editors, or authors. ICON Group International, Inc., the editors, and the authors are not responsible for the content of any Web pages or publications referenced in this publication.
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Acknowledgements The collective knowledge generated from academic and applied research summarized in various references has been critical in the creation of this book which is best viewed as a comprehensive compilation and collection of information prepared by various official agencies which produce publications on arthritis. Books in this series draw from various agencies and institutions associated with the United States Department of Health and Human Services, and in particular, the Office of the Secretary of Health and Human Services (OS), the Administration for Children and Families (ACF), the Administration on Aging (AOA), the Agency for Healthcare Research and Quality (AHRQ), the Agency for Toxic Substances and Disease Registry (ATSDR), the Centers for Disease Control and Prevention (CDC), the Food and Drug Administration (FDA), the Healthcare Financing Administration (HCFA), the Health Resources and Services Administration (HRSA), the Indian Health Service (IHS), the institutions of the National Institutes of Health (NIH), the Program Support Center (PSC), and the Substance Abuse and Mental Health Services Administration (SAMHSA). In addition to these sources, information gathered from the National Library of Medicine, the United States Patent Office, the European Union, and their related organizations has been invaluable in the creation of this book. Some of the work represented was financially supported by the Research and Development Committee at INSEAD. This support is gratefully acknowledged. Finally, special thanks are owed to Tiffany Freeman for her excellent editorial support.
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About the Editors James N. Parker, M.D. Dr. James N. Parker received his Bachelor of Science degree in Psychobiology from the University of California, Riverside and his M.D. from the University of California, San Diego. In addition to authoring numerous research publications, he has lectured at various academic institutions. Dr. Parker is the medical editor for health books by ICON Health Publications.
Philip M. Parker, Ph.D. Philip M. Parker is the Eli Lilly Chair Professor of Innovation, Business and Society at INSEAD (Fontainebleau, France and Singapore). Dr. Parker has also been Professor at the University of California, San Diego and has taught courses at Harvard University, the Hong Kong University of Science and Technology, the Massachusetts Institute of Technology, Stanford University, and UCLA. Dr. Parker is the associate editor for ICON Health Publications.
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About ICON Health Publications To discover more about ICON Health Publications, simply check with your preferred online booksellers, including Barnes & Noble.com and Amazon.com which currently carry all of our titles. Or, feel free to contact us directly for bulk purchases or institutional discounts: ICON Group International, Inc. 4370 La Jolla Village Drive, Fourth Floor San Diego, CA 92122 USA Fax: 858-546-4341 Web site: www.icongrouponline.com/health
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Table of Contents FORWARD .......................................................................................................................................... 1 CHAPTER 1. STUDIES ON ARTHRITIS ................................................................................................ 3 Overview ....................................................................................................................................... 3 The Combined Health Information Database ................................................................................ 3 Federally Funded Research on Arthritis...................................................................................... 31 E-Journals: PubMed Central ....................................................................................................... 65 The National Library of Medicine: PubMed................................................................................ 87 CHAPTER 2. NUTRITION AND ARTHRITIS..................................................................................... 189 Overview ................................................................................................................................... 189 Finding Nutrition Studies on Arthritis .................................................................................... 189 Federal Resources on Nutrition................................................................................................. 198 Additional Web Resources......................................................................................................... 198 CHAPTER 3. ALTERNATIVE MEDICINE AND ARTHRITIS .............................................................. 207 Overview ................................................................................................................................... 207 The Combined Health Information Database ............................................................................ 207 National Center for Complementary and Alternative Medicine ............................................... 208 Additional Web Resources......................................................................................................... 233 General References..................................................................................................................... 258 CHAPTER 4. DISSERTATIONS ON ARTHRITIS ................................................................................ 259 Overview ................................................................................................................................... 259 Dissertations on Arthritis ......................................................................................................... 259 Keeping Current ........................................................................................................................ 266 CHAPTER 5. CLINICAL TRIALS AND ARTHRITIS ........................................................................... 267 Overview ................................................................................................................................... 267 Recent Trials on Arthritis ......................................................................................................... 267 Keeping Current on Clinical Trials ........................................................................................... 291 CHAPTER 6. PATENTS ON ARTHRITIS ........................................................................................... 293 Overview ................................................................................................................................... 293 Patents on Arthritis................................................................................................................... 293 Patent Applications on Arthritis............................................................................................... 420 Keeping Current ........................................................................................................................ 450 CHAPTER 7. BOOKS ON ARTHRITIS............................................................................................... 451 Overview ................................................................................................................................... 451 Book Summaries: Federal Agencies ........................................................................................... 451 Book Summaries: Online Booksellers ........................................................................................ 456 The National Library of Medicine Book Index........................................................................... 475 Chapters on Arthritis ................................................................................................................ 477 CHAPTER 8. MULTIMEDIA ON ARTHRITIS .................................................................................... 489 Overview ................................................................................................................................... 489 Video Recordings....................................................................................................................... 489 Audio Recordings ...................................................................................................................... 490 Bibliography: Multimedia on Arthritis ..................................................................................... 492 CHAPTER 9. PERIODICALS AND NEWS ON ARTHRITIS ................................................................. 495 Overview ................................................................................................................................... 495 News Services and Press Releases ............................................................................................. 495 Newsletters on Arthritis............................................................................................................ 501 Newsletter Articles .................................................................................................................... 503 Academic Periodicals covering Arthritis................................................................................... 515 APPENDIX A. PHYSICIAN RESOURCES.......................................................................................... 519 Overview ................................................................................................................................... 519 NIH Guidelines ......................................................................................................................... 519
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Contents NIH Databases ...........................................................................................................................521 Other Commercial Databases .....................................................................................................526 The Genome Project and Arthritis .............................................................................................526 APPENDIX B. PATIENT RESOURCES ...............................................................................................531 Overview ....................................................................................................................................531 Patient Guideline Sources ..........................................................................................................531 Finding Associations ..................................................................................................................564 APPENDIX C. RESEARCHING MEDICATIONS .................................................................................567 Overview ....................................................................................................................................567 U.S. Pharmacopeia .....................................................................................................................567 Commercial Databases ...............................................................................................................571 Researching Orphan Drugs .......................................................................................................572
ONLINE GLOSSARIES ................................................................................................................575 Online Dictionary Directories ...................................................................................................578 ARTHRITIS DICTIONARY.........................................................................................................579 INDEX...............................................................................................................................................690
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FORWARD In March 2001, the National Institutes of Health issued the following warning: "The number of Web sites offering health-related resources grows every day. Many sites provide valuable information, while others may have information that is unreliable or misleading."1 Furthermore, because of the rapid increase in Internet-based information, many hours can be wasted searching, selecting, and printing. Since only the smallest fraction of information dealing with arthritis is indexed in search engines, such as www.google.com or others, a non-systematic approach to Internet research can be not only time consuming, but also incomplete. This book was created for medical professionals, students, and members of the general public who want to know as much as possible about arthritis, using the most advanced research tools available and spending the least amount of time doing so. In addition to offering a structured and comprehensive bibliography, the pages that follow will tell you where and how to find reliable information covering virtually all topics related to arthritis, from the essentials to the most advanced areas of research. Public, academic, government, and peer-reviewed research studies are emphasized. Various abstracts are reproduced to give you some of the latest official information available to date on arthritis. Abundant guidance is given on how to obtain free-of-charge primary research results via the Internet. While this book focuses on the field of medicine, when some sources provide access to non-medical information relating to arthritis, these are noted in the text. E-book and electronic versions of this book are fully interactive with each of the Internet sites mentioned (clicking on a hyperlink automatically opens your browser to the site indicated). If you are using the hard copy version of this book, you can access a cited Web site by typing the provided Web address directly into your Internet browser. You may find it useful to refer to synonyms or related terms when accessing these Internet databases. NOTE: At the time of publication, the Web addresses were functional. However, some links may fail due to URL address changes, which is a common occurrence on the Internet. For readers unfamiliar with the Internet, detailed instructions are offered on how to access electronic resources. For readers unfamiliar with medical terminology, a comprehensive glossary is provided. For readers without access to Internet resources, a directory of medical libraries, that have or can locate references cited here, is given. We hope these resources will prove useful to the widest possible audience seeking information on arthritis. The Editors
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From the NIH, National Cancer Institute (NCI): http://www.cancer.gov/cancerinfo/ten-things-to-know.
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CHAPTER 1. STUDIES ON ARTHRITIS Overview In this chapter, we will show you how to locate peer-reviewed references and studies on arthritis.
The Combined Health Information Database The Combined Health Information Database summarizes studies across numerous federal agencies. To limit your investigation to research studies and arthritis, you will need to use the advanced search options. First, go to http://chid.nih.gov/index.html. From there, select the “Detailed Search” option (or go directly to that page with the following hyperlink: http://chid.nih.gov/detail/detail.html). The trick in extracting studies is found in the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Journal Article.” At the top of the search form, select the number of records you would like to see (we recommend 100) and check the box to display “whole records.” We recommend that you type “arthritis” (or synonyms) into the “For these words:” box. Consider using the option “anywhere in record” to make your search as broad as possible. If you want to limit the search to only a particular field, such as the title of the journal, then select this option in the “Search in these fields” drop box. The following is what you can expect from this type of search: ·
Arthritis 101: Temporomandibular Joint Disorders Source: Arthritis Today. 15(5): 36,39. September-October 2001. Summary: This journal article provides people who have temporomandibular joint (TMJ) disorders (TMDs), which affect the jaw joint and supporting muscles, with information on diagnosis and treatment. Myofascial pain is the most common form of TMD. The TMJ is also susceptible to arthritis, including rheumatoid arthritis, juvenile rheumatoid arthritis, and osteoarthritis. Symptoms of TMD include pain, popping and locking of the TMJ, headaches, earaches, and dizziness. Diagnosis is based on a physical examination, a review of dental records, and a description of symptoms. Self management includes using hot or cold packs to ease pain, eating soft foods, and avoiding chewing gum. Other measures that might be helpful include physical therapy, nonsteroidal antiinflammatory drugs, and relaxation exercises. Cortisone injections or
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analgesics may also be useful. If surgery is recommended, a second opinion should be sought. The TMJ Association organized a meeting to promote a better understanding of TMD and to identify future areas of research. 4 figures. ·
Intraindividual Variability in Cognitive Performance in Older Adults: Comparison of Adults With Mild Dementia, Adults With Arthritis, and Healthy Adults Source: Neuropsychology. 14(4): 588-598. 2000. Summary: This article looks at intraindividual variability in cognitive performance in older adults with dementia (n=13), older adults with arthritis (n=17), and healthy older adults (n=15). Participants completed two reaction-time and two episodic-memory tasks on four occasions. The intraindividual variability in latency was significantly greater in the group with mild dementia than in the neurologically intact groups. Individual differences in variability were stable over time and across cognitive domains. Intraindividual variability was also related to level of performance and was uniquely predictive of neurological status, independent of level of performance. These results suggest that intraindividual variability is a potentially useful indicator of cognitive functioning. 4 figures, 4 tables, 28 references. (AA-M).
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Predictors of Motor Vehicle Crashes in a Dementia Clinic Population: The Role of Gender and Arthritis (editorial) Source: Journal of the American Geriatric Society. 43(12): 1444-1445. December 1995. Summary: This letter to the editor reviews driving records for 249 patients seen in a dementia clinic in Vancouver, Canada, to determine which demographic variables or medical conditions contributed to the incidence of motor vehicle accidents. Of the subjects, 165 had dementia and 84 did not. The results suggest that more men than women have accidents because women were twice as likely as men to have stopped driving. Additionally, the combination of arthritis and use of nonsteroidal antiinflammatory medication yielded the greatest number of drivers with one or more motor vehicle crashes. These findings underscore the need to address other medical conditions and the use of pharmaceutical agents when evaluating the driving status of older adults. 1 table, 9 references.
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Reactive Arthritis: Newer Developments Source: Rheumatic Disease Clinics of North America. 29(1): 37-59. February 2003. Summary: This journal article provides heath professionals with information on reactive arthritis (ReA). ReA is characterized by an aseptic inflammatory articular involvement occurring in a genetically predisposed individual secondary to an infectious process localized outside the joint. The classic microbes associated with ReA are enterobacterias and chlamydia but recent studies have shown that other bacterial species are found in synovial tissue and fluid. In addition, shigella, salmonella, yersinia, campylobacter, streptococcus, and intestinal parasites are associated with ReA. ReA usually refers to an acute or insidious oligoarthritis process after enteric (enteroarthritis) or urogenital (uroarthritis) infection. Conventional antirheumatic therapeutic modalities based on NSAIDs, sulfasalazine, and steroids are effective in the majority of patients. In more refractory cases, the use of second-line agents including methotrexate and more recently biological agents such as etanercept and infliximab has been found highly effective. The role of antibiotics remains not well established, although they appear to be effective in acute ReA of urogenital origin. 2 figures and 139 references. (AAM).
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Current Approach to the Evaluation and Management of Acute Monarthritis Source: Physician Assistant. 27(3): 22-28. March 2003. Summary: This journal article for health professionals provides infomation on the diagnosis and treatment of monoarthritis. A complaint of monarthritis presents a diagnostic challenge to the primary care clinician due to the overlapping clinical features of the various monoarthropathies. Initial considerations should include infection and crystalline deposition diseases as etiologic possibilities. A complete history and physical examination, selected laboratory and radiographic studies, and analysis of joint aspirate are key in differentiating between joint sepsis, crystalline deposition diseases, and other common causes. The differential diagnosis of monarthritis includes septic arthritis, trauma and overuse, gout and pseudogout, and osteonecrosis. Reactive arthritis, malignancy, and other systemic rheumatic diseases such as psoriatic arthritis, rheumatoid arthritis, and systemic lupus erythematosus may also present with an acute monarthritis. Treatment is directed at the underlying disorder and, when indicated, should be guided by the results of the synovial fluid analysis. 5 figures, 3 tables, and 19 references. (AAM).
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Prescribing Assistive Devices for Patients With Rheumatoid Arthritis Source: Journal of Musculoskeletal Medicine. 19(1): 27-34. January 2002. Summary: This journal article provides health professionals with information on assistive devices for patients with rheumatoid arthritis (RA). The physical impairments and disability that accompany RA may require major adaptive changes in lifestyle. Assistive devices become an important component of this adaptation by allowing those with RA to complete many everyday tasks independently. These devices are prescribed by an occupational or physical therapist. Successful device prescription requires proper patient evaluation, patient education, and follow up. To maximize compliance, evaluation must take into account the demographic data and environment as well as the person's physical impairments. Demographic factors that relate to compliance with using assistive devices to perform the activities of daily living include age and gender. Individual factors concerning task performance and compliance in the use of assistive devices include type and severity of disability, lack of personal acceptance of assistive devices, perceived benefit of the device, and lack of confidence in usage. Some of the assistive devices that are more commonly used by patients with RA include those that help with walking and general mobility, dressing, bathing and grooming, preparing food, writing, working at a desk, and gardening. 5 figures, 2 tables, and 26 references. (AA-M).
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Recognizing and Managing Reactive Arthritis Source: Journal of Musculoskeletal Medicine. 19(1): 37-42. January 2002. Summary: This journal article provides health professionals with information on the diagnosis and management of reactive arthritis (ReA). This type of arthritis is a sterile inflammatory arthropathy in which the arthritis occurs in response to an antecedent infection, most typically one that involves the genitourinary or gastrointestinal tract. The most common symptom in this systemic disease is joint inflammation. Classically, ReA is characterized by an asymmetric oligoarthritis, predominantly of the lower extremities. Patients may also present with a monoarthritis or dactylitis. The site and nature of the event that triggers the infection may be difficult to identify in many cases, posing a diagnostic challenge. There is no one reliable diagnostic test for ReA, but some tests help categorize the disease process and rule out other diseases. The erythrocyte
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sedimentation rate is generally elevated but is nonspecific and often less elevated than it is in rheumatoid arthritis. Serum immunoglobulin (Ig) levels are generally normal, although an elevation of serum IgA levels is commonly seen in postdysenteric ReA. Salmonella, Shigella, Yersinia, and Chlamydia species are the microbes most commonly involved. Nonsteroidal antiinflammatory drugs form the basis of pharmacologic therapy, but corticosteroids and antibiotic treatment may have a role. Patient education is also an important part of the treatment program. 6 figures and 16 references. (AA-M). ·
Using Anakinra for Adult Rheumatoid Arthritis Source: Nurse Practitioner. 27(4): 62-65. April 2002. Summary: This journal article provides health professionals with information on using anakinra (Kineret) for treating rheumatoid arthritis (RA). Although the traditional approach to the pharmacologic treatment of RA consists of trying one drug at a time, a growing consensus among rheumatologists points to changing the stepped, pyramid approach to an inverted pyramid paradigm of early, aggressive intervention. Drugs from the biologic response modifiers (BRMs) classification may prove more effective than disease modifying antirheumatic drug therapy in preserving bone, preventing erosion of cartilage, and promoting joint form and function. BRMs inhibit or antagonize proinflammatory cytokines and related enzymes involved in joint destruction. Anakinra, a BRM, blocks interleukin (IL)-1-induced synovial inflammatory cell infiltration and blocks IL-1b binding. Anakinra reduces inflammation, pain, and disease activity, and it improves quality of life when administered as monotherapy or in combination with methotrexate. Anakinra was approved by the Food and Drug Administration in November 2001 as a daily subcutaneous injection of 100 milligrams for treating moderate to severe RA in people over 18. In studies, the most common adverse effect was injection site reactions; serious infection and neutropenia also occurred. 19 references.
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Role of Meat in the Expression of Rheumatoid Arthritis, The Source: British Journal of Nutrition. 84(5): 589-595. November 2000. Summary: This journal article provides health professionals with information on the role of meat in the expression of rheumatoid arthritis (RA). This disease is characterized by inflammation of the synovial tissues in the joints. The search for the causes of RA has not led to any general agreement on its etiology. Although approximately 150 studies have found dietary influences in RA, the level of scientific methodology for most of these studies is such that generally they are not accepted by the medical establishment. The article reviews numerous papers related to dietary components that are associated with RA. In addition, the ecological approach is used to examine the links between diet and RA. Multicountry data for the prevalence of RA in females from 8 and 15 countries were compared statistically with components of national dietary supply. Fat from meat and offal for the period 2 years before the prevalence data was found to have the highest statistical association with the prevalence of RA. The statistical correlations for meat and offal were almost as high as those for fat. Although similar correlations were found for temporal changes in indices of RA effects in several European countries between 1968 and 1978 as more meat was added to the national diets, the correlations were higher for meat than for fat. Agents in meat that may contribute to RA symptoms include nitrite and iron. 1 figure, 4 tables, and 70 references. (AA-M).
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Controlled Trial of Arthroscopic Surgery for Osteoarthritis of the Knee, A Source: New England Journal of Medicine. 347(2): 81-88. July 11, 2002. Summary: This journal article provides health professionals with information on a randomized, placebo-controlled trial that assessed the efficacy of arthroscopic surgery of the knee in relieving pain and improving function in patients with osteoarthritis (OA). The study population consisted of 180 patients with knee OA who were randomly assigned to receive arthroscopic debridement, arthroscopic lavage, or placebo surgery. Patients in the placebo group received skin incisions and underwent a simulated debridement without insertion of the arthroscope. Patients and assessors of outcome were blinded to the treatment group assignment. Outcomes were assessed at multiple points over a 24 month period with the use of five self reported scores (three on scales for pain and two on scales for function) and one objective test of walking and stair climbing. A total of 165 patients completed the trial. The study found that at no point did either of the intervention groups report less pain or better function than the placebo group. For example, there was no difference in knee pain between the placebo group and either the lavage group or the debridement group at 1 year or 2 years. Similarly, there was no significant difference in arthritis pain between the placebo group and the lavage group or the debridement group at 1 or 2 years. Furthermore, at no time point did either arthroscopic intervention group have significantly greater improvement in function than the placebo group. For example, there was no significant difference between the placebo group and either the lavage group or the debridement group in the self reported ability to walk and bend at 1 year or at 2 years. In fact, objectively measured walking and stair climbing were poorer in the debridement group than in the placebo group at 2 weeks and 1 year and showed a trend toward worse functioning at 2 years. Lacking evidence of the superiority of the arthroscopic treatments over the placebo procedure in relieving pain or improving function, researchers considered whether the 95 percent confidence intervals for the differences in outcomes between each arthroscopic procedure and the placebo procedure included clinically important differences. At almost all time points during follow up, the confidence intervals excluded the minimal important differences used in the study. The article concludes that the outcomes after arthroscopic lavage or arthroscopic debridement were no better than those after a placebo procedure. 2 figures, 3 tables, and 35 references. (AA-M).
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Rheumatoid Arthritis: Emerging Treatments Source: Consultant. 42(3): 297-301,305-306. March 2002. Summary: This journal article provides health professionals with information on the epidemiology, pathophysiology, diagnosis, management, and course of rheumatoid arthritis (RA). Women are affected by RA about three times as often as men. The presence of estrogen receptors on synovial cells and T cells suggests an important hormonal relationship, which may explain the increased prevalence of RA in women. RA appears to be genetically linked, with higher concordance in monozygotic than in dizygotic twins. RA is characterized by synovial inflammation and progressive erosion of cartilage and bone. Symptoms of RA usually develop between the third and sixth decades of life. The American College of Rheumatology classification criteria can help guide clinical diagnosis. Laboratory testing is useful in diagnosis as well as in assessing prognosis and monitoring the response to therapy. Evaluation includes an assessment of comorbid illness and lifestyle factors that may aggravate RA, including infection; renal insufficiency; and cardiovascular, chronic pulmonary, peptic ulcer, and lymphoproliferative diseases. Treatment involves a combination of patient education, physical and occupational therapies, consultations with a rheumatologist, and medical
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management. Early, aggressive treatment of RA may reduce joint destruction and long term disability. Therapy is generally initiated with a nonsteroidal antiinflammatory drug and a disease modifying antirheumatic drug such as methotrexate. Newer therapies are typically used in conjunction with methotrexate for patients who fail to achieve adequate benefit from this agent alone. Etanercept and infliximab, two new tumor necrosis factor alpha antagonists, are effective and well tolerated. Leflunomide, a reversible inhibitor of pyrimidine synthesis in RA, is at least as effective as methotrexate. Anakinra, an exogenous recombinant interleukin-1 receptor antagonist, helps prevent bone resorption, erosion, and destruction of joint cartilage. 2 figures, 5 tables, and 47 references. (AA-M). ·
Exercise Plan for Older Patients With Arthritis, An Source: Journal of Musculoskeletal Medicine. 19(4): 140-143,147-150. April 2002. Summary: This journal article for health professionals presents guidelines for determining when exercise is appropriate for older patients with arthritis and the factors involved in implementing an exercise program. Patients with osteoarthritis suffer pain, stiffness, and loss of mobility resulting from progressive deterioration of the cartilage lining the joints. Keeping joints moving with exercise can be an effective way to stabilize or slow the degenerative process, if the activity is convenient, safe, enjoyable, and goals are achievable. An exercise plan should be developed in phases in which progression from one to the next is gradual to help physician and patient anticipate difficulties and gauge progress. The initial evaluation helps in establishing objectives: gathering baseline data, identifying an area of the body to focus on first, and identifying potential contraindications to activities. Subsequent phases include range of motion exercises and isometric, isotonic, and recreational or functional strengthening exercises. 2 figures and 16 references. (AAM).
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Age of Arthritis, The Source: Time Magazine. 160(24): 70-79. December 9, 2002. Summary: This magazine article proposes that arthritis will become an epidemic as the baby boom generation enters their fifties. The twinge of pain in the knee or back may escalate into debilitating conditions such as osteoarthritis or rheumatoid arthritis. Approximately one-third of Americans suffer from some form of joint disease. Forty million people will have arthritis by 2020. Exercise, sports, and being overweight cause damage to joints. Gene mutations may weaken cartilage and make some people more susceptible than others to arthritic conditions. Doctors realize that osteoarthritis involves the bones, ligaments, and tendons as well as cartilage. Rheumatoid arthritis is also described. The structure of joints is outlined. Treatment for arthritis includes pain relievers, medicines to help decrease swelling, and anti-inflammatories. Exercise is recommended to help strengthen muscles. Alternative therapies such as glucosamine and chondroitin may relieve pain but have not been shown to rebuild cartilage. Joint replacement surgery may be necessary if other treatments are ineffective.
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Research Advances in Rheumatoid Arthritis Source: Journal of the American Medical Association. JAMA. 285(5): 648-650. February 7, 2001. Summary: This journal article provides health professionals with information on research advances in rheumatoid arthritis (RA). This common chronic inflammatory disease, which occurs worldwide and in all racial groups, is associated with progressive
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destruction of diarthrodial joints, substantial morbidity and economic burden, and a shortened lifespan. Although the etiology of RA is unknown, it is presumed that the disease is likely triggered either directly or indirectly by an infectious agent in a genetically predisposed person. Significant progress has been made in understanding the pathogenesis of RA, and increasingly effective therapies have been introduced, including antitumor necrosis factor alpha agents. Advances made in the past 25 years will pale in comparison to those anticipated for the next 25 years, including delineation of the genetic basis for disease susceptibility and severity, genetic definition of disease subtypes that differ in severity and response to therapy, and prompt initiation of effective individualized treatment based on genetic and environmental assessment. Reconstructive surgery will become increasingly unnecessary, and the morbidity, economic burden, and mortality due to RA will be reduced substantially. 12 references. (AA-M). ·
Determining the Efficacy of Glucosamine and Chondroitin for Osteoarthritis Source: Nurse Practitioner, The. 26(6): 44-46,49-52. June 2001. Summary: This journal article provides health professionals with information on the use of glucosamine and chondroitin in the treatment of osteoarthritis (OA). Although OA was once regarded as a simple consequence of aging and cartilage degeneration, researchers now believe that OA may be a group of overlapping diseases rather than a single disorder. The functional properties of articular cartilage are the core of OA pathogenesis. Components of articular cartilage are water, collagen, proteoglycans, chondrocytes, and other matrix components. Over time, the catabolism of proteoglycans and the increased loss of glycosaminoglycans result in the abrasion of cartilage and the formation of new bone within the joint. In healthy people, a balance of cartilage matrix turnover is maintained through synthesis and degradation. The failure to maintain this homeostatic balance because of reduced formation or increased catabolism is a possible explanation for OA. Treatment modalities focus on primary and secondary prevention. Primary prevention involves educating patients about joint protection, exercise, weight reduction, and the dangers of repetitive motion. Secondary prevention is mainly palliative and involves both nonpharmacologic and pharmacologic therapies to minimize pain. Glucosamine sulfate and chondroitin sulfate are being used by many patients for the treatment of OA. The article reviews human and animal studies on the use of these agents in treating OA. Despite findings in many of these studies supporting the efficacy of these agents for palliation of joint pain in patients with OA, the American College of Rheumatology Subcommittee on OA believes that it is too early to issue recommendations for use. Currently, the National Institute for Arthritis and Musculoskeletal and Skin Diseases, in collaboration with the National Center for Complementary and Alternative Medicine has begun a pivotal study to thoroughly evaluate these agents. 36 references. (AA-M).
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Amyloid Precursors and Amyloidosis in Inflammatory Arthritis Source: Current Opinion in Rheumatology. 13(1): 67-73. January 2001. Summary: This journal article provides health professionals with information on the role of serum amyloid A (SAA) in arthritis and associated diseases. SAA is the circulating precursor of amyloid A protein, the fibrillar component of amyloid deposits in secondary amyloidosis. Recent data demonstrating the multifunctional role of SAA in the pathogenesis of amyloidosis have yielded important insights into this potentially fatal consequence of chronic inflammation. SAA had been shown to participate in chemotaxis, cellular adhesion, cytokine production, and metalloproteinase secretion,
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and is thus integrally involved in the disease process. In addition to its production by the liver as part of the acute phase response, SAA is also expressed by several pathologic tissues such as atherosclerotic plaques and rheumatoid synovitis, as well as in the brains of patients with Alzheimer's disease. Its constitutive production in normal tissue suggests a role for SAA in host defense and tissue turnover. Many pathways are involved in the regulation of SAA, and as more becomes known about these, potential therapeutic targets may be identified. However, the prevention of secondary amyloidosis is best achieved by early and adequate treatment of patients with chronic inflammatory disorders. Suppression of the acute phase response and normalization of SAA levels are likely to significantly affect the incidence of amyloidosis in inflammatory arthritis. 92 references. (AA-M). ·
Emerging Insights Into the Cause of Rheumatoid Arthritis Source: Journal of Musculoskeletal Medicine. 18(10): 459-461,464,469-472. October 2001. Summary: This journal article, the first in a special series of articles on the diagnosis and management of rheumatoid arthritis (RA), provides health professionals with information on the genetic and nongenetic factors that influence the onset, course, and severity of RA. This disease results from an abnormal immune response that occurs in a genetically susceptible host, leading to self sustaining, chronic inflammation that affects joints and, sometimes, organs. The strongest genetic components are polymorphisms of the major histocompatibility complex class (MHC) II genes. The MHC region contains several loci that encode for human leukocyte antigen (HLA). Allelic polymorphisms of HLA genes have been associated with several autoimmune diseases. Clinical studies suggest that HLA-DREB1 alleles modify the expression of established RA. Several environmental stimuli, possibly bacteria, viruses, or retroviruses, may contribute to RA in susceptible hosts. The immune system of persons with RA has features of premature aging, including reduced thymic function and T cell diversity. Oligoclonal T cell populations with natural killer features are common. A synovial cellular infiltrate is a consistent feature in RA. The inflamed synovium, or pannus, invades the joint and produces focal bone erosions. Cytokines, especially tumor necrosis factor alpha, are important mediators of inflammation in the rheumatoid joint. Although rheumatoid factors can exist in persons who do not have RA, the presence of rheumatoid factor foretells a more severe course of disease. 4 figures, 1 table, and 30 references. (AA-M).
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When To Consider a COX-2 Inhibitor for Osteoarthritis of the Knee Source: JAAPA: Journal of the American Academy of Physician Assistants. 14(3): 13-14. March 2001. Summary: This journal article uses a case study question to provide health professionals with information on the use of cyclooxygenase-2 (COX-2) inhibitors in treating osteoarthritis (OA) of the knee. The patient in question is a 64 year old retired schoolteacher who has a history of OA and hypertension. She complains of tenderness and pain in her right knee. She takes nonprescription ibuprofen almost daily but complains that it causes heartburn. She asks about taking the newer COX-2 inhibitors. The article recommends that the patient be given acetaminophen first. Other options include the nonsteroidal antiinflammatory drugs (NSAIDs) etodolac or salsalate, or another agent. If the patient does not tolerate the NSAIDs or they do not relieve her symptoms, one of the COX-2 inhibitors can be considered. Celecoxib is indicated for signs and symptoms of OA, rheumatoid arthritis, and familial adenomatous polyposis, whereas rofecoxib is indicated for acute pain, OA, and primary dysmenorrhea. Although the COX-2 inhibitors have an excellent safety profile, they are quite costly in
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comparison with NSAIDs. The main adverse effects associated with the COX-2 inhibitors are diarrhea, dyspepsia, nausea, and edema; however, they pose less risk of gastrointestinal bleeding than standard NSAIDs. 1 table and 5 references. ·
Comparison of Cyclosporine, Sulfasalazine, and Symptomatic Therapy in the Treatment of Psoriatic Arthritis, A Source: Journal of Rheumatology. 28(10): 2274-2282. October 2001. Summary: This journal article provides health professionals with information on a study that compared the efficacy and tolerability of cyclosporine (CSA) with that of symptomatic therapy (ST) alone and sulfasalazine (SSZ) in the treatment of psoriatic arthritis (PsA). Twelve rheumatology centers recruited 99 patients with active PsA in a 24 week, prospective, randomized, open, controlled study. The patients were treated with CSA at a dose of 3 milligrams (mg)/kilogram (kg)/day or SSZ at a dose of 2,000 mg/day plus ST, or ST alone (nonsteroidal antiinflammatory drugs, analgesics, or prednisone at a dose of 5 mg or less per day). The primary end point was the 6 month change in pain. Analyses were based on an intention to treat principle. The study found that, in comparison with both SSZ and ST, there was a statistically significant difference in favor of CSA in terms of the mean changes in the pain score, which was considered the primary response variable. A significant decrease in favor of CSA versus ST alone was also observed for swollen joint count, tender joint count, joint/pain tenderness score, patient and physician global assessment by at least 1 point, total Arthritis Impact Measurement Scale score, and spondylitis functional index. There was a statistically significant difference in the American College of Rheumatology (ACR) 50 percent and ACR 70 percent response rates between the CSA and ST groups. Comparing the SSZ and ST alone groups, only the spondylitis functional index decreased significantly in the SSZ treated patients. The Psoriasis Area and Severity Index was significantly lower in the CSA group than in the ST and SSZ groups. Decrease in erythrocyte sedimentation rate was significant only in the SSZ versus the ST group, whereas reduction in C reactive protein was significant in the CSA treated patients compared with the ST group. The most common adverse event in the CSA group was mild, reversible kidney dysfunction. The article concludes that the results of the trial confirm that CSA is well tolerated by patients who have PsA and suggest that it is more efficacious than ST or SSZ. 2 figures, 4 tables, and 44 references. (AA-M).
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Stress Fracture in Long Term Methotrexate Treatment for Psoriatic Arthritis Source: Annals of the Rheumatic Diseases. 60(8): 736-738. August 2001. Summary: This journal article uses a case study to provide health professionals with information on the occurrence of stress fracture in long term methotrexate treatment for psoriatic arthritis. The case involved a 42 year old woman who presented at an outpatient rheumatology department with severe, incapacitating pain in her left leg. She had been diagnosed with psoriasis at age 17 and was treated with topical drugs. Periodically, she was prescribed etretinate and photochemotherapy as additional treatment. Oligoarthritis of her knees and ankles appeared at age 25. Nonsteroidal antiinflammatory drugs and an occasional intraarticular injection of corticosteroids controlled her symptoms. She developed a severe polyarthritis of her elbows, wrists, fingers, ankles, and metatarsophalangeal joints at age 37. Methotrexate (MTX) was used to manage the polyarthritis. The article presents findings from the physical examination, laboratory studies, and diagnostic imaging tests and discusses the course of treatment used to manage her condition. In addition, the article reports on osteoporotic fractures associated with MTX treatment. Evidence suggests that MTX may enhance osteoporosis,
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especially in patients who have inflammatory rheumatic diseases. In these patients, MTX might induce stress fractures. The article concludes by outlining the lessons learned from the case study. 2 figures and 28 references. ·
Arthritis: Timely Treatments for an Ageless Disease [2001 Revision] Source: US Food and Drug Administration. May-June 2000. Contact: Available from FDA Consumer Website: www.fda.gov/fdac/features/2000/300_arth.html. Summary: This journal article provides arthritis patients with information on new treatments for the disease. Arthritis refers to a group of more than 100 rheumatic diseases and conditions that cause pain, stiffness, and swelling in the joints. Osteoarthritis (OA) and rheumatoid arthritis (RA) are the two most common forms of arthritis. OA results from the wear and tear of normal activities, affecting twenty-one million people. RA is an autoimmune disease that occurs when the body's immune system mistakenly attacks the cell lining inside the joint. Traditionally, non-steroidal anti-inflammatory drugs NSAIDs)have been used to relieve pain in OA patients. Their use can cause gastrointestinal bleeding and ulcers. A new type of NSAID, known as COX-2 inhibitors, helps suppress arthritis with less stomach irritation. Celebrex was the first COX-2 inhibitor approved by the Food and Drug Administration (FDA) for use in treating OA, and Vioxx became the second, approved in 1999. Two nondrug alternatives, Hyalgan and Synvisc, were approved by the Center for Devices and Radiological Health in 1997 for the treatment of pain in OA. Treatments for RA have relied on a combination of NSAIDs and disease-modifying anti-rheumatic drugs (DMARDS) such as methotrexate and sulfasalazine. DMARDS work to slow inflammation and can alter the course of the disease. Physicians were previously using DMARDS for patients who failed to respond to other therapies but are now using them early and aggressively in the hope of slowing disease progression and damage to joints and internal organs. The most recently approved treatment regimen for RA is one that combines the genetically engineered biological drug infliximab with the drug methotrexate. Etanercept is the first biologic response modifier to receive FDA approval for treating patients who have moderate to severe RA. Although both infliximab and etanercept show promise in treating RA, the longterm risks and benefits are unknown. Arava is the first oral treatment approved for slowing the progression of RA. The Prosorba column, a single-use medical device that removes proteins believed to attack joint cells from the blood, is the first nondrug alternative for adult patients with moderate to severe RA. Other forms of arthritis treatment include range of motion, strengthening, and endurance exercises and unproven remedies such as the nutritional supplements glucosamine and chondroitan sulfate. Steps to prevent arthritis include reducing repetitive joint use and maintaining an ideal weight.
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Arthritis 101: Juvenile Rheumatoid Arthritis Source: Arthritis Today. 14(1): 32-33. January-February 2000. Summary: This journal article uses a question and answer format to provide people who have children with juvenile rheumatoid arthritis (JRA) with information. There are three forms of childhood arthritis. Systemic onset JRA affects many bodily systems, including the joints, spleen, lymph nodes, liver, and heart. Polyarticular JRA affects more than four joints in a symmetrical manner. Joints most commonly affected are the knees, ankles, hips, feet, and small joints of the hands. This form of JRA has two subtypes. The first is characterized by the presence of rheumatoid factor and DR4 genetic type. The
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second is characterized only by joint involvement. Pauciarticular JRA usually affects four or fewer joints in an asymmetrical manner. The joints most commonly affected are the knees, elbows, wrist, and ankles. This form of JRA has three subtypes. In the first subtype, children have antinuclear antibodies and a high risk of iridocyclitis. In the second subtype, arthritis affects the spine and other joints, and children may test positive for the HLA-B27 gene. In the third subtype, joint involvement is the only feature. Although the cause of JRA is unknown, contributing factors likely include genetics and environmental factors. JRA can occur in boys or girls of any age, but it usually begins during the toddler or early adolescent years. Generally, it affects more girls than boys. Diagnosis of JRA is based on a medical history, physical examination, and possibly laboratory tests. Although in many ways JRA is treated the same as adult rheumatoid arthritis (RA), many drugs used to treat RA are not approved for children. Large doses of aspirin are usually used first, followed by disease modifying antirheumatic drugs if the disease progresses. 4 figures. ·
Part 1: The Role of Exercise: Rehabilitation Strategies for Patients With Rheumatoid Arthritis Source: Journal of Musculoskeletal Medicine. 17(4): 191-194,196-198, 203-204. April 2000. Summary: This journal article, the first of two parts and the ninth article in a special series on the diagnosis and management of rheumatoid arthritis (RA), provides health professionals with information on rehabilitation strategies. The article focuses on the general principles of rehabilitation as they apply to persons who have RA and the role of exercise in promoting optimal strength and function. For optimal preservation of joint function and range of motion (ROM), the patient who has RA should begin a rehabilitation program early. A history and physical examination focusing on musculoskeletal problems and functional evaluation are essential prerequisites. Progressive exercise is a key component of any rehabilitation program. The type, intensity, and duration of exercise depend on disease activity and stage. Patients begin with passive and active ROM movements, adding strengthening and aerobic exercise as tolerance and mobility permit. Primary strengthening exercises are isometric, isotonic, and isokinetic. Isometric exercise involves having the patient contract his or her muscle against a stationary object such as a belt, table, or machine that has a fixed arm. After muscles have been trained isometrically, the patient needs to incorporate isotonic exercises into the program. These involve moving the joint for several repetitions against resistance offered by free weights, elastic bands, or a machine. Isokinetic exercise is done with a machine and offers no strengthening advantage over isometric exercise. The best aerobic exercises for patients who have RA are stationary bicycling and swimming. Exercising at 70 percent maximum capacity for just 15 minutes 3 times a week usually produces improvement in 8 to 12 weeks. 3 figures, 9 tables, and 19 references. (AA-M).
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Ayurvedic Medicine and Arthritis Source: Rheumatic Disease Clinics of North America. 26(1): 133-144. February 2000. Summary: This journal article provides health professionals with an overview of the use of Ayurvedic medicine in the treatment of arthritis. Ayurveda is a holistic science that promotes health through an appropriate diet and lifestyle. The tridosha theory is the core concept in health and disease. The three doshas are considered to govern biomotor, metabolic, and perservative activity as the primary physiological forces. Each dosha has its own characteristic anatomic, physiologic, and psychological expressions. Disease caused by one dosha is considered to be curable, although that caused by two is only
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controllable. Diseases caused by three doshas is incurable. The Ayurvedic treatment is highly individualized. Deviations in diet and behavior pattern from Ayurvedic norms are also evaluated for targeting therapy. The Ayurvedic pathogenesis links arthritis to the gut. Specifically, the affliction of the joints is attributed to the excess accumulation of a vicious substance called ama that is produced in the gut as a result of weakened digestion and metabolism, food indiscretions, and disturbed tridosha equilibrium. The ama, while spreading along channels connecting organs but not defined anatomically, vitiates them and causes destruction, leading to numerous diseases, including arthritis. Management consists chiefly of diet and lifestyle changes, the panchkarma process, and herbal drugs. Clinical ethnovalidation of the ancient therapy is needed to meet modern requirements and set up an interface with modern medicine. 22 references. (AA-M). ·
55-Year-Old Woman With Rheumatoid Arthritis, A Source: Journal of the American Medical Association. JAMA. 283(4): 524-531. January 26, 2000. Summary: This journal article provides health professionals with information on the diagnosis, epidemiology, pathology, pathogenesis, and treatment of rheumatoid arthritis (RA). This systemic inflammatory disorder is characterized by symmetrical polyarthritis that often leads to joint deformity and loss of function. The small joints of the hands, wrists, elbows, shoulders, knees, ankles, and feet are the most commonly affected sites. The prevalence increases with age and affects women two to three times more frequently than men. Although the etiology of RA is unknown, there is evidence of a complex interaction between genetic and environmental factors. Early pathological changes associated with RA include proliferation of the synovial lining cells, focal perivascular lymphocytic infiltration, and endothelial cell proliferation. As the disease progresses, synovial tissue grows over the articular surfaces. Diagnostic criteria include morning joint stiffness, objective evidence of symmetrical polyarticular joint inflammation, rheumatoid nodules, detection of serum rheumatoid factors, and evidence of radiographic changes. The diagnosis of RA is based mainly on the presence of these characteristic clinical features. The differential diagnosis of RA includes viral diseases, systemic lupus erythematosus, and overlap syndromes with other autoimmune disorders. The morbidity associated with RA results from acute and chronic synovial and systemic inflammation. Treatment must target all pathological processes. An important aspect of treatment is properly assessing the stage of the disease, the level of disease activity, and the functional status of the patient. Treatment should consist of pharmacological therapies and nonpharmacological therapies, including rest, physical and occupational therapy, exercise, nutritional counseling, and general measures to protect bones and joints. The medications used to treat RA can divided into classes that include analgesics, nonsteroidal antiinflammatory drugs, glucocorticoids, and slow acting antirheumatic drugs or disease modifying antirheumatic drugs. In addition, the article presents a case report of a 55 year old woman with RA and answers questions about treatment approaches. 2 tables and 60 references.
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Arthritis 101: Lyme Disease Source: Arthritis Today. 14(2): 34-35. March-April 2000. Summary: This journal article provides the general public and people who have arthritis with information on Lyme disease. This tick borne disease causes symptoms that can mimic those of mononucleosis, meningitis, multiple sclerosis, rheumatoid arthritis, and other diseases. The early localized stage of Lyme disease occurs 7 to 10 days after
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infection and is characterized by an expanding red rash and viral type symptoms. The early disseminated stage occurs after several weeks or months of infection. Additional symptoms, including nervous system problems, may appear. The late stage of the disease can occur from months to years after the initial infection. In this stage, arthritis pain and swelling may occur in a few large joints. Lyme disease is usually diagnosed from the signs and symptoms in the earlier stages. A blood test may help confirm the diagnosis. Treatment involves taking antibiotics. Although two vaccines have been developed, people should still take precautions such as clearing brush from a yard, wearing long sleeved shirts and long pants tucked into socks when walking through woods or high grasses, checking exposed skin regularly, and removing a tick gently. 2 figures. ·
Arthritis: Timely Treatments for an Ageless Disease Source: FDA Consumer. 34(3): 27-33. May-June 2000. Summary: This journal article provides people who have arthritis with information on new treatments for this chronic condition. Arthritis refers to a group of more than 100 rheumatic diseases and conditions that cause pain, stiffness, and swelling in the joints. The two most common forms of arthritis are osteoarthritis (OA) and rheumatoid arthritis (RA). OA results from wear and tear, whereas RA is an autoimmune disease that occurs when the body's own immune system mistakenly attacks the cell lining inside the joint. Traditional nonsteroidal anti-inflammatory drugs (NSAIDs) have been used for relief from OA pain, but their use can cause gastrointestinal bleeding and ulcers. However, a new type of NSAID, cyclooxygenase-2 (COX-2) inhibitors, helps suppress arthritis with less stomach irritation. Celebrex was the first COX-2 inhibitor approved by the Food and Drug Administration (FDA) for use in treating OA, and Vioxx became the second COX-2 inhibitor to receive FDA approval. Two nondrug alternatives, Hyalgan and Synvisc, were approved by the Center for Devices and Radiological Health in 1997 for the treatment of pain in OA. The most recently approved treatment regimen is one that combines the genetically engineered biological drug infliximab with the drug methotrexate. Etanercept is the first biologic response modifier to receive FDA approval for treating patients who have moderate to severe RA. Although both infliximab and etanercept show promise in treating RA, their long term risks and benefits are unknown. Arava is the first oral treatment approved for slowing the progression of RA. A nondrug alternative for adult patients who have moderate to severe RA and who have failed or cannot tolerate disease modifying antirheumatic drugs is the Prosorba column. This device removes proteins that are believed to attack joint cells from the blood. Other forms of treatment for arthritis include range of motion, strengthening, and endurance exercises and unproven remedies such as the nutritional supplements glucosamine and chondroitin sulfate. There are various steps people can take to prevent arthritis. 5 figures.
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Glucosamine and Chondroitin for Treatment of Osteoarthritis: A Systematic Quality Assessment and Meta-analysis Source: JAMA. Journal of the American Medical Association. 283(11): 1469-1475. March 15, 2000. Summary: This journal article provides health professionals with information on a study that evaluated the benefit of glucosamine and chondroitin preparations for osteoarthritis (OA) symptoms using meta analysis combined with systematic quality assessment of clinical trials of these preparations in knee or hip OA. Clinical trials of glucosamine and chondroitin compounds were identified by using electronic searches of MEDLINE and
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the Cochrane Controlled Trials Register. 'Osteoarthritis,' 'osteroarthrosis,' 'degenerative arthritis,' 'glucosamine,' 'chondroitin,' and 'glycosaminoglycans' were entered as medical subject heading terms and as textwords. Review articles, manuscripts, and supplements from rheumatology and OA journals were manually searched, and unpublished data were sought by contacting content experts, study authors, and manufacturers of glucosamine and chondroitin. Studies were included if they were published or unpublished double blind, randomized, placebo controlled trials of 4 or more weeks' duration that tested glucosamine or chondroitin for knee or hip OA and reported extractable data on the effect of treatment on symptoms. Fifteen of 37 studies were included in the analysis. Reviewers performed data extraction and scored each trial using a quality assessment instrument. Quality scores ranged from 12.3 percent to 55.4 percent of the maximum, with a mean of 35.5 percent. Only one study described adequate allocation concealment and two reported an intent to treat analysis. Most were supported or performed by a manufacturer. Funnel plots show significant asymmetry compatible with publication bias. Tests for heterogeneity were nonsignificant after removing one outlier trial. The aggregated effect sizes were 0.44 for glucosamine and 0.78 for chondroitin, but they were diminished when only high quality or large trials were considered. The effect sizes were relatively consistent for pain and functional outcomes. The article concludes that trials of glucosamine and chondroitin preparations demonstrate moderate to large effects on OA symptoms, but quality issues and likely publication bias suggest that these effects are exaggerated. Nevertheless, some degree of efficacy appears probable for these preparations. 2 figures, 2 tables, and 54 references. (AA-M). ·
Cervical Spine Complications in Rheumatoid Arthritis Patients Source: Postgraduate Medicine. 107(1): 199-200,205-208. January 2000. Summary: This journal article provides health professionals with information on a goal oriented approach to managing cervical spine complications in patients with rheumatoid arthritis (RA). RA is associated with changes in the cervical spine, including loss of articular cartilage, ligamentous destruction, and bone erosion. These changes may lead to various complications, including atlantoaxial subluxation, cranial settling, subaxial cervical subluxation, and peridontoid pannus formation. Warning signs of cervical involvement in RA include painful limitation of neck motion, suboccipital pain, paresthesias of the hands and feet, clumsiness of the hands, urinary retention or incontinence, and involuntary leg spasms. Treatment goals include relieving pain, establishing spinal stability, and decompressing the neural elements. Failure of conservative management indicates a need for surgical stabilization. The article describes the approach to surgical management of atlantoaxial subluxation, cranial settling, and subaxial subluxation and explains the procedure for treating patients who have radiographic evidence of neural element compromise. 4 figures, 1 table, and 21 references.
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Arthritis 101: Sjogren's Syndrome Source: Arthritis Today. 14(4): 32-33. July-August 2000. Summary: This journal article uses a question and answer format to provide people who have Sjogren's syndrome with information on the etiology, epidemiology, diagnosis, and treatment of this arthritis related disease affecting several organs. Sjogren's syndrome is an autoimmune disease in which lymphocytes attacks moisture producing glands, and, in some cases, the lungs, kidneys, liver, skin, nerves, or joints. Risk factors include being a postmenopausal woman, having an autoimmune disease, and having a
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family member with Sjogren's. Diagnosis is based on a complete physical examination; medical history evaluation; and various diagnostic tests, including the slit lamp test, the Schirmer test, a lip biopsy, and blood tests to detect antibodies. Although there is no cure for Sjogren's syndrome, it can be treated with medications and other measures to relieve the common symptoms of the condition. The article presents some general treatment modalities as well as treatments for some of the specific symptoms of Sjogren's. 1 figure. ·
Complementary and Alternative Therapies for Arthritis: Science or Fiction? Source: Journal of Musculoskeletal Medicine. 17(6): 330-332,334-340,345. June 2000. Summary: This journal article provides health professionals with information on complementary and alternative therapies for arthritis. The issue of alternative medicine as a legitimate medical treatment is a matter of ongoing debate in the United States. Despite evidence that these treatments may be beneficial, many physicians are reluctant to advise patients about their use. In addition, there are few, if any, well designed, long term clinical studies to corroborate benefits and outcomes from alternative treatments. The use of diet, nutritional supplements, botanicals, and acupuncture is increasing among patients who have chronic conditions. The article reviews studies on the effects of diet; nutrition supplements such as antioxidants, dehydroepiandrosterone, glucosamine and chondroitin sulfates, omega 3 fatty acids, and vitamin D; botanicals such as bromelain, evening primrose and borage oils, feverfew, and valerian; and acupuncture. Although more scientific studies are needed to assess benefit and risk, complementary and alternative medicine have shown promise in managing some rheumatic diseases, including osteoarthritis, rheumatoid arthritis, and systemic lupus erythematosus. Complementary and alternative medicine may act synergistically when used as an adjunct to conventional medical care. Objective evidence concerning available therapies, a clinical outline of practical advice, and a resource guide are tools that can help the clinician when counseling patients who are considering alternative therapies. 1 figure, 4 tables, and 39 references. (AA-M).
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Osteoarthritis of the Knee: A Special Report Source: Physician and Sportsmedicine. Special Report. May 2000. Contact: Available from McGraw-Hill Healthcare Information. 4530 West 77th Street, Floor 3, Minneapolis, MN 55435. (800) 525-5003 or (609) 426-7070 (for subscriptions) or (952) 835-3222 (for back issues). Summary: This special report presents a series of articles that provide health professionals with information on osteoarthritis (OA) of the knee. The first article reviews the pathophysiological characteristics of OA and discusses its etiology, diagnosis, and evaluation. OA is caused by multiple factors, including genetic, metabolic, biochemical, enzymatic, biomechanical, and environmental factors. The history, physical examination, and radiographic examination help establish the diagnosis. The second article offers an overview of the nonoperative management of OA of the knee. Nonoperative techniques can be effective in relieving pain and improving functional ability. Nonpharmacologic treatment options include decreasing physical activity, exercising, losing weight, using supports and braces, and undergoing physiotherapy. Topical treatments include nonsteroidal anti-inflammatory drugs (NSAIDs) and capsaicin. Systemic therapies include nonnarcotic and narcotic analgesics, antidepressants, NSAIDs, chondroitin, and glucosamine. Intra-articular therapies include corticosteroids and viscosupplementation. The third article discusses operative
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treatment for the arthritic knee, focusing on the role of arthroscopy, the indications for joint replacement, and the new area of articular cartilage restoration and resurfacing. The choice of procedure is based on the patient's age, the extent of disease, and the desired level of physical activity. The fourth article presents case reports of active patients with arthritis who underwent viscosupplementation. The fifth article uses a question and answer format to provide health professionals with information on traditional and innovative treatments for OA of the knee. The final article is a continuing medical education activity. 5 tables and 95 references. ·
Rehabilitation Strategies for Patients With Rheumatoid Arthritis, Part 2: Modalities, Orthoses, and Assistive Devices Source: Journal of Musculoskeletal Medicine. 17(7): 385-387,391-393, 397-398. July 2000. Summary: This journal article, the second of two parts on rehabilitation strategies for patients with rheumatoid arthritis (RA), provides health professionals with information on the role of joint protective modalities, assistive devices, and orthoses that help patients exercise and function at their best. Modalities, orthoses, assistive devices, and education are important partners to exercise and medical therapy for patients with RA. Thermal modalities help decrease pain and muscle spasm in joints subacutely or chronically affected by RA; however, heat should be avoided during acute inflammation. Deep heat delivered via ultrasound or microwave is recommended for subacute and chronic capsular and tendon tightness that occurs in a large joint such as the shoulder or hip. Cold is recommended for decreasing pain, muscle spasm, and edema. Vehicles for delivering cold include ice packs, crushed ice, gel packs, and bags of frozen peas. Physical modalities that may increase comfort include massage, electrical stimulation, and, for patients with neck and back syndromes, traction. Orthoses help decrease inflammation, relieve pain, align and rest joints, and improve function, particularly in the hands, wrists, feet, and ankles. Orthoses can be static or dynamic. Assistive devices include large handled tools, sporting equipment, and kitchen utensils. Education improves compliance. Many patients resort to such alternatives as acupuncture or acupressure when conventional treatment brings no relief. Orthopedic referral is appropriate when joint realignment, stabilization, or reconstruction is necessary. 5 figures, 2 tables, and 10 references. (AA-M).
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Gastrointestinal Toxicity With Celecoxib vs Nonsteroidal Antiinflammatory Drugs for Osteoarthritis and Rheumatoid Arthritis: The CLASS Study: A Randomized Controlled Trial Source: Journal of the American Medical Association. JAMA. 284(10): 1247-1255. September 13, 2000. Summary: This journal article provides health professionals with information on a prospective, randomized double-blind study that determined whether celecoxib, a cyclooxygenase-2 (COX-2) inhibitor, is associated with a lower incidence of significant upper gastrointestinal (GI) toxic effects and other adverse effects compared with conventional nonsteroidal antiinflammatory drugs (NSAIDs). The study, known as the Celecoxib Long Term Arthritis Safety Study, was conducted at 386 centers in the United States and Canada from September 1998 to March 2000. A total of 8,059 patients aged 18 years or older with osteoarthritis (OA) or rheumatoid arthritis (RA) were enrolled in the study, and 7,968 received at least one dose of study drug. A total of 4,573 patients received treatment for 6 months. Patients were randomly assigned to receive 400 milligrams of celecoxib twice a day, 800 milligrams of ibuprofen three times a day, or 75 milligrams of diclofenac twice a day. Aspirin use for cardiovascular prophylaxis was
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permitted. Of the 7,968 patients receiving at least one dose of the study drug, 3,987 patients were treated with celecoxib, 1,985 patients received ibuprofen, and 1,996 were treated with diclofenac. For all patients, the annualized incidence rates of upper GI ulcer complications alone and combined with symptomatic ulcers for celecoxib versus NSAIDs were 0.76 percent versus 1.45 percent and 2.08 percent versus 3.54 percent, respectively. For patients not taking aspirin, the annualized incidence rates of upper GI ulcer complications alone and combined with symptomatic ulcers for celecoxib versus NSAIDs were 0.44 percent versus 1.27 percent and 1.40 percent versus 2.91 percent. For patients taking aspirin, the annualized incidence rates of upper GI ulcer complications alone and combined with symptomatic ulcers for celecoxib versus NSAIDs were 2.01 percent versus 2.12 percent and 4.70 percent versus 6.00 percent. Fewer patients treated with celecoxib than with NSAIDs experienced chronic GI blood loss, GI intolerance, hepatotoxicity, or renal toxicity. No difference was noted in the incidence of cardiovascular events between celecoxib and NSAIDs, regardless of aspirin use. The article concludes that celecoxib, at dosages greater than those indicated clinically, was associated with a lower incidence of symptomatic ulcers and ulcer complications combined, as well as other clinically important toxic effects, than NSAIDs at standard dosages. This supports the hypothesis that COX-2 agents exhibit fewer GI toxic effects. Findings have significant implications with respect to drug therapy for the symptomatic treatment of RA and OA. 39 references. ·
Elderly-Onset Rheumatoid Arthritis Source: Rheumatic Disease Clinics of North America. 26(3): 517-526. August 2000. Summary: This journal article provides health professionals with information on the etiology, clinical manifestations, diagnosis, and treatment of elderly onset rheumatoid arthritis (EORA). One third of the elderly population acquires RA after the age of 60, and the prevalence of the condition increases with age. Features that distinguish EORA from younger onset rheumatoid arthritis (YORA) include a more equal gender distribution; an acute onset; more frequent involvement of large, proximal joints; more systemic manifestations and a higher erythrocyte sedimentation rate at onset; a lower frequency of rheumatoid factor positivity; and a worse outcome. Immunosenescence and genetic and hormonal factors are probably important variables in the observed difference between EORA and YORA. In the elderly, rheumatoid arthritis often coexists with other chronic medical disorders that can alter function; change the structure of bones, joints, and muscles; and demand complicated medication regimens. This makes differential diagnosis difficult. Seronegative EORA makes up 1 percent to 48 percent of patients. There are two syndromes that may be indistinguishable from seronegative EORA: polymyalgia rheumatica and the syndrome of remitting seronegative symmetrical synovitis with pitting edema. Medications commonly used to treat EORA include nonsteroidal antiinflammatory drugs, low dose steroids, and disease modifying antirheumatic drugs. Life expectancy decreases in patients who have rheumatoid arthritis. 3 tables and 36 references. (AA-M).
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Crystal-Associated Arthritis in the Elderly Source: Rheumatic Disease Clinics of North America. 26(3): 527-546. August 2000. Summary: This journal article provides health professionals with information on the clinical features, diagnosis, and management of crystal associated arthritis in the elderly population. The understanding of the clinical syndromes of gout and pseudogout and the role of basic calcium crystals in arthritis has increased since the original descriptions of the involvement of crystals in arthritis. Gout is usually considered an affliction
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confined to middle aged men but it has an increasing prevalence in older populations, with unique and often atypical features. In classic gout, the typical initial attack occurs after years of sustained hyperuricemia and deposition of monosodium urate (MSU) in the synovial tissue. The initial attack is monoarticular in most patients. If the disease is untreated, attacks occur more frequently. Over the years, tophaceous deposits become apparent over the elbows, fingers, or other areas. Older patients who have gout are more likely to be women, to have polyarticular involvement, to have small joint finger involvement, and to develop tophi early in the course of their illness. There is also a greater association of gout with use of diuretics and renal disease in older patients. A diagnosis of gout can be made with certainty only by confirming the presence of MSU crystals in the synovial fluid or tissue. Various drugs are available to treat an acute attack of gout, including nonsteroidal antiinflammatory drugs, corticosteroids, corticotropin, and colchicine. Long term hypouricemic therapy involves using uricosuric agents or allopurinol. Calcium pyrophosphate dihydrate (CPPD) crystal deposition disease, or pseudogout, is also common in elderly patients. The most common clinical forms of CPPD are acute attacks of monoarthritis or polyarthritis, a chronic arthropathy associated with osteoarthritis, or an incidental asymptomatic process. The main differential diagnosis is with other crystal induced processes and with infection. The management of the patient with pseudogout is similar to the management of the patient with acute gout. Another crystal associated arthritis occurring in the elderly is basic calcium phosphate hydroxyapatite deposition disease. 6 figures, 2 tables, and 64 references. (AA-M). ·
Hyaluronate Therapy in Osteoarthritis Source: Seminars in Arthritis and Rheumatism. 30(2-Supplement 2): i-vi,1-25. October 2000. Summary: This supplemental journal provides health professionals with information on one of the new hyaluronates, Hyalgan, for the treatment of osteoarthritis (OA) of the knee. The articles in the journal examine hyaluronate from the perspective of its place in the medical care of a person with OA, the clinical data that support its use, and the evidence that it may have disease modifying properties. The first article reviews the pharmacologic modalities available for the treatment of OA of the knee, including acetaminophen, nonsteroidal antiinflammatory drugs (NSAIDs), topical analgesics, intraarticular corticosteroids, and intraarticular hyaluronic acid (HA). The article also summarizes clinical trials of intraarticular HA therapy and discusses its role. The next article reviews the comparative clinical trial data on HA, focusing on its efficacy in placebo controlled trials and comparative trials with intraarticular corticosteroids and NSAIDs. The article also comments on the safety of HA. The final article reviews the cellular and immunologic effects of hyaluronate that could affect disease progression. Topics include the characteristics, synthesis, and biological function of endogenous hyaluronan; the pathology of OA; the effects of HA on synoviocytes and chrondroblasts and on inflammation; and the structure modifying effects of HA. 2 figures, 8 tables, and 106 references.
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Updated Consensus Statement on Tumour Necrosis Factor Blocking Agents for the Treatment of Rheumatoid Arthritis (May 2000) Source: Annals of Rheumatic Diseases. 59(Supplement 1): i1-i2. November 2000. Summary: This journal article provides health professionals with an updated consensus statement on the use of tumor necrosis factor (TNF) blocking agents for the treatment of rheumatoid arthritis (RA). These agents should normally be used for active RA or
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juvenile chronic arthritis (JCA) after a full trial of an effective disease modifying antirheumatic drug has been ineffective. TNF blocking agents, when used in adequate doses and sufficiently frequent dosing regimens, should produce significant, documentable improvement in symptoms, signs, and laboratory parameters within 4 to 16 weeks. Quantifiable disease activity measures should be followed. If improvement has not occurred within 4 to 16 weeks, alternative treatments or regimens should be considered. TNF blocking agents should not be started or should be discontinued when serious infections occur. These agents should also be stopped if there is clinical evidence of drug induced lupus like syndrome. Studies regarding selected areas of efficacy, toxicity, and the general use of TNF blocking agents are needed to help further define the most appropriate use of these agents. 11 references. ·
Arthrocentesis To Diagnose and Treat Acute Gouty Arthritis in the Great Toe Source: JAAPA: Official Journal of the American Academy of Physician Assistants. 13(10): 93-94,96. October 2000. Summary: This journal article provides health professionals with information on the use of arthrocentesis to diagnose and treat acute gouty arthritis. Although a high level of uric acid in the blood suggests gout, it can be confirmed only by identification of urate crystals in fluid aspirated from the joint. Arthrocentesis with fluid aspiration may relieve the pain of acute gouty arthritis, but the clinician may find it necessary to inject a corticosteroid directly into the joint space before removing the aspiration needle. The article explains how arthrocentesis is performed, presents postoperative instructions the physician should give the patient, and identifies contraindications and complications. 1 figure, 2 tables, and 5 references.
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Use of Glucosamine Sulfate and Chondroitin Sulfate in the Treatment of Osteoarthritis Source: Physician Assistant. 24(11): 46,49-50,52-55. November 2000. Summary: This journal article provides health professionals with information on the use of glucosamine sulfate and chondroitin sulfate in the treatment of osteoarthritis (OA). Glucosamine sulfate and chondroitin sulfate are dietary supplements that have received publicity in the lay press as a cure for arthritis. Both of these chemicals are essential in the production and function of normal, healthy articular cartilage. The article reviews the pathogenesis and traditional management of OA. Treatment usually includes physical, pharmacologic, and surgical measures. To date, the only definitive, but limited, treatment option is surgery. Therefore, alternative treatment options such as dietary supplements are attractive to people who have OA. Both glucosamine and chondroitin have mild antiinflammatory effects; however, the mechanism is different from that of nonsteroid antiinflammatory drugs (NSAIDs) and is not fully understood. The antiinflammatory effect of glucosamine may be related to the stimulation of proteoglycan biosynthesis that stabilizes cell membranes. The antiinflammatory effect of chondroitin is believed to be due to a dose dependent decrease in collagenolytic activity within articular cartilage. Although adverse effects are more commonly reported with the use of chondroitin rather than glucosamine, these effects are minimal. People who have comorbid conditions such as diabetes should be counseled prior to using glucosamine and chondroitin. The article also reviews several clinical trials comparing glucosamine and chondroitin with placebo or NSAIDs. Clinical trials have consistently shown glucosamine and chondroitin to be as effective as NSAIDs for symptom relief, with the benefit of fewer gastrointestinal and renal adverse effects. 4 tables and 17 references. (AA-M).
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Arthritis 101: The Shoulder Source: Arthritis Today. 14(6): 40-42. November-December 2000. Summary: This journal article provides people who have shoulder problems with information on the structure of the shoulder and common shoulder problems. The bony structure of the shoulder consists of the scapula, the coracoid process, the clavicle, the acromion, and the humerus. More than 20 different muscles and tendons, as well as ligaments, support and stabilize the shoulder. Bursae lubricate and reduce friction as the bones and connective tissue move. The shoulder joint is the ball and socket glenohumeral joint. Common shoulder problems include rheumatoid arthritis, adhesive capsulitis, dislocation, and rotator cuff tears. The article identifies people who are at risk for these problems, describes each of them, and explains how they are treated. 5 figures.
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Psoriatic Arthritis: Diagnosis and Management of a Diverse Disease Source: Journal of Musculoskeletal Medicine. 17(3): 169-177. March 2000. Summary: This journal article provides health professionals with information on the epidemiology, pathogenesis, clinical features, diagnosis, and management of psoriatic arthritis (PsA). This form of arthritis, which is associated with psoriasis, is a clinically diverse disease that includes cutaneous lesions along with some features of both rheumatoid arthritis and seronegative spondyloarthropathies such as dactylitis, bony erosions, and sacroiliitis. Immunologic, genetic, and environmental factors probably contribute to PsA. There are five disease subtypes, and their features may overlap. Although sometimes considered a more benign rheumatic process, PsA can vary from a mild monarthritis or oligoarthritis to an erosive polyarthritis that requires early effective immunosuppressive therapy with methotrexate or second line agents such as cyclosporine and sulfasalazine. Intervention with physical or occupational therapy is often overlooked, except for patients with advanced joint damage and functional loss. However, early intervention with exercise instruction, appropriate splinting, and assistive devices can be very effective in alleviating symptoms and preserving function. Various topical agents such as emollients, keratolytics, and corticosteroids can be effective in treating limited skin disease. Early recognition of skin lesions, articular involvement, other associated features, and specific human leukocyte antigen markers will ensure timely management of this condition. 4 figures, 4 tables, and 33 references. (AA-M).
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Fever and Arthritis: Narrowing the Diagnosis Source: Journal of Musculoskeletal Medicine. 17(11): 676-682,687. November 2000. Summary: This journal article provides health professionals with information on the major causes of fever and arthritis and approaches to diagnosis and management. The coexistence of arthritis and fever has important diagnostic and therapeutic ramifications. Fever can be a manifestation of an infectious process that demands emergent treatment. Acute bacterial arthritis is a rheumatologic emergency that should be managed very aggressively to prevent joint destruction. Types of bacterial arthritis include gonococcal arthritis; infective endocarditis; and arthritis associated with Lyme disease, syphilis, tuberculosis, and Whipple disease. Fungal infections may also be associated with arthritis. Acute arthritis is unusual in fungal infections, except in Candida and Blastomyces infections. Viral arthritis usually presents with a self limited, symmetric picture resembling that of rheumatoid arthritis. Reactive arthritis is an inflammatory disorder caused by the body's immune reaction to a microorganism present in a distant mucosal site. Acute rheumatic fever is a classic example of a reactive arthritis. Fever and
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arthritis can also be caused by a variety of noninfectious diseases or the superimposition of an infection onto a systemic inflammatory disorder such as systemic lupus erythematosus, crystal induced diseases, and drug reactions. The clinical algorithm used in the differential diagnosis is dominated by the facts gleaned primarily from the history and physical examination, with support from laboratory, radiologic, and microbiologic testing. Therapy involves the prompt administration of antibiotics if there is any suspicion of bacterial infection. No specific therapy is available for virus associated arthritis. Nonsteroidal antiinflammatory drugs (NSAIDs) are the first line treatment for reactive arthritis and crystal induced diseases. Other connective tissue disorders are treated with NSAIDs, corticosteroids, and disease modifying or immunosuppressive drugs. 2 figures, 4 tables, and 21 references. (AA-M). ·
From the CDC: Facts and Figures About Arthritis and Rheumatic Diseases Source: Journal of Musculoskeletal Medicine. 17(1): 46. January 2000. Summary: This journal article provides health professionals with highlights of some of the results from a survey conducted by the Centers for Disease Control and Prevention (CDC) about the impact of arthritis and rheumatic diseases on the U.S. health care system. Findings include the following: Arthritis affects nearly 43 million people, the cost of arthritis was $65 billion in 1992, women are affected by arthritis and other rheumatic conditions more than men, and many people younger than 65 are affected by arthritis. The CDC also used additional data to determine how often arthritis and rheumatic diseases cause patients to visit the doctor, enter the hospital, or receive home health care. In 1997, 744,000 people with arthritis and other rheumatic diseases accounted for 30,914,000 discharges from short stay hospitals. They consumed 4 million days of care. People with arthritis and rheumatic diseases were responsible for 44 million ambulatory care visits, with women accounting for 63 percent of these visits. 1 figure and 1 reference.
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Osteoarthritis: New Insights: Part 1: The Disease and Its Risk Factors Source: Annals of Internal Medicine. 133(8): 635-646. October 17, 2000. Summary: This journal article, the first of a two part summary of a National Institutes of Health conference on osteoarthritis (OA), provides health professionals with information on what OA is and on risk factors that predispose to it. The conference brought together experts on OA from diverse backgrounds and provided a multidisciplinary and comprehensive summary of recent advances in the prevention of OA onset, progression, and disability. OA is the most common form of arthritis, affecting millions of people in the United States. It is a complex disease whose etiology bridges biomechanics and biochemistry. Evidence is growing for the role of systemic factors such as ethnicity, genetics, dietary intake, estrogen use, and bone density, as well as local biomechanical factors such as muscle weakness, obesity, and joint laxity, in the development of OA. These risk factors are particularly important in weight bearing joints, and modifying them may present opportunities for prevention of pain and disability. The article discusses these systemic and biomechanical risk factors and examines the impact of OA on disability. 3 figures, 3 tables, and 120 references. (AA-M).
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Quality of Care for Patients With Rheumatoid Arthritis Source: Journal of the American Medical Association. JAMA. 284(8): 984-992. August 23/30, 2000.
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Summary: This journal article provides health professionals with information on a study that assessed the quality of the health care that patients with rheumatoid arthritis (RA) receive for their arthritis and comorbid diseases. The primary data source for the study was a historical cohort of 1,355 adult patients with RA enrolled in the fee for service or discounted fee for service plans of a nationwide U.S. insurance company. Patients were identified and followed up through administrative data between 1991 and 1995. Quality scores for arthritis, comorbid disease, and health care maintenance were developed from performance on explicit process measures that related to each of these domains and described the percentage of indicated health care processes performed within each domain during each person year of the study. The study found that, during 4,598 person years of followup, quality scores were 62 percent for arthritis care, 52 percent for comorbid disease care, and 42 percent for health maintenance care. Across all domains, care patterns including relevant specialists yielded performance scores 30 percent to 187 percent higher than those that did not, and 45 percent to 67 percent of person years were associated with patterns of care that did not include a relevant specialist. The presence of primary care without specialty care yielded health care maintenance scores that were 43 percent higher than those for patterns that included neither primary nor relevant specialty care. The article concludes that, in this population, health care quality appears to be suboptimal for arthritis, comorbid disease, and health care maintenance. Patterns of care that included relevant specialists were associated with substantially higher quality across all domains. Patterns that included generalists were associated with substantially higher quality health care maintenance than patterns that included neither a generalist nor a relevant specialist. The optimal roles of primary care physicians and specialists in the care of patients with complex conditions should be reassessed. 6 tables and 60 references. (AA-M). ·
Psoriatic Arthritis: Evolving Concepts Source: Current Opinion in Rheumatology. 12(4): 274-280. July 2000. Summary: This journal article provides health professionals with information on the epidemiology, etiology, pathogenesis, pathology, clinical manifestations, diagnosis, and treatment of psoriatic arthritis. Research reviewed in the article reflects recent advances made in basic research and the clinical management of psoriatic arthritis in 1999. Some of these advances are destined to modify the current approach to the disease. Problems related to nosology and epidemiology, the two still controversial aspects, are discussed. Genetic susceptibility to psoriasis and psoriatic arthritis and the inciting role played by some bacteria are confirmed, and attention is focused on the role of T cells, cytokines, adhesion molecules, and angiogenetic factors in the skin and synovial membrane. Two main clinical patterns of articular involvement may be easily detected in psoriatic arthritis. One is peripheral, and the other is axial. A unified concept has been proposed for the classification of clinical subsets of psoriatic arthritis based on common and primary entheseal involvement. Modern imaging techniques enable early articular changes to be discovered, support innovative pathogenetic hypotheses, and allow new therapeutic approaches. Drug therapy has been shown to induce substantial improvement in skin and articular disease manifestations. Combined drug treatment may be of particular interest in clinical forms of psoriatic arthritis not responding to standard or less aggressive therapeutic regimens. 4 tables and 50 references. (AA-M).
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Efficacy of Fish Oil Concentrate in the Treatment of Rheumatoid Arthritis Source: Journal of Rheumatology. 27(10): 2343-2346. October 2000.
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Summary: This journal article provides health professionals with information on a 15 week randomized, placebo controlled, double blind, noncrossover study that determined the efficacy of fish oil derived from fatty acid supplementation in people with rheumatoid arthritis (RA) whose fatty acid intake in the background diet was less than 10 grams (g) per day. Fifty participants were recruited for it. The treatment capsule was 60 percent triglycerides supplemented at a rate of 40 milligrams (mg) per kilogram (kg) of body weight, and the control capsule was 50/50 corn/olive oil. Analysis of nine clinical variables indicates that there was a significant difference between the control and treatment groups. Five participants in the treatment group and three in the control group met the American College of Rheumatology preliminary criteria for improvement in RA at the 20 percent level. The treatment group achieved a significant change from baseline to 15 weeks in all clinical variables except total joint count, erythrocyte sedimentation rate, and C-reactive protein. Dietary supplementation resulted in a significant increase in eicosapentaenoic acid in plasma and monocyte lipids in the supplemented group. Findings suggest that fish oil supplementation that delivers fatty acids at a dose of 40 mg/kg body weight per day, with a dietary fatty acid intake of less than 10 g per day in the background diet, results in substantial cellular incorporation of fatty acids and improvements in clinical status in patients with RA. 3 tables and 16 references. (AA-M). ·
Glucosamine for Arthritis: Hope or Hype? Source: Patient Care. 33(12): 17-18,28. July 15, 1999. Summary: This journal article provides health professionals with information on the efficacy of glucosamine and chondroitin in treating osteoarthritis (OA). A book published in 1997 touted the medical miracle of glucosamine and chondroitin supplements in treating OA. Both conventional and alternative clinicians are taking another look at these supplements, and the National Institutes of Health is organizing a large, randomized trial that may provide some definitive answers on their efficacy in treating OA. These substances, which are naturally produced in the body, are structural components of cartilage. The rationale for using glucosamine is that increasing the amount of available glucosamine would improve the ratio of cartilage repair to degradation. Studies have investigated the use of oral glucosamine versus placebo, intramuscular glucosamine versus placebo, and oral glucosamine versus ibuprofen. Results suggest that glucosamine may provide some therapeutic benefits for patients with OA. Although the Arthritis Foundation continues to advocate using the American College of Rheumatology treatment guidelines for OA, it now offers advice to patients considering the use of glucosamine. 9 references.
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Latest Approaches to Rheumatoid Arthritis Treatment, The Source: Patient Care. 33(12): 69-72,74,77,84,87-88,90. July 15, 1999. Summary: This journal article provides health professionals with information on the latest pharmacologic approaches to treating rheumatoid arthritis (RA). RA is a chronic, systemic, inflammatory autoimmune disease of unknown cause. The traditional therapeutic pyramid model relies on the initial and prolonged use of nonsteroid antiinflammatory drugs (NSAIDs). Slow acting antirheumatic drugs or disease modifying antirheumatic drugs (DMARDs) are used when milder therapies fail. Newer models for treating RA include the step down bridge approach and the sawtooth strategy. In the former, treatment begins with a fast acting corticosteroid plus methotrexate (MTX) to control inflammation. This is replaced with a slower acting drug once inflammation is reduced. With the sawtooth strategy, a DMARD is used early in the process and, as it
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loses efficacy, it is replaced by other similar agents. The article discusses the use of conventional NSAIDs such as aspirin, newer NSAIDs such as celecoxib and rofexocib, and COX-2 inhibitors in treating RA. In addition, the article presents the mechanism of action and common toxicities of various second-line treatments for RA, including , gold compounds, hydroxychloroquine, sulfasalazine, cytotoxic and immunosuppressive agents, azathioprine, and cyclophosphamide. Other topics include the role of corticosteroids and combination and investigational or emerging therapies in treating RA. Investigational therapeutic agents that show promise are monoclonal antibodies to CD4, soluble tumor necrosis factor receptor fusion protein, antitumor necrosis factoralpha monoclonal antibody, interleukin-1 receptor antagonists, interleukin-10, T-cell receptor peptide vaccination, and MTX-plus emerging therapies. 4 tables and 39 references. ·
Osteoarthritis, Shoulder Impingement, Cervical Radiculopathy, Plantar Fasciitis Source: Patient Care. 33(12): 176-178,181-182,184,187-188,191-192,194, 197-198,201-202. July 15, 1999. Summary: This journal article provides health professionals with information on diagnosing and treating osteoarthritis (OA), shoulder impingement syndrome, cervical radiculopathy, and plantar fasciitis. The diagnostic dilemma posed by OA of the knee and hip lies in differentiating OA from other causes of pain and stiffness. Although radiography is the diagnostic gold standard for OA, objective diagnostic criteria are still needed for arthritis. Another diagnostic problem is trying to predict when early stage OA is likely to progress to a more advanced, disabling stage. Pain caused by OA may be managed with nonsteroidal anti-inflammatory drugs (NSAIDs), opioid analgesics, cyclo-oxygenase-2 inhibitors, intra-articular corticosteroid injections, and injections of hyaluronic acid. Weight management is also important for overweight patients with OA of the knee or hip. Unloading braces may also be helpful. Many patients with OA are using the nutritional supplements glucosamine and chondroitin. Referral to an orthopedic surgeon may be necessary if all nonsurgical treatment options have been exhausted in a patient who has end-stage disease. Although shoulder impingement is common, accurate diagnosis requires an understanding of the anatomy and biomechanics of the shoulder. Diagnosis is based on information obtained from the medical history, physical examination, and diagnostic tests. Following an accurate diagnosis, conservative treatment approaches, including rest, anti-inflammatory therapy, and range-of-motion exercises may be used. Long-acting corticosteroid injections may be needed for more advanced disease. Neck pain is very common and has many causes. Diagnosis is based on information obtained from the medical history, physical examination, and diagnostic tests. Conservative treatment includes immobilization, anti-inflammatory treatment, and physical therapy. Referral for surgical intervention may be needed if these methods fail. Plantar fasciitis is a very common, painful condition of sudden onset. The typical symptom is pain on the anterior medial aspect of the heel. Diagnosis is based on information obtained from the medical history, physical examination, and diagnostic tests. A comprehensive therapeutic program for plantar fasciitis should include using NSAIDs, modifying activities, performing exercises to stretch the Achilles tendon, wearing shoes with an arch support, and using a tension splint. 3 figures, 6 tables, and 16 references.
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Determining Surgical Priorities in Rheumatoid Arthritis Source: Comprehensive Therapy. 25(2): 101-107. February 1999.
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Summary: This journal article provides health professionals with information on surgical priorities in patients with rheumatoid arthritis. Consideration should be given to the patient's needs and expectations in developing a surgical plan. The first area of priority for the orthopedic surgeon is managing the involvement of the cervical spine. Early detection and treatment of cervical spine disease are important to ensure the wellbeing of the patient. The most common manifestation of cervical spine disease in the patient with rheumatoid arthritis is atlantoaxial subluxation. A life-threatening manifestation of cervical spine involvement is basilar invagination. Subaxial subluxation is also a common condition. Although cervical spine disease is prevalent in patients with rheumatoid arthritis and the natural history is progressive, only 15 percent of patients ultimately have surgery. Surgical intervention usually involves posterior spinal fusion and instrumentation. The article describes surgical procedures used in upper and lower extremity reconstruction, focusing on procedures for the shoulder, elbow, shoulder-elbow, wrist, hand, wrist-hand, hip, knee, and ankle-hindfoot. Procedures undertaken to save life or prevent neurologic demise take precedence over procedures to alleviate pain or correct disabling deformities. 36 references. ·
Causes of Pain in Children With Arthritis Source: Rheumatic Disease Clinics of North America. 25(1): 31-53. February 1999. Summary: This journal article provides health professionals with information on the causes of pain in children who have arthritis. Pain is generally considered to be a clinically significant symptom for many children who have juvenile rheumatoid arthritis (JRA). JRA is a heterogeneous group of chronic inflammatory arthritides. The onset of JRA is defined by the pattern of disease in the first 6 months. The types of onset include systemic JRA, pauciarticular JRA, and polyarticular JRA. The most common causes of painful arthritis in children are infectious in nature. Children often have musculoskeletal pain not accompanied by arthritis. Chronic pain syndromes are common in children. Although the course of disease is unpredictable in all types of juvenile chronic arthritis, it most often follows a fluctuating course with periods of flare and remission. Psychosocial stress and daily mood may contribute to disease severity, symptoms, and functional ability in children who have JRA. Although pain in children who have JRA has been underrecognized and undertreated, studies have shown that pain is a significant problem for many of these children. Newly developed pain assessment tools designed specifically for children are now available. The treatment of pain in children who have JRA has focused on controlling the underlying disease with medications and providing symptomatic relief with acetaminophen, heat or cold, splints, adaptive devices, and physical therapy. The mainstay of drug treatment for the pain of JRA is nonsteroidal anti-inflammatory drugs accompanied by acetaminophen for acutely painful events. The remittive agent of choice in children who have multiple active joints and unremitting pain is methotrexate. Opioids are used to provide pain relief in acute situations. Systemic steroids, however, should be avoided whenever possible. The complexity of pain in children who have JRA is best managed using a multidisciplinary approach that includes aggressive traditional medical management and incorporates interventions that address psychosocial variables such as coping strategies and perceptions of disease. Cognitive behavioral therapy can address these issues without interfering in the medical management of JRA. 5 figures, 2 tables, and 72 references.
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Costs of Rheumatoid Arthritis: An International Long-Term View Source: Seminars in Arthritis and Rheumatism. 29(5): 305-320. April 2000.
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Summary: This journal article provides health professionals with information on a study that reviewed the literature from the major Organization for Economic Cooperation and Development countries on the measurable direct and indirect costs of rheumatoid arthritis (RA) in industrialized countries from a societal perspective and developed a template for international use. A literature search using MEDLINE and other sources identified 153 relevant published articles, press releases, and other documents in English and other languages on the costs of RA and rheumatism. Only 12 publications provided sufficient information in terms of total costs of RA or detailed monetary information on either direct or indirect costs. Findings indicate that mean direct costs derived from RA only studies are $5,425, indirect costs are $9,744, and total costs are $15,238 per patient per year. The literature suggests a prevalence of RA between 0.5 percent and 1.1 percent of the population in Western industrialized societies. This equates to a societal cost of $121.9 million per 1 million population per year, or $97.7 million per 1 million population based on all 12 studies. Between one fourth and one half of the costs of RA are direct medical costs. Hospitalization is the most important single factor in direct costs, especially in moderate and severe RA. Costs of medication represent a comparatively small portion of direct costs. However, evidence shows that patient visits for drug treatment and safety monitoring are a major factor in overall cost. A trend that may have an impact on the direct costs of RA is the increasing use of outpatient rather than inpatient treatment. Indirect costs are often ignored when estimating the burden of disease on society, partly because they are more difficult to measure than direct costs. They do not represent actual payments or the flow of money, but rather lost economic opportunities. Indirect costs caused by work disability can be substantially higher than direct costs, particularly in working age patients. In these patients, indirect costs exceed direct costs by a factor of two to three. Although work disability may be uncommon in early RA, indirect costs escalate with disease progression. The total costs of RA to society, and the different cost components such as direct and indirect costs, are broadly comparable in industrialized countries by their order of magnitude. Major confounding factors for international comparison are different study methodologies and patient samples. The article concludes that the cost template developed in the article can be used to estimate the likely costs of RA to society for industrialized countries. It will probably underestimate indirect costs because of their incomplete coverage in the studies examined. A long term perspective is needed for chronic diseases such as RA to assess the future effects of early interventions. Treatment in the early stages of RA that effectively reduces long term disability has the potential for substantial savings to society. 3 figures, 6 tables, and 68 references. (AA-M). ·
Longterm Therapy of Psoriatic Arthritis: Intramuscular Gold or Methotrexate? Source: Journal of Rheumatology. 27(8): 1922-1927. August 2000. Summary: This journal article provides health professionals with information on a study that compared the efficacy and toxicity of methotrexate (MTX) and intramuscular (im) gold in the treatment of psoriatic arthritis (PsA). Medical records from all patients with PsA attending the gold and MTX clinics at an arthritis center in Vancouver, British Columbia, Canada, between 1971 and 1995 were reviewed. The odds of a clinical response, defined as at least a 50 percent reduction in active joint count from initial to last visit or for at least 6 months, and the relative risk of discontinuing therapy associated with MTX or im gold treatment were calculated after controlling for significant baseline covariates using logistic regression and Cox regression analyses, respectively. The frequency of side effects and the reasons for treatment cessation were also compared between treatment groups. Eighty-one patients received 111 treatment courses: 43 of MTX and 68 of im gold. In the univariate analysis, there was a marked
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difference in the proportion of treatment courses resulting in clinical responses between treatment groups: a 50 percent reduction in joint count was achieved in 25 of 43 MTX courses compared with 24 of 68 im gold courses. In the logistic regression analysis, the likelihood of a clinical response was 8.9 times greater with MTX than im gold. Patients who had not used a second line agent prior to initiation of the study drug and patients with shorter PsA duration and higher erythrocyte sedimentation rate (ESR) were more likely to achieve a clinical response. Those who had not used a prior second line agent had 2.9 times the odds of achieving a clinical response as users. For every 1 year increase in PsA duration prior to introducing the study drug, patients were 5 percent less likely to achieve a clinical response. For every 1 millimeter increase in ESR, patients were 2 percent more likely to achieve a clinical response. In the univariate analysis, a greater proportion of gold courses were discontinued. When taking length of followup into consideration, the frequency of treatment discontinuation was 33.4 per 100 person years of followup for im gold but only 12.8 per 100 person years for MTX. In the Cox regression analysis, patients were five times more likely to discontinue therapy with im gold than with MTX. Prior users of second line agents were 1.65 times more likely to discontinue therapy than nonusers. No major toxicity occurred, and frequency of side effects was similar for both treatments. The article concludes that MTX and im gold are safe and well tolerated in the treatment of PsA. Data suggest that earlier treatment may be associated with a better response. 1 figure, 5 tables, and 36 references. (AA-M). ·
Arthritis 101: The Eyes Source: Arthritis Today. 13(3): 30-31. May-June 1999. Summary: This journal article provides people who have arthritis and related conditions with information on common arthritis related eye problems, which are classified according to the form of arthritis or condition with which they are associated. Giant cell arteritis, an inflammation of the blood vessels that supply the head, may occur in people who have polymyalgia rheumatica. Ankylosing spondylitis and juvenile rheumatoid arthritis are associated with iritis, an inflammation of the iris. Scleritis, a chronic inflammation of the blood vessels in the whites of the eyes, occurs in about 1 percent of those who have rheumatoid arthritis. Dry eyes are a key symptom of Sjogren's syndrome. People who have lupus may experience cotton wool spots, which are white, puffy patches that appear on the retina and can be seen during an eye examination. In addition, some medications used to treat arthritis-related disease, including hydroxychloroquine and prednisone, can damage the eye. Regular eye examinations are important in detecting and treating eye problems early. 1 table.
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Rheumatoid Arthritis: A Review and Suggested Dental Care Considerations Source: Journal of the American Dental Association. 130(5): 689-698. May 1999. Summary: This journal article provides dental health care workers with information from a study of the impact of rheumatoid arthritis (RA) and its treatment on the provision of oral health care. An extensive review of the medical literature in English on RA and dental care was undertaken. Although a MEDLINE search spanned the years from 1975 to the present, the most recent literature was prioritized. Appropriate medical and dental textbooks were also used. Nearly 200 articles and 7 textbooks were reviewed. Major features of RA, including its pathophysiology, diagnosis, clinical features, and treatment, were identified. The cause is unknown, but the etiology appears to be multifactorial and may involve infectious, genetic, endocrine, and immune participation. There is no specific laboratory test to diagnose RA. Although rheumatoid factors are found in more than two-thirds of adult patients with RA, they are not specific
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to it. The latest set of criteria for diagnosing RA was developed by studying patients who had already been diagnosed. The objective of RA therapies is to restore or maintain quality of life by relieving pain, reducing joint inflammation, and preventing joint destruction and deformity. Nonsteroidal anti-inflammatory drugs are the first-line treatment. Corticosteroids, another option, have both anti-inflammatory and immunosuppressive effects. Disease-modifying antirheumatic drugs, which have the potential to reduce disease activity or prevent joint damage, include gold, sulfasalazine, hydroxychloroquine, D-penicillamine, azathioprine, and leflunomide. Methotrexate has become a popular choice because of its immunosuppressive and anti-inflammatory effects. One of the latest and more novel approaches to treatment is cytokine therapy. However, long-term use of methotrexate and other antirheumatics can lead to various oral manifestations. The article discusses the clinical implications of RA in dental practice and provides guidelines on the dental management of people who have the disease. Considerations include the patient's ability to maintain adequate oral hygiene, xerostomia and its related complications, the patient's susceptibility to infections, impaired hemostasis, and untoward drug actions and interactions. 4 tables and 57 references. (AA-M). ·
Antibiotics for Rheumatoid Arthritis?: Minocycline Shows Promise in Some Patients Source: Postgraduate Medicine. 105(4): 95-98. April 1999. Summary: This journal article provides health professionals with information on the use of the antibiotic minocycline for the treatment of rheumatoid arthritis. Although studies in the United States and Europe have validated the usefulness of minocycline, most rheumatologists are not convinced of the value of antibiotic therapy for this form of arthritis. Three double-blind, controlled studies and two open trials have reported the efficacy of minocycline in treating rheumatoid arthritis. The mechanism of action of minocycline and related compounds is unclear; however, the antirheumatic effect could be related to immunomodulatory and anti-inflammatory properties. Minocycline may be a reasonable alternative for treating patients with a benign prognosis, but not for those with severe and potentially very destructive disease. 3 tables and 25 references.
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Arthritis 101: Gout Source: Arthritis Today. 13(1): 26-27. January-February 1999. Summary: This journal article provides people who have gout with information on this painful form of arthritis. Gout, which is caused by the deposition of uric acid crystals in the joint, usually appears suddenly. If allowed to progress, the pain and inflammation of gout can resemble that of rheumatoid arthritis. The article explains why uric acid may accumulate in bodily tissues and who is most susceptible to getting gout. It also lists factors that can aggravate gout: use of diuretic medications, obesity, use of alcohol, kidney failure, and a diet rich in purines. Other topics are how gout is diagnosed using a patient's medical history, a physical examination, and laboratory tests; what joints are affected by gout; and how it is treated, namely, with anti-inflammatory medications, nonsteroidal anti-inflammatory drugs, and glucocorticoid medications. 5 figures.
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Effect of Arthrocentesis of the Temporomandibular Joint in Patients With Rheumatoid Arthritis Source: Journal of Oral and Maxillofacial Surgery. 57(5): 537-540. May 1999. Summary: This journal article presents health professionals with the findings of a study that evaluated the effect of arthrocentesis of the temporomandibular joint (TMJ) in
Studies 31
patients with rheumatoid arthritis (RA). Twelve female patients with previous documented RA underwent baseline assessment with erythrocyte sedimentation rate, physical examination of TMJ function, and visual analog pain scale (VAPS). The VAPS and jaw function changes were recorded at 2-week intervals for 6 weeks after lysis and lavage under local anesthesia in an ambulatory setting. The study found that maximal incisal opening (MIO) improved soon after arthrocentesis. As important was the finding that MIO did not decrease in those patients who were not initially limited. In addition, overall change in VAPS was significant. Improvement in the post-treatment biweekly VAPS suggests that some physiologic or mechanical changes occurred within the joint space. The article concludes that TMJ arthrocentesis is a useful adjunct in the short-term management of the symptoms of RA. A critique of the study follows the article. 2 figures, 2 tables, and 25 references. (AA-M).
Federally Funded Research on Arthritis The U.S. Government supports a variety of research studies relating to arthritis. These studies are tracked by the Office of Extramural Research at the National Institutes of Health.2 CRISP (Computerized Retrieval of Information on Scientific Projects) is a searchable database of federally funded biomedical research projects conducted at universities, hospitals, and other institutions. Search the CRISP Web site at http://crisp.cit.nih.gov/crisp/crisp_query.generate_screen. You will have the option to perform targeted searches by various criteria, including geography, date, and topics related to arthritis. For most of the studies, the agencies reporting into CRISP provide summaries or abstracts. As opposed to clinical trial research using patients, many federally funded studies use animals or simulated models to explore arthritis. The following is typical of the type of information found when searching the CRISP database for arthritis: ·
Project Title: 5 FLUOROURACIL (5 FU) PLUS LEUCOVORIN IN TREATMENT OF RHEUMATOID ARTHRITIS Principal Investigator & Institution: Bunch, Thomas W.; Mayo Clinic Rochester 200 1St St Sw Rochester, Mn 55905 Timing: Fiscal Year 2001 Summary: The main objective of this study is to provide patients that have refractory rheumatoid arthritis with a better treatment option. Rheumatoid arthritis affects 1-2 percent of the population, and current treatments are inadequately efficacious for many patients. Immunosuppressive agents have been shown to clearly suppress the immunopathogenic mechanisms response for much of the disease activity. This is a clinical trial to determine the maximally tolerated dose of 5-FU and leucovorin when given on a daily x 5 schedule in patients with rheumatoid arthritis, to define toxicity and to document any clinical benefit of this drug combination in patients with rheumatoid arthritis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
Healthcare projects are funded by the National Institutes of Health (NIH), Substance Abuse and Mental Health Services (SAMHSA), Health Resources and Services Administration (HRSA), Food and Drug Administration (FDA), Centers for Disease Control and Prevention (CDCP), Agency for Healthcare Research and Quality (AHRQ), and Office of Assistant Secretary of Health (OASH).
2
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Project Title: ACTIVATION OF COLLAGENASE IN RHEUMATOID ARTHRITIS Principal Investigator & Institution: Windsor, L Jack. Oral Biology; Indiana Univ-Purdue Univ at Indianapolis 620 Union Drive, Room 618 Indianapolis, in 462025167 Timing: Fiscal Year 2001; Project Start 1-SEP-1997; Project End 1-AUG-2003 Summary: (Adapted from the applicant's abstract) - Rheumatoid arthritis is characterized by chronic inflammation and joint degeneration. This erosion of the joint is likely due to an imbalance of extracellular matrix synthesis and metabolism induced, in part, by members of the matrix metalloproteinase (MMP) family. The MMPs are zincdependent endopeptidases that are capable of degrading most of the components of the extracellular matrix. Active collagenase has been identified in the synovial fluid and in tissue extracts from patients with rheumatoid arthritis as well as in conditioned media from cytokine-stimulated synovial fibroblasts. It has been suggested that this activation of collagenase was initiated via the plasminogen cascade and/or involves stromelysin-1. However, the activation pathway of collagenase is a pivotal step in collagen degradation that still remains poorly understood. The overall aim of this study is to identify and characterize the mode of activation of fibroblast-type collagenase (collagenase-1) by synovial fibroblasts and manipulate its activation to determine if control of this process could be beneficial in the treatment of rheumatoid arthritis. The following specific aims are proposed to accomplish these goals: Specific aim 1 - Human synovial fibroblast cell lines capable of mediating destruction of a reconstituted matrix consisting of type I collagen fibrils will be identified and characterized. Collagen degradation initiated by these cells will be blocked by addition of inhibitory antibodies to collagenase-1 to demonstrate that this collagen degradation is collagenase -1 dependent. Intermediates in the activation of collagenase-1 will be identified and characterized by alpha2macroglobulin and TIMP (tissue inhibitor of metalloproteinases) capture techniques as well as by their reactivity in a fluorescent maleimide. In order to determine processing sites, amino-terminal sequencing will be carried out using activation intermediates purified by antibody affinity chromatography or by immunoprecipitation. Specific aim 2 - The investigators propose to distinguish the roles stromelysin and other MMPs play in the activation of collagenase-1 by synovial fibroblasts through addition of inhibitory antibodies made to each enzyme. Inhibitory antibodies to TIMP-1 may be included to provide an imbalance of enzymes to inhibitors which might lead to the activation of collagenase-1. Activation intermediates will be identified and characterized. Specific aim 3 - Once a synovial fibroblast cell line is identified that activates collagenase-1 independent of stromelysin-1 and other MMPs, it will be used to identify the mechanism(s) or factor(s) that are responsible for CL-1 activation. The feasibility of this specific aim is limited and depends on identifying a synovial fibroblast cell line that meets these criteria. The long-term goal of this project is to identify drugs or other reagents (antibodies) that can block the mechanism by which cells activate collagenase-1 and the other MMPs in order to prevent the continuous or intermittent destruction of the joints as seen in rheumatoid arthritis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ADENOSINE-3 AGONISTS FOR THE SUPPRESSION OF ARTHRITIS Principal Investigator & Institution: Szabo, Csaba; Vice President for Research; Inotek Pharmaceuticals Corporation 100 Cummings Ctr, Ste 419E Beverly, Ma 01915 Timing: Fiscal Year 2002; Project Start 5-SEP-1999; Project End 1-AUG-2004 Summary: (provided by the applicant): Based on promising in vitro and in vivo data, the applicants are developing novel classes of compounds with anti-inflammatory effects,
Studies 33
and with anti-arthritic potential. In this proposal, we present evidence that selected ligands of the adenosine-3 receptor are (1) inhibitors of the production of macrophagederived pro-inflammatory mediators and enhancers of the production of antiinflammatory mediators in vitro and in vivo (2) potent anti-inflammatory agents in a variety of inflammatory conditions including collagen-induced arthritis, and endotoxininduced systemic inflammation. The applicants intend to develop a selected adenosine 3 receptor agonist as an anti-arthritic drug. The applicants have collaborated with a prominent group in the field of adenosine receptor ligands, and have identified candidates, with selectivity towards the adenosine 3 subtype in human systems, which are deemed suitable leads for further drug development, efficacy studies, and eventual formal pharmacokinetic and toxicology studies. The specific aims of the present proposal are (1) to identify a lead adenosine-3 ligand, with acceptable efficacy profile in human systems (2) to perform efficacy studies with the compound in terms of suppression of pro-inflammatory mediators in human cell systems (3) to synthesize larger, GLP and GMP-quality quantities of a lead adenosine-3 agonist compound, and (4) to perform in-house and subcontracted pharmacokinetic and toxicity studies in two species according to FDA requirements. The current scope of work will bring the applicants forward to the level of an IND application for Phase I clinical testing of a selected adenosine-3 ligand. PROPOSED COMMERCIAL APPLICATION: The domestic market for a novel, effective therapy for arthritis is estimated at >$1 billion per annum. Global markets are estimated at $4 billion. Current market entrants are incompletely effective: Arthritis-related morbidity is substantial, with chronic disability, loss of employment, and exercise intolerance. A novel A3 receptor agonist may represent a useful anti-inflammatory adjunct to current therapeutic regimens; funding of the current SBIR Phase II will allow for starting human safety trials in 2 years. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: ANALYSIS OF GENETIC AND NONGENETIC RISK FACTORS IN RHEUMATOID ARTHRITIS Principal Investigator & Institution: Criswell, Lindsey A.; University of California San Francisco 500 Parnassus Ave San Francisco, Ca 94122 Timing: Fiscal Year 2001 Summary: Rheumatoid arthritis (RA) is a chronic, disabling illness of unknown cause. Although both genetic and non-genetic factors are clearly important in disease onset and progression, little is known about specific risk factors. Furthermore, interactions among genetic and non-genetic factors are likely to be important, yet this remains an underexplored area of investigation. Substantial evidence implicates the Major Histocompatibility Complex (MHC) region in RA susceptibility. However, existing studies fail to define precisely which of the numerous candidate genes in this region influence disease risk, and whether they have independent or interactive effects. Specifically, strong evidence supports a role for the HLA-DRB1 "shared epitope," however, there is strong evidence that other MHC region loci likely influence RA risk or severity. Non-MHC genes must also be important, yet little is known about other genetic risk factors. Preliminary data by our group and others suggest a role for T cell receptor B (TCRB) genes in RA susceptibility. Finally, although non-genetic factors are estimated to explain at least 50% of RA risk, little is known about specific non-genetic risk factors. In this study, we will focus on two gene regions and two categories of nongenetic factors that are implicated in RA etiology based on pathophysiologic considerations and previous genetic and epidemiologic studies. Specifically, we will examine four candidates within or near the MHC region (HLA-DRB1, -DMA, tumor
34 Arthritis
necrosis factor exposure to cigarette smoke. Our analysis will explicitly assess the presence of independent and interactive effects upon certain patient and disease characteristics. Our choice of analytic method, the transmission disequilibrium test, will allow us to study an ethnically diverse sample while maintaining false positive associations arising from population admixture. The results of this study will: 1) more precisely define the MHC contribution to RA; 2) evaluate the role of the TCRB gene complex; 3) provide new and important information about discrete non-genetic risk factors in RA onset and disease expression; and 5) provide important information about potential sources of genetic heterogeneity that will inform the design and analysis of future genetic epidemiologic studies of RA. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: ARTHRITIS
ANDROGEN
AS
ADJUNCT
THERAPY
IN
RHEUMATOID
Principal Investigator & Institution: Davis, John C. Medicine; University of California San Francisco 500 Parnassus Ave San Francisco, Ca 94122 Timing: Fiscal Year 2001; Project Start 0-SEP-1999; Project End 0-JUN-2003 Summary: Rheumatoid arthritis (RA) is a chronic, debilitating multisystem disease affecting nearly two million persons in the United States alone. The incidence of RA in men under the age of forty-five is less than that reported in women, however the incidence approaches that of women in older age groups of men. This increased incidence in males coincides with decreasing levels of sex hormones. A hypogonadic condition characterized by low serum testosterone has been previously described in male RA patients compared with age-matched controls with osteoarthritis, ankylosing spondylitis and healthy controls. Patients with RA have significant disability with decreased function over time. Androgens have the potential to increase nitrogen retention, lean body mass, strength, and body weight which could slow the decline in function. Patients with RA also have both local and systemic forms of osteoporosis. There is evidence that androgens may stimulate the proliferation and differentiation of osteoblasts and osteoblast-like cells in vitro which may help reduce the rate of bone loss in RA. Previous studies in both animal models and humans seem to suggest that androgen administration may be beneficial in a number of autoimmune diseases including RA. In this study, we will examine the role of transdermal testosterone versus placebo in male patients with RA over a two-year period. Specifically, we will examine (1) the effect of testosterone on lean body mass and muscle strength with the use of whole body dual xray absorptiometry (DXA) scan and muscle strength testing, (2) the effect of testosterone on bone mineral density by DXA scan of the spine and hip, and (3) the effect of testosterone on disease specific measures of quality of life with validated instruments for quality of life. Additionally, measure of disease activity and side effects will also be assessed. The results of this study will (1) help to define the role of androgen administration and its effects on function through assessment of muscle mass and strength, (2) explore the potential benefits of testosterone therapy on bone mineral density in patients with both localized and systemic forms of osteoporosis, (3) define changes in quality of life in patients with RA treated with androgen, and (4) help to define the potential role of androgen therapy in other systemic illnesses where muscle wasting has a profound impact on quality of life (e.g. both inflammatory and noninflammatory muscle disease). In addition, this K-23 grant will provide opportunity for further career development through mentorship provided by an committee with multiple areas of expertise and formal education in the areas of clinical research design and conduct, outcome assessment development and analysis, and clinical trial analysis.
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Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: ANGIOGENESIS & ALPHA V INTEGRINS IN RHEUMATOID ARTHRITIS Principal Investigator & Institution: Storgard, Chris M.; Mayo Clinic Rochester 200 1St St Sw Rochester, Mn 55905 Timing: Fiscal Year 2001; Project Start 7-SEP-1999; Project End 0-JUN-2004 Summary: Angiogenesis is central to the pathophysiology of rheumatoid arthritis (RA), and anti-angiogenic therapy targeting vascular integrin alphavbeta3, a crucial effector of the angiogenic process, may provide a novel approach to the treatment of this disease. The Specific Aims of this Mentored Clinical Scientist Development Award are [1] To characterize the dominant integrin pathway promoting angiogenesis in human RA, [2] To evaluate the effects of rational combination therapy targeting angiogenesis, cytokineinduced inflammation, and T cell mediated immunity, to determine the relative contribution of angiogenesis to the pathophysiology of RA, and provide pre-clinical evaluation of potential synergistic therapeutic effects, and [3] To examine the molecular mechanism of alpha V integrin-mediated endothelial cell survival during angiogenesis. The proposed research plan, in addition to providing valuable information, will equip the applicant with the necessary skills and techniques to investigate molecular mechanisms of cell function and signal transduction and perform anti-angiogenic gene delivery strategies as an independent investigator. Antagonists of alphavbeta3 are presently being evaluated in phase I/II cancer trials, and the results of this proposed study will provide the basis for alphavbeta3 antagonist therapy in future human arthritis trials. The strength of this career development award is based on the Mentor, Dr. David Cheresh, an international leader in angiogenesis research with a solid history of fostering the development of independent researchers. In addition, The Scripps Graduate Program in Macromolecular and Cellular Structure and Chemistry, in conjunction with The Scripps Research Institute and the Cheresh Laboratory, provide an outstanding training environment with exposure to state-of-the-art technology, permitting collaboration and intellectual exchange with many leading investigators. This comprehensive career development plan, in addition to the proposed research project will guarantee successful maturation of the applicant from physician to physician-scientist. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ARTHRITIS
ANTI-ANGIOGENIC
GENE
THERAPY
FOR
RHEUMATOID
Principal Investigator & Institution: Kasahara, Noriyuki; None; University of Southern California 2250 Alcazar Street, Csc-219 Los Angeles, Ca 90033 Timing: Fiscal Year 2001; Project Start 0-SEP-1999; Project End 1-JUL-2002 Summary: The purpose of these studies is to evaluate the therapeutic potential of the angiogenesis inhibitors thrombospondin-1, angiostatin, and endostatin, for gene therapy of rheumatoid arthritis. Using lentiviral and helper-dependent adenoviral vectors as gene delivery systems for these angiogenesis inhibitors, we propose to develop an intraarticular treatment for rheumatoid arthritis. A considerable body of experimental and clinical data has documented that the pathogenetic process in rheumatoid arthritis involves the induction of a neovascular response. The process of new blood vessel formation, or angiogenesis, involves the interaction of substances that either stimulate or inhibit endothelial cell proliferation and migration. During pathologic processes such
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as rheumatoid arthritis, increased expression of angiogenic stimulators or decreased production of inhibitors alters the balance of positive and negative inputs of endothelial cell proliferation in favor of active neovascularization. We hypothesize that by increasing the concentration of these angiogenesis inhibitors in the synovial tissues during chronic inflammation, we may prevent the induction of new blood vessels and retard disease progression. The proposed experiments will allow us to: 1) optimize delivery and expression of transgenes encoding the angiogenesis inhibitors thrombospondin-1, endostatin and angiostatin, following intra- articular administration of lentiviral and helper-dependent adenoviral vectors, 2) to determine the extent of systemic absorption and investigate the systemic effects of intra- articularly delivered anti-angiogenic lentiviral and adenoviral vectors, 3) to determine the in vivo chemopreventive effects of increased local expression of angiogenesis inhibitors on the establishment of arthritic disease, and 4) to determine the ability of lentiviral-and adenoviral-mediated delivery and local overexpression of anti-angiogenic genes to inhibit disease progression and angiogenesis in established arthritis. The development of an effective anti-angiogenic therapy for rheumatoid arthritis utilizing a relatively non-invasive intra- articular gene delivery strategy could have significant impact on patient quality of life, and potentially improve long-term outcome. In addition, by taking advantage of the ease of access by the intra-articular route, we anticipate that it will be possible to establish high local concentrations of potent angiogenic inhibitors while minimizing potentially adverse effects associated with systemic administration. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: ANTIBIOTIC THERAPY FOR RHEUMATOID ARTHRITIS (ATRA TRIAL) Principal Investigator & Institution: St Clair, Eugene W.; Duke University Durham, Nc 27706 Timing: Fiscal Year 2001 Summary: Previous randomized, controlled clinical trials suggest that oral tetracyclines may reduce the symptoms of joint inflammation in rheumatoid arthritis (RA). This class of antibiotics has well-described antimicrobial effects as well as anti-collagenase activity. Collagenase is an enzyme that degrades cartilage and bone and is believed to be important in the pathogenesis of RA. This study evaluated the safety and potential clinical efficacy of I.V. doxycycline therapy in 31 patients with RA and explored whether any improvements in arthritis from the doxycycline were due to its antibacterial actions or ability to reduce the activity of collagenase. The three objectives of this study were: 1) To determine the feasibility, safety, and potential clinical efficacy of I.V. doxycycline therapy in RA and explore whether this agent ameliorates clinical manifestations of this disease by suppressing bacterial infection or matrix metalloproteinases (MMP) activity; 2) To determine whether daily and weekly treatment with I.V. doxycycline can reduce urinary excretion of collagen crosslinks in patients with RA and potentially retard joint damage; and 3) To explore the potential effects of daily and weekly I.V. doxcycline therapy on biochemical markers of cartilage proteoglycan degradation; and 4) to determine whether IV doxycycline can reduce expression of nitric oxide synthase type 2 expressed by circulatory monocytes. Patients were randomized into 3 groups: Group I received I.V. doxycycline and oral placebo, Group II will received I.V. placebo and oral azithromycin, and Group III received I.V. and oral placebo. The I.V. therapy was delivered through a peripheral long-line catheter. The initial treatment phase consisted of daily infusions and oral therapy for 21 days. The second treatment phase consisted of weekly infusions administered from week 4 through 11. Results: The study is closed and
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a Final Report was submitted to the NIH on December 29, 1998. Thirty-one patients were enrolled between April of 1995 and February 1998. The study population included various ethnic backgrounds, such as African- American, Caucasian, and Native American and was predominantly female (24/7). Only 4 patients withdrew from the trial before the day 112 visit. Three patients discontinued the study drug after day 28 because of worsening arthritis and one patient withdrew at day 56 when she was diagnosed with breast cancer. Thirteen (42%) of the patients experienced at least one infusion-related event during the trial. These events included catheter site tenderness/pain/redness, symptoms of burning during the infusion, site-related skin rash from adhesive tape, catheter infiltration, signs of localized infection at the catheter site, clotting of the catheter or line, and thrombophlebitis. None of these events were classified as serious. Most of the patients experienced at least 1 adverse event, which were most commonly gastrointestinal or neurologic in origin. The most frequent adverse events apart from the infusion-related complications included headache (8 patients), abdominal pain (6 patients), fatigue (6 patients), nausea/vomiting (5 patients, vaginitis (5 patients), loose stools/diarrhea 93 patients), dizziness/lightheadedness (3 patients), and decreased appetite (3 patients). The results of the present study do not provide evidence that i.v. doxycycline therapy reduces the signs or symptoms of RA. These data must be interpreted with caution because the study was not designed to provide adequate statistical power to answer this question. The present study does show that this treatment approach is feasible and does not cause unacceptable toxicities. However, no significant differences were noted among treatment groups in the primary endpoints. The tender joint count dropped only slightly in all of the 3 treatment groups. This result is compatible with little or no immediate clinical effect from the 3 weeks of i.v. doxycycline therapy. Significance: There are no future plans since doxycycline did not improve the primary endpoints. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: ARTHRITIS AND PHYSICAL TREATMENT Principal Investigator & Institution: Sun, Hui B. Anatomy and Cell Biology; Indiana Univ-Purdue Univ at Indianapolis 620 Union Drive, Room 618 Indianapolis, in 462025167 Timing: Fiscal Year 2002; Project Start 5-AUG-2002; Project End 1-JUL-2005 Summary: (provided by applicant): The long-term objectives of this proposal are to elucidate the effects of mechanical stimuli to tissue degradation of rheumatoid arthritis and to develop a physical treatment for relieving pain and stiffness of arthritic joints. Using two human synovial cell cultures isolated from rheumatoid arthritis patients, we have recently found that mechanical shearing at a few dyn/cm 2 transiently decreases the transcriptional levels of matrix metalloproteinase (MMP)-1, MMP-13 genes as well as ets-1 transcription factor, while the same shearing increases the mRNA levels of tissue inhibitor of metalloproteinase (TIMP)-1, TIMP-2 and c-fos. These preliminary gene expression results suggest a potential use of mechanical shear stress as a therapeutic tool and allow us to test the following hypothesis: An appropriate nonstationary temporal profile of gentle mechanical shear stress at a few dyn/cm2 can maintain simultaneously a reduced mRNA level of MMP-1, 3, and -13 as well as an increased mRNA level of TIMP-1 and 2 through the down-regulation of ets-1 transcription factor. Two specific aims of this project are (i) to evaluate the proposed five non-stationary shear stress profiles for decreasing MMP rRNAs and increasing TIMP mRNAs, and (ii) to identify the function of ets-1 on mechanical stress-induced response in the simultaneous regulation of MMPs and TIMPs. We will isolate RNA from the
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stress-treated synovial cell cultures and determine the cDNAs levels of the specific MMPs and TIMPs as well as AP-1 and ets gene family members using a reverse transcription-polymerase chain reaction procedure. We will also measure the level of MMP proteins by immunoblotting and determine MMP activities by using zymography and a fibril degradation assay. By transfecting ets-1, we will test the function of ets-1 under mechanical stimuli. The proposed project will contribute to answer whether a non-invasive physical treatment can be developed for preventing from tissue degradation in arthritis joints. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: ARTHRITIS ACCOMMODATIONS
DISABILITY:
MULTIPLICITY
AND
Principal Investigator & Institution: Verbrugge, Lois M. Senior Research Scientist; Gerontology; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, Mi 481091274 Timing: Fiscal Year 2001; Project Start 2-SEP-2000; Project End 0-JUN-2003 Summary: (adapted from the investigator's abstract): This project studies multiplicity of disabilities and scope of accommodations among US adults with arthritis disability. The conceptual framework for the analyses is the disablement process, which relates person and environment factors to disability and participation outcomes. The data source is the National Health Interview Survey Disability Supplement (NHIS-D) conducted in 199495 for the US community-dwelling population. Both the NHIS-D baseline interview (Phase I-all household members) and follow-up interview (Phase II: persons with disability) are used. Arthritis disability is defined as having one or more disabilities attributed to arthritis. Two spans of ICS codes for arthritis are used: Arthritis and Other Rheumatic Conditions (Broad coverage of joint and connective tissue conditions) and Arthritis (Subgroup of osteo, rheumatoid and axial arthritis). Disabilities and accommodations in various domains (Personal care, household management, home, work, transportation) are covered. Descriptive analyses provide national-level estimates of disabilities, buffers, and barriers for arthritis-disabled persons versus persons with disabilities due to other conditions. Multivariate models of social participation are estimated with sociodemographic, disability, and accommodations predictors. Two outcomes are studied: nonproductive main activity (an objective feature) and disability identity (subjective). Cross-sectional and longitudinal models are estimated. We hypothesize that participation is facilitated by buffers, but hampered by barriers and extensive disability. Results of the project will be disseminated not only in journal publications, but also in presentations to public health and medical professions. The project has two distinctive contributions: (1) Multiplicity: disability and accommodations are described in compact whole-persons ways. (2) Accommodations: buffers that enhance and barriers that inhibit the involvement of arthritis-disabled persons in their community are identified. Buffers and barriers are modifiable factors, so the results will give sound clues about accommodations that can be vigorously promoted to help arthritis-disabled persons. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: ARTHRITIS EDUCATION CAMPAIGN: PAIN AND EXERCISE Principal Investigator & Institution: Watts, H G. Vice President; State of the Art, Inc. 4455 Connecticut Ave Nw, Ste B-2 Washington, Dc 20008 Timing: Fiscal Year 2002; Project Start 1-JUL-2002; Project End 0-JUN-2003
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Summary: (provided by investigator): State of the Art is developing a healthcommunication and education campaign-"Arthritis Education Campaign: Pain and Exercise (AEC). AEC will include a 13-part broadcast television series (one season), which will be edited to create a video set, and a companion workbook. The goal of AEC is to lessen pain disability and health distress of people with arthritis. AEC will teach people with arthritis, ages 45 and older, how to exercise with arthritis to reduce pain and motivate them to adopt exercise and other self-management techniques. The aims of Phase I are to determine the beliefs about arthritis and exercise held by people with arthritis and to develop and validate the content and message for the series and workbook. Phase I research will include: key informant interviews, creative plan development, board of advisor review/creative plan revision, and focus group testing. Phase I of AEC will use qualitative and quantitative research designs that will consist of key informant interviews and focus group testing with some quantitative testing. AEC will develop and apply an innovative format that combines traditional exercise instruction and documentary clips to address psychosocial issues and motivate people with arthritis. This innovative format will offer instructional and emotional support. PROPOSED COMMERCIAL APPLICATION: The television broadcast will be offered to network, cable, and public television stations. American Public Television, a major content provider to PBS stations, has already expressed interest in AEC. The video set and workbook will be distributed through physicians, health professionals, and organizations that serve people with arthritis. State of the Art has successfully marketed many other patient education materials to this market and already has contacts and established relationships to assist in the marketing. The market for products for people with arthritis is large. Arthritis is the leading cause of disability in the United States and is projected to affect nearly 60 million people in 2020. There is currently no broadcast exercise show for people with arthritis on the air. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: ATHEROCLEROSIS IN RHEUMATOID ARTHRITIS COHORT Principal Investigator & Institution: Del Rincon, Inmaculada; Medicine; University of Texas Hlth Sci Ctr San Ant 7703 Floyd Curl Dr San Antonio, Tx 78229 Timing: Fiscal Year 2001; Project Start 8-JUL-2001; Project End 0-JUN-2006 Summary: This K 23 Career Development Award will accomplish the double objective of training the candidate in patient-oriented research, and advancing current knowledge of the relationship between inflammation and atherosclerosis. For the career development component, the candidate will participate in the Master of Science in Clinical Investigation program, established at her institution with funding from a K30 Award from the NHLBI. This outstanding program is tailored to the candidate's needs, and will provide an in depth exposure to study design, data management and analysis, research ethics and scientific writing. The candidate will benefit from a rich environment of national experts in epidemiology, vascular imaging, cardiology, neurology, rheumatology and biostatistics. The objective of the research component is to examine to what extent atherosclerosis and cardiovascular morbidity are explained by systemic inflammation in rheumatoid arthritis (RA), accounting for the competing influence of established cardiovascular risk factors. The candidate will pursue three Specific Aims: (1) To determine the extent of atherosclerosis that is explained by cumulative systemic inflammation in RA; (2) To determine the role of inflammation in the progression of atherosclerosis in patients with RA; and (3) To determine the role of ongoing inflammatory disease activity as a risk factor for cardiac and cerebrovascular atherothrombotic events in RA. For Specific Aim 1, 680 members of an established
40 Arthritis
cohort of RA patients will undergo two non-invasive procedures to measure atherosclerosis: high resolution B-mode ultrasound of the carotid intima- media thickness (IMT) and ankle-arm systolic blood pressure index. These measures will be compared to the severity of joint damage, which reflects cumulative inflammation in RA. For Specific Aim 2, the candidate will examine the influence of inflammation on the progression of carotid IMT over three years. For Specific Aim 3, the candidate will assess the influence of ongoing inflammatory disease activity on the incidence of cardiac and cerebrovascular events in the RA cohort. This research is a novel approach to understanding the contribution of inflammation to atherosclerosis, and will point the way for future research into the mechanisms of atherogenesis. In addition, it will have implications for the management of patients with RA and other inflammatory diseases, by extending the current indications for anti- inflammatory therapy to the prevention of atherosclerosis. This would ultimately lengthen life expectancy and improve the quality of life of people with inflammatory diseases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: AVONEX IN JUVENILE RHEUMATOID ARTHRITIS Principal Investigator & Institution: Sundel, Robert;; Children's Hospital (Boston) Boston, Ma 021155737 Timing: Fiscal Year 2001 Summary: This pilot study will evaluate the safety and efficacy of interferon B in the treatment of polyarticular juvenile rheumatoid arthritis (JRA), and to establish a dosing range for this medication in the treatment of polyarticular JRA. JRA is an incurable idiopathic condition that affects at least 70,000 children in the United States (Cassidy JT, Nelson AM, The frequency of juvenile arthritis. J Rheumatol 1988; 15:535). Polyarticular disease, which makes up at least 1/3 of this number, is one of the most severe subtypes owing to its tendency to cause pain and damage of multiple joints. A recent summary of outcomes in polyarticular JRA reported that 45% of children with this form of arthritis have active disease 10 years after onset of symptoms, and 54% have radiographic evidence of joint damage (Levinson JE, Wallace CA, J Rheumatol 1992; 19:6). Although new medications-especially methotrexate-appear to have improved the prognosis of children with polyarticular JRA, a uniformly safe and effective therapy is elusive. Interferon B is an ideal agent to test as a novel therapy for polyarticular JRA. Large scale use in patients of all ages with autoimmune disease has documented its safety, and it inhibits many of the processes thought to be central to the pathogenesis of joint inflammation in JRA (Cirell R, Tyring SK. Major therapeutic use of interferons. Clin Immunother 1995; 3:27-87). Subjects will receive each of two dosages by intramuscular injection once weekly of interferon B for 12 weeks each in a cross-over fashion. The order in which each patient receives each dose will be randomized, and both patient and physician will be blinded to the dose being administered. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: BEHAVIORAL TREATMENTS FOR RHEUMATOID ARTHRITIS Principal Investigator & Institution: Nicassio, Perry M. None; University of California Los Angeles 10920 Wilshire Blvd., Suite 1200 Los Angeles, Ca 90024 Timing: Fiscal Year 2003; Project Start 1-AUG-2003; Project End 1-JUL-2008 Summary: (provided by applicant): Behavioral interventions for rheumatoid arthritis (IRA) have had a salutary impact on patients' ability to manage difficult symptoms and other demands of this medical condition. Yet, the effects of behavioral treatments for RA
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on underlying disease activity and mood disturbance are largely undetermined. The proposed project compares cognitive-behavioral therapy (CBT), Tai Chi Chih (TCC), a form of movement-based meditation, and education control (EC) on measures of psychological adaptation (e.g., helplessness, coping), mood disturbance, sleep quality, pro-inflammatory cytokines, and RA disease severity. An important feature of the CBT intervention is that it incorporates strategies to enhance mood and diminish depressive symptoms. TCC has recently shown promise as an effective intervention in increasing physical activity and health functioning in older adults. Because of its emphasis on relaxation and exercise, TCC offers an interesting theoretical contrast to CBT. Two Ph.D. level psychologists will administer the CBT and EC interventions, while a highly experienced TCC instructor will administer the TCC protocol. A total of 210 IRA patients will be randomly assigned after a pre-treatment evaluation to one of the three interventions and will be assessed again at Week 8 of treatment, at post-treatment (Weeks 16-17), 8-month follow-up, and 1-year follow-up. A primary objective of the study will be to compare the clinical efficacy of CBT and TCC against EC. CBT and TCC are expected to contribute to significantly greater improvement in psychosocial functioning and IRA disease severity than EC. CBT, in turn, is hypothesized to lead to greater improvement than TCC on clinical endpoints because it teaches a variety of skills that patients can use to manage RA. This study will also explore the mechanisms through which CBT and TCC promote improvement in IRA disease severity. We anticipate, for example, that improvement in RA disease severity resulting from CBT and TCC will be mediated by reductions in pro-inflammatory cytokines (IL-1, TNF, IL6). Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: BIOMECHANICAL FACTORS IN RHEUMATOID ARTHRITIS Principal Investigator & Institution: Guilak, Farshid; Associate Professor; Surgery; Duke University Durham, Nc 27706 Timing: Fiscal Year 2003; Project Start 0-JUN-2003; Project End 1-MAR-2006 Summary: (provided by applicant): Rheumatoid arthritis is a chronic arthropathy characterized by inflammation, proliferation and destruction of the articular cartilage. Although historically cartilage has been considered to be an "innocent bystander" of the disease, recent evidence suggests that the degradation of cartilage in arthritis involves an imbalance of the anabolic and catabolic activities of the articular chondrocytes, secondary to synovitis and joint inflammation. Chondrocyte metabolic activity is strongly influenced by soluble mediators (e.g., cytokines) and biophysical factors (e.g., mechanical stress). In particular, biomechanical factors may play an important role in the onset and progression of degenerative arthritis secondary to joint inflammation in rheumatoid arthritis. However, the sequence of biomechanical and biochemical processes regulating these events in vivo is still unclear. The primary hypothesis of this study is that, in rheumatoid arthritis, a loss of cartilage biomechanical function and the presence of inflammatory cytokines alters the metabolic response of chondrocytes to mechanical stress. Aim 1 of this project is to measure the mechanical properties of the cartilage extracellular and pericellular matrices in RA, and to incorporate this data in a theoretical model of the micromechanical environment of the cell. In Aim 2, we will determine the role of stress magnitude in the stimulation of nitric oxide and prostaglandin E2 production by chondrocytes, and determine the influence of these inflammatory mediators on matrix turnover. In Aim 3, we will determine whether mechanical stress has an additive or antagonistic effect on with certain inflammatory cytokines (interleukin 1, tumor necrosis factor alpha, and interleukin 17) in controlling
42 Arthritis
the PGE2 synthesis and matrix metabolism. Currently, there is little information on the biomechanical changes in articular cartilage with RA. Understanding the biomechanical and molecular mechanisms of chondrocyte response to physiologic loading in an inflammatory environment may enable new therapies that are specific to the stage of the disease. As many pharmacologic therapies for RA are focusing on the NOS2 and COX2 pathways, investigation of the interaction of physical therapies with these pathways will hopefully lead to more safe and effective treatments for RA. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: ARTHRITIS
CLINICALLY
IMPORTANT
CHANGES
IN
RHEUMATOID
Principal Investigator & Institution: Ward, Michael M. Associate Professor; Medicine; Stanford University Stanford, Ca 94305 Timing: Fiscal Year 2001; Project Start 0-SEP-1999; Project End 1-AUG-2002 Summary: Proper interpretation of the results of controlled clinical trials requires an assessment of not only the statistical significance of treatment differences but also of the clinical importance of such differences. Efforts to define criteria for important improvement in rheumatoid arthritis (RA) have thus far not considered the patient's perspective, even though patients' values represent the normative standard on which improvements should be judged. The specific aims of this project are to determine if group criteria for important improvement in arthritis activity measures can be defined by assessing the agreement among patients of judgments of important changes in arthritis activity, and to determine if preference measures are useful measures of the importance of clinical changes. Because the importance of changes can be meaningfully judged only for measures that are sensitive to change, the sensitivity to change of arthritis activity measures will also be assessed. This observational case series study will measure changes in 12 arthritis activity measures, changes in patient preference measures, and judgments of the importance of changes in arthritis activity over one to four months in 240 patients with active RA. Consensus among patients regarding the magnitude of change in each measure considered important would allow group criteria for important improvement to be defined that were based on patients' valuations. Lack of consensus among patients, and therefore inability to define meaningful group criteria for important improvement, may indicate that clinical trials should include endpoints that more directly reflect patients' valuations of health, such as preference measures. This study will therefore also examine the reliability, construct validity, and sensitivity to change of patient preference measures, and will determine if preference measures better reflect changes judged to be important than do changes in traditional arthritis activity measures. This study will allow investigators to plan studies with knowledge of clinically important differences in arthritis activity measures, and will help clinicians and patients to understand better the relative benefits of different treatments. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: ARTHRITIS
COPING
SKILLS
TRAINING
FOR
EARLY
RHEUMATOID
Principal Investigator & Institution: Keefe, Francis J. Professor and Associate Director; Psychiatry; Duke University Durham, Nc 27706 Timing: Fiscal Year 2002; Project Start 7-SEP-2002; Project End 1-AUG-2006 Summary: (provided by applicant): Rheumatoid arthritis (RA) is the most common inflammatory polyarthritis and a major health problem. Although medical interventions
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are being used much earlier in the course of RA, these interventions do not address the challenges of coping with the early stages of this disease. To date, only one, very recent study has evaluated the efficacy of coping skills training (CST) during the early course of RA. Although its findings suggest CST may be helpful, the study had methodological limitations (e.g. lack of control for attention, relatively short-term follow-up). It also used a traditional CST intervention that did not specifically address the unique challenges posed by the early course of RA. The proposed study seeks to determine whether a comprehensive coping skills training intervention can improve pain, psychological disability, and physical disability in patients with early RA. 225 patients with early RA will be assigned to 1 of 3 conditions: 1) Comprehensive Coping Skills Training, 2) Arthritis Education, or 3) Standard Care. Patients in the comprehensive coping skills training condition will receive training in a variety of cognitive and behavioral coping strategies and training in specific techniques for improving communication, setting short- and long-term goals, and enhancing maintenance. Patients in the arthritis education condition will attend sessions providing them with detailed information on rheumatoid arthritis and its treatment. Patients in the standard care condition will continue to receive the standard medical care provided to RA patients. Measures of pain, physical disability, and psychological disability and traditional clinical outcome measures will be collected pre- and post- treatment and at 6, 12, and 18 months follow-up. A self-efficacy scale and daily measures of coping, life events, mood, and pain will be gathered at each evaluation in order to analyze how these variables relate to long-term outcome. If comprehensive CST is effective, it could lead to new research and a greater integration of CST methods into the medical management of early RA. Future studies could examine whether comprehensive CST alters the long-term disease course of persons with RA. Finally, future studies could examine whether comprehensive CST alters the immune responses of RA patients to daily stressors. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: DEFECTS IN ACTIVATION-INDUCED T CELL DEATH IN ARTHRITIS Principal Investigator & Institution: Zhang, Jian;; Rush-Presbyterian-St Lukes Medical Ctr Chicago, Il 60612 Timing: Fiscal Year 2001; Project Start 1-MAR-2001; Project End 9-FEB-2004 Summary: (Taken from the application): Activation-induced cell death (AICD)in T cells is the major mechanism for peripheral tolerance. Repeated stimulation of T cells via their antigen receptor (TCR) induces co-expression of Fas and Fas ligand (FasL) on the surface of T cells and the Fas-FasL interaction leads to the "suicide" or "fratricide" of T cells. Plate-bound (surface-immobilized) anti-TCR antibody (e.g., anti-CD3 antibody) can mimic (auto)antigen-mediated T cell activation and AICD, and is a useful tool to study intracellular signaling mechanisms in T cells in vitro. Proteoglycan-induced arthritis is a novel autoimmune murine model induced by systemic immunization of BALB/c mice with cartilage proteoglycans. The development of the disease is based upon cross-reactive immune responses between the immunizing human and mouse (self) cartilage proteoglycans in genetically susceptible BALB/c mice. In this autoimmune arthritis model, an aberrant proliferation of peripheral CD4+ T cells was found in vitro in response to TCR stimulation. The hyper-proliferation of CD4+ T cells was associated with low levels of AICD and an unexpectedly high ratio of IFN-y, to IL-4 in arthritic mice. These observations together suggest that Th1 cells from arthritic mice may be resistant to AICD. The overall hypothesis of this proposal is that a defect(s) in
44 Arthritis
the Fas-mediated signaling pathway lead to a deficiency in peripheral deletion of autoreactive Th1 type cells. As a result, autoreactlve Th1 cells accumulate in the periphery, leading to the breakdown of self-tolerance, and provoking inflammation in synovial joints by an antigen-driven mechanism. In this proposal, we will investigate whether and how defects in the intracellular regulators (FLIP, Bcl-2, and cell cycle modulators) of Fas-mediated signaling pathway results in impaired AICD of CD4+ T cells in proteoglycan-induced arthritis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: DEVELOPMENT OF A BOTANICAL ANTI-ARTHRITIS DRUG, PMI001 Principal Investigator & Institution: Fridlender, Bertold;; Phytomedics, Inc. 65 Stults Rd Dayton, Nj 08810 Timing: Fiscal Year 2002; Project Start 0-SEP-2002; Project End 1-MAR-2003 Summary: (provided by applicant): An extract of the roots of Tripterygium wilfordii, a plant with a long history of medicinal use in China, demonstrated great promise as a potential prescription botanical drug for rheumatoid arthritis. In-vitro, in-vivo and human clinical studies performed in the U.S.A. and in China indicate that the extract of Tripierygium roots (PMI-001) is effective against arthritis and other autoimmune disorders. PMI-001 contains triptolide and other related molecules that inhibit IL-2 release and COX-2 transcription, a dual mechanism that is unique among current arthritis treatments. The main difficulty to PMI-001 development as a successful botanical drug has been obtaining a supply of roots that are consistent in quantity, quality and efficacy. The proposed work will establish large-scale greenhouse based hydroponic cultivation of Tripterygium in order to optimize PMI-001 safety and efficacy and assure its continuous and cost-effective supply. This will be accomplished through determining optimum conditions for plant propagation, cultivation, harvesting and extraction. In addition, analytical methods and efficacy bioassays will be developed and validated, establishing the framework for the future QAIQC methods and GMP procedures necessary for the FDA approval of this novel, safe and efficacious product. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: DEVELOPMENT OF CASPASE INHBITORS FOR ARTHRITIS Principal Investigator & Institution: Flanagan, W Michael.; Sunesis Pharmaceuticals, Inc. 341 Oyster Point Blvd South San Francisco, Ca 94080 Timing: Fiscal Year 2003; Project Start 1-SEP-2003; Project End 1-AUG-2005 Summary: (provided by applicant): The long-term objective of this proposal is to apply a unique and powerful "extended tethering" technology to discover novel therapeutics for the treatment: of arthritis. Small molecule caspase-1 inhibitors represent a new class of arthritis therapeutics with the advantages of oral availability and decreased toxicity. Covalent tethering, a technology developed at Sunesis Pharmaceuticals involves a "screen-then-link" process that allows a greater survey of chemical diversity space than is achievable using the large compound libraries typically screened by pharmaceutical firms. A variation of this approach, known as extended tethering identified a high potency cell-active caspase-1 inhibitor during Phase I. Extended tethering is particularly powerful for enzyme targets such as caspase-l that contain an active site cysteine residue and for which active site binding determinants are well characterized. Moreover, extended tethering provides not only an efficient means of ligand discovery but also a direct path to lead optimization since the target protein is used as a template for the
Studies 45
construction of its: own inhibitor. Our Phase II proposal capitalizes on the promising caspase-1 inhibitor identified by extended tethering in Phase I and proposes to carry it forward through lead optimization and to pre-clinical development. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: DISABLEMENT PROCESS IN RHEUMATOID ARTHRITIS Principal Investigator & Institution: Escalante, Agustin; Associate Professor; Medicine; University of Texas Hlth Sci Ctr San Ant 7703 Floyd Curl Dr San Antonio, Tx 78229 Timing: Fiscal Year 2001; Project Start 1-AUG-1999; Project End 1-MAY-2004 Summary: (adapted from investigator's abstract): The broad objective of this research is to understand disability in rheumatoid arthritis (RA) within the theoretical framework of The Disablement Process Model. This model postulates a main disease-disability pathway in which pathology causes impairments, which lead to functional limitations, which, in turn, cause disability. Risk factors that precede and interventions or exacerbation's that follow the onset of the process of disablement, modify the main pathway. The specific aims of this application are: (1) To define the temporal sequence of events in the development of disability due to RA attributable to altered articular structure; (2) To define the temporal sequence of events leading to disability in RA attributable to pain; (3) To define the temporal sequence of events leading to disability in RA attributable to symptoms of depression; (4) To evaluate the modifying effect of medical interventions and co-morbidity. The models and hypotheses of this application are based on cross-sectional analyses on a cohort of 455 persons with RA participating in Dr. Escalante's current ORALE Study (Outcome of Rheumatoid Arthritis Longitudinal Evaluation). The ORALE cohort will be augmented to 760 members by the end of the first year of this application. Four yearly follow-ups are planned after the initial baseline assessment, to be conducted during the first through fourth years of this 5-year application. Main pathway factors that will be assessed include the inflammatory response, serum rheumatoid factor, bone destruction and extra-articular signs and symptoms, corresponding to pathology; articular signs and symptoms, strength, ambulation and manual dexterity, corresponding to impairments; activities of daily living, under functional limitations; and physical disability. Risk factors are age, gender and ethnicity, the HLA-DRB1 genotype, education, occupation, income, functional health literacy and acculturation. Psychosocial modifiers include and social support, learned helplessness, self-efficacy, coping strategies, stress, symptoms of depression, and coexistent medical conditions. Interventions to be measured include anti-rheumatic drugs and joint surgery, the lag between disease onset and initiation of anti-rheumatic therapy, compliance, and rehabilitation interventions. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: EXERCISE ADHERENCE AND OUTCOMES AMONG PERSONS WITH OSTEOARTHRITIS Principal Investigator & Institution: Hughes, Susan L. Professor; University of Illinois at Chicago Suite 304 Aob, M/C 672 Chicago, Il 60612 Timing: Fiscal Year 2001 Summary: CDC data indicate that 7% of the US population aged 55-64 experience limitation in activity due to arthritis, increasing to 19% for persons over age 84. When these data are projected to the year 2020, the number of persons with arthritis is estimated to increase by 57% and activity limitation by 66% (U.S., DHHS, 1994). Current data indicate that lower- extremity joint impairment is a serious risk factor for future
46 Arthritis
disability. Previous exercise interventions have demonstrated short-term efficacy in improved interim performance measures (e.g., 6-minute distance walk) among older persons with lower-extremity osteoarthritis (OA). However, the long- term impact of a multiple component prevention intervention that blends exercise with education aimed at enhancing self-efficacy on maintenance of functional status is unknown. Using stages of behavioral change theory and social/cognitive learning theory, we hypothesize that a multiple component intervention that addresses lower-extremity muscle strength, fitness walking, and exercise and arthritis self-efficacy will delay disability onset. To test this hypothesis, we will convert a current NIAMS-funded randomized study of shortterm efficacy (8 weeks) of a multiple component intervention to a longitudinal trial. The longitudinal trial will obtain adherence measures quality over 24 months on 146 treatments and 146 control group participants. Adherence is defined as 2 hours per week of self-reported exercise activity. To reinforce adherence, we will invite graduates of the short-term intervention to participate in an on-going once weekly facility-based walking program. The facility-based program will be supplemented with individualized regiments and supplies need for ongoing home-based adherence. We will use GEE to assess whether the treatment group maintains a significantly higher level of adherence over 24 months than controls, will test a multivariate model that predicts adherence, and will examine the impact of self-efficacy on sustained improvement in interim performance and adherence, and the impact of sustained improvement in interim performance on functional status outcomes over time. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: HEART DISEASE IN RHEUMATOID ARTHRITIS Principal Investigator & Institution: Gabriel, Sherine E. Professor; Mayo Clinic Rochester 200 1St St Sw Rochester, Mn 55905 Timing: Fiscal Year 2001; Project Start 1-SEP-2000; Project End 1-AUG-2005 Summary: (Applicant's Abstract) The hypotheses to be tested in this proposal are built on findings from two intriguing, but rather disparate lines of investigation. The first is the recent data suggesting that the excess mortality experienced by people with rheumatoid arthritis (RA) may result from increased rates of coronary heart disease (CHD) among RA patients compared to the general population. The second is the rapidly growing body of evidence indicating that chronic systemic inflammation (such as that which occurs in RA) plays an important role of chronic inflammation in CHD. We propose 3 specific aims to investigate this subject: First, we will use a cohort study to test the hypothesis that the incidence of acute MI (the central manifestation of CHD) is higher in RA subjects compared to controls. Second, we will identify high-risk RA subgroups and, using a novel adaptation of the case-cohort design, investigate interactions between RA and the major CHD risk factors (e.g. smoking, hyperlipidemia, exogenous estrogens). Third, we will conduct studies on archived autopsy heart tissue to test the hypothesis that coronary atherosclerosis is more extensive in RA subjects compared to matched controls. A unique set of circumstances allows us to address each of these aims rigorously and efficiently. We will incorporate and extend our already assembled population-based RA incidence cohort and identify validated definite acute MI outcomes using the cardiovascular surveillance techniques developed through out NIH-funded companion study, "Coronary Disease Morbidity and Mortality in a Population" (HL59205). Our population-based data resources, with essentially complete enumeration of a geographically defined population, allowed us to design an analytic plan which nearly quadruples the statistical power of our risk factor analyses, compared with typical cohort analyses. Third, the availability of extensive autopsy material (the
Studies 47
autopsy rate in this community is four-fold higher than the national rate and all autopsies have been performed at the same center since 1930) provides us with a unique opportunity to assess the pathologic characteristics of atherosclerosis among RA subjects compared to controls. When combined with our experienced multidisciplinary investigative team, these resources lend us a capability, not available elsewhere, to rigorously examine the risks and determinants of coronary heart disease in patients with RA. These results will lay the foundation for a program of research aimed at elucidating the mechanisms for CHD in RA patients and at improving our understanding of the role of inflammation in the pathogenesis of CHD in the general population. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: IMPROVING VOCATIONAL OUTCOMES IN ARTHRITIS Principal Investigator & Institution: Maisiak, Richard S. Professor; University of Alabama at Birmingham Uab Station Birmingham, Al 35294 Timing: Fiscal Year 2001 Summary: The long-term objectives of the proposed research project are to (1) enhance program participation and (2) improve the vocational outcome of persons with work disability due to arthritis and related musculoskeletal disorders (ARMD), who are actively seeking vocational rehabilitation services. It is hypothesized that persons with work disability due to ARMD seeking vocational rehabilitation (VR) services, who are exposed to an "Agency Access Intervention", are more likely to gain entrance to the VR system and be determined eligible for services than are similar persons not exposed to the intervention. Further, it is hypothesized that persons with work disability due to ARMD who are determined to be eligible for VR services, and, who are exposed to an "Agency Enhancement Intervention" during the provision of services are more likely to become and remain employed, upon completion of the VR program, than are similar persons not exposed to the intervention. The research design is a randomized, controlled, field experiment comparing the vocational outcomes of the group receiving the two-part intervention to those not receiving the intervention, and it allows evaluation of each component of the intervention separately. The intervention consists of training sessions to help prospective VR clients with ARMD successfully enter and complete the VR program, and training sessions for a randomly selected group of VR professionals to help them serve VR clients with ARMD more effectively. If this intervention strategy proves capable of significantly increasing (a) VR utilization rates, (b) post-service employment rates, and (c) duration of post-service employment in a previously underserved group with historically poor VR outcomes, it could have significant role in reducing the immense impact, nationally, of work disability due to arthritis and musculoskeletal disorders. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: INFLUENCE OF SEX AND HLA ON RHEUMATOID ARTHRITIS Principal Investigator & Institution: Moxley, George F. Associate Professor; Internal Medicine; Virginia Commonwealth University Richmond, Va 232980568 Timing: Fiscal Year 2001; Project Start 7-SEP-1999; Project End 0-JUN-2004 Summary: This application is to support a Midcareer Investigator Award allowing continued patient-oriented investigation into the genetic basis of rheumatoid arthritis (RA). The immediate goal is to examine how sex and HLA interact in RA heredity, while the long-term goal is to describe RA disease mechanisms in such detail that effective prevention or therapy will be possible. This award will provide career development
48 Arthritis
support to protect time for this patient-oriented clinical research, develop new research skills, and do mentoring of junior investigators. The applicant will continue studies of sex influence on HLA penetrance in rheumatoid arthritis. The current studies have shown that RA is independently associated with several disease susceptibility loci in the HLA region, not just DRB1 variants but also independently with tumor necrosis factor (TNFalpha) variants. The future studies will define the functional correlates of TNF variants by identifying unrelated persons with common HLA genotypes and then examining inducible TNF production and MHC class II density in peripheral blood cells. Such results will be used to develop multivariate models to determine whether these explain sex differences in HLA penetrance. A second ongoing project, in cooperation with investigators at Case Western Reserve University, is to identify RA families suitable for genetic studies. A third project is proposed for this application. RA families will be studied to determine whether there is segregation distortion of RAassociated HLA haplotypes, that is, whether a child (either affected or not) is more likely than expected to inherit a RA-associated HLA haplotype from a mother with the HLA haplotype or a father with the HLA haplotype. Such parent-of-origin effects might represent genomic imprinting. Dr. Moxley has already demonstrated mentoring success, guiding junior investigators through design, performance, problem- solving, analysis, and publication. Virginia Commonwealth University has a rich patient population and strong programs to educate investigators in clinical research and biostatistics. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: INORGANIC PYROPHOSPHATE METABOLISM IN ARTHRITIS Principal Investigator & Institution: Ryan, Lawrence M. Professor; Medicine; Medical College of Wisconsin Po Box26509 Milwaukee, Wi 532264801 Timing: Fiscal Year 2002; Project Start 1-MAY-1987; Project End 1-MAR-2007 Summary: (provided by applicant): Calcium pyrophosphate dihydrate (CPPD) crystal deposition disease is a common form of arthritis, particularly in the elderly. Prevalence approaches 50 percent in those over 80. CPPD crystals cause acute attacks of gout-like arthritis, but more importantly are associated with debilitating degenerative arthritis. In vitro and in vivo data strongly suggest that these crystals cause or amplify cartilage degeneration. This proposal focuses on the source of inorganic pyrophosphate (PPi), the anion constituent of CPPD crystals. Disordered PPi metabolism is clearly implicated in CPPD crystal deposition. Specific emphasis will be placed on mechanisms underlying PPi generation in extracellular cartilage matrix where crystals form. The effector arm of extracellular PPi (ePPi) generation involves the ectoenzyme nucleoside triphosphate pyrophosphohydrolase (NTPPPH), which generates ePPi from extracellular nucleoside triphosphates such as ATP. NTPPPH activity is highly expressed in articular cartilage. The availability of extracellular ATP substrate for NTPPPH is rate-limiting for generation of ePPi and the most likely cellular source of that ATP is the chondrocyte. These studies are designed to determine the effects of factors that modulate ePPi formation upon the release of ATP from chondrocytes. Specific emphasis is placed on growth factors (transforming growth factor-beta and insulin-like growth factor-I), on chondrocyte donor age, on transduction pathways (protein kinase C and cAMP-related), and on purine receptors (P1and P2). All of the aforementioned influence ePPi elaboration by chondrocytes. The second goal of this proposal is to determine the mechanisms of ATP egress from chondrocytes. Specific focus will be on ATP binding cassette proteins (analogues of human ABC1 and p-glycoprotein expressed in chondrocytes), a gap junction protein (connexin 43), and ANK protein as possible
Studies 49
transporters. The intent of these studies is to develop insights into the pathogenesis of CPPD deposition disease so that therapeutic options may be generated. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: INTERACTIVE EDUCATION FOR SELF-MANAGEMENT OF ARTHRITIS Principal Investigator & Institution: Brink, Susan G. Principal; Healthmark Multimedia, Llc 1201 Connecticut Ave Nw, #250 Washington, Dc 20036 Timing: Fiscal Year 2002; Project Start 1-JUL-2002; Project End 0-JUN-2003 Summary: (provided by applicant): Arthritis affects over 40 million people in the U.S. The most prevalent form of arthritis is osteoarthritis (OA) affecting over 20 million people, mostly adults over the age of 45. As a chronic condition of adults, the prevalence of OA will surely increase as the population ages. Studies of arthritis education programs indicate that patient involvement in a self-management program can lead to decreases in pain, depression and disability and increases in self-efficacy. HealthMark Multimedia proposes to develop a prototype education and self-management program for people with arthritis using an interactive web site format. If feasible, this approach will increase the educational options available to those with OA. The web site will use Stages of Change concepts from the Transtheoretical Model to help those with OA identify needed behavior changes and strategies and to make and maintain those changes. Social Learning Theory will inform the multimedia approach to behavior change within each stage. In Phase II the web site will be expanded to address multiple issues in self-management of OA. Print materials will be written to provide information to health care providers on how they can help their patients with OA make use of the web site. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: INTRARTICULAR SLPI THERAPY FOR RHEUMATOID ARTHRITIS Principal Investigator & Institution: Labhasetwar, Vinod D. Associate Professor; Pharmaceutical Sciences; University of Nebraska Medical Center Omaha, Ne 681987835 Timing: Fiscal Year 2001; Project Start 8-SEP-2001; Project End 1-JUL-2003 Summary: (provided by applicant): Rheumatoid arthritis (RA) is a chronic inflammatory disease, characterized by the loss of joint structure and function, resulting in significant pain and morbidity. In this proposal, we plan to investigate a new therapeutic strategy for the treatment of RA. In normal joints, the cartilage matrix turnover is maintained due to a balance between the activities of proteases and protease inhibitors. This balance is lost in arthritic joints, resulting in a greater protease activity, leading to cartilage and bone degeneration. Secretory leukocyte protease inhibitor (SLPI) has been identified as an endogenous potent protease inhibitor that maintains the critical balance against the proteases in the joint. Since SLPI is not produced by the joint tissue and the arthritic joints loose their ability to sequester SLP1 from the blood, it is hypothesized that intra articular administration of SLPI in a sustained release formulation would be effective in reinstating the balance between the proteases and protease inhibitors, and in inhibiting the progression of the disease. SLPI is also considered to be involved in protecting the cartilage growth factor (Link N) in the joint from protease-mediated degradation. The link N promotes the synthesis of proteoglycan and collagen, which are required for maintaining normal cartilage composition in the joint. Therefore, localized SLPI therapy could also lead to regeneration of the cartilage matrix and restoration of joint functions. Therefore, the objective of the proposed studies is to determine the efficacy of sustained
50 Arthritis
intra articular delivery of SLPI using an injectable thermo reversible (TR) gel system in RA. The specific aims of the research program are: (1) To formulate a sustained release TR gel system for SLP1 using biodegradable and biocompatible Polyethylene oxide-Poly (L-Lactide)-Polyethylene oxide copolymer, and to evaluate the gel for sustained protein release properties, (2) To investigate the kinetics of intra articularly injected SLPI-gel system to provide localized and sustained delivery of the protein, and to determine the therapeutic efficacy of the gel to inhibit the progression of the disease in a rat streptococcal. cell wall-induced model of inflammatory erosive arthritis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: JUVENILE RHEUMATOID ARTHRITIS: MRI ANALYSIS Principal Investigator & Institution: Dardzinski, Bernard;; Children's Hospital Med Ctr (Cincinnati) 3333 Burnet Ave Cincinnati, Oh 45229 Timing: Fiscal Year 2001; Project Start 1-SEP-2001; Project End 0-JUN-2006 Summary: Juvenile rheumatoid arthritis (JRA) is the most common chronic inflammatory arthritis of childhood. The end result of ongoing synovial inflammation is degradation of articular cartilage. Whether the control of synovitis halts further cartilage degradation is not known. Irreversible thinning and erosion of cartilage leads to significant morbidity and loss of function. Magnetic resonance imaging (MRI) is proven to be a useful modality for depicting articular cartilage and synovium in both children and adults with inflammatory arthritis. Quantitative T2 mapping of articular cartilage in adults has shown that increased T2 relaxation time is an early marker of cartilage injury. This application will test the hypothesis that increased T2 relaxation time in articular cartilage of the knee in children with JRA reflects early cartilage injury. This quantitative method might possibly detect potentially reversible articular cartilage changes prior to irreversible cartilage erosions detected by conventional MRI. The longitudinal relationship between serial short-term changes in articular cartilage T2 relaxation time, degree of synovial inflammation, and clinical evaluation of disease activity will be determined. Articular cartilage T2 relaxation time in children with limited disease duration undergoing therapy will be quantified and monitored for reversibility. Serum and synovial fluid biomarkers will be measured and compared with alterations in articular cartilage T2 relaxation time. We will determine whether changes in T2 relaxation time profiles are predictive of articular cartilage erosions in children with JRA, and quantify and monitor reversibility of articular cartilage T2 relaxation time changes in children with longer disease duration. The long-term goal of this research is to provide a noninvasive, quantitative measure of early and potentially reversible degeneration in articular cartilage of children. These studies may extend the utility of MRI to quantitatively validate clinical outcomes in rheumatic diseases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: LEUKOCYTE MICROARRAYS IN JUVENILE RHEUMATOID ARTHRITIS Principal Investigator & Institution: Jarvis, James N. Associate Professor; Pediatrics; University of Oklahoma Hlth Sciences Ctr Health Sciences Center Oklahoma City, Ok 73126 Timing: Fiscal Year 2002; Project Start 3-SEP-2002; Project End 1-MAY-2004 Summary: (provided by applicant): Juvenile rheumatoid arthritis (JRA) is a family of illnesses characterized by chronic inflammation and hyperplasia of the synovial linings of joints. Its causes are unknown, and responses to treatment are often poor and
Studies 51
associated with significant morbidity. Current theories of JRA pathogenesis have focused entirely on the role of T cells and adaptive immunity, failing to account for welldescribed abnormalities that implicate innate immunity in the disease process. We postulate that JRA pathogenesis involves complex interactions between innate and adaptive immunity. Traditional scientific approaches that focus narrowly and in depth on specific aspects of inflammation or immunity cannot grasp the complex pathogenesis at a single glance. DNA microarrays offer an ideal method for investigating these molecular interactions. Our preliminary experiments using DNA microarrays examined gene expression in peripheral blood buffy coat preparations from three children with polyarticular-onset JRA (poly-JRA). Our preliminary results indicate that the number of differentially expressed genes (compared to healthy age-matched controls) is 25-50 from an array of 2,400 genes. We now propose to continue to use buffy coat leukocyte preparations as the first step in identifying genes differentially expressed in additional children with active poly-JRA (Year 1). Once strong candidate genes have been identified, we will verify their expression and identify cellular localization in a single step using purified cell fractions (monocytes, granulocytes, and lymphocytes) and reverse transcriptase polymerase chain reaction (Year 2). We expect these pilot studies will provide the foundation for novel insights into the intersecting roles on innate and adaptive immunity in polyarticular JRA. Furthermore, these studies are likely to provide the basis for the elucidation of important prognostic markers and targets of novel therapies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: LEUKOTRIENE B4 RECEPTORS IN RHEUMATOID ARTHRITIS Principal Investigator & Institution: Bodduluri, Haribabu; Pathology and Lab Medicine; University of Louisville University of Louisville Louisville, Ky 40292 Timing: Fiscal Year 2003; Project Start 1-MAR-2003; Project End 8-FEB-2007 Summary: (provided by applicant): Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory disease. Neutrophils are found in large numbers in rheumatoid synovium and have been suggested to be involved in clinical signs of inflammation and pain associated with RA. Neutrophil activation during host defense and inflammation is mediated by G-protein coupled receptors (GPCRs) for chemoattractants. Leukotriene B4 (LTB4), a potent chemoattractant for neutrophils activates its receptor (BLT-1) to mediate diverse physiological effects in neutrophils. A second LTB4 receptor (BLT-2) with distinct antagonist specificity and tissue distribution was recently described. GPCRs are regulated by receptor phosphorylation leading to desensitization as well as down regulation. We will test the hypothesis that LTB4 acting through the high affinity receptor BLT-1 mediates its effects on neutrophils in RA, while LTB4 acting through BLT-2 modulates T-lymphocyte activation and function in RA. The goal of the current studies is to develop comprehensive in vivo and in vitro models to determine the role of LTB4 and the relative contributions of BLT-1 and BLT-2 in the development of murine RA. In specific aim 1 we will define the role of BLT-1 in the development and progression of collagen induced arthritis in the BLT-1 deficient mice we have already generated by targeted gene disruption. In specific aim 2 we will use the well-established RBL-2H3 cell model to determine the differences in signaling, desensitization, internalization and antagonist specificity of BLT-1 and BLT-2. These studies take advantage of the novel video microscopy and live cell imaging methods we have recently developed. Leukotrienes are involved in the pathophysiology of many acute and chronic inflammatory diseases such as systemic anaphylaxis, atherosclerosis, RA and asthma. Understanding the precise function of distinct LTB4 receptors in mice
52 Arthritis
deficient in specific receptors and defining the role of these receptors in RA will identify novel targets for therapeutic intervention of RA. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: LIFESTYLE INTERVENTIONS IN SENIORS WITH ARTHRITIS Principal Investigator & Institution: Eittinger, Walter H.; Wake Forest University 2240 Reynolda Rd Winston-Salem, Nc 27106 Timing: Fiscal Year 2001 Summary: The Lifestyles Intervention for Seniors with Arthritis (LISA) Trial is a singleblind, controlled clinical trial to test the efficacy of weight loss on disability and disease progression in older people with knee osteoarthritis. Three hundred obese, sedentary people, age sixty and older, with symptomatic knee osteoarthritis will be randomized to receive: usual care, a structured aerobic exercise intervention, a dietary weight loss intervention or a combined exercise-weight loss intervention. Participants in the study will be followed for thirty months. The primary outcome measure is physical disability. Secondary outcome measures include performance measures of function, exercise capacity, health-related quality of life, biomechanics of gait, knee pain and disease progression by x-ray. The cost effectiveness of the interventions will be determined. This study will determine the relative efficacies of exercise, weight loss and combined intervention in the management of osteoarthritis of the knee in older people. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: NATURAL VITAMIN E IN CONTROLLING SYMPTOMS OF RHEUMATOID ARTHRITIS Principal Investigator & Institution: Roubenoff, Ronenn;; New England Medical Center Hospitals 750 Washington St Boston, Ma 021111533 Timing: Fiscal Year 2001 Summary: We will study the efficacy and safety of supplemental vitamin E therapy in patients with Rheumatoid Arthritis (RA). Since most patients in the United States are treated with at least one and as many as four medications, it is not realistic to study vitamin E therapy in the absence of other medications. Moreover, it is not likely that vitamin E would be used as the sole drug treatment in many Rheumatoid Arthritis patients even with its demonstrated benefit. Thus, the most important clinical trial should be designed to examine the potential use of vitamin E as an alternative/adjunct to NSAID in the typical multi-modality treatment of RA. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: NEUROGENIC CONTRIBUTIONS TO CHRONIC ARTHRITIS Principal Investigator & Institution: Westlund-High, Karin N. Professor; University of Texas Medical Br Galveston 301 University Blvd Galveston, Tx 77555 Timing: Fiscal Year 2001; Project Start 1-FEB-1974; Project End 1-JUL-2006 Summary: Our exciting experimental data generated from the last several years indicate the novel role that glutamate receptors mediated neurogenic events play as a key factor in inflammatory nociceptive processes. Glutamate receptor antagonists given the spinal cord dorsal horn eliminate half of the joint swelling induced in rat inflammation models. Our recent finding that knee injections of glutamate receptor agonists increase joint blood flow, plasma/protein extravasation, joint swelling, and nerve activation intimates peripheral glutamate involvement. This may account for glutamate increases in
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inflamed joints in animal models and in clinic patients with active arthritis. In clinical samples, glutamate is high in joints with active arthritis and is independent of levels in the patients other joints or in the plasma. Preliminary data presented inflammatory cascades through stimulation of tumor necrosis factor (TNF-alpha) release since glutamate added to synovial cell cultures increases TNF-alpha levels detected in the culture supernatant. Together these findings led to the hypothesis for the studies proposed that glutamate receptor mediated events play a critical role in persistent nociceptive responses and initiation of inflammatory cascades. Specific Aim 1 is to determine the types of glutamate receptors in the knee joint involved in the changes in nociceptive and inflammatory parameters. Specific Aim 2 is to establish that it is the small sensory nerves innervating the knee joint that contain and contribute to the release of glutamate in the joint. Specific Aim 3 will establish that glutamate contributes to the release of the inflammatory mediator, TNF-alpha, using clonal human synovial cell cultures. Specific Aim 4 is to determine whether the glutamate receptor promoted TNFalpha release from synovial cell cultures. Specific Aim 4 is mediated by activation of glutamate- mediated NFkappaB signal transduction pathways. These studies will eventually seek mechanisms that may lead to translational approaches to abrogation of the inflammatory state through pharmacological interventions directed at glutamate receptor-mediated signal transduction pathways. These studies will utilize anatomical, behavioral, electrophysiological, biochemical, and molecular methods to examine models in some cases after stroke, these studies seek a better understanding of the interactions of neurogenic and immune processes in the hope that reversal of joint inflammation for patients is possible. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: NEUTROPHIL PHENOTYPING IN PERIODIC AND CHRONIC ARTHRITIS Principal Investigator & Institution: Centola, Michael B. Adjunct Associate Professor; Oklahoma Medical Research Foundation Oklahoma City, Ok 73104 Timing: Fiscal Year 2001 Summary: Intra-articular migration and activation of neutrophils may play a principal role in the joint erosion of inflammatory arthritis. DNA microarrays provide a means to profile gene expression in neutrophils from inflamed joints of patients with arthritis. Gene profiling may identify neutrophil regulators of intra-articular inflammation, and define key similarities and differences among inflammatory arthridities. The arthritis in patients with familial Mediterranean fever (FMF) is caused by mutations in MEFV, a gene encoding an inflammatory regulator that is specifically expressed in myeloid cells. FMF arthritis is unusual in that most inflammatory cells are neutrophils, and episodes of arthritis are transient. It therefore represents a unique human model to uncouple the initiation phase of synovitis from the chronic phase. Three specific aims are proposed: First, we will use immunohistochemistry and ELISAs to define the nature of intraarticular leukocyte infiltrates and cytokine profiles in FMF arthritis. These data will be compared with known profiles in other forms of arthritis. Second, we will perform microarray analysis from collected RNA samples of neutrophils form the active joints and peripheral blood of patients with period (FMF), chronic (rheumatoid and psoriatic), reactive, and infectious arthritis and from peripheral blood neutrophils of controls. Differentially expressed genes will be analyzed, with particular attention to identifying regulators of inflammation and defining subphenotypes within a specific disease. Third, we will test the functions of specific neutrophil gene products in modulating leukocyte adhesion and signaling. The MEFV gene performed to determine whether pyrin, will be
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expressed in myeloid cell lines, and microarray analysis of RNA from the cells will be differentially expressed known or novel gene products in FMF or other forms of arthritis will be tested in assays of leukocyte adhesion, transendothelial migration, chemotaxis, and other functions. These studies will define mediators of intra-articular neutrophil migration and activation, and may provide insights into the mechanisms that regulate leukocyte recruitment in other forms of inflammation. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: ARTHRITIS
PATHOGENESIS
OF
BONE
EROSION
IN
RHEUMATOID
Principal Investigator & Institution: Gravallese, Ellen M.; Beth Israel Deaconess Medical Center E/Es-214 Boston, Ma 02215 Timing: Fiscal Year 2003; Project Start 1-JAN-2003; Project End 1-DEC-2007 Summary: (provided by applicant): Rheumatoid arthritis (RA) is a chronic inflammatory disease that often produces severe destruction of articular cartilage and bone. Considerable evidence indicates that bone erosions in RA are produced by osteoclasts (OCs). An essential factor for the differentiation and activation of osteoclasts is receptoractivator of NF-KB ligand (RANKL), which mediates its effects via a specific cell surface receptor, receptor-activator of NF-kB (RANK). Recently, a novel secreted form of RANKL (secRANKL) has been identified which appears to be regulated by a unique promoter. The studies outlined in this proposal are designed to test the hypothesis that that there is enhanced local expression of RANKL at sites of bone erosion in RA and that regulation of RANKL expression in cells at sites of bone erosion is a critical determinant of focal bone loss. Specific Aim 1 will test the hypothesis that RANKL production by cells derived from RA synovium is critical in the pathogenesis of osteoclastic bone erosion. This Aim will address the following questions: What are the exact cellular sources of RANKL at sites of bone erosion in RA? Where is RANKL expressed in relation to OPG expression and to RANK positive OC precursors? Retrieved human tissues will be utilized initially to answer these questions. Cellular expression profiles will be confirmed and the temporal expression of these factors will be determined in two murine models of inflammatory arthritis: collagen-induced arthritis (CIA), and the KJBxN model. Dispersed cells from RA synovium will be used to determine the expression of RANKL isoforms in relevant cell types. Finally, the activity of the secRANKL isoform in osteoclastogenesis will be determined in an in vitro co-culture model of osteoclastogenesis. Specific Aim 2 will test the hypothesis that T cell-derived RANKL is required for bone erosion in RA. Arthritis will be generated in mice in which T cells provide the only source of RANKL, and in genetically engineered mouse strains lacking T cells, in order to definitively determine the role of T cell-derived RANKL in bone erosion. Specific Aim 3 will identify regulatory elements responsible for the constitutive and inducible expression of the membrane-bound RANKL isoform in cell types present in RA, and will test the hypothesis that the NFAT family of transcription factors is critical in the inducible regulation of the memRANKL gene. RT-PCR analysis of RANKL expressing cell-types present in focal RA bone erosions demonstrates differential constitutive and inducible expression of the two known RANKL isoforms. Preliminary data also demonstrate a potential role of NFATs in RANKL regulation in T cells. This Aim will provide data on the regulation of RANKL gene expression in cell types present in bone erosion in RA and may lead to new therapeutic strategies for preventing bone destruction in this disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PERIODONTAL DISEASE AND RHEUMATOID ARTHRITIS Principal Investigator & Institution: Mccracken, Michael S. Prosthodontics; University of Alabama at Birmingham Uab Station Birmingham, Al 35294 Timing: Fiscal Year 2002; Project Start 1-JUL-2002; Project End 0-JUN-2007 Summary: (provided by applicant) Candidate: Michael McCracken, DDS, PhD, is motivated and committed to an academic career involving clinical research. He has demonstrated his ability to complete projects and work independently in the past, and shows the qualtities necessary to become a productive researcher with the education and training provided by this grant. Mentors: Larry Moreland, MD, has as long track record of mentoring clinical researchers. He is the PI of the NIH-funded K30 program at UAB and is the Director of the Pittman General Clinical Research Center. Dr. Marjorie Jeffcoat has also mentored many young investigators, and is Chair of Periodontics at the UAB School of Dentistry and PI on the Oral Health Research Training Grant. Dr. Moreland and Dr. Jeffcoat have collaborated successfully on several previous projects, and are committed to the research outlined in this proposal. Dr. George Howard is the Chair of the Department of Biostatistics in the School of Public Health. He will work with the candidate with the didactic training portion of the training and with statistical support of the research. Dr. Graciela alarcon has a long history in outcomes research in musculoskeletal diseases. Environment: The UAB Medical Center provides depth and diversity of clinical research endeavors as well as the state-of-the-art physical resources that are necessary to support this K23 application. UAB is situated on more than 70 square blocks in the city of Birmingham. With over 16,000 faculty, staff and employees, an annual budget for l999-2000 of over $1.15 billion dollars, and extramural funding exceeding $286 million dollars in 1998-1999, UAB provides a solid environment for this training program. Research: The proposal for this training opportunity is to investigate the severity of periodontal disease in patients with rheumatoid arthritis. The hypothesis is that patients with inflammatory rheumatoid arthritis are more susceptible to inflammation of the periodontal tissues. Furthermore, it is hypothesized that among patients with rheumatoid arthritis, an association exists between the rate of progression of inflammatory arthritis and the progression of periodontal disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ARTHRITIS
PHARMACOGENETICS
OF METHOTREXATE
THERAPY IN
Principal Investigator & Institution: Whitehead, Alexander S. Professor; Pharmacology; University of Pennsylvania 3451 Walnut Street Philadelphia, Pa 19104 Timing: Fiscal Year 2002; Project Start 5-SEP-2002; Project End 1-AUG-2007 Summary: (provided by applicant): Inflammatory diseases, including arthritis, are often associated with reduced life expectancy, due in part to an excess of cardiovascular disease deaths. Low dose methotrexate (MTX) therapy is a mainstay for the long-term management of arthritis. Arthritis patients with cardiovascular disease who are treated with MTX have higher cardiovascular mortality rates than their peers treated with alternative disease-modifying anti-rheumatoid drugs (DMARDs). In addition, there is considerable inter-individual variation in the clinical efficacy of MTX, and about 30% of patents experience unacceptable toxicity. Objective methods to identify those for whom MTX therapy will be effective and minimally toxic, without greatly enhancing cardiovascular disease risk, would therefore contribute significantly to the clinical management of arthritis and other inflammatory conditions. MTX inhibits dihydrofolate reductase, an enzyme involved in purine synthesis and a component of the broader
56 Arthritis
folate/Hcy metabolic axis. Methylenetetrahydrofolate reductase (MTHFR) is pivotal in controlling the distribution of folate derivatives between the two main constituent pathways that serve cellular methylation reactions and nucleic acid synthesis. In addition, methionine synthase (MTR), cystathionine Beta-synthase (CBS), and methionine synthase reductase (MTRR) are involved in reactions that control Hcy concentrations. Functional polymorphisms of MTHFR, MTR, CBS and MTRR significantly modify intracellular levels of folate derivatives and/or circulating Hcy levels, thereby increasing the risk of Hcy-associated pathologies. These polymorphisms, alone or in combination, may "prime" the folate/Hcy metabolic axis to respond to MTX by adopting an extreme pathogenic phenotype, and may also be significant determinants of the efficacy and toxicity associated with the drug. We will access the above in a pharmacogenetic analysis of 300 arthritis patients who are about to embark on MTX therapy. Pre-treatment and in-treatment folate derivative, B vitamin and Hcy concentrations will be determined together with MTHFR, MTR, CBS, and MTRR genotypes to establish whether there are particular phenotypic and/or genotypic variables that can be used to predict MTX efficacy and toxicity, and the likelihood of MTX-mediated enhancement of Hcy-associated disease risk. This research may establish the genetic parameters that mandate the treatment of arthritic patients with either MTX or an alternative DMARD. It has the potential to facilitate individualized treatment protocols that are less empirical and therefore more effective, and to reduce the incidence of cardiovascular co-morbidity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: PHYSICAL THERAPY, AN ANTIFLAMMATORY SIGNAL ON ARTHRITIS Principal Investigator & Institution: Agarwal, Sudha; Associate Professor; Dental Medicine; University of Pittsburgh at Pittsburgh 350 Thackeray Hall Pittsburgh, Pa 15260 Timing: Fiscal Year 2001; Project Start 9-SEP-2001; Project End 0-JUN-2004 Summary: (provided by applicant): Osteoarthritis and rheumatoid arthritis are diseases of complex etiopathology associated with progressive inflammation and cartilage destruction. Rehabilitative physical therapies such as continuous passive motion (CPM)/exercise yield beneficial effects on arthritic joints as well as on post-surgical arthritic joints by an as-yet-unknown mechanism, but one that is likely to involve mechanical activation of cells. Since inflammatory cytokines like IL-1B play a major role in cartilage destruction, it is the hypothesis that mechanical strain exerts antiinflammatory effects on arthritic joints by blocking proinflammatory signals and subsequent gene induction induced by IL-1. This is based on the facts that, in vitro, chondrocytes respond to cyclic tensile strain (CTS) by suppression of IL-1-dependent proteins that are responsible for cartilage degradation. CTS simultaneously induces gene exression of proteins inhibited by IL- 1B, that are reparative in nature. These effects of CTS are mediated via inhibition of IL-1B-induced nuclear factor (NF)-kB translocation to the nucleus, as well as the synthesis of its subunit. CTS exerts these effects at concentrations of IL-1B similar to those present in inflamed synovial joints, suggesting the clinical relevance of actions of mechanical strain. In this proposal the PIs wish to confirm in vitro findings using an in vivo model system of antigen induced arthrits (AIA) and an apparatus that subjects arthritic joints to CPM. Long term goals are to understand the molecular mechanisms of stress-induced anti-inflammatory responses that limit the degeneration in joint diseases and constitute the basis for rehabilitative physical therapies like CPM. Specifically, the PIs will (i) determine if CPM therapy
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exerts its beneficial effects on the arthritic joints by regulating the synthesis of catabolic proteins or their inhibitors. (ii) determine if CPM therapy exerts its beneficial effects on arthritic joints via induction of matrix-associated proteins. (iii) determine if the intracellular mechanisms of CPM in vivo are mediated via inhibition of nuclear factor (NF)-kB subunits p65 and p50 synthesis in the tissues of knee joints from CPM treated and untreated rabbits with AIA. This understanding of the signalling pathways that mediate the beneficial effects of mechanical strain is necessary for defining the biological basis for the efficacy of CPM/exercise, for the development of defined parameters for safe application of physical therapies to accelerate cartilage repair as well as for the use of CPM in novel non-invasive rehabilitative therapies for not only cartilage repatr but also for other diseases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: PULSE THERAPY IN SYSTEMIC JUVENILE RHEUMATOID ARTHRITIS Principal Investigator & Institution: Lovell, Daniel J. Professor; Children's Hospital Med Ctr (Cincinnati) 3333 Burnet Ave Cincinnati, Oh 45229 Timing: Fiscal Year 2000; Project Start 0-SEP-1998; Project End 1-OCT-2003 Summary: (adapted from applicant's abstract): Systemic juvenile rheumatoid arthritis (sJRA) is associated with significant long term morbidity and mortality. Current therapies including methotrexate are considered ameliorative rather than remission inducing or curative. There have been anecdotal reports suggesting that pulse therapy with intravenous corticosteroids, cyclophosphamide, and methotrexate may induce prolonged remissions in sJRA. Therefore, the objectives of this study are to determine and compare the ability of two pulse therapy regimens to induce remission in sJRA of less than 12 months duration during a 9-month, open-label, randomized, actively controlled clinical trial. The first pulse therapy regimen is composed of intravenous methylprednisalone 30 mg per kg per day (1 gram max) for three consecutive days, intravenous cyclophosphamide 0.4 grams per meter2 BSA on the third day, and up to 20 mg per meter2 per week of methotrexate. The second pulse therapy regimen is identical to the first, except no cyclophosphamide is given. Up to five cycles of these regimens may be given over a 9-month period. Patients in both groups may also receive background medications including a non-steroidal, anti-inflammatory drug and up to 0.5 mg/kg/d of oral prednizone. The primary outcome to measure the effect of this therapy will be the proportion of patients who achieve clinical remission according to the ACR criteria for remission in rheumatoid arthritis. Secondary outcome measures of effectiveness include proportion of patients who demonstrate clinical response according to the preliminary definition of improvement for JRA. In addition, time per remission and the duration of remission will be compared between the two groups among patients who do remit. Specific Aim 2 is to determine and compare the short and intermediate term (18 months) safety profiles of the pulse therapy regimens as defined in Specific Aim 1. Long term goals of the project are to determine and compare the longer-term safety profiles of this treatment regimen. This will involve analysis of patient/parent-derived data obtained by mail or phone follow-up to detect significant medical problems and reproductive or neoplastic complications. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: RELAXATION RESPONSE,SOMATIC STYLE & RHEUMATOID ARTHRITIS Principal Investigator & Institution: Barsky, Arthur J. Professor; Brigham and Women's Hospital 75 Francis Street Boston, Ma 02115 Timing: Fiscal Year 2001; Project Start 5-JUL-2001; Project End 0-JUN-2006 Summary: This is a three-armed randomized, controlled intervention trial to determine the effect of relaxation response training (RR) and of relaxation training combined with cognitive/behavioral therapy (RRCBT) on the symptoms, functional ability, role impairment, and medical care utilization of patients with rheumatoid arthritis (RA). We will also examine the role of selected attitudes and beliefs expected to moderate the treatment response and predict outcome. These same attitudes and beliefs are also hypothesized to predict the incidence of medication side-effects and to be associated with the inter- individual variability in RA symptoms seen among patients with RA of comparable severity and extent. Three-hundred and seventy- five RA patients will undergo a baseline assessment of the independent variables (including hypochondriacal health anxiety, bodily amplification, normative beliefs about health, and alexithymia) and covariates (including RA severity, life stress, social support, and psychological distress). They will then be randomly assigned to RR, RRCBT, or an attention control group. The outcome variables (RA symptoms, functional ability, role impairment, and medical care utilization) will be measured immediately after treatment, and 6 and 12 (the primary outcome) months later. The effect of treatment will be determined by comparing each intervention group to the control group, and by within-subject comparisons before and after treatment. Additional group analyses will be conducted to determine the influence of cognitive and attitudinal variables on outcome. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: RHEUMATOID ARTHRITIS: PREDICTORS OF THERAPEUTIC RESPONSE Principal Investigator & Institution: O'dell, James R. Professor and Chief of Rheumatology; Internal Medicine; University of Nebraska Medical Center Omaha, Ne 681987835 Timing: Fiscal Year 2001; Project Start 0-SEP-2000; Project End 1-AUG-2003 Summary: (investigator's abstract): Rheumatoid arthritis (RA) is a common, chronic disease that causes substantial morbidity and mortality while utilizing a large portion of health care resources. While recent therapeutic approaches have provided significant improvement in patients' functional status and well being, the selection of specific therapy remains empiric and highly variable. The ability to use surrogate markers to predict which patient is likely to respond to certain anti-rheumatic therapy would offer major advantages in the management of this chronic and progressive disease. Recent evidence has suggested a clear role for proinflammatory cytokines, membrane metalloproteinases, and genetic factors in influencing the severity and progressive nature of the disease. Thus, it is reasonable to suggest that the status of these factors may allow the characterization of patients into 'responder' versus 'non-responder' groups. The intent of this proposal is to utilize material from carefully controlled clinical trials where patient groups have been identified as either responding or not responding to specific therapies. This material will be evaluated for various cytokine, MMP, and genetic factors that may predict response to therapy. The hypothesis is that determining specific patient cytokine profiles, membrane metalloproteinase levels, and/or genetic phenotypes may predict the 'responder/non-responder' status of patients with specific
Studies 59
therapy intervention. This hypothesis will be tested by three specific aims which are: Specific Aim #1 - correlate the response of patients with RA to specific therapies with changes in cytokine, matrix metalloproteinases and/or acute phase protein levels. Specific Aim #2 - correlate the response of patients with RA to specific therapies with HLA-DRB1 subtyping and non-MHC gene polymorphism. Specific Aim #3 - develop strategies for initiating prospective clinical trails using predictive cytokine, matrix metalloproteinase, and genetic factors. The unique strength of this proposal is the patient serum and DNA sample bank that is available from several controlled, randomized, blinded, clinical protocols that clearly define patients as responder or nonresponder. Retrospective analysis of this information can be utilized to plan prospective clinical trials using potentially predictive patterns of cytokine, matrix metalloproteinases, and genetic factors. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: ROLE OF CYTOKINES IN RHEUMATOID ARTHRITIS Principal Investigator & Institution: Tsark, Eleanor C.; City of Hope National Medical Center Duarte, Ca 91010 Timing: Fiscal Year 2001; Project Start 1-SEP-2001 Summary: Rheumatoid arthritis (RA) is an autoimmune disease characterized by infiltration of T cells and antigen presenting cells (APC) from the blood into the synovial joint. Activation of both cell types results in destruction of tissue within the joint. This tissue destruction leads to an abundance of self proteins available for uptake by phagocytic APC. Presentation of self peptide:MHC complexes by APC is believed to lead to activation and expansion of autoreactive T cells. The most convincing evidence implicating a role for antigen presentation in RA is the observation that inheritance of certain subtypes of the HLA-DR4 allele predisposes people to developing RA. The nature of the self peptides being presented by these DR4 subtypes is currently not known, but studies performed in animal models have provided some candidate autoantigens. The following studies are proposed: Aim 1: Determine the array of epitopes derived from candidate autoantigens expressed by normal peripheral blood APC and determine how cytokines modulate presentation of these epitopes; Aim 2: Determine the array of epitopes derived from candidate autoantigens expressed by APC obtained from RA patients and determine how cytokines modulate presentation of these epitopes; Aim 3: Determine if mature dendritic cells obtained from rheumatoid synovia display enhanced ability to process and present soluble autoantigens due to the presence of inflammatory cytokines. T cell hybridomas which recognize peptides derived from human type II collagen HCgp39 and calreticulin in the context of DR4 have been generated by immunizing human DR4 transgenic mice with these candidate autoantigens. These T cell hybridomas can then be used to study presentation of these epitopes by APC from human DR4 donors with and without rheumatoid arthritis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: SOCIAL DETERMINANTS OF ARTHRITIS OUTCOMES Principal Investigator & Institution: Callahan, Leigh A.; University of North Carolina Chapel Hill Office of Sponsored Research Chapel Hill, Nc 27599 Timing: Fiscal Year 2003; Project Start 1-JAN-2003; Project End 1-DEC-2007 Summary: The strong association throughout the developed world between lower levels of individual socioeconomic status (SES) and poorer health outcomes from many diseases including arthritis is well established. Although not yet well studied in
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arthritis, recent data suggest that community social determinants, e.g., the socioeconomic environment of an individual's neighborhood, may be operant in this regard, as well. It is of considerable interest that the association of community social determinants with health outcomes appears to be independent of an individual's SES, at least in some clinical situations. Both Healthy People 2010 and the National Arthritis Action Plan place high priority on reducing disparities in health outcomes in this country. Development of effective prevention strategies will require a) precise recognition of individual and community variables that are associated with health outcomes and b) evaluation of the putative mediating mechanisms. The long-term goal of the proposed project is to better understand why people of lower SES have poorer arthritis outcomes. The immediate objective of this project is to define the individual and community social characteristics that contribute to arthritis outcomes using a community-based cohort of individuals derived from a family practice network. This objective will be accomplished through the following specific aims: (1) to test for a significant independent relationship between community level SES and prevalence of arthritis; (2) to test for a significant independent relationship between community level SES and health related quality of life in persons with arthritis; and (3) to test hypothesized "individual-in-context" mediators of the relationship between community level SES and arthritis health outcomes. This project could establish whether there are independent significant contextual effects of communities on the prevalence, severity and progression of arthritis. If these associations are found, potential mediators can be explored to establish the bridge between the observation of associations and implementing and designing prevention strategies. The results of these analyses will guide health policies and the focus of prevention strategies, i.e., at the community and/or individual level. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: STRESS AND ADAPTATION TO RHEUMATOID ARTHRITIS Principal Investigator & Institution: Zautra, Alex J. Professor and Program Director; Psychology; Arizona State University P.O. Box 873503 Tempe, Az 852873503 Timing: Fiscal Year 2001; Project Start 0-APR-1994; Project End 1-MAY-2005 Summary: Description (adapted from investigator's abstract): This research is designed to determine the extent to which variations in cognitive behavior therapy reduce disease activity and improve the mental health of older adults with rheumatoid arthritis (RA). The study combines field assessments, laboratory tests of stress reactivity and clinical evaluations of the mental and physical health of subjects in a longitudinal design. After pre-testing, 210 RA patients will be randomly selected in one of three treatments: Cognitive-Behavior Therapy for Pain (CBT-P), Cognitive-Behavior Therapy for Depression (CBT-D) or Education Group only (EG), which serves as a control. The distinction between pain and depression as foci of CBT in RA is supported by previously funded research by the investigator on interpersonal stress and disease activity in persons with arthritis. Illness severity, depressive symptoms and interpersonal difficulties are expected to predict psychological and physiologic stress responses in participants. Stress reactivity measures are expected to predict the course of illness over time. Those receiving CBT-D are expected to show the greatest improvement in physical functioning, mental health and disease activity. Successful treatment is expected to alter stress responses, leading to better physical and mental health over time. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: STUDY ADMINISTERING MYCOPHENOLATE MOFETIL FOR ACTIVE RHEUMATOID ARTHRITIS Principal Investigator & Institution: Merkel, Peter A.; Boston University Medical Campus 715 Albany St, 560 Boston, Ma 02118 Timing: Fiscal Year 2001 Summary: This study is an extension of the double-blind, randomized, parallel group, multicenter comparison of the efficacy and safety of Mycophenolate Mofetil and placebo in patients with active Rheumatoid Arthritis. The design is an open label trial of MMF therapy in RA patients for a minimum of 6 months and will have a duration of approximately 1 year, evaluating the long-term safety profile. Five patients are anticipated to participate in this extension study. Patients who are eligible to be included in this study are those who have completed the 6 month blinded treatment protocol and continuing abstinence of contradictions or exclusion factors relating to safety as defined in the protocol of the blinded study. Concurrent Glucocorticoids (<=10mg/d Prednisolone or equivalent) &/or NSAID use will be allowed if the patient has been treated with them through out the blinded study. Patients will begin the study at the last visit of the blinded study & MMF will be dispensed. They will return 2 weeks and 4 weeks later and then for once a month visits for the following two months. Later visits will take place every 6 weeks. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: SYNOVIAL CADHERIN IN RHEUMATOID ARTHRITIS Principal Investigator & Institution: Brenner, Michael B. Professor; Brigham and Women's Hospital 75 Francis Street Boston, Ma 02115 Timing: Fiscal Year 2002; Project Start 1-JUL-2002; Project End 0-JUN-2007 Summary: (provided by applicant) Cadherins are integral membrane adhesion proteins that mediate homophilic adhesion (bind to cadherins of the same type) on cells within a tissue. During development they mediate the sorting of cells into tissues and in adults the integrity and architecture of tissues. Cadherin expression and signaling are also known to participate in regulating cell proliferation, migration and invasion. For example, loss of E-cadherin (E-cad) expression that mediates integrity of the epithelium, is associated with epithelial cell progression to malignancy, invasion and metastases. Normal synovium is a tissue of a few cells thick composed of Type A, monocyte-like synoviocytes (MLS) and Type B, fibroblast-like synoviocytes (FLS). Yet the synovial lining is neither a true epithelium nor endothelium as it lacks a basement membrane. We hypothesize that a distinct cadherin might be expressed on synoviocytes and play a role in making the synovium a tissue. We identified cadherin-11 (cad-11) expressed by the type B FLS, but not by fibroblasts in skin, gut, or various other tissues. Here we show preliminary data that cad-11 influences the proliferation, adhesion and cytoskeletal organization of FLS. Thus, we propose to define the role of cad-11 in influencing the proliferation of FLS cultured in the presence of cad-11 expressing cells or plate-bound cad-11 fusion proteins coated on plastic wells. Effects on the major signaling pathways affecting FLS activation, proliferation, apoptosis, migration and invasion will be determined, since these features bear relevance to the abnormal proliferation and invasion characteristics of synovial cells in the rheumatoid pannus. We have previously described that lymphocytes bind E-cadherin via the alphaEbeta7 leukocyte integrin (a heterophilic interaction). Here, we propose to identify the lymphocyte receptor that mediates adhesion to cad-11, as it may play an important role in lymphocyte adhesion and localization in the inflamed synovium. Finally, we have
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confirmed expression of cad-11 in a mouse model of synovitis and will administer anticad-11 mAb and cad-11-Fc to assess the potential value of cad-11 as a therapeutic target in inflammatory synovitis. Together, these studies are likely to yield new insights into the biology of synoviocytes and identify a new biotherapeutic target (the synovial cadherin) having potential relevance to rheumatoid arthritis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: THREE DOSES RHEUMATOID ARTHRITIS
OF
MELOXICAM
W/
DICLOFENAC
FOR
Principal Investigator & Institution: Dooley, Mary A.; University of North Carolina Chapel Hill Office of Sponsored Research Chapel Hill, Nc 27599 Timing: Fiscal Year 2001 Summary: This abstract is not available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: TOLEROGENIC STEM CELL TRANSPLANTATION FOR ARTHRITIS Principal Investigator & Institution: Messner, Ronald P. Professor; Medicine; University of Minnesota Twin Cities 200 Oak Street Se Minneapolis, Mn 554552070 Timing: Fiscal Year 2001; Project Start 0-SEP-1999; Project End 0-JUN-2003 Summary: Immunoablation followed by autologous stem cell transplantation holds the promise of providing a cure for some types of severe autoimmune disease. The goal of this proposal is to examine the therapeutic potential of autologous stem cell transplantation by studying the effects of a pseudoautologous bone marrow transplant (PA-BMT) on fully-developed collagen-induced arthritis (CIA) in mice. We postulate that stem cell transplantation will provide a window of opportunity in which treatments that were formerly effective only when given before the onset of disease will now be therapeutic in mice with established disease. We will thus exploit the process of reconstitution of the immune system to reestablish the tolerance that was broken when autoimmunity was induced. The key to this process will be the use of specific treatments to render the reemerging immune system tolerant to the antigen(s) driving the autoimmune process. CIA, a well- characterized model of inflammatory polyarthritis, was chosen because it is partially responsive to immune ablation and rescue with either allogeneic or syngeneic bone marrow cells. It thus provides a model in which the proposed treatments can be judged by their ability to improve or worsen the results of transplantation alone. Preliminary experiments indicate that induction of tolerance to type II collagen in naive mice is significantly enhanced by the prior use of PA-BMT. Initial experiments will determine the optimum protocol for a PA-BMT as judged by the level of CIA activity that persists after the transplant. Subsequent experiments will evaluate the potential of post-transplant immunotherapy to eliminate the residual CIA activity that persists after transplant. The special case of antigen-specific therapy will be examined first. Protocols using collagen, which are capable of inducing tolerance if given before but not after arthritis, will be tested to determine if they regain effectiveness when used in the immediate post transplant period. The second set of experiments will explore the concept of non-CII specific immunotherapy with the aim of shifting the balance to favor tolerance rather than active response to autoantigens during rematuration of the immune system. The response of arthritis to the treatments will be correlated with studies of the level of immunologic reconstitution as well as in vivo and in vitro T and B cell responses to CII. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: TREATMENT OF ARTHRITIS WITH INTERLEUKINS Principal Investigator & Institution: Lauermann, Vit;; Rubicon Laboratory, Inc. 7904 Springway Rd Baltimore, Md 21204 Timing: Fiscal Year 2003; Project Start 1-MAY-2003; Project End 0-APR-2004 Summary: (provided by applicant): The overall goal of this project is to develop a therapeutic method for targeted delivery of IL-4 to arthritic joints. Rheumatoid arthritis is an autoimmune disease characterized by progressive cartilage and bone erosion. Cytokines are important modulators of immune responses and IL-4 is an attractive cytokine for treating arthritis. Local administration of IL-4 has therapeutic effects in patients with moderate arthritis. However, the therapeutic efficacy of the cytokine is limited due to its toxicity. To improve the cytokine therapeutic effect, its concentration in a disease site has to be increased without causing undesirable side effects. The proposed method suppresses the biological activity of the administered cytokine until it reaches proximity of a target cell. The cytokine is then rendered active and concentrates in a disease site. The cytokine concentration in arthritic joints can reach levels that have desired therapeutic effects without systemic toxicity. This targeted delivery approach can be adapted for other cytokines and diseases and can be used as adjuvant to other treatments or stand alone. In Phase I we will develop the biological reagents and test them in vitro. We will use these reagents in Phase II in preclinical studies evaluating treatment of arthritis in animals. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: TREATMENT OF EARLY AGGRESSIVE RHEUMATOID ARTHRITIS TEAR Principal Investigator & Institution: Moreland, Larry W. Professor of Medicine and Associate Dean; Medicine; University of Alabama at Birmingham Uab Station Birmingham, Al 35294 Timing: Fiscal Year 2001; Project Start 7-SEP-2001; Project End 6-SEP-2003 Summary: (provided by applicant): Combinations of biologic agents and traditional disease modifying antirheumatic drugs (DMARDs) are being increasingly used in early RA. The effectiveness and side effects of different regimens, however, are unlikely to be compared in clinical trials performed by pharmaceutical companies. The proposed multicenter trial, Treatment of Early Aggressive Rheumatoid Arthritis (TEAR), represents the first pre-planned 5-year trial of biologic/DMARD combinations in early RA. Thus, the TEAR trial might provide information of value to RA patients, rheurnatologists and the Food & Drug Administration. The proposed trial is a 3-arm study comparing 2 different combinations (anti-TNF plus methotrexate versus methotrexate plus hydroxychloroquine plus sulfasalazine) versus monotherapy (methotrexate) in patients with early RA who have an "aggressive" clinical phenotype defined by presence of erosions on hand or feet radiographs, or positive serum rheumatoid factor, plus active synovitis of multiple joints. A steering committee of clinical researchers involved with RA trials has been formed to design the TEAR trial. The clinical trials planning grant is needed for the following specific aims: (1) to conduct meetings and conference calls of steering committee to write the grant for funding of the TEAR trial; (2) to develop study materials including data collection instruments, design and preparation for the quality control procedures, informed consent prototype, manual of operations and procedures (MOPP); (3) to secure definite commitments for participation from pharmaceutical companies and clinical research sites; (4) to design appropriate pharmacogenetic studies that potentially would identify patients who have
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a significant positive clinical response in this trial; and (6) to perform preliminary analysis of existing data to refine the outcomes to be used in this clinical trial. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: ARTHRITIS
WHY IS
CARDIAC
RISK
INCREASED IN RHEUMATIOD
Principal Investigator & Institution: Solomon, Daniel H.; Brigham and Women's Hospital 75 Francis Street Boston, Ma 02115 Timing: Fiscal Year 2002; Project Start 6-SEP-2002; Project End 1-AUG-2004 Summary: (provided by applicant): While rheumatoid arthritis is primarily considered a condition affecting the joints and impairing function, past data suggest that cardiac disease represents the number one cause of mortality in rheumatoid arthritis. However, the adjusted rates of cardiovascular death and myocardial infarction in rheumatoid arthritis are poorly characterized. Additionally, whether the increased cardiovascular risk is because of the medications used for rheumatoid arthritis or the underlying disease severity is unknown. The proposed research has two major aims: 1) to quantify the rates of cardiovascular death and myocardial infarction in patients with rheumatoid arthritis after controlling for known cardiovascular risk factors and 2) to determine the contribution of rheumatoid arthritis medication exposure and disease severity to cardiovascular disease rates. Prior work on this issue has largely been conducted in referral populations and attempts to control for known cardiovascular risk factors have been poor. We propose to study this issue in a large Medicare/Medicaid database that we have extensive experience working with. This database contains information on over 2 million patients followed for 10 years and includes diagnoses and procedures for all physician and inpatient visits. As well, prescription data from a large pharmacy benefits program has been integrated into this database allowing for a complete characterization of an individual patients medication exposure. While any one diagnosis of rheumatoid arthritis may not be accurate in such a database, the project entails a validation substudy to develop an algorithm for selecting patients with a high probability of having rheumatoid arthritis. The proposed project will be an important advance in this area because of the large number of patients with rheumatoid arthritis to be included (over 5,000), the community-based nature of their care, the ability to control for known cardiovascular risk factors, the extensive medication information allowing for us to explore key hypotheses regarding corticosteroid exposure, and the attempt to simultaneously control for disease severity Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: WORK DISABILITY-- PERSONS WITH RHEUMATOID ARTHRITIS Principal Investigator & Institution: Allaire, Saralynn;; Boston University Medical Campus 715 Albany St, 560 Boston, Ma 02118 Timing: Fiscal Year 2001; Project Start 4-SEP-2001; Project End 1-AUG-2006 Summary: Work disability is a major burden of rheumatoid arthritis (RA). The most cited study of RA work disability was conducted 15 years ago. Since then, remarkable changes in the macro-economy, in the nature of work, in governmental income support programs, and in the treatment of the disease have occurred. As these are likely to have affected RA work disability, new and more sensitive data are clearly needed. The study's primary aim is to assess work disability among employed persons with RA using a prospective study design. The secondary aims are to assess RA work disability in two increasingly important subgroups, retirement aged persons and minorities, and
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to assess current risk factors for RA work disability. Risk factors of particular interest are work characteristics that reflect the changing nature of work and consistent use of disease modifying anti-rheumatic drugs. We will study two measures of work disability, work cessation and limitation in ability to work. Subjects will be drawn from patients with RA participating in the National Data Bank for Rheumatic Diseases, a large, national cohort of arthritis patients. 4615 employed subjects with RA aged 18 through 67 will form the full sample; subsets of subjects will be used for some specific aims. Additional patients will be recruited into the NDB cohort to ensure that newly diagnosed patients are included. Subjects will be assessed at the beginning of the project and yearly thereafter for three years for both work disability and factors affecting it. Work cessation is any work stoppage age 65. Limitation in ability to work will be measured using the Work Limitations Questionnaire (WLQ). Incidence of work cessation will be estimated using the Kaplan-Meier method. Trends over time in the WLQ will be examined using random effects regression models. The same methods will be used to examine work disability among retirement-aged subjects. ANCOVA and Cox regression will be used to examine differences in work disability between minorities and Whites. Cox regression, mixed-effects and 1ogistic regression analyses will assess the strength of risk factors. Because of large sample sizes, power estimates indicate results can be determined with fine precision. The information gained will be used for resource allocation, for determining which groups of persons with RA have special needs, and for designing targeted interventions to help persons with RA maintain employment. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
E-Journals: PubMed Central3 PubMed Central (PMC) is a digital archive of life sciences journal literature developed and managed by the National Center for Biotechnology Information (NCBI) at the U.S. National Library of Medicine (NLM).4 Access to this growing archive of e-journals is free and unrestricted.5 To search, go to http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Pmc, and type “arthritis” (or synonyms) into the search box. This search gives you access to fulltext articles. The following is a sample of items found for arthritis in the PubMed Central database: ·
A follow-up to "Anti-cytokine therapy in chronic destructive arthritis" by Wim B van den Berg. by Brennan FM. 2001; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=128897
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A multinational randomized, controlled, clinical trial of etoricoxib in the treatment of rheumatoid arthritis [ISRCTN25142273]. by Collantes E, Curtis SP, Lee KW, Casas N, McCarthy T, Melian A, Zhao PL, Rodgers DB, McCormick CL, Lee M, Lines CR, Gertz BJ. 2002; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=115849
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A new model for rheumatoid arthritis? by McDevitt H. 2000; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=129990
Adapted from the National Library of Medicine: http://www.pubmedcentral.nih.gov/about/intro.html. With PubMed Central, NCBI is taking the lead in preservation and maintenance of open access to electronic literature, just as NLM has done for decades with printed biomedical literature. PubMed Central aims to become a world-class library of the digital age. 5 The value of PubMed Central, in addition to its role as an archive, lies in the availability of data from diverse sources stored in a common format in a single repository. Many journals already have online publishing operations, and there is a growing tendency to publish material online only, to the exclusion of print. 3 4
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A novel mechanism for the regulation of IFN-[gamma] inducible protein-10 expression in rheumatoid arthritis. by Hanaoka R, Kasama T, Muramatsu M, Yajima N, Shiozawa F, Miwa Y, Negishi M, Ide H, Miyaoka H, Uchida H, Adachi M. 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=165028
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A possible cause of joint destruction in septic arthritis. by Krieg AM. 1999; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=128861
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A revival of the B cell paradigm for rheumatoid arthritis pathogenesis? by Benoist C, Mathis D. 2000; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=129991
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Ablation of interleukin-12 exacerbates Lyme arthritis in SCID mice.. by Anguita J, Samanta S, Barthold SW, Fikrig E. 1997 Oct; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=175621
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Activation of Natural Killer Cells in Arthritis-Susceptible but Not Arthritis-Resistant Mouse Strains following Borrelia burgdorferi Infection. by Brown CR, Reiner SL. 1998 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=108650
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Activation of synovial fibroblasts in rheumatoid arthritis: lack of expression of the tumour suppressor PTEN at sites of invasive growth and destruction. by Pap T, Franz JK, Hummel KM, Jeisy E, Gay R, Gay S. 2000; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=17804
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Acute-phase serum amyloid A production by rheumatoid arthritis synovial tissue. by O'Hara R, Murphy EP, Whitehead AS, FitzGerald O, Bresnihan B. 2000; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=17807
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Administration of Interleukin 12 in Combination with Type II Collagen Induces Severe Arthritis in DBA/1 Mice. by Germann T, Szeliga J, Hess H, Storkel S, Podlaski FJ, Gately MK, Schmitt E, Rude E. 1995 May 23; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=41799
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Alpha-Toxin and Gamma-Toxin Jointly Promote Staphylococcus aureus Virulence in Murine Septic Arthritis. by Nilsson IM, Hartford O, Foster T, Tarkowski A. 1999 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=96427
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Analysis of a Viridans Group Strain Reveals a Case of Bacteremia Due to Lancefield Group G Alpha-Hemolytic Streptococcus dysgalactiae subsp. equisimilis in a Patient with Pyomyositis and Reactive Arthritis. by Woo PC, Teng JL, Lau SK, Lum PN, Leung KW, Wong KL, Li KW, Lam KC, Yuen KY. 2003 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=149685
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Anti-C5 Monoclonal Antibody Therapy Prevents Collagen-Induced Arthritis and Ameliorates Established Disease. by Wang Y, Rollins SA, Madri JA, Matis LA. 1995 Sep 12; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=41086
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Anti-cytokine therapy in chronic destructive arthritis. by van den Berg WB. 2001; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=128880
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Anti-TNF-[alpha] antibody allows healing of joint damage in polyarthritic transgenic mice. by Shealy DJ, Wooley PH, Emmell E, Volk A, Rosenberg A, Treacy G, Wagner CL, Mayton L, Griswold DE, Song XY. 2002; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=125301
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Anti-Tumor Necrosis Factor Ameliorates Joint Disease in Murine Collagen- Induced Arthritis. by Williams RO, Feldmann M, Maini RN. 1992 Oct 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=50217
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Apoptosis and p53 expression in rat adjuvant arthritis. by Tak PP, Klapwijk MS, Broersen SF, van de Geest DA, Overbeek M, Firestein GS. 2000; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=17810
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Arthritis and Osteomyelitis due to Aspergillus fumigatus: A 17 years old boy with chronic granulomatous disease. by Bodur H, Ozoran K, Colpan A, Balaban N, Tabak Y, Kulacoglu S. 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=150380
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Arthritis Research: more than a journal (http://arthritis-research.com). by Lipsky PE, Maini RN. 1999; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=128859
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Arthritis Research: the move to publish research articles in full online only. by Lipsky PE, Maini RN. 2002; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=128922
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Arthritis severity and spirochete burden are determined by serotype in the Borrelia turicatae-mouse model of Lyme disease.. by Pennington PM, Allred CD, West CS, Alvarez R, Barbour AG. 1997 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=174589
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Articular cartilage and changes in Arthritis: Cell biology of osteoarthritis. by Sandell LJ, Aigner T. 2001; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=128887
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Articular cartilage and changes in arthritis: Matrix degradation. by Mort JS, Billington CJ. 2001; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=128908
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Assessment of a genetic contribution to osteoarthritis of the hip: sibling study. by Lanyon P, Muir K, Doherty S, Doherty M. 2000 Nov 11; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=27520
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Association of MHC and rheumatoid arthritis: Association of RA with HLA-DR4 - the role of repertoire selection. by Roudier J. 2000; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=130006
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Association of MHC and rheumatoid arthritis: HLA-DR4 and rheumatoid arthritis studies in mice and men. by Fugger L, Svejgaard A. 2000; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=130004
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Association of MHC and rheumatoid arthritis: Regulatory role of HLA class II molecules in animal models of RA - studies on transgenic/knockout mice. by Taneja V, David CS. 2000; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=130003
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Association of MHC and rheumatoid arthritis: Why is rheumatoid arthritis associated with the MHC genetic region? An introduction. by Holmdahl R. 2000; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=130002
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Association of MHC and rheumatoid arthritis:HLA polymorphisms in phenotypic variants of rheumatoid arthritis. by Weyand CM, Goronzy JJ. 2000; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=130005
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B cells in rheumatoid arthritis. by Kim HJ, Berek C. 2000; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=129995
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B lymphocytopenia in rheumatoid arthritis is associated with the DRB1 shared epitope and increased acute phase response. by Wagner U, Kaltenhauser S, Pierer M, Wilke B, Arnold S, Hantzschel H. 2002; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=125293
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B7-1 and B7-2 monoclonal antibodies modulate the severity of murine Lyme arthritis.. by Anguita J, Roth R, Samanta S, Gee RJ, Barthold SW, Mamula M, Fikrig E. 1997 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=175428
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Bacterial Cell Wall-Induced Arthritis: Chemical Composition and Tissue Distribution of Four Lactobacillus Strains. by Simelyte E, Rimpilainen M, Lehtonen L, Zhang X, Toivanen P. 2000 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=97639
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Biased T-Cell Antigen Receptor Repertoire in Lyme Arthritis. by Roessner K, Trivedi H, Gaur L, Howard D, Aversa J, Cooper SM, Sigal LH, Budd RC. 1998 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=108020
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Blockade of collagen-induced arthritis post-onset by antibody to granulocytemacrophage colony-stimulating factor (GM-CSF): requirement for GM-CSF in the effector phase of disease. by Cook AD, Braine EL, Campbell IK, Rich MJ, Hamilton JA. 2001; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=64841
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Body mass indices in patients with disabling hip osteoarthritis. by Marks R, Allegrante JP. 2002; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=83842
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Bone loss: Quantitative imaging techniques for assessing bone mass in rheumatoid arthritis. by Njeh CF, Genant HK. 2000; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=128873
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Bone loss: Therapeutic approaches for preventing bone loss in inflammatory arthritis. by Rehman Q, Lane NE. 2001; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=128900
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Borrelia burgdorferi-specific T lymphocytes induce severe destructive Lyme arthritis.. by Lim LC, England DM, DuChateau BK, Glowacki NJ, Schell RF. 1995 Apr; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=173166
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Can SOCS make arthritis better? by Ivashkiv LB, Tassiulas I. 2003 Mar 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=153773
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Cardiovascular risk in rheumatoid arthritis versus osteoarthritis: acute phase response related decreased insulin sensitivity and high-density lipoprotein cholesterol as well as clustering of metabolic syndrome features in rheumatoid arthritis. by Dessein PH, Stanwix AE, Joffe BI. 2002; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=125299
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CD4+CD25+ immunoregulatory T cells may not be involved in controlling autoimmune arthritis. by Bardos T, Czipri M, Vermes C, Finnegan A, Mikecz K, Zhang J. 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=165034
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Cell-cell interactions in synovitis: Antigen presenting cells and T cell interaction in rheumatoid arthritis. by Aarvak T, Natvig JB. 2001; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=128879
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Cell-cell interactions in synovitis: Interactions between T cells and B cells in rheumatoid arthritis. by Weyand CM, Goronzy JJ, Takemura S, Kurtin PJ. 2000; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=128875
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Cellular Immunity in Osteoarthritis: Novel Concepts for an Old Disease. by Liossis SN, Tsokos GC. 1998 Jul; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=95594
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Citrullination: a small change for a protein with great consequences for rheumatoid arthritis. by van Venrooij WJ, Pruijn GJ. 2000; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=130012
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Clearance of Borrelia burgdorferi May Not Be Required for Resistance to Experimental Lyme Arthritis. by Brown CR, Reiner SL. 1998 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=108164
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Clonal expansion is a characteristic feature of the B-cell repertoire of patients with rheumatoid arthritis. by Itoh K, Patki V, Furie RA, Chartash EK, Jain RI, Lane L, Asnis SE, Chiorazzi N. 2000; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=17803
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Clopidogrel associated with acute arthritis. by Garg A, Radvan J, Hopkinson N. 2000 Feb 19; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=27292
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Coinfection with Borrelia burgdorferi and the Agent of Human Granulocytic Ehrlichiosis Alters Murine Immune Responses, Pathogen Burden, and Severity of Lyme Arthritis. by Thomas V, Anguita J, Barthold SW, Fikrig E. 2001 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=98295
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Collagen-induced arthritis is exacerbated in IL-10-deficient mice. by Finnegan A, Kaplan CD, Cao Y, Eibel H, Glant TT, Zhang J. 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=154422
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Combined antibiotic and free radical trap treatment is effective at combating Staphylococcus-aureus-induced septic arthritis. by Sakiniene E, Collins LV. 2002; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=111022
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Competitive-Inhibition Enzyme-Linked Immunosorbent Assay for Detection of Serum Antibodies to Caprine Arthritis-Encephalitis Virus: Diagnostic Tool for
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Successful Eradication. by Herrmann LM, Cheevers WP, McGuire TC, Adams DS, Hutton MM, Gavin WG, Knowles DP. 2003 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=150544 ·
Conducting clinical trials over the internet: feasibility study Can randomised controlled trials be successfully conducted over the internet? The authors report a feasibility study of such a trial in patients with osteoarthritis of the knee. by McAlindon T, Formica M, Kabbara K, LaValley M, Lehmer M. 2003 Aug 30; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=188386
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Correlation of the score for subjective pain with physical disability, clinical and radiographic scores in recent onset rheumatoid arthritis. by Sarzi-Puttini P, Fiorini T, Panni B, Turiel M, Cazzola M, Atzeni F. 2002; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=117789
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Costimulating aberrant T cell responses by B7-H1 autoantibodies in rheumatoid arthritis. by Dong H, Strome SE, Matteson EL, Moder KG, Flies DB, Zhu G, Tamura H, Driscoll CL, Chen L. 2003 Feb 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=151851
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Cross-Reactivity between the Rheumatoid Arthritis-Associated Motif EQKRAA and Structurally Related Sequences Found in Proteus mirabilis. by Tiwana H, Wilson C, Alvarez A, Abuknesha R, Bansal S, Ebringer A. 1999 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=96580
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Cytokine mRNA and protein expression in primary-culture and repeated-passage synovial fibroblasts from patients with rheumatoid arthritis. by Hirth A, Skapenko A, Kinne RW, Emmrich F, Schulze-Koops H, Sack U. 2002; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=83845
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Cytokine, activation marker, and chemokine receptor expression by individual CD4+ memory T cells in rheumatoid arthritis synovium. by Nanki T, E Lipsky P. 2000; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=17818
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Cytokines in Mycoplasma hyorhinis-Induced Arthritis in Pigs Bred Selectively for High and Low Immune Responses. by Jayagopala Reddy NR, Wilkie BN, Borgs P, Mallard BA. 2000 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=97260
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Cytokine-stimulated T cells induce macrophage IL-10 production dependent on phosphatidylinositol 3-kinase and p70S6K: implications for rheumatoid arthritis. by Foey A, Green P, Foxwell B, Feldmann M, Brennan F. 2002; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=64854
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Decomplementation by cobra venom factor suppresses Yersinia-induced arthritis in rats.. by Gaede KI, Baumeister E, Heesemann J. 1995 Sep; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=173512
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Decreased effector memory CD45RA+ CD62L- CD8+ T cells and increased central memory CD45RA- CD62L+ CD8+ T cells in peripheral blood of rheumatoid arthritis patients. by Maldonado A, Mueller YM, Thomas P, Bojczuk P, O'Connors C, Katsikis PD. 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=165030
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Definition of MHC and T cell receptor contacts in the HLA-DR4restricted immunodominant epitope in type II collagen and characterization of collageninduced arthritis in HLA-DR4 and human CD4 transgenic mice. by Andersson EC, Hansen BE, Jacobsen H, Madsen LS, Andersen CB, Engberg J, Rothbard JB, McDevitt GS, Malmstrom V, Holmdahl R, Svejgaard A, Fugger L. 1998 Jun 23; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=22687
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Destructive Arthritis in Vaccinated Interferon Gamma-Deficient Mice Challenged with Borrelia burgdorferi: Modulation by Tumor Necrosis Factor Alpha. by Christopherson JA, Munson EL, England DM, Croke CL, Remington MC, Molitor ML, DeCoster DJ, Callister SM, Schell RF. 2003 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=145283
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Detection of Mycobacterium tuberculosis Group Organisms in Human and Mouse Joint Tissue by Reverse Transcriptase PCR: Prevalence in Diseased Synovial Tissue Suggests Lack of Specific Association with Rheumatoid Arthritis. by Kempsell KE, Cox CJ, McColm AA, Bagshaw JA, Reece R, Veale DJ, Emery P, Isaacs JD, Gaston JS, Crowe JS. 2001 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=98089
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Dietary Glycine Prevents Peptidoglycan Polysaccharide-Induced Reactive Arthritis in the Rat: Role for Glycine-Gated Chloride Channel. by Li X, Bradford BU, Wheeler MD, Stimpson SA, Pink HM, Brodie TA, Schwab JH, Thurman RG. 2001 Sep; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=98707
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Differential clinical efficacy of anti-CD4 monoclonal antibodies in rat adjuvant arthritis is paralleled by differential influence on NF-[kappa]B binding activity and TNF-[alpha] secretion of T cells. by Pohlers D, Schmidt-Weber CB, Franch A, Kuhlmann J, Brauer R, Emmrich F, Kinne RW. 2002; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=111020
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Differential expression of the angiogenic Tie receptor family in arthritic and normal synovial tissue. by Shahrara S, Volin MV, Connors MA, Haines GK, Koch AE. 2002; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=111023
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Differentiation of B Cells in the Nonlymphoid Tissue of the Synovial Membrane of Patients with Rheumatoid Arthritis. by Schroder AE, Greiner A, Seyfert C, Berek C. 1996 Jan 9; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=40210
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Dipeptidyl peptidase I activates neutrophil-derived serine proteases and regulates the development of acute experimental arthritis. by Adkison AM, Raptis SZ, Kelley DG, Pham CT. 2002 Feb 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=150852
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Direct adenovirus-mediated gene transfer of interleukin 1 and tumor necrosis factor [alpha] soluble receptors to rabbit knees with experimental arthritis has local and distal anti-arthritic effects. by Ghivizzani SC, Lechman ER, Kang R, Tio C, Kolls J, Evans CH, Robbins PD. 1998 Apr 14; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=22538
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Direct Molecular Typing of Borrelia burgdorferi Sensu Lato Species in Synovial Samples from Patients with Lyme Arthritis. by Jaulhac B, Heller R, Limbach FX, Hansmann Y, Lipsker D, Monteil H, Sibilia J, Piemont Y. 2000 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=86617
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Disease activity and risk of lymphoma in patients with rheumatoid arthritis: nested case-control study. by Baecklund E, Ekbom A, Sparen P, Feltelius N, Klareskog L. 1998 Jul 18; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=28610
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Disease-Inducible Transgene Expression from a Recombinant Adeno-Associated Virus Vector in a Rat Arthritis Model. by Pan RY, Xiao X, Chen SL, Li J, Lin LC, Wang HJ, Tsao YP. 1999 Apr; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=104105
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Distinct Characteristics of Resistance to Borrelia burgdorferi-Induced Arthritis in C57BL/6N Mice. by Ma Y, Seiler KP, Eichwald EJ, Weis JH, Teuscher C, Weis JJ. 1998 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=107872
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Divergent T-Cell Cytokine Patterns in Inflammatory Arthritis. by Simon AK, Seipelt E, Sieper J. 1994 Aug 30; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=44646
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Dominant recognition of a Borrelia burgdorferi outer surface protein A peptide by T helper cells in patients with treatment-resistant Lyme arthritis.. by Kamradt T, LenglJanssen B, Strauss AF, Bansal G, Steere AC. 1996 Apr; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=173916
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Dominant T-Cell-Receptor [beta] Chain Variable Region V[beta]14+ Clones in Juvenile Rheumatoid Arthritis. by Grom AA, Thompson SD, Luyrink L, Passo M, Choi E, Glass DN. 1993 Dec 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=47930
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Dual Role of Interleukin-10 in Murine Lyme Disease: Regulation of Arthritis Severity and Host Defense. by Brown JP, Zachary JF, Teuscher C, Weis JJ, Wooten RM. 1999 Oct; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=96863
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E and P Selectins Are Not Required for Resistance to Severe Murine Lyme Arthritis. by Seiler KP, Ma Y, Weis JH, Frenette PS, Hynes RO, Wagner DD, Weis JJ. 1998 Sep; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=108558
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Effects of disease modifying agents and dietary intervention on insulin resistance and dyslipidemia in inflammatory arthritis: a pilot study. by Dessein PH, Joffe BI, Stanwix AE. 2002; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=153842
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Efficacy of knee tape in the management of osteoarthritis of the knee: blinded randomised controlled trial. by Hinman RS, Crossley KM, McConnell J, Bennell KL. 2003 Jul 19; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=165705
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Efficacy of treatment with glycosaminoglycans on experimental collagen-induced arthritis in rats. by Campo GM, Avenoso A, Campo S, Ferlazzo AM, Altavilla D, Calatroni A. 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=165044
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Efficacy, tolerability, and upper gastrointestinal safety of celecoxib for treatment of osteoarthritis and rheumatoid arthritis: systematic review of randomised controlled trials. by Deeks JJ, Smith LA, Bradley MD. 2002 Sep 21; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=126301
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Efficient adenoviral infection with I[kappa]B[alpha] reveals that macrophage tumor necrosis factor [alpha] production in rheumatoid arthritis is NF-[kappa]B dependent. by Foxwell B, Browne K, Bondeson J, Clarke C, de Martin R, Brennan F, Feldmann M. 1998 Jul 7; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=20955
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Endogenous regulation of a therapeutic transgene restores homeostasis in arthritic joints. by Miagkov AV, Varley AW, Munford RS, Makarov SS. 2002 May 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=150962
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Enhanced expression of genes involved in coagulation and fibrinolysis in murine arthritis. by Salvi R, Peclat V, So A, Busso N. 2000; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=17822
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Essential role for proteinase-activated receptor-2 in arthritis. by Ferrell WR, Lockhart JC, Kelso EB, Dunning L, Plevin R, Meek SE, Smith AJ, Hunter GD, McLean JS, McGarry F, Ramage R, Jiang L, Kanke T, Kawagoe J. 2003 Jan 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=151840
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Essential role of the cryptic epitope SLAYGLR within osteopontin in a murine model of rheumatoid arthritis. by Yamamoto N, Sakai F, Kon S, Morimoto J, Kimura C, Yamazaki H, Okazaki I, Seki N, Fujii T, Uede T. 2003 Jul 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=164290
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Experimental arthritis induced by a clinical Mycoplasma fermentans isolate. by Rivera A, Yanez A, Leon-Tello G, Gil C, Giono S, Barba E, Cedillo L. 2002; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=116578
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Experimental Lyme Arthritis in the Absence of Interleukin-4 or Gamma Interferon. by Brown CR, Reiner SL. 1999 Jul; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=116514
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Expression and function of wingless and frizzled homologs in rheumatoid arthritis. by Sen M, Lauterbach K, El-Gabalawy H, Firestein GS, Corr M, Carson DA. 2000 Mar 14; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=16008
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Expression of Adhesion Molecules in Synovia of Patients with Treatment-Resistant Lyme Arthritis. by Akin E, Aversa J, Steere AC. 2001 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=98084
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FcgammaR expression on macrophages is related to severity and chronicity of synovial inflammation and cartilage destruction during experimental immune-
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complex-mediated arthritis (ICA). by Blom AB, van Lent PL, van Vuuren H, Holthuysen AE, Jacobs C, van de Putte LB, van de Winkel JG, van den Berg WB. 2000; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=17821 ·
Fibroblast biology: Development and differentiation of synovial fibroblasts in arthritis. by Edwards JC. 2000; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=130134
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Fibroblast biology: Effector signals released by the synovial fibroblast in arthritis. by Ritchlin C. 2000; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=130136
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Fibroblast biology: Role of synovial fibroblasts in the pathogenesis of rheumatoid arthritis. by Pap T, Muller-Ladner U, Gay RE, Gay S. 2000; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=130137
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Fibroblast biology: Signals targeting the synovial fibroblast in arthritis. by Konttinen YT, Li TF, Hukkanen M, Ma J, Xu JW, Virtanen I. 2000; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=130135
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Fibroblast biology: Synovial fibroblasts in rheumatoid arthritis - leading role or chorus line? by Kontoyiannis D, Kollias G. 2000; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=130133
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Future of adenoviruses in the gene therapy of arthritis. by Evans CH, Ghivizzani SC, Oligino TA, Robbins PD. 2001; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=128890
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Gamma Interferon and Interleukin-10 Gene Expression in Synovial Tissues from Patients with Early Stages of Chlamydia-Associated Arthritis and Undifferentiated Oligoarthritis and from Healthy Volunteers. by Kotake S, Schumacher HR Jr, Arayssi TK, Gerard HC, Branigan PJ, Hudson AP, Yarboro CH, Klippel JH, Wilder RL. 1999 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=116026
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Gamma Interferon Is Not Required for Arthritis Resistance in the Murine Lyme Disease Model. by Glickstein L, Edelstein M, Dong JZ. 2001 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=98381
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Gene expression induced by interleukin-17 in fibroblast-like synoviocytes of patients with rheumatoid arthritis: upregulation of hyaluronan-binding protein TSG-6. by Kehlen A, Pachnio A, Thiele K, Langner J. 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=165059
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Gene therapy for established murine collagen-induced arthritis by local and systemic adenovirus-mediated delivery of interleukin-4. by Kim SH, Evans CH, Kim S, Oligino T, Ghivizzani SC, Robbins PD. 2000; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=17812
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Gene therapy in rheumatoid arthritis: how to target joint destruction? by Pap T, Muller-Ladner U, Gay R, Gay S. 1999; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=128862
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Gene therapy moves forward - The Second International Meeting on Gene and Cell Therapies of Arthritis and Related Disorders, 17-18 May 2001, Montpellier, France. by Robbins PD, Jorgensen C, Evans CH. 2001; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=128905
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Genetic Control of Experimental Lyme Arthritis in the Absence of Specific Immunity. by Brown CR, Reiner SL. 1999 Apr; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=96554
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Genetic epidemiology: Approaches to the genetic analysis of rheumatoid arthritis. by John S, Worthington J. 2001; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=128899
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Genetics of rheumatoid arthritis: confronting complexity. by Gregersen PK. 1999; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=128868
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Genotypic Characterization of Seven Strains of Mycoplasma fermentans Isolated from Synovial Fluids of Patients with Arthritis. by Schaeverbeke T, Clerc M, Lequen L, Charron A, Bebear C, de Barbeyrac B, Bannwarth B, Dehais J, Bebear C. 1998 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=104804
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Granulocyte-Macrophage Colony-Stimulating Factor in Staphylococcus aureusInduced Arthritis. by Verdrengh M, Tarkowski A. 1998 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=107983
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Hip disability and osteoarthritis outcome score (HOOS) -- validity and responsiveness in total hip replacement. by Nilsdotter AK, Lohmander LS, Klassbo M, Roos EM. 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=161815
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Home based exercise programme for knee pain and knee osteoarthritis: randomised controlled trial. by Thomas KS, Muir KR, Doherty M, Jones AC, O'Reilly SC, Bassey EJ. 2002 Oct 5; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=128377
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Hormone replacement therapy in rheumatoid arthritis is associated with lower serum levels of soluble IL-6 receptor and higher insulin-like growth factor 1. by d'Elia HF, Mattsson LA, Ohlsson C, Nordborg E, Carlsten H. 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=165058
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Host Range of Small-Ruminant Lentivirus Cytopathic Variants Determined with a Selectable Caprine Arthritis- Encephalitis Virus Pseudotype System. by Hotzel I, Cheevers WP. 2001 Aug 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=114973
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Human parvovirus B19 as a causative agent for rheumatoid arthritis. by Takahashi Y, Murai C, Shibata S, Munakata Y, Ishii T, Ishii K, Saitoh T, Sawai T, Sugamura K, Sasaki T. 1998 Jul 7; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=20958
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Hyposecretion of the adrenal androgen dehydroepiandrosterone sulfate and its relation to clinical variables in inflammatory arthritis. by Dessein PH, Joffe BI, Stanwix AE, Moomal Z. 2001; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=30711
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Identification of Mycoplasma fermentans in Synovial Fluid Samples from Arthritis Patients with Inflammatory Disease. by Johnson S, Sidebottom D, Bruckner F, Collins D. 2000 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=86027
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Identification of rat susceptibility loci for adjuvant-oil-induced arthritis. by Lorentzen JC, Glaser A, Jacobsson L, Galli J, Fakhrai-rad H, Klareskog L, Luthman H. 1998 May 26; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=27729
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IFN-[gamma] production in response to in vitro stimulation with collagen type II in rheumatoid arthritis is associated with HLA-DRB1*0401 and HLA-DQ8. by Berg L, Ronnelid J, Sanjeevi CB, Lampa J, Klareskog L. 2000; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=17806
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IgVH genes from different anatomical regions, with different histopathological patterns, of a rheumatoid arthritis patient suggest cyclic re-entry of mature synovial B-cells in the hypermutation process. by Souto-Carneiro MM, Krenn V, Hermann R, Konig A, Muller-Hermelink HK. 2000; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=17813
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IL-17 derived from juxta-articular bone and synovium contributes to joint degradation in rheumatoid arthritis. by Chabaud M, Lubberts E, Joosten L, van den Berg W, Miossec P. 2001; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=30709
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Immune Response of HLA-DQ8 Transgenic Mice to Peptides from the Third Hypervariable Region of HLA-DRB1 Correlates with Predisposition to Rheumatoid Arthritis. by Zanelli E, Krco CJ, Baisch JM, Cheng S, David CS. 1996 Mar 5; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=39864
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In vivo efficacy of azithromycin in treatment of systemic infection and septic arthritis induced by type IV group B Streptococcus strains in mice: comparative study with erythromycin and penicillin G.. by Tissi L, von Hunolstein C, Mosci P, Campanelli C, Bistoni F, Orefici G. 1995 Sep; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=162860
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Increased translocation of Escherichia coli and development of arthritis in vitamin Adeficient rats.. by Wiedermann U, Hanson LA, Bremell T, Kahu H, Dahlgren UI. 1995 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=173417
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Inducible costimulator is essential for collagen-induced arthritis. by Nurieva RI, Treuting P, Duong J, Flavell RA, Dong C. 2003 Mar 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=151904
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Infection of Synovial Fibroblasts in Culture by Yersinia enterocolitica and Salmonella enterica Serovar Enteritidis: Ultrastructural Investigation with Respect to the Pathogenesis of Reactive Arthritis. by Meyer-Bahlburg A, Brinkhoff J, Krenn V, Trebesius K, Heesemann J, Huppertz HI. 2001 Dec; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=98891
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Insights into rheumatoid arthritis derived from the Sa immune system. by Menard HA, Lapointe E, Rochdi MD, Zhou ZJ. 2000; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=128869
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Interleukin 6 plays a key role in the development of antigen-induced arthritis. by Ohshima S, Saeki Y, Mima T, Sasai M, Nishioka K, Nomura S, Kopf M, Katada Y, Tanaka T, Suemura M, Kishimoto T. 1998 Jul 7; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=20957
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Interleukin-4 (IL-4) and IL-13 Signaling Pathways Do Not Regulate Borrelia burgdorferi-Induced Arthritis in Mice: IgG1 Is Not Required for Host Control of Tissue Spirochetes. by Potter MR, Noben-Trauth N, Weis JH, Teuscher C, Weis JJ. 2000 Oct; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=101512
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Internet hand x-rays: A comparison of joint space narrowing and erosion scores (Sharp/Genant) of plain versus digitized x-rays in rheumatoid arthritis patients. by Arbillaga HO, Montgomery GP, Cabarrus LP, Watson MM, Martin L, Edworthy SM. 2002; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=113251
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Investigation of infectious agents associated with arthritis by reverse transcription PCR of bacterial rRNA. by Cox CJ, Kempsell KE, Gaston JS. 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=154423
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Involvement of CD4+ T lymphocytes in induction of severe destructive Lyme arthritis in inbred LSH hamsters.. by Lim LC, England DM, Glowacki NJ, DuChateau BK, Schell RF. 1995 Dec; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=173690
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Involvement of Endogeneous Tumor Necrosis Factor [alpha] and Transforming Growth Factor [beta] During Induction of Collagen Type II Arthritis in Mice. by Thorbecke GJ, Shah R, Leu CH, Kuruvilla AP, Hardison AM, Palladino MA. 1992 Aug 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=49712
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Is day care equivalent to inpatient care for active rheumatoid arthritis? Randomised controlled clinical and economic evaluation. by Lambert CM, Hurst NP, Forbes JF, Lochhead A, Macleod M, Nuki G. 1998 Mar 28; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=28498
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Is it Crohn's disease? A severe systemic granulomatous reaction to sulfasalazine in patient with rheumatoid arthritis. by Quallich LG, Greenson J, Haftel HM, Fontana RJ. 2001; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=56591
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Isolation and characterization of rheumatoid arthritis synovial fibroblasts from primary culture --- primary culture cells markedly differ from fourth-passage cells. by Zimmermann T, Kunisch E, Pfeiffer R, Hirth A, Stahl HD, Sack U, Laube A, Liesaus E, Roth A, Palombo-Kinne E, Emmrich F, Kinne RW. 2001; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=17827
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Isolation of Pantoea agglomerans in Two Cases of Septic Monoarthritis after Plant Thorn and Wood Sliver Injuries. by De Champs C, Le Seaux S, Dubost JJ, Boisgard S, Sauvezie B, Sirot J. 2000 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=88752
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Joint-specific and systemic autoreactivity in the development of inflammatory arthritis. by Fugger L. 2000; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=129986
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Lack of Functional Receptors Is the Only Barrier That Prevents Caprine ArthritisEncephalitis Virus from Infecting Human Cells. by Mselli-Lakhal L, Favier C, Leung K, Guiguen F, Grezel D, Miossec P, Mornex JF, Narayan O, Querat G, Chebloune Y. 2000 Sep 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=116344
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Leptin in septic arthritis: decreased levels during infection and amelioration of disease activity upon its administration. by Hultgren OH, Tarkowski A. 2001; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=64851
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Leukotriene B4 Plays a Critical Role in the Progression of Collagen- Induced Arthritis. by Griffiths RJ, Pettipher ER, Koch K, Farrell CA, Breslow R, Conklyn MJ, Smith MA, Hackman BC, Wimberly DJ, Milici AJ, Scampoli DN, Cheng JB, Pillar JS, Pazoles CJ, Doherty NS, Melvin LS, Reiter LA, Biggars MS, Falkner FC, Mitchell DY, Liston TE, Showell HJ. 1995 Jan 17; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=42772
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Limited T-Cell Receptor [beta]-Chain Heterogeneity Among Interleukin 2 ReceptorPositive Synovial T Cells Suggests a Role for Superantigen in Rheumatoid Arthritis. by Howell MD, Diveley JP, Lundeen KA, Esty A, Winters ST, Carlo DJ, Brostoff SW. 1991 Dec 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=53044
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Localization of non-Mhc collagen-induced arthritis susceptibility loci in DBA /1j mice. by McIndoe RA, Bohlman B, Chi E, Schuster E, Lindhardt M, Hood L. 1999 Mar 2; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=26762
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Lyme Arthritis Resolution with Antiserum to a 37-Kilodalton Borrelia burgdorferi Protein. by Feng S, Hodzic E, Barthold SW. 2000 Jul; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=101718
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Macrophages and enriched populations of T lymphocytes interact synergistically for the induction of severe, destructive Lyme arthritis.. by DuChateau BK, Jensen JR, England DM, Callister SM, Lovrich SD, Schell RF. 1997 Jul; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=175398
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Macrophages exposed to Borrelia burgdorferi induce Lyme arthritis in hamsters.. by Du Chateau BK, England DM, Callister SM, Lim LC, Lovrich SD, Schell RF. 1996 Jul; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=174108
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Macrophages in rheumatoid arthritis. by Kinne RW, Brauer R, Stuhlmuller B, PalomboKinne E, Burmester GR. 2000; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=130001
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Mechanisms of bone loss in inflammatory arthritis: diagnosis and therapeutic implications. by Goldring SR, Gravallese EM. 2000; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=129989
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Mechanisms of TNF-[alpha] -- and RANKL-mediated osteoclastogenesis and bone resorption in psoriatic arthritis. by Ritchlin CT, Haas-Smith SA, Li P, Hicks DG, Schwarz EM. 2003 Mar 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=153764
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Meta-analysis of short term low dose prednisolone versus placebo and non-steroidal anti-inflammatory drugs in rheumatoid arthritis. by Gotzsche PC, Johansen HK. 1998 Mar 14; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=28482
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Model studies directed toward the application of boron neutron capture therapy to rheumatoid arthritis: Boron delivery by liposomes in rat collagen-induced arthritis. by Watson-Clark RA, Banquerigo ML, Shelly K, Hawthorne MF, Brahn E. 1998 Mar 3; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=19402
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Modulation of Cytokine Profiles by the Mycoplasma Superantigen Mycoplasma arthritidis Mitogen Parallels Susceptibility to Arthritis Induced by M. arthritidis. by Mu HH, Sawitzke AD, Cole BC. 2000 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=97259
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Molecular profile of synovial fibroblasts in rheumatoid arthritis depends on the stage of proliferation. by Masuda K, Masuda R, Neidhart M, Simmen BR, Michel BA, MullerLadner U, Gay RE, Gay S. 2002; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=125298
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Monoarticular antigen-induced arthritis leads to pronounced bilateral upregulation of the expression of neurokinin 1 and bradykinin 2 receptors in dorsal root ganglion neurons of rats. by Segond von Banchet G, Petrow PK, Brauer R, Schaible HG. 2000; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=17819
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Monoclonal Antibodies to Conformational Epitopes of the Surface Glycoprotein of Caprine Arthritis-Encephalitis Virus: Potential Application to Competitive-Inhibition Enzyme-Linked Immunosorbent Assay for Detecting Antibodies in Goat Sera. by Ozyoruk F, Cheevers WP, Hullinger GA, McGuire TC, Hutton M, Knowles DP. 2001 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=96009
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Mosaic chromosomal aberrations in synovial fibroblasts of patients with rheumatoid arthritis, osteoarthritis, and other inflammatory joint diseases. by Kinne RW, Liehr T, Beensen V, Kunisch E, Zimmermann T, Holland H, Pfeiffer R, Stahl HD, Lungershausen W, Hein G, Roth A, Emmrich F, Claussen U, Froster UG. 2001; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=64845
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New susceptibility locus for rheumatoid arthritis suggested by a genome-wide linkage study. by Cornelis F, Faure S, Martinez M, Prud'homme JF, Fritz P, Dib C, Alves H, Barrera P, de Vries N, Balsa A, Pascual-Salcedo D, Maenaut K, Westhovens R, Migliorini P, Tran TH, Delaye A, Prince N, Lefevre C, Thomas G, Poirier M, Soubigou S,
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NF-[kappa]B activation provides the potential link between inflammation and hyperplasia in the arthritic joint. by Miagkov AV, Kovalenko DV, Brown CE, Didsbury JR, Cogswell JP, Stimpson SA, Baldwin AS, Makarov SS. 1998 Nov 10; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=24931
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NF-kappaB in rheumatoid arthritis: a pivotal regulator of inflammation, hyperplasia, and tissue destruction. by Makarov SS. 2001; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=128895
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Occurrence of Severe Destructive Lyme Arthritis in Hamsters Vaccinated with Outer Surface Protein A and Challenged with Borrelia burgdorferi. by Croke CL, Munson EL, Lovrich SD, Christopherson JA, Remington MC, England DM, Callister SM, Schell RF. 2000 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=97189
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On the Belief that Arthritis Pain is Related to the Weather. by Redelmeier DA, Tversky A. 1996 Apr 2; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=39730
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One-Step Reverse Transcriptase PCR Method for Detection of Borrelia burgdorferi mRNA in Mouse Lyme Arthritis Tissue Samples. by Limbach FX, Jaulhac B, Piemont Y, Kuntz JL, Monteil H, Sibilia J. 1999 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=85022
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Osteoarthritis Associated with Mild Chondrodysplasia in Transgenic Mice Expressing [alpha]1(IX) Collagen Chains with a Central Deletion. by Nakata K, Ono K, Miyazaki J, Olsen BR, Muragaki Y, Adachi E, Yamamura K, Kimura T. 1993 Apr 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=46198
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Osteopontin deficiency protects joints against destruction in anti-type II collagen antibody-induced arthritis in mice. by Yumoto K, Ishijima M, Rittling SR, Tsuji K, Tsuchiya Y, Kon S, Nifuji A, Uede T, Denhardt DT, Noda M. 2002 Apr 2; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=123686
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Outer Surface Protein A and Arthritis in Hamsters. by Parenti DL. 2000 Dec; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=97844
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p53 in rheumatoid arthritis: friend or foe? by Muller-Ladner U, Nishioka K. 2000; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=129999
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Peptide-induced nasal tolerance for a mycobacterial heat shock protein 60 T cell epitope in rats suppresses both adjuvant arthritis and nonmicrobially induced experimental arthritis. by Prakken BJ, van der Zee R, Anderton SM, van Kooten PJ, Kuis W, van Eden W. 1997 Apr 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=20361
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Perforin and Granzyme A Expression Identifying Cytolytic Lymphocytes in Rheumatoid Arthritis. by Griffiths GM, Alpert S, Lambert E, McGuire J, Weissman IL. 1992 Jan 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=48276
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Perinatal characteristics and risk of rheumatoid arthritis. by Jacobsson LT, Jacobsson ME, Askling J, Knowler WC. 2003 May 17; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=155691
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Perturbation of the T cell repertoire in rheumatoid arthritis. by Wagner UG, Koetz K, Weyand CM, Goronzy JJ. 1998 Nov 24; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=24393
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Potent antiarthritic properties of a glucocorticoid derivative, NCX-1015, in an experimental model of arthritis. by Paul-Clark MJ, Mancini L, Del Soldato P, Flower RJ, Perretti M. 2002 Feb 5; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=122250
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Predominant selection of T cells specific for the glycosylated collagen type II epitope (263 --270) in humanized transgenic mice and in rheumatoid arthritis. by Backlund J, Carlsen S, Hoger T, Holm B, Fugger L, Kihlberg J, Burkhardt H, Holmdahl R. 2002 Jul 23; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=126607
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Preferential induction of septic arthritis and mortality by superantigen-producing staphylococci.. by Bremell T, Tarkowski A. 1995 Oct; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=173591
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Prevention of collagen-induced arthritis in mice by a polyphenolic fraction from green tea. by Haqqi TM, Anthony DD, Gupta S, Ahmad N, Lee MS, Kumar GK, Mukhtar H. 1999 Apr 13; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=16365
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Priming with tat-Deleted Caprine Arthritis Encephalitis Virus (CAEV) Proviral DNA or Live Virus Protects Goats from Challenge with Pathogenic CAEV. by Harmache A, Vitu C, Guiguen F, Russo P, Bertoni G, Pepin M, Vigne R, Suzan M. 1998 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=109888
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Protection against cartilage and bone destruction by systemic interleukin-4 treatment in established murine type II collagen-induced arthritis. by Joosten LA, Lubberts E, Helsen MM, Saxne T, Coenen-de Roo CJ, Heinegard D, van den Berg WB. 1999; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=17779
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Protection against peroxynitrite-induced fibroblast injury and arthritis development by inhibition of poly(ADP-ribose) synthase. by Szabo C, Virag L, Cuzzocrea S, Scott GS, Hake P, O'Connor MP, Zingarelli B, Salzman A, Kun E. 1998 Mar 31; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=19929
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Protection of rats against Mycoplasma arthritidis-induced arthritis by active and passive immunizations with two surface antigens.. by Washburn LR, Weaver EJ. 1997 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=170526
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Purinergic Regulation of Bradykinin-Induced Plasma Extravasation and AdjuvantInduced Arthritis in the Rat. by Green PG, Basbaum AI, Helms C, Levine JD. 1991 May 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=51618
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Randomised double blind trial of etoricoxib and indometacin in treatment of acute gouty arthritis. by Schumacher HR Jr, Boice JA, Daikh DI, Mukhopadhyay S, Malmstrom K, Ng J, Tate GA, Molina J. 2002 Jun 22; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=116444
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Reactivation of arthritis induced by small bowel bacterial overgrowth in rats: role of cytokines, bacteria, and bacterial polymers.. by Lichtman SN, Wang J, Sartor RB, Zhang C, Bender D, Dalldorf FG, Schwab JH. 1995 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=173300
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Regional analysis of p53 mutations in rheumatoid arthritis synovium. by Yamanishi Y, Boyle DL, Rosengren S, Green DR, Zvaifler NJ, Firestein GS. 2002 Jul 23; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=126618
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Regulatory Role of Interleukin-10 in Experimental Group B Streptococcal Arthritis. by Puliti M, von Hunolstein C, Verwaerde C, Bistoni F, Orefici G, Tissi L. 2002 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=128010
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Relative importance of genetic effects in rheumatoid arthritis: historical cohort study of Danish nationwide twin population. by Svendsen AJ, Holm NV, Kyvik K, Petersen PH, Junker P. 2002 Feb 2; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=65056
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Reply to "Outer Surface Protein A and Arthritis in Hamsters". by Schell RF. 2000 Dec; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=116981
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Response to Fionula Brennan's Commentary "A follow-up to 'Anti-cytokine therapy in chronic destructive arthritis' by Wim B van den Berg". by van den Berg WB. 2001; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=128898
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Restricted Heterogeneity in T-Cell Antigen Receptor V[beta] Gene Usage in the Lymph Nodes and Arthritic Joints of Mice. by Haqqi TM, Anderson GD, Banerjee S, David CS. 1992 Feb 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=48427
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Results of a phase-I/II randomized, masked, placebo-controlled trial of recombinant human interleukin-11 (rhIL-11) in the treatment of subjects with active rheumatoid arthritis. by Moreland L, Gugliotti R, King K, Chase W, Weisman M, Greco T, Fife R, Korn J, Simms R, Tesser J, Hillson J, Caldwell J, Schnitzer T, Lyons D, Schwertschlag U. 2001; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=34114
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Reverse Transcriptase-PCR Analysis of Bacterial rRNA for Detection and Characterization of Bacterial Species in Arthritis Synovial Tissue. by Kempsell KE, Cox CJ, Hurle M, Wong A, Wilkie S, Zanders ED, Gaston JS, Crowe JS. 2000 Oct; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=101566
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Rheumatoid arthritis associated autoantibodies in patients with synovitis of recent onset. by Goldbach-Mansky R, Lee J, McCoy A, Hoxworth J, Yarboro C, Smolen JS, Steiner G, Rosen A, Zhang C, Menard HA, Zhou ZJ, Palosuo T, Van Venrooij WJ, Wilder RL, Klippel JH, Schumacher HR Jr, EI-Gabalawy HS. 2000; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=17811
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Rheumatoid arthritis viewed using a headache paradigm. by Holmdahl R. 2000; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=129997
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Rheumatoid arthritis, gold therapy, contact allergy and blood cytokines. by Svensson A, Moller H, Bjorkner B, Bruze M, Leden I, Theander J, Ohlsson K, Linder C. 2002; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=65540
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Rheumatology: 9. Physical and occupational therapy in the management of arthritis. by Clark BM. 2000 Oct 17; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=80550
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Role of IL-12 in Staphylococcus aureus-triggered arthritis and sepsis. by Hultgren OH, Stenson M, Tarkowski A. 2001; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=17823
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Role of intercellular adhesion molecule 1 in pathogenesis of staphylococcal arthritis and in host defense against staphylococcal bacteremia.. by Verdrengh M, Springer TA, Gutierrez-Ramos JC, Tarkowski A. 1996 Jul; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=174143
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Role of neutrophils in experimental septicemia and septic arthritis induced by Staphylococcus aureus.. by Verdrengh M, Tarkowski A. 1997 Jul; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=175355
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Role of Osteopontin in Murine Lyme Arthritis and Host Defense against Borrelia burgdorferi. by Potter MR, Rittling SR, Denhardt DT, Roper RJ, Weis JH, Teuscher C, Weis JJ. 2002 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=127811
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Role of the proteasome and NF-[kappa]B in streptococcal cell wall-induced polyarthritis. by Palombella VJ, Conner EM, Fuseler JW, Destree A, Davis JM, Laroux FS, Wolf RE, Huang J, Brand S, Elliott PJ, Lazarus D, McCormack T, Parent L, Stein R, Adams J, Grisham MB. 1998 Dec 22; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=28102
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Role of the staphylococcal accessory gene regulator (sar) in septic arthritis.. by Nilsson IM, Bremell T, Ryden C, Cheung AL, Tarkowski A. 1996 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=174395
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Role of Tumor Necrosis Factor Alpha, Interleukin-1[beta], and Interleukin-6 in a Mouse Model of Group B Streptococcal Arthritis. by Tissi L, Puliti M, Barluzzi R, Orefici G, von Hunolstein C, Bistoni F. 1999 Sep; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=96776
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Serum cartilage oligomeric matrix protein (COMP) decreases in rheumatoid arthritis patients treated with infliximab or etanercept. by Crnkic M, Mansson B, Larsson L, Geborek P, Heinegard D, Saxne T. 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=165057
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Severity of Group B Streptococcal Arthritis in Selected Strains of Laboratory Mice. by Puliti M, Bistoni F, von Hunolstein C, Orefici G, Tissi L. 2001 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=97917
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Simple and Rapid Method for Production of Whole-Virus Antigen for Serodiagnosis of Caprine Arthritis-Encephalitis Virus by Enzyme-Linked Immunosorbent Assay. by Simard C, Kibenge MT, Singh P, Dixon P. 2001 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=96062
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Single Base Mutation in the Type II Procollagen Gene (COL2A1) as a Cause of Primary Osteoarthritis Associated with a Mild Chondrodysplasia. by Ala-Kokko L, Baldwin CT, Moskowitz RW, Prockop DJ. 1990 Sep 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=54577
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Smoking --gender interaction and risk for rheumatoid arthritis. by Krishnan E, Sokka T, Hannonen P. 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=165046
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Somatic mutations in the p53 tumor suppressor gene in rheumatoid arthritis synovium. by Firestein GS, Echeverri F, Yeo M, Zvaifler NJ, Green DR. 1997 Sep 30; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=23522
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Species-Specific Serodiagnosis of Lyme Arthritis and Neuroborreliosis Due to Borrelia burgdorferi Sensu Stricto, B. afzelii, and B. garinii by Using Decorin Binding Protein A. by Heikkila T, Seppala I, Saxen H, Panelius J, Yrjanainen H, Lahdenne P. 2002 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=153353
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Staphylococcal peptidoglycans induce arthritis. by Liu ZQ, Deng GM, Foster S, Tarkowski A. 2001; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=64849
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Structural Requirements for Recognition of the HLA-Dw14 Class II Epitope: A Key HLA Determinant Associated with Rheumatoid Arthritis. by Hiraiwa A, Yamanaka K, Kwok WW, Mickelson EM, Masewicz S, Hansen JA, Radka SF, Nepom GT. 1990 Oct 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=54890
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Studies of the specificity and cross-reactions of antibodies to lipid A found in juvenile arthritis.. by Miller JJ, Olds LC. 1995 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=170125
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Successful immunotherapy with matrix metalloproteinase-derived peptides in adjuvant arthritis depends on the timing of peptide administration. by van Bilsen JH, Wagenaar-Hilbers JP, van der Cammen MJ, van Dijk ME, van Eden W, Wauben MH. 2002; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=125294
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Suppression of Experimental Arthritis by Gene Transfer of Interleukin 1 Receptor Antagonist cDNA. by Makarov SS, Olsen JC, Johnston WN, Anderle SK, Brown RR, Baldwin AS, Haskill JS, Schwab JH. 1996 Jan 9; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=40246
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Suppression of murine collagen-induced arthritis by targeted apoptosis of synovial neovasculature. by Gerlag DM, Borges E, Tak PP, Ellerby HM, Bredesen DE, Pasqualini R, Ruoslahti E, Firestein GS. 2001; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=64846
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Suppressor of cytokine signaling-1 regulates acute inflammatory arthritis and T cell activation. by Egan PJ, Lawlor KE, Alexander WS, Wicks IP. 2003 Mar 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=153765
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Synergy between Anti-CD4 and Anti-Tumor Necrosis Factor in the Amelioration of Established Collagen-Induced Arthritis. by Williams RO, Mason LJ, Feldmann M, Maini RN. 1994 Mar 29; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=43450
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Synovial cytokine mRNA expression during arthritis triggered by CpG motifs of bacterial DNA. by Deng GM, Tarkowski A. 2001; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=17824
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Synovial stromal cells from rheumatoid arthritis patients attract monocytes by producing MCP-1 and IL-8. by Hayashida K, Nanki T, Girschick H, Yavuz S, Ochi T, Lipsky PE. 2001; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=17828
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Systemic Versus Cartilage-Specific Expression of a Type II Collagen-Specific T-Cell Epitope Determines the Level of Tolerance and Susceptibility to Arthritis. by Malmstrom V, Michaelsson E, Burkhardt H, Mattsson R, Vuorio E, Holmdahl R. 1996 Apr 30; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=39564
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T cell homeostasis in patients with rheumatoid arthritis. by Koetz K, Bryl E, Spickschen K, O'Fallon WM, Goronzy JJ, Weyand CM. 2000 Aug 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=16846
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T Cells and T-Cell Cytokine Transcripts in the Synovial Membrane in Patients with Osteoarthritis. by Sakkas LI, Scanzello C, Johanson N, Burkholder J, Mitra A, Salgame P, Katsetos CD, Platsoucas CD. 1998 Jul; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=95595
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T cells that are naturally tolerant to cartilage-derived type II collagen are involved in the development of collagen-induced arthritis. by Malmstrom V, Backlund J, Jansson L, Kihlberg J, Holmdahl R. 2000; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=17814
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T-cell activation without proliferation in juvenile idiopathic arthritis. by Black AP, Bhayani H, Ryder CA, Gardner-Medwin JM, Southwood TR. 2002; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=111019
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Th1 and Th2 cytokines regulate proteoglycan-specific autoantibody isotypes and arthritis. by Kaplan C, Valdez JC, Chandrasekaran R, Eibel H, Mikecz K, Glant TT, Finnegan A. 2002; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=64852
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The angiogenesis inhibitor protease-activated kringles 1 --5 reduces the severity of murine collagen-induced arthritis. by Sumariwalla PF, Cao Y, Wu HL, Feldmann M, Paleolog EM. 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=154428
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The Arthritis Research non-peer-review depository. by Lipsky PE, Maini RN. 2000; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=129985
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The expansion of CD4+CD28- T cells in patients with rheumatoid arthritis. by Pawlik A, Ostanek L, Brzosko I, Brzosko M, Masiuk M, Machalinski B, Gawronska-Szklarz B. 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=165060
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The genetics of rheumatoid arthritis and the need for animal models to find and understand the underlying genes. by Jirholt J, Lindqvist AK, Holmdahl R. 2001; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=128884
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The Immunoglobulin (IgG) Antibody Response to OspA and OspB Correlates with Severe and Prolonged Lyme Arthritis and the IgG Response to P35 Correlates with Mild and Brief Arthritis. by Akin E, McHugh GL, Flavell RA, Fikrig E, Steere AC. 1999 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=96293
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The nonpsychoactive cannabis constituent cannabidiol is an oral anti-arthritic therapeutic in murine collagen-induced arthritis. by Malfait AM, Gallily R, Sumariwalla PF, Malik AS, Andreakos E, Mechoulam R, Feldmann M. 2000 Aug 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=16904
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The role of prostaglandin E2 receptors in the pathogenesis of rheumatoid arthritis. by McCoy JM, Wicks JR, Audoly LP. 2002 Sep 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=151107
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The role of staphylococcal polysaccharide microcapsule expression in septicemia and septic arthritis.. by Nilsson IM, Lee JC, Bremell T, Ryden C, Tarkowski A. 1997 Oct; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=175605
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The T-Cell-Receptor Repertoire in the Synovial Fluid of a Patient with Rheumatoid Arthritis is Polyclonal. by Uematsu Y, Wege H, Straus A, Ott M, Bannwarth W, Lanchbury J, Panayi G, Steinmetz M. 1991 Oct 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=52543
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T-helper-cell cytokines in the early evolution of murine Lyme arthritis.. by Kang I, Barthold SW, Persing DH, Bockenstedt LK. 1997 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=175438
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Ticlopidine associated with acute arthritis. by Dakik HA, Salti I, Haidar R, Uthman IW. 2002 Jan 5; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=61656
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Upregulated hypoxia inducible factor-1[alpha] and -2[alpha] pathway in rheumatoid arthritis and osteoarthritis. by Giatromanolaki A, Sivridis E, Maltezos E, Athanassou N, Papazoglou D, Gatter KC, Harris AL, Koukourakis MI. 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=165055
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Urinary Excretion of Thiol Compounds in Patients with Rheumatoid Arthritis. by Rojkovich B, Nagy E, Prohle T, Poor G, Gergely P. 1999 Sep; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=95754
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Urokinase, a constitutive component of the inflamed synovial fluid, induces arthritis. by Jin T, Tarkowski A, Carmeliet P, Bokarewa M. 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=154426
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Use of soluble peptide --DR4 tetramers to detect synovial T cells specific for cartilage antigens in patients with rheumatoid arthritis. by Kotzin BL, Falta MT, Crawford F, Rosloniec EF, Bill J, Marrack P, Kappler J. 2000 Jan 4; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=26656
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Use of Two-Dimensional Gel Electrophoresis To Measure Changes in Synovial Fluid Proteins from Patients with Rheumatoid Arthritis Treated with Antibody to CD4. by Smith MA, Bains SK, Betts JC, Choy EH, Zanders ED. 2001 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=96017
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Variability and Immunogenicity of Caprine Arthritis-Encephalitis Virus Surface Glycoprotein. by Valas S, Benoit C, Baudry C, Perrin G, Mamoun RZ. 2000 Jul 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=112118
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VLA-4-dependent and -independent pathways in cell contact-induced proinflammatory cytokine production by synovial nurse-like cells from rheumatoid arthritis patients. by Takeuchi E, Tanaka T, Umemoto E, Tomita T, Shi K, Takahi K, Suzuki R, Ochi T, Miyasaka M. 2002; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=153839
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Waldenstrom's Disease Complicated by Recurrent Meningococcal Arthritis. by Singwe-Ngandeu M, Buchs N, Rohner P, Gabay C. 2001 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=88284
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What can we do about osteoarthritis? by Lohmander LS. 2000; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=129992
The National Library of Medicine: PubMed One of the quickest and most comprehensive ways to find academic studies in both English and other languages is to use PubMed, maintained by the National Library of Medicine.6 The advantage of PubMed over previously mentioned sources is that it covers a greater number of domestic and foreign references. It is also free to use. If the publisher has a Web PubMed was developed by the National Center for Biotechnology Information (NCBI) at the National Library of Medicine (NLM) at the National Institutes of Health (NIH). The PubMed database was developed in conjunction with publishers of biomedical literature as a search tool for accessing literature citations and linking to full-text journal articles at Web sites of participating publishers. Publishers that participate in PubMed supply NLM with their citations electronically prior to or at the time of publication.
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site that offers full text of its journals, PubMed will provide links to that site, as well as to sites offering other related data. User registration, a subscription fee, or some other type of fee may be required to access the full text of articles in some journals. To generate your own bibliography of studies dealing with arthritis, simply go to the PubMed Web site at http://www.ncbi.nlm.nih.gov/pubmed. Type “arthritis” (or synonyms) into the search box, and click “Go.” The following is the type of output you can expect from PubMed for “arthritis” (hyperlinks lead to article summaries): ·
A case of multiple sclerosis associated with rheumatoid arthritis and positive anticardiolipin antibodies. Author(s): Mpofu S, Moots RJ. Source: Annals of the Rheumatic Diseases. 2003 April; 62(4): 376. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12634248&dopt=Abstract
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A case of orbital myositis associated with rheumatoid arthritis. Author(s): Fadini GP. Source: Annals of the Rheumatic Diseases. 2003 April; 62(4): 383; Author Reply 383-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12634254&dopt=Abstract
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A child with vitamin D deficiency rickets and suppurative arthritis. Author(s): Weinstein M. Source: The Pediatric Infectious Disease Journal. 2003 March; 22(3): 290-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12664884&dopt=Abstract
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A clinical practice guideline for treatment of septic arthritis in children: efficacy in improving process of care and effect on outcome of septic arthritis of the hip. Author(s): Kocher MS, Mandiga R, Murphy JM, Goldmann D, Harper M, Sundel R, Ecklund K, Kasser JR. Source: The Journal of Bone and Joint Surgery. American Volume. 2003 June; 85-A(6): 994-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12783993&dopt=Abstract
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A comparison of self-reports of distress and affective disorder diagnoses in rheumatoid arthritis: a receiver operator characteristic analysis. Author(s): McQuillan J, Fifield J, Sheehan TJ, Reisine S, Tennen H, Hesselbrock V, Rothfield N. Source: Arthritis and Rheumatism. 2003 June 15; 49(3): 368-76. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12794793&dopt=Abstract
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A comparison of ultrasonography and magnetic resonance imaging in the evaluation of temporomandibular joint involvement in rheumatoid arthritis and psoriatic arthritis. Author(s): Melchiorre D, Calderazzi A, Maddali Bongi S, Cristofani R, Bazzichi L, Eligi C, Maresca M, Ciompi M. Source: Rheumatology (Oxford, England). 2003 May; 42(5): 673-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12709544&dopt=Abstract
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A controlled longitudinal study of the social functioning of children with juvenile rheumatoid arthritis. Author(s): Reiter-Purtill J, Gerhardt CA, Vannatta K, Passo MH, Noll RB. Source: Journal of Pediatric Psychology. 2003 January-February; 28(1): 17-28. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12490627&dopt=Abstract
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A host of novel agents for treating psoriasis, psoriatic arthritis stir interest. Author(s): Lamberg L. Source: Jama : the Journal of the American Medical Association. 2003 June 4; 289(21): 2779-80, 2783. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12783895&dopt=Abstract
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A longitudinal study of rheumatoid arthritis in South Africans. Author(s): Tikly M, Zannettou N, Hopley M. Source: Medgenmed [electronic Resource] : Medscape General Medicine. 2003 February 5; 5(1): 2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12827063&dopt=Abstract
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A novel anti-inflammatory role for simvastatin in inflammatory arthritis. Author(s): Leung BP, Sattar N, Crilly A, Prach M, McCarey DW, Payne H, Madhok R, Campbell C, Gracie JA, Liew FY, McInnes IB. Source: Journal of Immunology (Baltimore, Md. : 1950). 2003 February 1; 170(3): 1524-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12538717&dopt=Abstract
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A poly(ADP-ribose) polymerase haplotype spanning the promoter region confers susceptibility to rheumatoid arthritis. Author(s): Pascual M, Lopez-Nevot MA, Caliz R, Ferrer MA, Balsa A, Pascual-Salcedo D, Martin J. Source: Arthritis and Rheumatism. 2003 March; 48(3): 638-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12632415&dopt=Abstract
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A polyarticular onset predicts erosive and deforming disease in psoriatic arthritis. Author(s): Queiro-Silva R, Torre-Alonso JC, Tinture-Eguren T, Lopez-Lagunas I. Source: Annals of the Rheumatic Diseases. 2003 January; 62(1): 68-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12480674&dopt=Abstract
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A prospective study of sicca symptoms in patients with rheumatoid arthritis. Author(s): Brun JG, Madland TM, Jonsson R. Source: Arthritis and Rheumatism. 2003 April 15; 49(2): 187-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12687509&dopt=Abstract
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A question of transformation: the synovial fibroblast in rheumatoid arthritis. Author(s): Davis LS. Source: American Journal of Pathology. 2003 May; 162(5): 1399-402. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12707022&dopt=Abstract
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A randomized double blind, placebo controlled trial of topical Tripterygium wilfordii in rheumatoid arthritis: reanalysis using logistic regression analysis. Author(s): Cibere J, Deng Z, Lin Y, Ou R, He Y, Wang Z, Thorne A, Lehman AJ, Tsang IK, Esdaile JM. Source: The Journal of Rheumatology. 2003 March; 30(3): 465-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12610802&dopt=Abstract
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A rare case of juxtaarticular osteoid osteoma of the calcaneus initially misdiagnosed as juvenile chronic arthritis. Author(s): Christodoulou A, Ploumis A, Karkavelas G, Terzidis I, Tsagias I. Source: Arthritis and Rheumatism. 2003 March; 48(3): 776-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12632432&dopt=Abstract
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A rationale for the use of summary measurements for the assessment of the effects of rheumatoid arthritis therapies. Author(s): Schiff M. Source: Clinical Therapeutics. 2003 March; 25(3): 993-1001. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12852713&dopt=Abstract
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A simplified disease activity index for rheumatoid arthritis for use in clinical practice. Author(s): Smolen JS, Breedveld FC, Schiff MH, Kalden JR, Emery P, Eberl G, van Riel PL, Tugwell P. Source: Rheumatology (Oxford, England). 2003 February; 42(2): 244-57. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12595618&dopt=Abstract
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A single infusion of infliximab increases the serum endostatin level in patients with rheumatoid arthritis. Author(s): Kucharz EJ, Gozdzik J, Kopec M, Kotulska A, Lewicki M, Pieczyrak R, Widuchowska M, Zakliczynska H, Szarzynska-Ruda M, Zycinska-Debska E. Source: Clin Exp Rheumatol. 2003 March-April; 21(2): 273-4. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12747296&dopt=Abstract
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A susceptibility gene for psoriatic arthritis maps to chromosome 16q: evidence for imprinting. Author(s): Karason A, Gudjonsson JE, Upmanyu R, Antonsdottir AA, Hauksson VB, Runasdottir EH, Jonsson HH, Gudbjartsson DF, Frigge ML, Kong A, Stefansson K, Valdimarsson H, Gulcher JR. Source: American Journal of Human Genetics. 2003 January; 72(1): 125-31. Epub 2002 December 09. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12474146&dopt=Abstract
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Abandoned therapies and unpublished trials in rheumatoid arthritis. Author(s): Keystone EC. Source: Current Opinion in Rheumatology. 2003 May; 15(3): 253-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12707578&dopt=Abstract
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Aberrant activation of B cells in patients with rheumatoid arthritis. Author(s): Lindenau S, Scholze S, Odendahl M, Dorner T, Radbruch A, Burmester GR, Berek C. Source: Annals of the New York Academy of Sciences. 2003 April; 987: 246-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12727646&dopt=Abstract
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Abnormal IgA levels in patients with rheumatoid arthritis. Author(s): Badcock LJ, Clarke S, Jones PW, Dawes PT, Mattey DL. Source: Annals of the Rheumatic Diseases. 2003 January; 62(1): 83-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12480680&dopt=Abstract
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Abnormal vitamin B(6) status is associated with severity of symptoms in patients with rheumatoid arthritis. Author(s): Chiang EP, Bagley PJ, Selhub J, Nadeau M, Roubenoff R. Source: The American Journal of Medicine. 2003 March; 114(4): 283-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12681455&dopt=Abstract
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Abrupt condylar destruction of the mandibula in juvenile idiopathic arthritis. Author(s): Twilt M, van der Giesen E, Mobers SM, ten Cate R, van Suijlekom-Smit LW. Source: Annals of the Rheumatic Diseases. 2003 April; 62(4): 366-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12634241&dopt=Abstract
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Acetabular revision with impacted morselized cancellous bone graft and a cemented cup in patients with rheumatoid arthritis: three to fourteen-year follow-up. Author(s): Schreurs BW, Thien TM, de Waal Malefijt MC, Buma P, Veth RP, Slooff TJ. Source: The Journal of Bone and Joint Surgery. American Volume. 2003 April; 85-A(4): 647-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12672840&dopt=Abstract
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Acral and ear papules and arthritis. Author(s): Petro A, Wegman PA, Su LD. Source: Archives of Dermatology. 2003 May; 139(5): 657-62. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12756106&dopt=Abstract
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Acute posterior interosseous nerve palsy caused by septic arthritis of the elbow: a case report. Author(s): Kato H, Iwasaki N, Minami A, Kamishima T. Source: The Journal of Hand Surgery. 2003 January; 28(1): 44-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12563636&dopt=Abstract
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Acute septic arthritis of the hip in children in northern Australia. Author(s): Gandini D. Source: Anz Journal of Surgery. 2003 March; 73(3): 136-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12608977&dopt=Abstract
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Acute septic arthritis of the hip in children in Northern Australia. Author(s): Graham HK. Source: Anz Journal of Surgery. 2003 March; 73(3): 91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12608961&dopt=Abstract
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Adalimumab, a fully human anti-tumor necrosis factor alpha monoclonal antibody, for the treatment of rheumatoid arthritis in patients taking concomitant methotrexate: the ARMADA trial. Author(s): Weinblatt ME, Keystone EC, Furst DE, Moreland LW, Weisman MH, Birbara CA, Teoh LA, Fischkoff SA, Chartash EK. Source: Arthritis and Rheumatism. 2003 January; 48(1): 35-45. Erratum In: Arthritis Rheum. 2003 March; 48(3): 855. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12528101&dopt=Abstract
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Adaptation and validation of the Turkish version of the Rheumatoid Arthritis Quality of Life Scale. Author(s): Kutlay S, Kucukdeveci AA, Gonul D, Tennant A. Source: Rheumatology International. 2003 January; 23(1): 21-6. Epub 2002 October 22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12548438&dopt=Abstract
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Add-on or step-up trials for new drug development in rheumatoid arthritis: a new standard? Author(s): Boers M. Source: Arthritis and Rheumatism. 2003 June; 48(6): 1481-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12794813&dopt=Abstract
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Addressing the safety of anakinra in patients with rheumatoid arthritis. Author(s): Fleischmann RM. Source: Rheumatology (Oxford, England). 2003 May; 42 Suppl 2: Ii29-35. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12817093&dopt=Abstract
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Administrative data as a tool for arthritis surveillance: estimating prevalence and utilization of services. Author(s): Powell KE, Diseker RA 3rd, Presley RJ, Tolsma D, Harris S, Mertz KJ, Viel K, Conn DL, McClellan W. Source: Journal of Public Health Management and Practice : Jphmp. 2003 July-August; 9(4): 291-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12836511&dopt=Abstract
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Adrenomedullin in synovial fluids from patients with rheumatoid arthritis inhibits interleukin 6 production from synoviocytes. Author(s): Nanke Y, Kotake S, Yonemoto K, Saito S, Tomatsu T, Kamatani N. Source: Annals of the Rheumatic Diseases. 2003 January; 62(1): 82-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12480679&dopt=Abstract
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Advances in the management of septic arthritis. Author(s): Garcia-De La Torre I. Source: Rheumatic Diseases Clinics of North America. 2003 February; 29(1): 61-75. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12635500&dopt=Abstract
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Age at menarche in juvenile rheumatoid arthritis. Author(s): Rusconi R, Corona F, Grassi A, Carnelli V. Source: J Pediatr Endocrinol Metab. 2003 March; 16 Suppl 2: 285-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12729405&dopt=Abstract
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Albumin-based drug delivery as novel therapeutic approach for rheumatoid arthritis. Author(s): Wunder A, Muller-Ladner U, Stelzer EH, Funk J, Neumann E, Stehle G, Pap T, Sinn H, Gay S, Fiehn C. Source: Journal of Immunology (Baltimore, Md. : 1950). 2003 May 1; 170(9): 4793-801. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12707361&dopt=Abstract
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Allele and antigen-specific treatment of rheumatoid arthritis: a double blind, placebo controlled phase 1 trial. Author(s): Kavanaugh A, Genovese M, Baughman J, Kivitz A, Bulpitt K, Olsen N, Weisman M, Matteson E, Furst D, van Vollenhoven R, Anderson J, Cohen S, Wei N, Meijerink J, Jacobs C, Mocci S. Source: The Journal of Rheumatology. 2003 March; 30(3): 449-54. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12610799&dopt=Abstract
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American Pain Society releases new guidelines for arthritis pain. Author(s): American Pain Society. Source: Home Healthcare Nurse. 2003 June; 21(6): 413-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12841185&dopt=Abstract
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Aminotransferase levels during treatment of rheumatoid arthritis with leflunomide in clinical practice. Author(s): Hoi A, Littlejohn GO. Source: Annals of the Rheumatic Diseases. 2003 April; 62(4): 379. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12634251&dopt=Abstract
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Amyloid arthropathy resembling seronegative rheumatoid arthritis in a patient with IgD-kappa multiple myeloma. Author(s): Fujishima M, Komatsuda A, Imai H, Wakui H, Watanabe W, Sawada K. Source: Intern Med. 2003 January; 42(1): 121-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12583633&dopt=Abstract
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An alternative perspective on treatment for diabetes, hypertension, and rheumatoid arthritis: comment on the editorial by Pincus et al. Author(s): Harrington T, Walsh MB. Source: Arthritis and Rheumatism. 2003 February; 48(2): 575-6; Author Reply 576-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12571871&dopt=Abstract
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An exceptional radiographic presentation of bilateral insufficiency fractures of the proximal tibia in a patient with rheumatoid arthritis. Author(s): Vanhoof J, Landewe S, Vandevenne J, Geusens P. Source: Annals of the Rheumatic Diseases. 2003 March; 62(3): 277-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12594125&dopt=Abstract
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An experimental study of a Mediterranean diet intervention for patients with rheumatoid arthritis. Author(s): Skoldstam L, Hagfors L, Johansson G. Source: Annals of the Rheumatic Diseases. 2003 March; 62(3): 208-14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12594104&dopt=Abstract
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An index of the three core data set patient questionnaire measures distinguishes efficacy of active treatment from that of placebo as effectively as the American College of Rheumatology 20% response criteria (ACR20) or the Disease Activity Score (DAS) in a rheumatoid arthritis clinical trial. Author(s): Pincus T, Strand V, Koch G, Amara I, Crawford B, Wolfe F, Cohen S, Felson D. Source: Arthritis and Rheumatism. 2003 March; 48(3): 625-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12632413&dopt=Abstract
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An open label study to establish dosing recommendations for nabumetone in juvenile rheumatoid arthritis. Author(s): Goodman S, Howard P, Haig A, Flavin S, Macdonald B. Source: The Journal of Rheumatology. 2003 April; 30(4): 829-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12672207&dopt=Abstract
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An open-label trial of the selective cyclo-oxygenase-2 inhibitor, rofecoxib, in inflammatory bowel disease-associated peripheral arthritis and arthralgia. Author(s): Reinisch W, Miehsler W, Dejaco C, Harrer M, Waldhoer T, Lichtenberger C, Vogelsang H. Source: Alimentary Pharmacology & Therapeutics. 2003 June 1; 17(11): 1371-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12786631&dopt=Abstract
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Anakinra, a recombinant human interleukin-1 receptor antagonist (r-metHuIL-1ra), in patients with rheumatoid arthritis: A large, international, multicenter, placebocontrolled trial. Author(s): Fleischmann RM, Schechtman J, Bennett R, Handel ML, Burmester GR, Tesser J, Modafferi D, Poulakos J, Sun G. Source: Arthritis and Rheumatism. 2003 April; 48(4): 927-34. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12687534&dopt=Abstract
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Anakinra: the first interleukin-1 inhibitor in the treatment of rheumatoid arthritis. Author(s): Kary S, Burmester GR. Source: Int J Clin Pract. 2003 April; 57(3): 231-4. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12723729&dopt=Abstract
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Analysis of a viridans group strain reveals a case of bacteremia due to lancefield group G alpha-hemolytic Streptococcus dysgalactiae subsp equisimilis in a patient with pyomyositis and reactive arthritis. Author(s): Woo PC, Teng JL, Lau SK, Lum PN, Leung KW, Wong KL, Li KW, Lam KC, Yuen KY. Source: Journal of Clinical Microbiology. 2003 February; 41(2): 613-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12574255&dopt=Abstract
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Analysis of the cell infiltrate and expression of proinflammatory cytokines and matrix metalloproteinases in arthroscopic synovial biopsies: comparison with synovial samples from patients with end stage, destructive rheumatoid arthritis. Author(s): Smeets TJ, Barg EC, Kraan MC, Smith MD, Breedveld FC, Tak PP. Source: Annals of the Rheumatic Diseases. 2003 July; 62(7): 635-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12810425&dopt=Abstract
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Angiopoietin-1 is expressed in the synovium of patients with rheumatoid arthritis and is induced by tumour necrosis factor alpha. Author(s): Gravallese EM, Pettit AR, Lee R, Madore R, Manning C, Tsay A, Gaspar J, Goldring MB, Goldring SR, Oettgen P. Source: Annals of the Rheumatic Diseases. 2003 February; 62(2): 100-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12525377&dopt=Abstract
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Angiopoietins, growth factors, and vascular morphology in early arthritis. Author(s): Fearon U, Griosios K, Fraser A, Reece R, Emery P, Jones PF, Veale DJ. Source: The Journal of Rheumatology. 2003 February; 30(2): 260-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12563678&dopt=Abstract
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Ankle arthritis. Author(s): Thomas RH, Daniels TR. Source: The Journal of Bone and Joint Surgery. American Volume. 2003 May; 85-A(5): 923-36. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12728047&dopt=Abstract
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Ankylosis of the temporomandibular joint as a sequela of septic arthritis and neonatal sepsis. Author(s): Regev E, Koplewitz BZ, Nitzan DW, Bar-Ziv J. Source: The Pediatric Infectious Disease Journal. 2003 January; 22(1): 99-101. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12553307&dopt=Abstract
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Antibiotic treatment and long term prognosis of reactive arthritis. Author(s): Laasila K, Laasonen L, Leirisalo-Repo M. Source: Annals of the Rheumatic Diseases. 2003 July; 62(7): 655-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12810429&dopt=Abstract
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Antibody-mediated stripping of CD4 from lymphocyte cell surface in patients with rheumatoid arthritis. Author(s): Hepburn TW, Totoritis MC, Davis CB. Source: Rheumatology (Oxford, England). 2003 January; 42(1): 54-61. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12509613&dopt=Abstract
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Anticitrullinated protein/peptide antibody assays in early rheumatoid arthritis for predicting five year radiographic damage. Author(s): Meyer O, Labarre C, Dougados M, Goupille P, Cantagrel A, Dubois A, Nicaise-Roland P, Sibilia J, Combe B. Source: Annals of the Rheumatic Diseases. 2003 February; 62(2): 120-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12525380&dopt=Abstract
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Anti-cyclic citrullinated peptide (anti-CCP) antibodies in children with juvenile idiopathic arthritis. Author(s): van Rossum M, van Soesbergen R, de Kort S, ten Cate R, Zwinderman AH, de Jong B, Dijkmans B, van Venrooij WJ. Source: The Journal of Rheumatology. 2003 April; 30(4): 825-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12672206&dopt=Abstract
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Anti-cyclic citrullinated peptide antibodies in advanced rheumatoid arthritis. Author(s): Pinheiro GC, Scheinberg MA, Aparecida da Silva M, Maciel S. Source: Annals of Internal Medicine. 2003 August 5; 139(3): 234-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12899598&dopt=Abstract
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Anti-cyclic citrullinated peptide antibodies, IgM and IgA rheumatoid factors in the diagnosis and prognosis of rheumatoid arthritis. Author(s): Bas S, Genevay S, Meyer O, Gabay C. Source: Rheumatology (Oxford, England). 2003 May; 42(5): 677-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12709545&dopt=Abstract
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Anti-cyclic citrullinated peptide antibody in early rheumatoid arthritis: comment on the editorial by Scott. Author(s): van Venrooij WJ, van de Putte LB, van den Hoogen FH. Source: Arthritis and Rheumatism. 2003 March; 48(3): 857; Author Reply 857-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12632446&dopt=Abstract
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Anti-cytokines and cytokines in the treatment of rheumatoid arthritis. Author(s): Taylor PC. Source: Current Pharmaceutical Design. 2003; 9(14): 1095-106. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12769749&dopt=Abstract
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Anti-glomerular basement membrane antibody-associated renal failure in a patient with leflunomide-treated rheumatoid arthritis. Author(s): Bruyn GA, Veenstra RP, Halma C, Grond J. Source: Arthritis and Rheumatism. 2003 April; 48(4): 1164-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12687568&dopt=Abstract
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Anti-inflammatory effects of a low arachidonic acid diet and fish oil in patients with rheumatoid arthritis. Author(s): Adam O, Beringer C, Kless T, Lemmen C, Adam A, Wiseman M, Adam P, Klimmek R, Forth W. Source: Rheumatology International. 2003 January; 23(1): 27-36. Epub 2002 September 06. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12548439&dopt=Abstract
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Anti-inflammatory effects of leflunomide on cultured synovial macrophages from patients with rheumatoid arthritis. Author(s): Cutolo M, Sulli A, Ghiorzo P, Pizzorni C, Craviotto C, Villaggio B. Source: Annals of the Rheumatic Diseases. 2003 April; 62(4): 297-302. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12634225&dopt=Abstract
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Anti-interleukin-6 receptor antibody therapy reduces vascular endothelial growth factor production in rheumatoid arthritis. Author(s): Nakahara H, Song J, Sugimoto M, Hagihara K, Kishimoto T, Yoshizaki K, Nishimoto N. Source: Arthritis and Rheumatism. 2003 June; 48(6): 1521-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12794819&dopt=Abstract
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Antinuclear antibodies following infliximab treatment in patients with rheumatoid arthritis or spondylarthropathy. Author(s): De Rycke L, Kruithof E, Van Damme N, Hoffman IE, Van den Bossche N, Van den Bosch F, Veys EM, De Keyser F. Source: Arthritis and Rheumatism. 2003 April; 48(4): 1015-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12687543&dopt=Abstract
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Antioxidant micronutrients and risk of rheumatoid arthritis in a cohort of older women. Author(s): Cerhan JR, Saag KG, Merlino LA, Mikuls TR, Criswell LA. Source: American Journal of Epidemiology. 2003 February 15; 157(4): 345-54. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12578805&dopt=Abstract
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Anti-TNFalpha therapy for rheumatoid arthritis: an update. Author(s): Taylor PC. Source: Intern Med. 2003 January; 42(1): 15-20. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12583612&dopt=Abstract
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Anti-tumour necrosis factor treatment in a patient with anorexia nervosa and juvenile idiopathic arthritis. Author(s): Barber J, Sheeran T, Mulherin D. Source: Annals of the Rheumatic Diseases. 2003 May; 62(5): 490-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12695170&dopt=Abstract
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Apoptosis in rheumatoid arthritis. Author(s): Baier A, Meineckel I, Gay S, Pap T. Source: Current Opinion in Rheumatology. 2003 May; 15(3): 274-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12707581&dopt=Abstract
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Apoptosis of peripheral blood lymphocytes in patients with juvenile idiopathic arthritis. Author(s): Smolewska E, Brozik H, Smolewski P, Biernacka-Zielinska M, Darzynkiewicz Z, Stanczyk J. Source: Annals of the Rheumatic Diseases. 2003 August; 62(8): 761-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12860732&dopt=Abstract
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Applying low disease activity criteria using the DAS28 to assess stability in patients with rheumatoid arthritis. Author(s): Vrijhoef HJ, Diederiks JP, Spreeuwenberg C, Van der Linden S. Source: Annals of the Rheumatic Diseases. 2003 May; 62(5): 419-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12695152&dopt=Abstract
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Aromatic trap analysis of free radicals production in experimental collagen-induced arthritis in the rat: protective effect of glycosaminoglycans treatment. Author(s): Campo GM, Avenoso A, Campo S, Ferlazzo A, Altavilla D, Micali C, Calatroni A. Source: Free Radical Research. 2003 March; 37(3): 257-68. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12688421&dopt=Abstract
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Art, artists, and arthritis. Author(s): Levine H. Source: Md Med. 2003 Winter; 4(1): 36-7. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12652862&dopt=Abstract
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Arterial stiffness and central blood pressure, as determined by pulse wave analysis, in rheumatoid arthritis. Author(s): Klocke R, Cockcroft JR, Taylor GJ, Hall IR, Blake DR. Source: Annals of the Rheumatic Diseases. 2003 May; 62(5): 414-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12695151&dopt=Abstract
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Arthritis and interstitial granulomatous dermatitis (Ackerman syndrome) with pulmonary silicosis. Author(s): Kroesen S, Itin PH, Hasler P. Source: Seminars in Arthritis and Rheumatism. 2003 April; 32(5): 334-40. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12701044&dopt=Abstract
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Arthritis and osteotomies in anterior cruciate ligament reconstruction. Author(s): Stein BE, Williams RJ 3rd, Wickiewicz TL. Source: The Orthopedic Clinics of North America. 2003 January; 34(1): 169-81. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12735208&dopt=Abstract
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Arthritis and uveitis in children. A pediatric rheumatology perspective. Author(s): Petty RE, Smith JR, Rosenbaum JT. Source: American Journal of Ophthalmology. 2003 June; 135(6): 879-84. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12788129&dopt=Abstract
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Arthritis as a cause of prolonged in-patient admission in acute medical beds. Author(s): Keough A, Kirwan JR. Source: Rheumatology (Oxford, England). 2003 June; 42(6): 810-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12771446&dopt=Abstract
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Arthritis as an unusual manifestation of Kikuchi-Fujimoto disease. Author(s): Douglas M, Bradbury R, Kannangara S, Mitchell D. Source: Rheumatology (Oxford, England). 2003 August; 42(8): 1010-2. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12869674&dopt=Abstract
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Arthritis associated with enteric infection. Author(s): Hill Gaston JS, Lillicrap MS. Source: Best Practice & Research. Clinical Rheumatology. 2003 April; 17(2): 219-39. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12787523&dopt=Abstract
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Arthritis associated with tuberculosis. Author(s): Malaviya AN, Kotwal PP. Source: Best Practice & Research. Clinical Rheumatology. 2003 April; 17(2): 319-43. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12787528&dopt=Abstract
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Arthritis following stomatitis in a sixteen-month-old child. Author(s): Yagupsky P, Press J. Source: The Pediatric Infectious Disease Journal. 2003 June; 22(6): 573-4, 576-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12828161&dopt=Abstract
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Arthritis Foundation community-based physical activity programs: effectiveness and implementation issues. Author(s): Boutaugh ML. Source: Arthritis and Rheumatism. 2003 June 15; 49(3): 463-70. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12794805&dopt=Abstract
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Arthritis in older adults. Current therapy with self-management as centerpiece. Author(s): Luggen AS. Source: Adv Nurse Pract. 2003 March; 11(3): 26-35; Quiz 36. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12683167&dopt=Abstract
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Arthritis self-management education programs: a meta-analysis of the effect on pain and disability. Author(s): Warsi A, LaValley MP, Wang PS, Avorn J, Solomon DH. Source: Arthritis and Rheumatism. 2003 August; 48(8): 2207-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12905474&dopt=Abstract
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Arthritis-related shunt nephritis in an adult. Author(s): Legoupil N, Ronco P, Berenbaum F. Source: Rheumatology (Oxford, England). 2003 May; 42(5): 698-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12709554&dopt=Abstract
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Arthrodesis of the shoulder after septic arthritis. Long-term results. Author(s): Wick M, Muller EJ, Ambacher T, Hebler U, Muhr G, Kutscha-Lissberg F. Source: The Journal of Bone and Joint Surgery. British Volume. 2003 July; 85(5): 666-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12892187&dopt=Abstract
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Arthroplasty of the shoulder in rheumatoid arthritis with rotator cuff dysfunction. Author(s): Woodruff MJ, Cohen AP, Bradley JG. Source: International Orthopaedics. 2003; 27(1): 7-10. Epub 2002 October 23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12582801&dopt=Abstract
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Arthroscopic treatment of septic arthritis of the hip. Author(s): Kim SJ, Choi NH, Ko SH, Linton JA, Park HW. Source: Clinical Orthopaedics and Related Research. 2003 February; (407): 211-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12567149&dopt=Abstract
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Arthrosonography of hip and knee joints in the follow up of juvenile rheumatoid arthritis. Author(s): Frosch M, Foell D, Ganser G, Roth J. Source: Annals of the Rheumatic Diseases. 2003 March; 62(3): 242-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12594110&dopt=Abstract
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Assessing the value of rheumatoid arthritis treatment alternatives: the potential effect of tumor necrosis factor inhibitors. Author(s): Mizutani W. Source: Manag Care Interface. 2003 March; 16(3): 44-50, 55. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12715413&dopt=Abstract
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Assessment of the test characteristics of C-reactive protein for septic arthritis in children. Author(s): Levine MJ, McGuire KJ, McGowan KL, Flynn JM. Source: Journal of Pediatric Orthopedics. 2003 May-June; 23(3): 373-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12724603&dopt=Abstract
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Association between carotid atherosclerosis and markers of inflammation in rheumatoid arthritis patients and healthy subjects. Author(s): Del Rincon I, Williams K, Stern MP, Freeman GL, O'Leary DH, Escalante A. Source: Arthritis and Rheumatism. 2003 July; 48(7): 1833-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12847676&dopt=Abstract
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Association of depression and rheumatoid arthritis. Author(s): Dickens C, Jackson J, Tomenson B, Hay E, Creed F. Source: Psychosomatics. 2003 May-June; 44(3): 209-15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12724502&dopt=Abstract
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Association of interleukin-18 expression with enhanced levels of both interleukin1beta and tumor necrosis factor alpha in knee synovial tissue of patients with rheumatoid arthritis. Author(s): Joosten LA, Radstake TR, Lubberts E, van den Bersselaar LA, van Riel PL, van Lent PL, Barrera P, van den Berg WB. Source: Arthritis and Rheumatism. 2003 February; 48(2): 339-47. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12571842&dopt=Abstract
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Association of polymorphisms of the tumour necrosis factor receptors I and II and rheumatoid arthritis. Author(s): Bayley JP, Bakker AM, Kaijzel EL, Huizinga TW, Verweij CL. Source: Rheumatology (Oxford, England). 2003 August; 42(8): 969-71. Epub 2003 March 31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12730509&dopt=Abstract
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Association of the -2849 interleukin-10 promoter polymorphism with autoantibody production and joint destruction in rheumatoid arthritis. Author(s): Lard LR, van Gaalen FA, Schonkeren JJ, Pieterman EJ, Stoeken G, Vos K, Nelissen RG, Westendorp RG, Hoeben RC, Breedveld FC, Toes RE, Huizinga TW. Source: Arthritis and Rheumatism. 2003 July; 48(7): 1841-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12847677&dopt=Abstract
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Asymptomatic erosive peripheral psoriatic arthritis: a frequent finding in Italian patients. Author(s): Palazzi C, D'Agostino L, D'Amico E, Pennese E, Petricca A. Source: Rheumatology (Oxford, England). 2003 July; 42(7): 909-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12826714&dopt=Abstract
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Atlantoaxial arthrodesis for vertebrobasilar insufficiency due to rheumatoid arthritis: a case report. Author(s): Maekawa T, Sasai K, Iida H, Yamashita K, Sakaida M. Source: The Journal of Bone and Joint Surgery. American Volume. 2003 April; 85-A(4): 711-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12672850&dopt=Abstract
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Atlantoaxial disorders in rheumatoid arthritis associate with the destruction of peripheral and shoulder joints, and decreased bone mineral density. Author(s): Neva MH, Kotaniemi A, Kaarela K, Lehtinen JT, Belt EA, Kauppi M. Source: Clin Exp Rheumatol. 2003 March-April; 21(2): 179-84. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12747271&dopt=Abstract
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Autoantibodies can be prognostic markers of an erosive disease in early rheumatoid arthritis. Author(s): Vencovsky J, Machacek S, Sedova L, Kafkova J, Gatterova J, Pesakova V, Ruzickova S. Source: Annals of the Rheumatic Diseases. 2003 May; 62(5): 427-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12695154&dopt=Abstract
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Autologous haematopoietic stem cell transplantation in juvenile idiopathic arthritis. Author(s): Wedderburn LR, Abinun M, Palmer P, Foster HE. Source: Archives of Disease in Childhood. 2003 March; 88(3): 201-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12598377&dopt=Abstract
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Bacterial components in the synovial tissue of patients with advanced rheumatoid arthritis or osteoarthritis: analysis with gas chromatography-mass spectrometry and pan-bacterial polymerase chain reaction. Author(s): Chen T, Rimpilainen M, Luukkainen R, Mottonen T, Yli-Jama T, Jalava J, Vainio O, Toivanen P. Source: Arthritis and Rheumatism. 2003 June 15; 49(3): 328-34. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12794787&dopt=Abstract
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Baseline balance and functional decline in older adults with knee pain: the Observational Arthritis Study in Seniors. Author(s): Marsh AP, Rejeski WJ, Lang W, Miller ME, Messier SP. Source: Journal of the American Geriatrics Society. 2003 March; 51(3): 331-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12588576&dopt=Abstract
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Benefit-risk assessment of infliximab in the treatment of rheumatoid arthritis. Author(s): Mikuls TR, Moreland LW. Source: Drug Safety : an International Journal of Medical Toxicology and Drug Experience. 2003; 26(1): 23-32. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12495361&dopt=Abstract
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Binding of outer surface protein A and human lymphocyte function-associated antigen 1 peptides to HLA-DR molecules associated with antibiotic treatmentresistant Lyme arthritis. Author(s): Steere AC, Falk B, Drouin EE, Baxter-Lowe LA, Hammer J, Nepom GT. Source: Arthritis and Rheumatism. 2003 February; 48(2): 534-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12571864&dopt=Abstract
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Biologic therapies for juvenile arthritis. Author(s): Wilkinson N, Jackson G, Gardner-Medwin J. Source: Archives of Disease in Childhood. 2003 March; 88(3): 186-91. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12598373&dopt=Abstract
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Biological response modifiers in the management of rheumatoid arthritis. Author(s): Louie SG, Park B, Yoon H. Source: American Journal of Health-System Pharmacy : Ajhp : Official Journal of the American Society of Health-System Pharmacists. 2003 February 15; 60(4): 346-55. Review. Erratum In: Am J Health Syst Pharm.2003 June 1; 60(11): 1095. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12625216&dopt=Abstract
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BiP, a putative autoantigen in rheumatoid arthritis, stimulates IL-10-producing CD8positive T cells from normal individuals. Author(s): Bodman-Smith MD, Corrigall VM, Kemeny DM, Panayi GS. Source: Rheumatology (Oxford, England). 2003 May; 42(5): 637-44. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12709539&dopt=Abstract
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Bisphosphonates for arthritis--a confusing rationale. Author(s): Maksymowych WP. Source: The Journal of Rheumatology. 2003 March; 30(3): 430-4. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12610795&dopt=Abstract
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Bone edema scored on magnetic resonance imaging scans of the dominant carpus at presentation predicts radiographic joint damage of the hands and feet six years later in patients with rheumatoid arthritis. Author(s): McQueen FM, Benton N, Perry D, Crabbe J, Robinson E, Yeoman S, McLean L, Stewart N. Source: Arthritis and Rheumatism. 2003 July; 48(7): 1814-27. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12847674&dopt=Abstract
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Bone resorption and inflammatory inhibition efficacy of intermittent cyclical etidronate therapy in rheumatoid arthritis. Author(s): Hasegawa J, Nagashima M, Yamamoto M, Nishijima T, Katsumata S, Yoshino S. Source: The Journal of Rheumatology. 2003 March; 30(3): 474-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12610804&dopt=Abstract
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Brain abscess in rheumatoid arthritis. Author(s): Lee CS, Chang CK. Source: Annals of the Rheumatic Diseases. 2003 July; 62(7): 689-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12810444&dopt=Abstract
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Brief report: adjustment to juvenile rheumatoid arthritis: a family systems perspective. Author(s): Helgeson VS, Janicki D, Lerner J, Barbarin O. Source: Journal of Pediatric Psychology. 2003 July-August; 28(5): 347-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12808011&dopt=Abstract
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Brief report: child-rearing practices of caregivers with and without a child with juvenile rheumatoid arthritis: perspectives of caregivers and professionals. Author(s): Gerhardt CA, Vannatta K, McKellop JM, Taylor J, Passo M, Reiter-Purtill J, Zeller M, Noll RB. Source: Journal of Pediatric Psychology. 2003 June; 28(4): 275-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12730284&dopt=Abstract
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By the way, doctor. I've heard about a new rheumatoid arthritis drug that I'd only have to take every two weeks. What do you know about it? Author(s): Robb-Nicholson C. Source: Harvard Women's Health Watch. 2003 May; 10(9): 8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12763730&dopt=Abstract
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Can diagnostic triage by general practitioners or rheumatology nurses improve the positive predictive value of referrals to early arthritis clinics? Author(s): Gormley GJ, Steele WK, Gilliland A, Leggett P, Wright GD, Bell AL, Matthews C, Meenagh G, Wylie E, Mulligan R, Stevenson M, O'Reilly D, Taggart AJ. Source: Rheumatology (Oxford, England). 2003 June; 42(6): 763-8. Epub 2003 March 31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12730536&dopt=Abstract
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Can hepatitis C virus infection and interferon-alpha undo the HLADRB1*0402/DQB1*0302 protection against rheumatoid arthritis? Author(s): La Civita L, Fadda P, Gaudiano C, Bentivenga C, Olivieri I. Source: Rheumatology (Oxford, England). 2003 February; 42(2): 383-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12595642&dopt=Abstract
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Candida septic arthritis of the hip in a young patient without predisposing factors. Author(s): Kawanabe K, Hayashi H, Miyamoto M, Tamura J, Shimizu M, Nakamura T. Source: The Journal of Bone and Joint Surgery. British Volume. 2003 July; 85(5): 734-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12892201&dopt=Abstract
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Cardiovascular morbidity and mortality in women diagnosed with rheumatoid arthritis. Author(s): Solomon DH, Karlson EW, Rimm EB, Cannuscio CC, Mandl LA, Manson JE, Stampfer MJ, Curhan GC. Source: Circulation. 2003 March 11; 107(9): 1303-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12628952&dopt=Abstract
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Cardiovascular thrombotic events in arthritis trials of the cyclooxygenase-2 inhibitor celecoxib. Author(s): White WB, Faich G, Borer JS, Makuch RW. Source: The American Journal of Cardiology. 2003 August 15; 92(4): 411-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12914871&dopt=Abstract
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Cartilage destruction mediated by synovial fibroblasts does not depend on proliferation in rheumatoid arthritis. Author(s): Seemayer CA, Kuchen S, Kuenzler P, Rihoskova V, Rethage J, Aicher WK, Michel BA, Gay RE, Kyburz D, Neidhart M, Gay S. Source: American Journal of Pathology. 2003 May; 162(5): 1549-57. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12707039&dopt=Abstract
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Case number 26: massive cholesterol crystal deposition: unusual location in rheumatoid arthritis. Author(s): Balint PV, Kane D, Sturrock RD. Source: Annals of the Rheumatic Diseases. 2003 June; 62(6): 512. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12759285&dopt=Abstract
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CD34-selected versus unmanipulated grafts for severe rheumatoid arthritis: comment on the article by Moore et al. Author(s): Van Laar JM, Pavletic SZ. Source: Arthritis and Rheumatism. 2003 May; 48(5): 1463-4; Author Reply 1464-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12746925&dopt=Abstract
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CD44 in rheumatoid arthritis. Author(s): Naor D, Nedvetzki S. Source: Arthritis Research & Therapy. 2003; 5(3): 105-15. Epub 2003 February 28. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12723975&dopt=Abstract
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Cementless acetabular replacement in patients with rheumatoid arthritis: a 6- to 14year prospective study. Author(s): Katsimihas M, Taylor AH, Lee MB, Sarangi PP, Learmonth ID. Source: The Journal of Arthroplasty. 2003 January; 18(1): 16-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12555177&dopt=Abstract
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Cervical spine disease in rheumatoid arthritis: how common a finding? How uncommon a problem? Author(s): Matteson EL. Source: Arthritis and Rheumatism. 2003 July; 48(7): 1775-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12847668&dopt=Abstract
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Changes in self-efficacy and health status over 5 years: a longitudinal observational study of 306 patients with rheumatoid arthritis. Author(s): Brekke M, Hjortdahl P, Kvien TK. Source: Arthritis and Rheumatism. 2003 June 15; 49(3): 342-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12794789&dopt=Abstract
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Chemokine blockade and chronic inflammatory disease: proof of concept in patients with rheumatoid arthritis. Author(s): Haringman JJ, Kraan MC, Smeets TJ, Zwinderman KH, Tak PP. Source: Annals of the Rheumatic Diseases. 2003 August; 62(8): 715-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12860725&dopt=Abstract
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Chemokines and chemokine receptors in rheumatoid arthritis. Author(s): Szekanecz Z, Kim J, Koch AE. Source: Seminars in Immunology. 2003 February; 15(1): 15-21. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12495637&dopt=Abstract
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Chronic arthritis: current perspectives. Author(s): Singh S. Source: Indian Pediatrics. 2003 May; 40(5): 393-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12768039&dopt=Abstract
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Chronic joint symptoms and prior arthritis diagnosis in community surveys: implications for arthritis prevalence estimates. Author(s): Feinglass J, Nelson C, Lawther T, Chang RW. Source: Public Health Reports (Washington, D.C. : 1974). 2003 May-June; 118(3): 230-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12766218&dopt=Abstract
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Chronic pulmonary toxicity of methotrexate and rheumatoid arthritis. Author(s): Provenzano G. Source: Rheumatology (Oxford, England). 2003 June; 42(6): 802-3; Author Reply 803-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12771440&dopt=Abstract
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Clinical and psychological outcome from a randomized controlled trial of patientinitiated direct-access hospital follow-up for rheumatoid arthritis extended to 4 years. Author(s): Kirwan JR, Mitchell K, Hewlett S, Hehir M, Pollock J, Memel D, Bennett B. Source: Rheumatology (Oxford, England). 2003 March; 42(3): 422-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12626791&dopt=Abstract
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Clinical and radiological effects of anakinra in patients with rheumatoid arthritis. Author(s): Bresnihan B, Cobby M. Source: Rheumatology (Oxford, England). 2003 May; 42 Suppl 2: Ii22-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12817092&dopt=Abstract
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Clinical features of patients with systemic sclerosis accompanied by rheumatoid arthritis. Author(s): Jinnin M, Ihn H, Yamane K, Asano Y, Yazawa N, Tamaki K. Source: Clin Exp Rheumatol. 2003 January-February; 21(1): 91-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12673896&dopt=Abstract
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Clinical observation on treatment of rheumatoid arthritis with fengshi xiandan in 53 cases. Author(s): Shen Y, Qu Q, Wang D. Source: J Tradit Chin Med. 2003 March; 23(1): 21-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12747191&dopt=Abstract
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Clinical relevance of peripheral vascular occlusive disease in patients with rheumatoid arthritis and systemic lupus erythematosus. Author(s): Henke PK, Sukheepod P, Proctor MC, Upchurch GR Jr, Stanley JC. Source: Journal of Vascular Surgery : Official Publication, the Society for Vascular Surgery [and] International Society for Cardiovascular Surgery, North American Chapter. 2003 July; 38(1): 111-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12844099&dopt=Abstract
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Clonal analysis of B cells in the synovial membrane of patients with rheumatoid arthritis. Author(s): Shiokawa S, Matsumato N, Nishimura J. Source: Scandinavian Journal of Rheumatology. 2003; 32(1): 12-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12635940&dopt=Abstract
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Clonally expanded CD4+CD28null T cells in rheumatoid arthritis use distinct combinations of T cell receptor BV and BJ elements. Author(s): Wagner U, Pierer M, Kaltenhauser S, Wilke B, Seidel W, Arnold S, Hantzschel H. Source: European Journal of Immunology. 2003 January; 33(1): 79-84. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12594835&dopt=Abstract
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Combined oral cyclosporin and methotrexate therapy in patients with rheumatoid arthritis elevates methotrexate levels and reduces 7-hydroxymethotrexate levels when compared with methotrexate alone. Author(s): Fox RI, Morgan SL, Smith HT, Robbins BA, Choc MG, Baggott JE. Source: Rheumatology (Oxford, England). 2003 August; 42(8): 989-94. Epub 2003 April 16. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12730515&dopt=Abstract
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Comparing parental distress, family functioning, and the role of social support for caregivers with and without a child with juvenile rheumatoid arthritis. Author(s): Gerhardt CA, Vannatta K, McKellop JM, Zeller M, Taylor J, Passo M, Noll RB. Source: Journal of Pediatric Psychology. 2003 January-February; 28(1): 5-15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12490626&dopt=Abstract
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Comparison between women and men with recent onset rheumatoid arthritis of disease activity and functional ability over two years (the TIRA project). Author(s): Hallert E, Thyberg I, Hass U, Skargren E, Skogh T. Source: Annals of the Rheumatic Diseases. 2003 July; 62(7): 667-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12810432&dopt=Abstract
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Computerized measurement of magnetic resonance imaging erosion volumes in patients with rheumatoid arthritis: a comparison with existing magnetic resonance imaging scoring systems and standard clinical outcome measures. Author(s): Bird P, Lassere M, Shnier R, Edmonds J. Source: Arthritis and Rheumatism. 2003 March; 48(3): 614-24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12632412&dopt=Abstract
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Concepts of arthritis in India's medical traditions: Ayurvedic and Unani perspectives. Author(s): Pugh JF. Source: Social Science & Medicine (1982). 2003 January; 56(2): 415-24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12473325&dopt=Abstract
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Confronting life with rheumatoid arthritis. Author(s): Melanson PM, Downe-Wamboldt B. Source: Journal of Advanced Nursing. 2003 April; 42(2): 125-33. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12670381&dopt=Abstract
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Consent to research in arthritis: quantity of information versus quality. Author(s): Hewlett S. Source: Arthritis and Rheumatism. 2003 June 15; 49(3): 281-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12794780&dopt=Abstract
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Consequences of increased systolic blood pressure in patients with osteoarthritis and rheumatoid arthritis. Author(s): Singh G, Miller JD, Huse DM, Pettitt D, D'Agostino RB, Russell MW. Source: The Journal of Rheumatology. 2003 April; 30(4): 714-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12672188&dopt=Abstract
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Consistent low prevalence of arthritis in quebec: findings from a provincial variation study in Canada based on several canadian population health surveys. Author(s): Wang PP, Badley EM. Source: The Journal of Rheumatology. 2003 January; 30(1): 126-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12508401&dopt=Abstract
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Contrast-enhanced power Doppler ultrasonography of the metacarpophalangeal joints in rheumatoid arthritis. Author(s): Szkudlarek M, Court-Payen M, Strandberg C, Klarlund M, Klausen T, Ostergaard M. Source: European Radiology. 2003 January; 13(1): 163-8. Epub 2002 July 18. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12541125&dopt=Abstract
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Contribution of patient related differences to multidrug resistance in rheumatoid arthritis. Author(s): Morgan C, Lunt M, Brightwell H, Bradburn P, Fallow W, Lay M, Silman A, Bruce IN. Source: Annals of the Rheumatic Diseases. 2003 January; 62(1): 15-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12480663&dopt=Abstract
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Control perceptions in patients with rheumatoid arthritis: the impact of the medical consultation. Author(s): Ryan S, Hassell A, Dawes P, Kendall S. Source: Rheumatology (Oxford, England). 2003 January; 42(1): 135-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12509626&dopt=Abstract
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Copper and zinc intake and serum levels in patients with juvenile rheumatoid arthritis. Author(s): Silverio Amancio OM, Alves Chaud DM, Yanaguibashi G, Esteves Hilario MO. Source: European Journal of Clinical Nutrition. 2003 May; 57(5): 706-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12771972&dopt=Abstract
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Correlation of serum levels of adenosine deaminase activity and its isoenzymes with disease activity in rheumatoid arthritis. Author(s): Sari RA, Taysi S, Yilmaz O, Bakan N. Source: Clin Exp Rheumatol. 2003 January-February; 21(1): 87-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12673895&dopt=Abstract
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Correlation of single time-point damage scores with observed progression of radiographic damage during the first 6 years of rheumatoid arthritis. Author(s): Paulus HE, Oh M, Sharp JT, Gold RH, Wong WK, Park GS, Bulpitt KJ; Western Consortium of Praticing Rheumatologists. Source: The Journal of Rheumatology. 2003 April; 30(4): 705-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12672187&dopt=Abstract
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Cortisol elimination from plasma in premenopausal women with rheumatoid arthritis. Author(s): Rovensky J, Imrich R, Koska J, Kovalancik M, Killinger Z, Payer J, Vigas M, Jezova D. Source: Annals of the Rheumatic Diseases. 2003 July; 62(7): 674-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12810434&dopt=Abstract
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Cost effectiveness and cost utility analysis of multidisciplinary care in patients with rheumatoid arthritis: a randomised comparison of clinical nurse specialist care, inpatient team care, and day patient team care. Author(s): van den Hout WB, Tijhuis GJ, Hazes JM, Breedveld FC, Vliet Vlieland TP. Source: Annals of the Rheumatic Diseases. 2003 April; 62(4): 308-15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12634227&dopt=Abstract
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Cost-effectiveness of low dose corticosteroids versus non-steroidal anti-inflammatory drugs and COX-2 specific inhibitors in the long-term treatment of rheumatoid arthritis. Author(s): Bae SC, Corzillius M, Kuntz KM, Liang MH. Source: Rheumatology (Oxford, England). 2003 January; 42(1): 46-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12509612&dopt=Abstract
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Costimulating aberrant T cell responses by B7-H1 autoantibodies in rheumatoid arthritis. Author(s): Dong H, Strome SE, Matteson EL, Moder KG, Flies DB, Zhu G, Tamura H, Driscoll CL, Chen L. Source: The Journal of Clinical Investigation. 2003 February; 111(3): 363-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12569162&dopt=Abstract
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Costs and predictors of costs in rheumatoid arthritis: a prevalence-based study. Author(s): Lajas C, Abasolo L, Bellajdel B, Hernandez-Garcia C, Carmona L, Vargas E, Lazaro P, Jover JA. Source: Arthritis and Rheumatism. 2003 February 15; 49(1): 64-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12579595&dopt=Abstract
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Costs of rheumatoid arthritis in Germany: a micro-costing approach based on healthcare payer's data sources. Author(s): Ruof J, Hulsemann JL, Mittendorf T, Handelmann S, von der Schulenburg JM, Zeidler H, Merkesdal S. Source: Annals of the Rheumatic Diseases. 2003 June; 62(6): 544-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12759292&dopt=Abstract
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Course of radiographic damage over 10 years in a cohort with early rheumatoid arthritis. Author(s): Lindqvist E, Jonsson K, Saxne T, Eberhardt K. Source: Annals of the Rheumatic Diseases. 2003 July; 62(7): 611-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12810421&dopt=Abstract
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Current drug therapy for rheumatoid arthritis. Author(s): Kawai S. Source: Journal of Orthopaedic Science : Official Journal of the Japanese Orthopaedic Association. 2003; 8(2): 259-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12665969&dopt=Abstract
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Cyclooxygenase-2: from arthritis treatment to new indications for the prevention and treatment of cancer. Author(s): Yamamoto DS, Viale PH. Source: Clinical Journal of Oncology Nursing. 2003 January-February; 7(1): 21-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12629931&dopt=Abstract
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Cyclosporin A monotherapy versus cyclosporin A and methotrexate combination therapy in patients with early rheumatoid arthritis: a double blind randomised placebo controlled trial. Author(s): Gerards AH, Landewe RB, Prins AP, Bruijn GA, Goei The HS, Laan RF, Dijkmans BA. Source: Annals of the Rheumatic Diseases. 2003 April; 62(4): 291-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12634224&dopt=Abstract
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Cyclosporin treatment in psoriatic arthritis: a cause of severe leg pain. Author(s): Lawson CA, Fraser A, Veale DJ, Emery P. Source: Annals of the Rheumatic Diseases. 2003 May; 62(5): 489. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12695169&dopt=Abstract
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Cytokine gene polymorphisms: association with psoriatic arthritis susceptibility and severity. Author(s): Balding J, Kane D, Livingstone W, Mynett-Johnson L, Bresnihan B, Smith O, FitzGerald O. Source: Arthritis and Rheumatism. 2003 May; 48(5): 1408-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12746914&dopt=Abstract
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Cytokines in the pathogenesis of rheumatoid arthritis and collagen-induced arthritis. Author(s): Lubberts E, van den Berg WB. Source: Advances in Experimental Medicine and Biology. 2003; 520: 194-202. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12613579&dopt=Abstract
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Daily pain and symptoms in children with polyarticular arthritis. Author(s): Schanberg LE, Anthony KK, Gil KM, Maurin EC. Source: Arthritis and Rheumatism. 2003 May; 48(5): 1390-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12746912&dopt=Abstract
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Declining use of orthopedic surgery in patients with rheumatoid arthritis? Results of a long-term, population-based assessment. Author(s): da Silva E, Doran MF, Crowson CS, O'Fallon WM, Matteson EL. Source: Arthritis and Rheumatism. 2003 April 15; 49(2): 216-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12687513&dopt=Abstract
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Decreasing pain and depression in a health promotion program for people with rheumatoid arthritis. Author(s): Oh H, Seo W. Source: Journal of Nursing Scholarship : an Official Publication of Sigma Theta Tau International Honor Society of Nursing / Sigma Theta Tau. 2003; 35(2): 127-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12854292&dopt=Abstract
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Degenerative sternoclavicular arthritis and hyperostosis. Author(s): Noble JS. Source: Clinics in Sports Medicine. 2003 April; 22(2): 407-22, Ix. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12825539&dopt=Abstract
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Delayed presentation of septic arthritis of a lumbar facet joint after diagnostic facet joint injection. Author(s): Orpen NM, Birch NC. Source: Journal of Spinal Disorders & Techniques. 2003 June; 16(3): 285-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12792344&dopt=Abstract
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Detection of Borrelia burgdorferi by species-specific and broad-range PCR of synovial fluid and synovial tissue of Lyme arthritis patients before and after antibiotic treatment. Author(s): Lipowsky C, Altwegg M, Michel BA, Bruhlmann P. Source: Clin Exp Rheumatol. 2003 March-April; 21(2): 271-2. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12747294&dopt=Abstract
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Determinants of physical function in rheumatoid arthritis: association with the disease process. Author(s): Hazes JM. Source: Rheumatology (Oxford, England). 2003 May; 42 Suppl 2: Ii17-21. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12817091&dopt=Abstract
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Development of a new instrument for rheumatoid arthritis: the Cedars-Sinai HealthRelated Quality of Life instrument (CSHQ-RA). Author(s): Weisman MH, Paulus HE, Russak SM, Lubeck DP, Chiou CF, Sengupta N, Ofman JJ, Borenstein J, Moadel AB, Sherbourne CD. Source: Arthritis and Rheumatism. 2003 February 15; 49(1): 78-84. Erratum In: Arthritis Rheum. 2003 June 15; 49(3): 477. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12579597&dopt=Abstract
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Development of a work instability scale for rheumatoid arthritis. Author(s): Gilworth G, Chamberlain MA, Harvey A, Woodhouse A, Smith J, Smyth MG, Tennant A. Source: Arthritis and Rheumatism. 2003 June 15; 49(3): 349-54. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12794790&dopt=Abstract
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Development of an instrument to measure disability in parenting activity among women with rheumatoid arthritis. Author(s): Katz PP, Pasch LA, Wong B. Source: Arthritis and Rheumatism. 2003 April; 48(4): 935-43. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12687535&dopt=Abstract
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Development of rheumatoid arthritis is not associated with two polymorphisms in the Crohn's disease gene CARD15. Author(s): Steer S, Fisher SA, Fife M, Cuthbert A, Newton J, Wordsworth P, Lewis CM, Mathew CG, Lanchbury JS. Source: Rheumatology (Oxford, England). 2003 February; 42(2): 304-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12595627&dopt=Abstract
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Diagnostic value of high-resolution B-mode and doppler sonography for imaging of hand and finger joints in rheumatoid arthritis. Author(s): Weidekamm C, Koller M, Weber M, Kainberger F. Source: Arthritis and Rheumatism. 2003 February; 48(2): 325-33. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12571840&dopt=Abstract
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Differential peptide binding motif for three juvenile arthritis associated HLA-DQ molecules. Author(s): Ihle J, Fleckenstein B, Terreaux C, Beck H, Albert ED, Dannecker GE. Source: Clin Exp Rheumatol. 2003 March-April; 21(2): 257-62. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12747287&dopt=Abstract
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Differentiation of psoas muscle abscess from septic arthritis of the hip in children. Author(s): Jain AK, Aggarwal AN, Letts M, Monson R, Song J. Source: Clinical Orthopaedics and Related Research. 2003 June; (411): 346; Author Reply 347. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12782894&dopt=Abstract
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Dipeptidyl peptidase IV on activated T cells as a target molecule for therapy of rheumatoid arthritis. Author(s): Williams YN, Baba H, Hayashi S, Ikai H, Sugita T, Tanaka S, Miyasaka N, Kubota T. Source: Clinical and Experimental Immunology. 2003 January; 131(1): 68-74. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12519388&dopt=Abstract
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Disability models: implications for arthritis exercise and physical activity interventions. Author(s): Jette AM, Keysor JJ. Source: Arthritis and Rheumatism. 2003 February 15; 49(1): 114-20. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12579601&dopt=Abstract
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Disease activity and health status in rheumatoid arthritis: a case-control comparison between Norway and Lithuania. Author(s): Dadoniene J, Uhlig T, Stropuviene S, Venalis A, Boonen A, Kvien TK. Source: Annals of the Rheumatic Diseases. 2003 March; 62(3): 231-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12594108&dopt=Abstract
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Does activation of the innate immune system contribute to the development of rheumatoid arthritis? Author(s): Klinman D. Source: Arthritis and Rheumatism. 2003 March; 48(3): 590-3. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12632408&dopt=Abstract
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Does concomitant osteoarthritis affect histopathologic changes in patients with rheumatoid arthritis? Comment on the article by Kraan et al. Author(s): Wei N. Source: Arthritis and Rheumatism. 2003 April; 48(4): 1161; Author Reply 1162. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12687564&dopt=Abstract
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Does glucosamine relieve arthritis joint pain? Author(s): Miller DC, Richardson J. Source: The Journal of Family Practice. 2003 August; 52(8): 645-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12899824&dopt=Abstract
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Does vascular endothelial growth factor play a role in interleukin-6 receptor antagonist therapy for rheumatoid arthritis? Author(s): Gentiletti J, Fava RA. Source: Arthritis and Rheumatism. 2003 June; 48(6): 1471-4. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12794810&dopt=Abstract
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Does yttrium radiosynovectomy increase the risk of cancer in patients with rheumatoid arthritis? Author(s): Vuorela J, Sokka T, Pukkala E, Hannonen P. Source: Annals of the Rheumatic Diseases. 2003 March; 62(3): 251-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12594113&dopt=Abstract
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Doppler sonographic findings in the long bicipital tendon sheath in patients with rheumatoid arthritis as compared with patients with degenerative diseases of the shoulder. Author(s): Strunk J, Lange U, Kurten B, Schmidt KL, Neeck G. Source: Arthritis and Rheumatism. 2003 July; 48(7): 1828-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12847675&dopt=Abstract
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Down-modulation of chemokine receptor cartilage expression in inflammatory arthritis. Author(s): Silvestri T, Meliconi R, Pulsatelli L, Dolzani P, Zizzi F, Frizziero L, Borzi RM, Facchini A. Source: Rheumatology (Oxford, England). 2003 January; 42(1): 14-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12509607&dopt=Abstract
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Drug-induced systemic lupus erythematosus associated with etanercept therapy in a child with juvenile idiopathic arthritis. Author(s): Lepore L, Marchetti F, Facchini S, Leone V, Ventura A. Source: Clin Exp Rheumatol. 2003 March-April; 21(2): 276-7. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12747299&dopt=Abstract
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Drug-related problems and quality of life in arthritis and low back pain sufferers. Author(s): Ernst ME, Iyer SS, Doucette WR. Source: Value in Health : the Journal of the International Society for Pharmacoeconomics and Outcomes Research. 2003 January-February; 6(1): 51-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12535238&dopt=Abstract
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Dynamic gadolinium-enhanced magnetic resonance imaging of the wrist in patients with rheumatoid arthritis can discriminate active from inactive disease. Author(s): Cimmino MA, Innocenti S, Livrone F, Magnaguagno F, Silvestri E, Garlaschi G. Source: Arthritis and Rheumatism. 2003 May; 48(5): 1207-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12746893&dopt=Abstract
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Early and extensive erosiveness in peripheral joints predicts atlantoaxial subluxations in patients with rheumatoid arthritis. Author(s): Neva MH, Isomaki P, Hannonen P, Kauppi M, Krishnan E, Sokka T. Source: Arthritis and Rheumatism. 2003 July; 48(7): 1808-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12847673&dopt=Abstract
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Early predictors of longterm outcome in patients with juvenile rheumatoid arthritis: subset-specific correlations. Author(s): Oen K, Malleson PN, Cabral DA, Rosenberg AM, Petty RE, Reed M, Schroeder ML, Cheang M. Source: The Journal of Rheumatology. 2003 March; 30(3): 585-93. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12610821&dopt=Abstract
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Economic evaluation of programs or interventions in the management of rheumatoid arthritis: defining a consensus-based reference case. Author(s): Maetzel A, Tugwell P, Boers M, Guillemin F, Coyle D, Drummond M, Wong JB, Gabriel SE; OMERACT 6 Economics Research Group. Source: The Journal of Rheumatology. 2003 April; 30(4): 891-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12672224&dopt=Abstract
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Effect of caffeine consumption on efficacy of methotrexate in rheumatoid arthritis. Author(s): Nesher G, Mates M, Zevin S. Source: Arthritis and Rheumatism. 2003 February; 48(2): 571-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12571869&dopt=Abstract
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Effect of cyclical intermittent etidronate therapy on circulating osteoprotegerin levels in patients with rheumatoid arthritis. Author(s): Valleala H, Mandelin J, Laasonen L, Koivula MK, Risteli J, Konttinen YT. Source: European Journal of Endocrinology / European Federation of Endocrine Societies. 2003 May; 148(5): 527-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12720535&dopt=Abstract
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Effect of valued activity disability, social comparisons, and satisfaction with ability on depressive symptoms in rheumatoid arthritis. Author(s): Neugebauer A, Katz PP, Pasch LA. Source: Health Psychology : Official Journal of the Division of Health Psychology, American Psychological Association. 2003 May; 22(3): 253-62. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12790252&dopt=Abstract
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Effectiveness of a measurement feedback system on outcome in rheumatoid arthritis: a controlled clinical trial. Author(s): Fransen J, Stucki G, Twisk J, Chamot AM, Gerster JC, Langenegger T, Seitz M, Michel BA; mebers of the Swiss Clinical Quality Management in Rheumatoid Arthritis (SCQM). Source: Annals of the Rheumatic Diseases. 2003 July; 62(7): 624-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12810423&dopt=Abstract
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Effects of disease management programs on functional status of patients with rheumatoid arthritis. Author(s): Badamgarav E, Croft JD Jr, Hohlbauch A, Louie JS, O'Dell J, Ofman JJ, Suarez-Almazor ME, Weaver A, White P, Katz P; Evidence-Based Medicine Working Groups in Rheumatology. Source: Arthritis and Rheumatism. 2003 June 15; 49(3): 377-87. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12794794&dopt=Abstract
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Effects of dynamic strength training on physical function, Valpar 9 work sample test, and working capacity in patients with recent-onset rheumatoid arthritis. Author(s): Hakkinen A, Sokka T, Lietsalmi AM, Kautiainen H, Hannonen P. Source: Arthritis and Rheumatism. 2003 February 15; 49(1): 71-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12579596&dopt=Abstract
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Effects of rheumatoid arthritis on sexual activity and relationships. Author(s): Hill J, Bird H, Thorpe R. Source: Rheumatology (Oxford, England). 2003 February; 42(2): 280-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12595623&dopt=Abstract
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Effects of treatment with etanercept (Enbrel, TNRF:Fc) on rheumatoid arthritis evaluated by Doppler ultrasonography. Author(s): Terslev L, Torp-Pedersen S, Qvistgaard E, Kristoffersen H, Rogind H, Danneskiold-Samsoe B, Bliddal H. Source: Annals of the Rheumatic Diseases. 2003 February; 62(2): 178-81. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12525391&dopt=Abstract
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Effects of tumor necrosis factor-alpha inhibitors on lung lesions with rheumatoid arthritis. Author(s): Inoue K, Takano H, Yanagisawa R, Yoshikawa T. Source: Chest. 2003 July; 124(1): 413-4; Author Reply 414. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12853558&dopt=Abstract
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Efficacy of etanercept for the treatment of juvenile idiopathic arthritis according to the onset type. Author(s): Quartier P, Taupin P, Bourdeaut F, Lemelle I, Pillet P, Bost M, Sibilia J, KonePaut I, Gandon-Laloum S, LeBideau M, Bader-Meunier B, Mouy R, Debre M, Landais P, Prieur AM. Source: Arthritis and Rheumatism. 2003 April; 48(4): 1093-101. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12687553&dopt=Abstract
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Efficacy of infliximab in psoriatic arthritis resistant to treatment with disease modifying antirheumatic drugs: an open pilot study. Author(s): Provenzano G, Termini A, Le Moli C, Rinaldi F. Source: Annals of the Rheumatic Diseases. 2003 July; 62(7): 680-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12810436&dopt=Abstract
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Efficiency of colchicine and corticosteroids in a leg ulceration with cholesterol embolism in a woman with rheumatoid arthritis. Author(s): Verneuil L, Ze Bekolo R, Dompmartin A, Comoz F, Marcelli C, Leroy D. Source: Rheumatology (Oxford, England). 2003 August; 42(8): 1014-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12869676&dopt=Abstract
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Elbow synovectomy on patients with juvenile rheumatoid arthritis. Author(s): Maenpaa H, Kuusela P, Lehtinen J, Savolainen A, Kautiainen H, Belt E. Source: Clinical Orthopaedics and Related Research. 2003 July; (412): 65-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12838054&dopt=Abstract
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Elevated angiogenin levels in synovial fluid from patients with inflammatory arthritis and secretion of angiogenin by cultured synovial fibroblasts. Author(s): Liote F, Champy R, Moenner M, Boval-Boizard B, Badet J. Source: Clinical and Experimental Immunology. 2003 April; 132(1): 163-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12653852&dopt=Abstract
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Elevated levels of synovial fluid antibodies reactive with the small proteoglycans biglycan and decorin in patients with rheumatoid arthritis or other joint diseases. Author(s): Polgar A, Falus A, Koo E, Ujfalussy I, Sesztak M, Szuts I, Konrad K, Hodinka L, Bene E, Meszaros G, Ortutay Z, Farkas E, Paksy A, Buzas EI. Source: Rheumatology (Oxford, England). 2003 April; 42(4): 522-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12649398&dopt=Abstract
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Eligibility of patients in routine care for major clinical trials of anti-tumor necrosis factor alpha agents in rheumatoid arthritis. Author(s): Sokka T, Pincus T. Source: Arthritis and Rheumatism. 2003 February; 48(2): 313-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12571838&dopt=Abstract
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Elucidation of the relationship between synovitis and bone damage: a randomized magnetic resonance imaging study of individual joints in patients with early rheumatoid arthritis. Author(s): Conaghan PG, O'Connor P, McGonagle D, Astin P, Wakefield RJ, Gibbon WW, Quinn M, Karim Z, Green MJ, Proudman S, Isaacs J, Emery P. Source: Arthritis and Rheumatism. 2003 January; 48(1): 64-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12528105&dopt=Abstract
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Epstein-Barr virus load in the peripheral blood of patients with rheumatoid arthritis: accurate quantification using real-time polymerase chain reaction. Author(s): Balandraud N, Meynard JB, Auger I, Sovran H, Mugnier B, Reviron D, Roudier J, Roudier C. Source: Arthritis and Rheumatism. 2003 May; 48(5): 1223-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12746895&dopt=Abstract
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Erosion healing in rheumatoid arthritis after anakinra treatment. Author(s): Rau R, Sander O, Wassenberg S. Source: Annals of the Rheumatic Diseases. 2003 July; 62(7): 671-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12810433&dopt=Abstract
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Erysipelothrix rhusiopathiae septic arthritis. Author(s): Ruiz ME, Richards JS, Kerr GS, Kan VL. Source: Arthritis and Rheumatism. 2003 April; 48(4): 1156-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12687560&dopt=Abstract
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Etanercept added to background methotrexate therapy in patients with rheumatoid arthritis: continued observations. Author(s): Kremer JM, Weinblatt ME, Bankhurst AD, Bulpitt KJ, Fleischmann RM, Jackson CG, Atkins KM, Feng A, Burge DJ. Source: Arthritis and Rheumatism. 2003 June; 48(6): 1493-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12794815&dopt=Abstract
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Etanercept treatment of rheumatoid arthritis in the “real world”. Author(s): Smith MD. Source: Annals of the Rheumatic Diseases. 2003 January; 62(1): 95-6; Author Reply 96. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12480688&dopt=Abstract
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Etanercept, a TNF antagonist for treatment for psoriatic arthritis and psoriasis. Author(s): Mease PJ. Source: Skin Therapy Letter. 2003 January; 8(1): 1-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12728284&dopt=Abstract
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Etanercept-induced lupus-like syndrome in a patient with rheumatoid arthritis. Author(s): Carlson E, Rothfield N. Source: Arthritis and Rheumatism. 2003 April; 48(4): 1165-6; Author Reply 1166. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12687569&dopt=Abstract
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Ethnic variation in the clinical manifestations of rheumatoid arthritis: role of HLADRB1 alleles. Author(s): Del Rincon I, Battafarano DF, Arroyo RA, Murphy FT, Fischbach M, Escalante A. Source: Arthritis and Rheumatism. 2003 April 15; 49(2): 200-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12687511&dopt=Abstract
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Evaluation of eutectic lidocaine/prilocaine cream (EMLA) for steroid joint injection in children with juvenile rheumatoid arthritis: a double blind, randomized, placebo controlled trial. Author(s): Uziel Y, Berkovitch M, Gazarian M, Koren G, Silverman ED, Schneider R, Laxer RM. Source: The Journal of Rheumatology. 2003 March; 30(3): 594-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12610822&dopt=Abstract
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Evaluation of respiratory status and mandibular movement after total temporomandibular joint replacement in patients with rheumatoid arthritis. Author(s): Mishima K, Yamada T, Sugahara T. Source: International Journal of Oral and Maxillofacial Surgery. 2003 June; 32(3): 275-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12767874&dopt=Abstract
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Evidence for the benefit of aerobic and strengthening exercise in rheumatoid arthritis. Author(s): Stenstrom CH, Minor MA. Source: Arthritis and Rheumatism. 2003 June 15; 49(3): 428-34. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12794800&dopt=Abstract
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Evolving concepts of rheumatoid arthritis. Author(s): Firestein GS. Source: Nature. 2003 May 15; 423(6937): 356-61. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12748655&dopt=Abstract
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Exercise and fitness in children with arthritis: evidence of benefits for exercise and physical activity. Author(s): Klepper SE. Source: Arthritis and Rheumatism. 2003 June 15; 49(3): 435-43. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12794801&dopt=Abstract
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Exercise-related goals and self-efficacy as correlates of aquatic exercise in individuals with arthritis. Author(s): Gyurcsik NC, Estabrooks PA, Frahm-Templar MJ. Source: Arthritis and Rheumatism. 2003 June 15; 49(3): 306-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12794784&dopt=Abstract
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Experiencing health in the context of rheumatoid arthritis. Author(s): Schmidt BJ, Brauer DJ, Peden-McAlpine C. Source: Nursing Science Quarterly. 2003 April; 16(2): 155-62. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12728834&dopt=Abstract
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Exploring the reciprocal relationship between immunity and inflammation in chronic inflammatory arthritis. Author(s): Cope AP. Source: Rheumatology (Oxford, England). 2003 June; 42(6): 716-31. Epub 2003 March 31. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12730506&dopt=Abstract
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Expression and regulation of Toll-like receptor 2 in rheumatoid arthritis synovium. Author(s): Seibl R, Birchler T, Loeliger S, Hossle JP, Gay RE, Saurenmann T, Michel BA, Seger RA, Gay S, Lauener RP. Source: American Journal of Pathology. 2003 April; 162(4): 1221-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12651614&dopt=Abstract
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Expression of activation-induced, T cell-derived, and chemokine-related cytokine/lymphotactin and its functional role in rheumatoid arthritis. Author(s): Blaschke S, Middel P, Dorner BG, Blaschke V, Hummel KM, Kroczek RA, Reich K, Benoehr P, Koziolek M, Muller GA. Source: Arthritis and Rheumatism. 2003 July; 48(7): 1858-72. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12847680&dopt=Abstract
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Expression of folylpolyglutamyl synthetase predicts poor response to methotrexate therapy in patients with rheumatoid arthritis. Author(s): Stranzl T, Wolf J, Leeb BF, Smolen JS, Pirker R, Filipits M. Source: Clin Exp Rheumatol. 2003 January-February; 21(1): 27-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12673886&dopt=Abstract
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Expression of lactoferrin on neutrophil granulocytes from synovial fluid and peripheral blood of patients with rheumatoid arthritis. Author(s): Caccavo D, Garzia P, Sebastiani GD, Ferri GM, Galluzzo S, Vadacca M, Rigon A, Afeltra A, Amoroso A. Source: The Journal of Rheumatology. 2003 February; 30(2): 220-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12563671&dopt=Abstract
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Expression of pleiotrophin, an embryonic growth and differentiation factor, in rheumatoid arthritis. Author(s): Pufe T, Bartscher M, Petersen W, Tillmann B, Mentlein R. Source: Arthritis and Rheumatism. 2003 March; 48(3): 660-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12632418&dopt=Abstract
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Expression of the dendritic cell-associated C-type lectin DC-SIGN by inflammatory matrix metalloproteinase-producing macrophages in rheumatoid arthritis synovium and interaction with intercellular adhesion molecule 3-positive T cells. Author(s): van Lent PL, Figdor CG, Barrera P, van Ginkel K, Sloetjes A, van den Berg WB, Torensma R. Source: Arthritis and Rheumatism. 2003 February; 48(2): 360-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12571844&dopt=Abstract
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Extra-articular disease manifestations in rheumatoid arthritis: incidence trends and risk factors over 46 years. Author(s): Turesson C, O'Fallon WM, Crowson CS, Gabriel SE, Matteson EL. Source: Annals of the Rheumatic Diseases. 2003 August; 62(8): 722-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12860726&dopt=Abstract
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Factors associated with toxicity, final dose, and efficacy of methotrexate in patients with rheumatoid arthritis. Author(s): Hoekstra M, van Ede AE, Haagsma CJ, van de Laar MA, Huizinga TW, Kruijsen MW, Laan RF. Source: Annals of the Rheumatic Diseases. 2003 May; 62(5): 423-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12695153&dopt=Abstract
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Factors influencing uptake of influenza vaccination in patients with rheumatoid arthritis. Author(s): Bridges MJ, Coady D, Kelly CA, Hamilton J, Heycock C. Source: Annals of the Rheumatic Diseases. 2003 July; 62(7): 685. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12810440&dopt=Abstract
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Factors related to severe uveitis at diagnosis in children with juvenile idiopathic arthritis in a screening program. Author(s): Chia A, Franco, Lee V, Graham EM, Edelsten C. Source: American Journal of Ophthalmology. 2003 June; 135(6): 757-62. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12788113&dopt=Abstract
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Fcgamma receptor expression levels on monocytes are elevated in rheumatoid arthritis patients with high erythrocyte sedimentation rate who do not use antirheumatic drugs. Author(s): Wijngaarden S, van Roon JA, Bijlsma JW, van de Winkel JG, Lafeber FP. Source: Rheumatology (Oxford, England). 2003 May; 42(5): 681-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12709546&dopt=Abstract
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FcgammaRIIIA-158V and rheumatoid arthritis: a confirmation study. Author(s): Morgan AW, Keyte VH, Babbage SJ, Robinson JI, Ponchel F, Barrett JH, Bhakta BB, Bingham SJ, Buch MH, Conaghan PG, Gough A, Green M, Lawson CA, Pease CT, Markham AF, Ollier WE, Emery P, Worthington J, Isaacs JD. Source: Rheumatology (Oxford, England). 2003 April; 42(4): 528-33. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12649399&dopt=Abstract
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FDA officials argue over safety of new arthritis drug. Author(s): Moynihan R. Source: Bmj (Clinical Research Ed.). 2003 March 15; 326(7389): 565. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12637379&dopt=Abstract
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Female sex increases risk for rheumatoid arthritis only in individuals encoding lowrisk HLA-DRB1 alleles. Author(s): de Vries N, Tak PP, Tijssen H, van Riel PL, van de Putte LB. Source: Arthritis and Rheumatism. 2003 June; 48(6): 1762-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12794845&dopt=Abstract
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Fibroblast-like synoviocytes from rheumatoid arthritis patients express less FLICEinhibitory protein than fibroblast-like synoviocytes from trauma patients: comment on the article by Schedel et al. Author(s): Tolboom TC, Medema JP, van Gaalen FA, Pieterman E, Huizinga TW, Toes RE. Source: Arthritis and Rheumatism. 2003 March; 48(3): 858-9; Author Reply 859. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12632447&dopt=Abstract
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Five-year followup of rheumatoid arthritis patients after early treatment with diseasemodifying antirheumatic drugs versus treatment according to the pyramid approach in the first year. Author(s): Verstappen SM, Jacobs JW, Bijlsma JW, Heurkens AH, van Booma-Frankfort C, Borg EJ, Hofman DM, van der Veen MJ; Utrecht Arthritis Cohort Study Group. Source: Arthritis and Rheumatism. 2003 July; 48(7): 1797-807. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12847672&dopt=Abstract
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Frequency of osteopenia in adolescents with early-onset juvenile idiopathic arthritis: a long-term outcome study of one hundred five patients. Author(s): Lien G, Flato B, Haugen M, Vinje O, Sorskaar D, Dale K, Johnston V, Egeland T, Forre O. Source: Arthritis and Rheumatism. 2003 August; 48(8): 2214-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12905475&dopt=Abstract
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Functional and prognostic relevance of the -173 polymorphism of the macrophage migration inhibitory factor gene in systemic-onset juvenile idiopathic arthritis. Author(s): De Benedetti F, Meazza C, Vivarelli M, Rossi F, Pistorio A, Lamb R, Lunt M, Thomson W, Ravelli A, Donn R, Martini A; British Paediatric Rheumatology Study Group. Source: Arthritis and Rheumatism. 2003 May; 48(5): 1398-407. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12746913&dopt=Abstract
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Functional characterization of adherent synovial fluid cells in rheumatoid arthritis: destructive potential in vitro and in vivo. Author(s): Neidhart M, Seemayer CA, Hummel KM, Michel BA, Gay RE, Gay S. Source: Arthritis and Rheumatism. 2003 July; 48(7): 1873-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12847681&dopt=Abstract
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Functional disability in rheumatoid arthritis patients compared with a community population in Finland. Author(s): Sokka T, Krishnan E, Hakkinen A, Hannonen P. Source: Arthritis and Rheumatism. 2003 January; 48(1): 59-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12528104&dopt=Abstract
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Gene therapy for arthritis. Author(s): Robbins PD, Evans CH, Chernajovsky Y. Source: Gene Therapy. 2003 May; 10(10): 902-11. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12732875&dopt=Abstract
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Genetic markers for the efficacy of tumour necrosis factor blocking therapy in rheumatoid arthritis. Author(s): Padyukov L, Lampa J, Heimburger M, Ernestam S, Cederholm T, Lundkvist I, Andersson P, Hermansson Y, Harju A, Klareskog L, Bratt J. Source: Annals of the Rheumatic Diseases. 2003 June; 62(6): 526-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12759288&dopt=Abstract
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Genetic studies in rheumatoid arthritis. Author(s): Grennan DM, Sanders PA. Source: Rheumatology (Oxford, England). 2003 March; 42(3): 490-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12626806&dopt=Abstract
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Geographically specific infections and arthritis, including rheumatic syndromes associated with certain fungi and parasites, Brucella species and Mycobacterium leprae. Author(s): McGill PE. Source: Best Practice & Research. Clinical Rheumatology. 2003 April; 17(2): 289-307. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12787526&dopt=Abstract
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Glucocorticoid receptor up-regulation in early rheumatoid arthritis treated with low dose prednisone or placebo. Author(s): Huisman AM, Siewertsz van Everdingen AA, Wenting MJ, Lafeber F, van Reesema DR, Jacobs JW, Bijlsma JW. Source: Clin Exp Rheumatol. 2003 March-April; 21(2): 217-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12747278&dopt=Abstract
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Glucosamine for arthritis. Author(s): Keller L. Source: Adv Nurse Pract. 2003 June; 11(6): 19-21, 100. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12807050&dopt=Abstract
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Glucose-6-phosphate isomerase is not a specific autoantigen in rheumatoid arthritis. Author(s): Herve CA, Wait R, Venables PJ. Source: Rheumatology (Oxford, England). 2003 August; 42(8): 986-8. Epub 2003 March 31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12730513&dopt=Abstract
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Gonococcal arthritis of the shoulder and septic extensor tenosynovitis of the wrist: sonographic appearances. Author(s): Craig JG, van Holsbeeck M, Alva M. Source: Journal of Ultrasound in Medicine : Official Journal of the American Institute of Ultrasound in Medicine. 2003 February; 22(2): 221-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12562127&dopt=Abstract
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Gonococcal arthritis. Author(s): Bardin T. Source: Best Practice & Research. Clinical Rheumatology. 2003 April; 17(2): 201-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12787521&dopt=Abstract
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Gower's sign in children with juvenile idiopathic arthritis. Author(s): Stathopulu E, Baildam E. Source: Rheumatology (Oxford, England). 2003 August; 42(8): 1002-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12869668&dopt=Abstract
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Group B streptococcus (Streptococcus agalactiae) pyogenic arthritis in nonpregnant adults. Author(s): Nolla JM, Gomez-Vaquero C, Corbella X, Ordonez S, Garcia-Gomez C, Perez A, Cabo J, Valverde J, Ariza J. Source: Medicine; Analytical Reviews of General Medicine, Neurology, Psychiatry, Dermatology, and Pediatrics. 2003 March; 82(2): 119-28. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12640188&dopt=Abstract
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Growth plate damage, a feature of juvenile idiopathic arthritis, can be induced by adenoviral gene transfer of oncostatin M: a comparative study in gene-deficient mice. Author(s): de Hooge AS, van de Loo FA, Bennink MB, Arntz OJ, Fiselier TJ, Franssen MJ, Joosten LA, Van Lent PL, Richards CD, van den Berg WB. Source: Arthritis and Rheumatism. 2003 June; 48(6): 1750-61. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12794844&dopt=Abstract
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Haemophagocytic syndrome in a rheumatoid arthritis patient treated with infliximab. Author(s): Aouba A, De Bandt M, Aslangul E, Atkhen N, Patri B. Source: Rheumatology (Oxford, England). 2003 June; 42(6): 800-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12771439&dopt=Abstract
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Hand bone densitometry in rheumatoid arthritis, a five year longitudinal study: an outcome measure and a prognostic marker. Author(s): Deodhar AA, Brabyn J, Pande I, Scott DL, Woolf AD. Source: Annals of the Rheumatic Diseases. 2003 August; 62(8): 767-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12860734&dopt=Abstract
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Health care utilization among older adults with arthritis. Author(s): Dunlop DD, Manheim LM, Song J, Chang RW. Source: Arthritis and Rheumatism. 2003 April 15; 49(2): 164-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12687506&dopt=Abstract
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Health related quality of life among adults reporting arthritis: analysis of data from the Behavioral Risk Factor Surveillance System, US, 1996-99. Author(s): Mili F, Helmick CG, Moriarty DG. Source: The Journal of Rheumatology. 2003 January; 30(1): 160-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12508407&dopt=Abstract
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Health status of patients with juvenile rheumatoid arthritis at 1 and 5 years after diagnosis. Author(s): Bowyer SL, Roettcher PA, Higgins GC, Adams B, Myers LK, Wallace C, Rennebohm R, Moore TL, Pepmueller PH, Spencer C, Wagner-Weiner L, Rabinovich E, Passo M, Lovell DJ, McCurdy D, Zemel L, Schikler KN, Szer I, Kurtin P, Lindsley C. Source: The Journal of Rheumatology. 2003 February; 30(2): 394-400. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12563701&dopt=Abstract
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Helicobacter pylori infection in rheumatoid arthritis: effect of drugs on prevalence and correlation with gastroduodenal lesions. Author(s): Kelly C, Saravanan V. Source: Rheumatology (Oxford, England). 2003 February; 42(2): 388; Author Reply 388. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12595646&dopt=Abstract
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Hemiarthroplasty for trapeziometacarpal arthritis - a useful alternative? Author(s): Phaltankar PM, Magnussen PA. Source: Journal of Hand Surgery (Edinburgh, Lothian). 2003 February; 28(1): 80-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12531675&dopt=Abstract
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Hepatitis B reactivation in a chronic hepatitis B surface antigen carrier with rheumatoid arthritis treated with infliximab and low dose methotrexate. Author(s): Ostuni P, Botsios C, Punzi L, Sfriso P, Todesco S. Source: Annals of the Rheumatic Diseases. 2003 July; 62(7): 686-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12810441&dopt=Abstract
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Hepatitis C virus and arthritis. Author(s): Olivieri I, Palazzi C, Padula A. Source: Rheumatic Diseases Clinics of North America. 2003 February; 29(1): 111-22. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12635503&dopt=Abstract
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Herbal medicines for the treatment of rheumatoid arthritis: a systematic review. Author(s): Soeken KL, Miller SA, Ernst E. Source: Rheumatology (Oxford, England). 2003 May; 42(5): 652-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12709541&dopt=Abstract
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Heterogeneous requirement of IkappaB kinase 2 for inflammatory cytokine and matrix metalloproteinase production in rheumatoid arthritis: implications for therapy. Author(s): Andreakos E, Smith C, Kiriakidis S, Monaco C, de Martin R, Brennan FM, Paleolog E, Feldmann M, Foxwell BM. Source: Arthritis and Rheumatism. 2003 July; 48(7): 1901-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12847684&dopt=Abstract
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High circulating levels of biologically inactive IL-6/SIL-6 receptor complexes in systemic juvenile idiopathic arthritis: evidence for serum factors interfering with the binding to gp130. Author(s): Pignatti P, Ciapponi L, Galle P, Hansen MB, Massa M, Meazza C, Paonessa G, Novick D, Ciliberto G, Martini A, De Benedetti F. Source: Clinical and Experimental Immunology. 2003 February; 131(2): 355-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12562400&dopt=Abstract
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High expression of Fas ligand by synovial fluid-derived gamma delta T cells in Lyme arthritis. Author(s): Roessner K, Wolfe J, Shi C, Sigal LH, Huber S, Budd RC. Source: Journal of Immunology (Baltimore, Md. : 1950). 2003 March 1; 170(5): 2702-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12594300&dopt=Abstract
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High mobility group box chromosomal protein 1 as a nuclear protein, cytokine, and potential therapeutic target in arthritis. Author(s): Ulloa L, Batliwalla FM, Andersson U, Gregersen PK, Tracey KJ. Source: Arthritis and Rheumatism. 2003 April; 48(4): 876-81. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12687528&dopt=Abstract
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High mobility group box chromosomal protein 1 plays a role in the pathogenesis of rheumatoid arthritis as a novel cytokine. Author(s): Taniguchi N, Kawahara K, Yone K, Hashiguchi T, Yamakuchi M, Goto M, Inoue K, Yamada S, Ijiri K, Matsunaga S, Nakajima T, Komiya S, Maruyama I. Source: Arthritis and Rheumatism. 2003 April; 48(4): 971-81. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12687539&dopt=Abstract
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High prevalence of thyroid autoantibodies in newly diagnosed rheumatoid arthritis patients. Author(s): Del Puente A, Savastano S, Nuzzo V, Esposito A, Lupoli G. Source: Clin Exp Rheumatol. 2003 January-February; 21(1): 137. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12673907&dopt=Abstract
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HLA antigens may influence the age of onset of psoriasis and psoriatic arthritis. Author(s): Queiro R, Torre JC, Gonzalez S, Lopez-Larrea C, Tinture T, Lopez-Lagunas I. Source: The Journal of Rheumatology. 2003 March; 30(3): 505-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12610809&dopt=Abstract
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HLA studies in psoriatic arthritis: current situation and future needs. Author(s): Gladman DD, Farewell VT. Source: The Journal of Rheumatology. 2003 January; 30(1): 4-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12508382&dopt=Abstract
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HLA-DRB1 status affects endothelial function in treated patients with rheumatoid arthritis. Author(s): Gonzalez-Juanatey C, Testa A, Garcia-Castelo A, Garcia-Porrua C, Llorca J, Vidan J, Hajeer AH, Ollier WE, Mattey DL, Gonzalez-Gay MA. Source: The American Journal of Medicine. 2003 June 1; 114(8): 647-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12798452&dopt=Abstract
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Human IgG Fc-binding phage antibodies constructed from synovial fluid CD38+ B cells of patients with rheumatoid arthritis show the imprints of an antigen-dependent process of somatic hypermutation and clonal selection. Author(s): Van Esch WJ, Reparon-Schuijt CC, Hamstra HJ, Van Kooten C, Logtenberg T, Breedveld FC, Verweij CL. Source: Clinical and Experimental Immunology. 2003 February; 131(2): 364-76. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12562401&dopt=Abstract
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Hydroxypyridinium collagen crosslinks in serum, urine, synovial fluid and synovial tissue in patients with rheumatoid arthritis compared with osteoarthritis. Author(s): Kaufmann J, Mueller A, Voigt A, Carl HD, Gursche A, Zacher J, Stein G, Hein G. Source: Rheumatology (Oxford, England). 2003 February; 42(2): 314-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12595629&dopt=Abstract
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Hyperhomocysteinemia in children with juvenile idiopathic arthritis is not influenced by methotrexate treatment and folic acid supplementation: a pilot study. Author(s): Huemer M, Fodinger M, Huemer C, Sailer-Hock M, Falger J, Rettenbacher A, Bernecker M, Artacker G, Kenzian H, Lang T, Stockler-Ipsiroglu S. Source: Clin Exp Rheumatol. 2003 March-April; 21(2): 249-55. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12747286&dopt=Abstract
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Hypertension in the patient with arthritis: have we been underestimating its significance? Author(s): Day R. Source: The Journal of Rheumatology. 2003 April; 30(4): 642-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12672178&dopt=Abstract
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Hypothalamic-pituitary-adrenocortical and gonadal functions in rheumatoid arthritis. Author(s): Cutolo M, Sulli A, Pizzorni C, Craviotto C, Straub RH. Source: Annals of the New York Academy of Sciences. 2003 May; 992: 107-17. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12794051&dopt=Abstract
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Hypothalamo-pituitary-adrenal axis dysregulation in patients with rheumatoid arthritis after the dexamethasone/corticotrophin releasing factor test. Author(s): Harbuz MS, Korendowych E, Jessop DS, Crown AL, Li pdfan SL, Kirwan JR. Source: The Journal of Endocrinology. 2003 July; 178(1): 55-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12844336&dopt=Abstract
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Identification of I kappa BL as the second major histocompatibility complex-linked susceptibility locus for rheumatoid arthritis. Author(s): Okamoto K, Makino S, Yoshikawa Y, Takaki A, Nagatsuka Y, Ota M, Tamiya G, Kimura A, Bahram S, Inoko H. Source: American Journal of Human Genetics. 2003 February; 72(2): 303-12. Epub 2002 December 31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12509789&dopt=Abstract
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Identifying quality care for arthritis. Author(s): Peterson C. Source: Healthplan. 2003 January-February; 44(1): 46-8, 50. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12611253&dopt=Abstract
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IL-17 promotes bone erosion in murine collagen-induced arthritis through loss of the receptor activator of NF-kappa B ligand/osteoprotegerin balance. Author(s): Lubberts E, van den Bersselaar L, Oppers-Walgreen B, Schwarzenberger P, Coenen-de Roo CJ, Kolls JK, Joosten LA, van den Berg WB. Source: Journal of Immunology (Baltimore, Md. : 1950). 2003 March 1; 170(5): 2655-62. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12594294&dopt=Abstract
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Imaging in rheumatoid arthritis--why MRI and ultrasonography can no longer be ignored. Author(s): Ostergaard M, Szkudlarek M. Source: Scandinavian Journal of Rheumatology. 2003; 32(2): 63-73. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12737323&dopt=Abstract
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Immune regulation in adjuvant-induced arthritis: possible implications for innovative therapeutic strategies in arthritis. Author(s): Van Eden W, Waksman BH. Source: Arthritis and Rheumatism. 2003 July; 48(7): 1788-96. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12847671&dopt=Abstract
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Impaired expression of erythrocyte glycosyl-phosphatidylinositol-anchored membrane CD59 in patients with psoriatic arthritis. Relation to terminal complement pathway activation. Author(s): Triolo G, Accardo-Palumbo A, Salli L, Ciccia F, Ferrante A, Tedesco L, Salli S, Giardina E, Pappalardo A, Licata G. Source: Clin Exp Rheumatol. 2003 March-April; 21(2): 225-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12747280&dopt=Abstract
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Implementing the National Arthritis Action Plan: new population-based approaches to increasing physical activity among people with arthritis. Author(s): Brady TJ, Sniezek JE. Source: Arthritis and Rheumatism. 2003 June 15; 49(3): 471-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12794806&dopt=Abstract
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Improved sleep may reduce arthritis pain. Author(s): Davis GC. Source: Holistic Nursing Practice. 2003 May-June; 17(3): 128-35. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12784896&dopt=Abstract
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Incidence of gastroduodenal ulcers in patients with rheumatoid arthritis after 12 weeks of rofecoxib, naproxen, or placebo: a multicentre, randomised, double blind study. Author(s): Hawkey CJ, Laine L, Simon T, Quan H, Shingo S, Evans J; Rofecoxib Rheumatoid Arthritis Endoscopy Study Group. Source: Gut. 2003 June; 52(6): 820-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12740337&dopt=Abstract
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Increase in cardiovascular and cerebrovascular disease prevalence in rheumatoid arthritis. Author(s): Wolfe F, Freundlich B, Straus WL. Source: The Journal of Rheumatology. 2003 January; 30(1): 36-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12508387&dopt=Abstract
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Increased expression of Fcgamma receptors II and III on macrophages of rheumatoid arthritis patients results in higher production of tumor necrosis factor alpha and matrix metalloproteinase. Author(s): Blom AB, Radstake TR, Holthuysen AE, Sloetjes AW, Pesman GJ, Sweep FG, van de Loo FA, Joosten LA, Barrera P, van Lent PL, van den Berg WB. Source: Arthritis and Rheumatism. 2003 April; 48(4): 1002-14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12687542&dopt=Abstract
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Increased inflammatory activity parallels increased basal nitric oxide production and blunted response to nitric oxide in vivo in rheumatoid arthritis. Author(s): Yki-Jarvinen H, Bergholm R, Leirisalo-Repo M. Source: Annals of the Rheumatic Diseases. 2003 July; 62(7): 630-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12810424&dopt=Abstract
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Increased perivascular synovial membrane expression of myeloid-related proteins in psoriatic arthritis. Author(s): Kane D, Roth J, Frosch M, Vogl T, Bresnihan B, FitzGerald O. Source: Arthritis and Rheumatism. 2003 June; 48(6): 1676-85. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12794836&dopt=Abstract
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Increased type I collagen degradation correlates with disease activity in reactive arthritis. Author(s): Kotaniemi A, Risteli J, Aho K, Hakala M. Source: Clin Exp Rheumatol. 2003 January-February; 21(1): 95-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12673897&dopt=Abstract
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Indian guidelines for the management of rheumatoid arthritis. Author(s): Lele RD. Source: J Assoc Physicians India. 2003 January; 51: 93-4; Author Reply 94. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12693480&dopt=Abstract
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Induction of p16 at sites of cartilage invasion in the SCID mouse coimplantation model of rheumatoid arthritis. Author(s): Kuenzler P, Kuchen S, Rihoskova V, Michel BA, Gay RE, Neidhart M, Gay S, Seemayer CA. Source: Arthritis and Rheumatism. 2003 July; 48(7): 2069-73. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12847703&dopt=Abstract
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Infection and arthritis. Infection of prosthetic joints. Author(s): Lidgren L, Knutson K, Stefansdottir A. Source: Best Practice & Research. Clinical Rheumatology. 2003 April; 17(2): 209-18. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12787522&dopt=Abstract
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Infections and biological therapy in rheumatoid arthritis. Author(s): Cunnane G, Doran M, Bresnihan B. Source: Best Practice & Research. Clinical Rheumatology. 2003 April; 17(2): 345-63. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12787529&dopt=Abstract
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Infections preceding early arthritis in southern Sweden: a prospective populationbased study. Author(s): Soderlin MK, Kautiainen H, Puolakkainen M, Hedman K, SoderlundVenermo M, Skogh T, Leirisalo-Repo M. Source: The Journal of Rheumatology. 2003 March; 30(3): 459-64. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12610801&dopt=Abstract
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Infectious complications of biologic treatments of rheumatoid arthritis. Author(s): Mohan AK, Cote TR, Siegel JN, Braun MM. Source: Current Opinion in Rheumatology. 2003 May; 15(3): 179-84. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12707568&dopt=Abstract
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Inflammatory arthritis in the elderly. Author(s): Kerr LD. Source: The Mount Sinai Journal of Medicine, New York. 2003 January; 70(1): 23-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12516006&dopt=Abstract
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Inflammatory arthritis presenting as scrotal pain. Author(s): Gordon MM, Buck C, Madhok R. Source: Rheumatology (Oxford, England). 2003 August; 42(8): 1003-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12869669&dopt=Abstract
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Inflammatory mediators and radiographic changes in temporomandibular joints of patients with rheumatoid arthritis. Author(s): Voog U, Alstergren P, Eliasson S, Leibur E, Kallikorm R, Kopp S. Source: Acta Odontologica Scandinavica. 2003 February; 61(1): 57-64. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12635783&dopt=Abstract
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Infliximab or etanercept in the treatment of children with refractory juvenile idiopathic arthritis: an open label study. Author(s): Lahdenne P, Vahasalo P, Honkanen V. Source: Annals of the Rheumatic Diseases. 2003 March; 62(3): 245-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12594111&dopt=Abstract
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Influence of therapy with chimeric monoclonal tumour necrosis factor-alpha antibodies on intracellular cytokine profiles of T lymphocytes and monocytes in rheumatoid arthritis patients. Author(s): Schuerwegh AJ, Van Offel JF, Stevens WJ, Bridts CH, De Clerck LS. Source: Rheumatology (Oxford, England). 2003 April; 42(4): 541-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12649401&dopt=Abstract
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Informed consent in a clinical trial of a novel treatment for rheumatoid arthritis. Author(s): Criscione LG, Sugarman J, Sanders L, Pisetsky DS, St Clair EW. Source: Arthritis and Rheumatism. 2003 June 15; 49(3): 361-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12794792&dopt=Abstract
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Infrared spectroscopy: shedding light on synovitis in patients with rheumatoid arthritis. Author(s): Canvin JM, Bernatsky S, Hitchon CA, Jackson M, Sowa MG, Mansfield JR, Eysel HH, Mantsch HH, El-Gabalawy HS. Source: Rheumatology (Oxford, England). 2003 January; 42(1): 76-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12509617&dopt=Abstract
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Inhibition of interleukin 10 signaling after Fc receptor ligation and during rheumatoid arthritis. Author(s): Ji JD, Tassiulas I, Park-Min KH, Aydin A, Mecklenbrauker I, Tarakhovsky A, Pricop L, Salmon JE, Ivashkiv LB. Source: The Journal of Experimental Medicine. 2003 June 2; 197(11): 1573-83. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12782719&dopt=Abstract
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Inhibitors of p38 mitogen-activated protein kinase for the treatment of rheumatoid arthritis. Author(s): Pargellis C, Regan J. Source: Curr Opin Investig Drugs. 2003 May; 4(5): 566-71. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12833650&dopt=Abstract
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Interactions between children with juvenile rheumatoid arthritis and their mothers. Author(s): Power TG, Dahlquist LM, Thompson SM, Warren R. Source: Journal of Pediatric Psychology. 2003 April-May; 28(3): 213-21. Erratum In: J Pediatr Psychol. 2003 July-August; 28(5): Following Page 373. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12654947&dopt=Abstract
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Interleukin 1 receptor antagonist anakinra improves functional status in patients with rheumatoid arthritis. Author(s): Cohen SB, Woolley JM, Chan W; Anakinra 960180 Study Group. Source: The Journal of Rheumatology. 2003 February; 30(2): 225-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12563672&dopt=Abstract
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Interleukin 10 treatment of patients with rheumatoid arthritis enhances Fc gamma receptor expression on monocytes and responsiveness to immune complex stimulation. Author(s): van Roon J, Wijngaarden S, Lafeber FP, Damen C, van de Winkel J, Bijlsma JW. Source: The Journal of Rheumatology. 2003 April; 30(4): 648-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12672180&dopt=Abstract
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Interleukin 7 stimulates tumour necrosis factor alpha and Th1 cytokine production in joints of patients with rheumatoid arthritis. Author(s): van Roon JA, Glaudemans KA, Bijlsma JW, Lafeber FP. Source: Annals of the Rheumatic Diseases. 2003 February; 62(2): 113-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12525379&dopt=Abstract
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Interleukin-10 receptor expression in systemic lupus erythematosus and rheumatoid arthritis. Author(s): Cairns AP, Crockard AD, Bell AL. Source: Clin Exp Rheumatol. 2003 January-February; 21(1): 83-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12673894&dopt=Abstract
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Interleukin-17 in rheumatoid arthritis: if T cells were to contribute to inflammation and destruction through synergy. Author(s): Miossec P. Source: Arthritis and Rheumatism. 2003 March; 48(3): 594-601. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12632409&dopt=Abstract
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Interobserver agreement in ultrasonography of the finger and toe joints in rheumatoid arthritis. Author(s): Szkudlarek M, Court-Payen M, Jacobsen S, Klarlund M, Thomsen HS, Ostergaard M. Source: Arthritis and Rheumatism. 2003 April; 48(4): 955-62. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12687537&dopt=Abstract
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Interobserver reliability of articular examination in juvenile idiopathic arthritis. Author(s): Senocak O, Unsal E, Akalin E, Ergor G. Source: Turk J Pediatr. 2003 January-March; 45(1): 29-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12718368&dopt=Abstract
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Interpretation of therapies for knee arthritis. Author(s): Christmas C, Moncada L. Source: Archives of Internal Medicine. 2003 August 11-25; 163(15): 1862. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12912728&dopt=Abstract
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Interpreting radiographic data in rheumatoid arthritis. Author(s): Ory PA. Source: Annals of the Rheumatic Diseases. 2003 July; 62(7): 597-604. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12810418&dopt=Abstract
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Intervention programs for arthritis and other rheumatic diseases. Author(s): Brady TJ, Kruger J, Helmick CG, Callahan LF, Boutaugh ML. Source: Health Education & Behavior : the Official Publication of the Society for Public Health Education. 2003 February; 30(1): 44-63. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12564667&dopt=Abstract
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Intra-articular corticosteroid injections in juvenile idiopathic arthritis. Author(s): Cleary AG, Murphy HD, Davidson JE. Source: Archives of Disease in Childhood. 2003 March; 88(3): 192-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12598375&dopt=Abstract
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Intravenous human recombinant tumor necrosis factor receptor p55-Fc IgG1 fusion protein Ro 45-2081 (lenercept): a double blind, placebo controlled dose-finding study in rheumatoid arthritis. Author(s): Rau R, Sander O, van Riel P, van de Putte L, Hasler F, Zaug M, Kneer J, van der Auwera P, Stevens RM; Rheumatology Group 791. Source: The Journal of Rheumatology. 2003 April; 30(4): 680-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12672184&dopt=Abstract
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Involvement of natural killer T cells in C57BL/6 mouse model of collagen-induced arthritis. Author(s): Wang CR. Source: J Microbiol Immunol Infect. 2003 March; 36(1): 15-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12741727&dopt=Abstract
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Is there still a role for traditional disease-modifying antirheumatic drugs (DMARDs) in rheumatoid arthritis? Author(s): Cannella AC, O'Dell JR. Source: Current Opinion in Rheumatology. 2003 May; 15(3): 185-92. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12707569&dopt=Abstract
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Is thiopurine methyltransferase genetic polymorphism a major factor for withdrawal of azathioprine in rheumatoid arthritis patients? Author(s): Corominas H, Domenech M, Laiz A, Gich I, Geli C, Diaz C, de Cuevillas F, Moreno M, Vazquez G, Baiget M. Source: Rheumatology (Oxford, England). 2003 January; 42(1): 40-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12509611&dopt=Abstract
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Isolated septic arthritis: meningococcal infection. Author(s): Joyce M, Laing A, Mullet H, Gilmore MF, Cormican M. Source: Journal of the Royal Society of Medicine. 2003 May; 96(5): 237-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12724437&dopt=Abstract
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Isolation and functional characterization of regulatory CD25brightCD4+ T cells from the target organ of patients with rheumatoid arthritis. Author(s): Cao D, Malmstrom V, Baecher-Allan C, Hafler D, Klareskog L, Trollmo C. Source: European Journal of Immunology. 2003 January; 33(1): 215-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12594850&dopt=Abstract
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Joint stiffness in a phantom limb: evidence of central nervous system involvement in rheumatoid arthritis. Author(s): Haigh RC, McCabe CS, Halligan PW, Blake DR. Source: Rheumatology (Oxford, England). 2003 July; 42(7): 888-92. Epub 2003 March 31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12730550&dopt=Abstract
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Kaposi's sarcoma in psoriatic arthritis. Author(s): Selvi E, De Stefano R, Manganelli S, Marcolongo R. Source: Rheumatology (Oxford, England). 2003 February; 42(2): 389. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12595648&dopt=Abstract
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Laboratory changes on anti-tumor necrosis factor treatment in rheumatoid arthritis. Author(s): Ziolkowska M, Maslinski W. Source: Current Opinion in Rheumatology. 2003 May; 15(3): 267-73. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12707580&dopt=Abstract
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Laboratory monitoring in pediatric acute osteomyelitis and septic arthritis. Author(s): Khachatourians AG, Patzakis MJ, Roidis N, Holtom PD. Source: Clinical Orthopaedics and Related Research. 2003 April; (409): 186-94. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12671501&dopt=Abstract
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Lack of association between -384 and 114 IL-2 gene polymorphisms and rheumatoid arthritis. Author(s): Fedetz M, Matesanz F, Caliz R, Ferrer MA, Collado MD, Alcina A, Martin J. Source: The Journal of Rheumatology. 2003 March; 30(3): 435-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12610796&dopt=Abstract
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Lack of association of Human T-cell lymphotrophic virus type 1(HTLV-1) infection and rheumatoid arthritis in an endemic area. Author(s): Sebastian D, Nayiager S, York DY, Mody GM. Source: Clinical Rheumatology. 2003 February; 22(1): 30-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12605314&dopt=Abstract
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Lack of trans-activation function for Maedi Visna virus and Caprine arthritis encephalitis virus Tat proteins. Author(s): Villet S, Faure C, Bouzar BA, Morin T, Verdier G, Chebloune Y, Legras C. Source: Virology. 2003 March 15; 307(2): 317-27. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12667801&dopt=Abstract
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Leflunomide for the treatment of rheumatoid arthritis. Author(s): Miceli-Richard C, Dougados M. Source: Expert Opinion on Pharmacotherapy. 2003 June; 4(6): 987-97. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12783594&dopt=Abstract
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Leflunomide for treating rheumatoid arthritis. Author(s): Osiri M, Shea B, Robinson V, Suarez-Almazor M, Strand V, Tugwell P, Wells G. Source: Cochrane Database Syst Rev. 2003; (1): Cd002047. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12535423&dopt=Abstract
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Liaison between rheumatoid arthritis and ulcerative colitis. Author(s): Aydin Y, Ozcakar L, Yildiz M, Akinci A. Source: Rheumatology International. 2003 January; 23(1): 47-8. Epub 2002 December 18. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12548442&dopt=Abstract
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Life-threatening reversible bone marrow toxicity in a rheumatoid arthritis patient switched from leflunomide to infliximab. Author(s): Marchesoni A, Arreghini M, Panni B, Battafarano N, Uziel L. Source: Rheumatology (Oxford, England). 2003 January; 42(1): 193-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12509641&dopt=Abstract
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Local production of B lymphocyte stimulator protein and APRIL in arthritic joints of patients with inflammatory arthritis. Author(s): Tan SM, Xu D, Roschke V, Perry JW, Arkfeld DG, Ehresmann GR, Migone TS, Hilbert DM, Stohl W. Source: Arthritis and Rheumatism. 2003 April; 48(4): 982-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12687540&dopt=Abstract
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Localization of MHC class II/human cartilage glycoprotein-39 complexes in synovia of rheumatoid arthritis patients using complex-specific monoclonal antibodies. Author(s): Steenbakkers PG, Baeten D, Rovers E, Veys EM, Rijnders AW, Meijerink J, De Keyser F, Boots AM. Source: Journal of Immunology (Baltimore, Md. : 1950). 2003 June 1; 170(11): 5719-27. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12759455&dopt=Abstract
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Long term structural effects of combination therapy in patients with early rheumatoid arthritis: five year follow up of a prospective double blind controlled study. Author(s): Maillefert JF, Combe B, Goupille P, Cantagrel A, Dougados M. Source: Annals of the Rheumatic Diseases. 2003 August; 62(8): 764-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12860733&dopt=Abstract
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Long-term anti-tumor necrosis factor antibody therapy in rheumatoid arthritis patients sensitizes the pituitary gland and favors adrenal androgen secretion. Author(s): Straub RH, Pongratz G, Scholmerich J, Kees F, Schaible TF, Antoni C, Kalden JR, Lorenz HM. Source: Arthritis and Rheumatism. 2003 June; 48(6): 1504-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12794817&dopt=Abstract
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Long-term efficacy and safety of etanercept in children with polyarticular-course juvenile rheumatoid arthritis: interim results from an ongoing multicenter, openlabel, extended-treatment trial. Author(s): Lovell DJ, Giannini EH, Reiff A, Jones OY, Schneider R, Olson JC, Stein LD, Gedalia A, Ilowite NT, Wallace CA, Lange M, Finck BK, Burge DJ; Pediatric Rheumatology Collaborative Study Group. Source: Arthritis and Rheumatism. 2003 January; 48(1): 218-26. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12528122&dopt=Abstract
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Long-term efficacy of a cognitive behavioural treatment from a randomized controlled trial for patients recently diagnosed with rheumatoid arthritis. Author(s): Sharpe L, Sensky T, Timberlake N, Ryan B, Allard S. Source: Rheumatology (Oxford, England). 2003 March; 42(3): 435-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12626793&dopt=Abstract
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Low dose methotrexate osteopathy in a patient with polyarticular juvenile idiopathic arthritis. Author(s): Rudler M, Pouchot J, Paycha F, Gentelle S, Grasland A, Vinceneux P. Source: Annals of the Rheumatic Diseases. 2003 June; 62(6): 588-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12759303&dopt=Abstract
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Low prevalence of antibodies to glucose-6-phosphate isomerase in patients with rheumatoid arthritis and a spectrum of other chronic autoimmune disorders. Author(s): Matsumoto I, Lee DM, Goldbach-Mansky R, Sumida T, Hitchon CA, Schur PH, Anderson RJ, Coblyn JS, Weinblatt ME, Brenner M, Duclos B, Pasquali JL, ElGabalawy H, Mathis D, Benoist C. Source: Arthritis and Rheumatism. 2003 April; 48(4): 944-54. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12687536&dopt=Abstract
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Low-dose glucocorticoids in early rheumatoid arthritis: discordant effects on bone mineral density and fractures? Author(s): van Everdingen AA, Siewertsz van Reesema DR, Jacobs JW, Bijlsma JW. Source: Clin Exp Rheumatol. 2003 March-April; 21(2): 155-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12747268&dopt=Abstract
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Lower level of synovial fluid interferon-gamma in HLA-B27-positive than in HLAB27-negative patients with Chlamydia trachomatis reactive arthritis. Author(s): Bas S, Kvien TK, Buchs N, Fulpius T, Gabay C. Source: Rheumatology (Oxford, England). 2003 March; 42(3): 461-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12626797&dopt=Abstract
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Lyme arthritis presenting as acute septic arthritis in children. Author(s): Willis AA, Widmann RF, Flynn JM, Green DW, Onel KB. Source: Journal of Pediatric Orthopedics. 2003 January-February; 23(1): 114-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12499956&dopt=Abstract
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Lymphoma subtypes in patients with rheumatoid arthritis: increased proportion of diffuse large B cell lymphoma. Author(s): Baecklund E, Sundstrom C, Ekbom A, Catrina AI, Biberfeld P, Feltelius N, Klareskog L. Source: Arthritis and Rheumatism. 2003 June; 48(6): 1543-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12794821&dopt=Abstract
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Macrophage activation syndrome following initiation of etanercept in a child with systemic onset juvenile rheumatoid arthritis. Author(s): Ramanan AV, Schneider R. Source: The Journal of Rheumatology. 2003 February; 30(2): 401-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12563702&dopt=Abstract
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Macrophage migration inhibitory factor: an emerging therapeutic target in rheumatoid arthritis. Author(s): Morand EF, Bucala R, Leech M. Source: Arthritis and Rheumatism. 2003 February; 48(2): 291-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12571836&dopt=Abstract
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Magnetic resonance imaging appearance of the hands and feet in patients with early rheumatoid arthritis. Author(s): Boutry N, Larde A, Lapegue F, Solau-Gervais E, Flipo RM, Cotten A. Source: The Journal of Rheumatology. 2003 April; 30(4): 671-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12672183&dopt=Abstract
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Magnetic resonance imaging in the evaluation of bone damage in rheumatoid arthritis: a more precise image or just a more expensive one? Author(s): Goldbach-Mansky R, Woodburn J, Yao L, Lipsky PE. Source: Arthritis and Rheumatism. 2003 March; 48(3): 585-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12632407&dopt=Abstract
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Magnetic resonance imaging of the fifth metatarsophalangeal joint compared with conventional radiography in patients with early rheumatoid arthritis. Author(s): Forslind K, Johanson A, Larsson EM, Svensson B. Source: Scandinavian Journal of Rheumatology. 2003; 32(3): 131-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12892248&dopt=Abstract
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Mandibular osteotomies in patients with juvenile rheumatoid arthritic disease. Author(s): Oye F, Bjornland T, Store G. Source: Scandinavian Journal of Rheumatology. 2003; 32(3): 168-73. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12892254&dopt=Abstract
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Measurement of disease activity in psoriatic arthritis. Extended report. Author(s): Ujfalussy I, Koo E. Source: Zeitschrift Fur Rheumatologie. 2003 February; 62(1): 60-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12624805&dopt=Abstract
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Measurement of soluble Fcgamma receptor type IIIa derived from macrophages in plasma: increase in patients with rheumatoid arthritis. Author(s): Masuda M, Morimoto T, Kobatake S, Nishimura N, Nakamoto K, Dong XH, Komiyama Y, Ogawa R, Takahashi H. Source: Clinical and Experimental Immunology. 2003 June; 132(3): 477-84. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12780696&dopt=Abstract
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Mechanisms of TNF-alpha- and RANKL-mediated osteoclastogenesis and bone resorption in psoriatic arthritis. Author(s): Ritchlin CT, Haas-Smith SA, Li P, Hicks DG, Schwarz EM. Source: The Journal of Clinical Investigation. 2003 March; 111(6): 821-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12639988&dopt=Abstract
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Mediterranean diet intervention in rheumatoid arthritis. Author(s): Kjeldsen-Kragh J. Source: Annals of the Rheumatic Diseases. 2003 March; 62(3): 193-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12594101&dopt=Abstract
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Melioidotic septic arthritis and its risk factors. Author(s): Kosuwon W, Taimglang T, Sirichativapee W, Jeeravipoolvarn P. Source: The Journal of Bone and Joint Surgery. American Volume. 2003 June; 85-A(6): 1058-61. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12784002&dopt=Abstract
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Meta-analysis of four rheumatoid arthritis genome-wide linkage studies: confirmation of a susceptibility locus on chromosome 16. Author(s): Fisher SA, Lanchbury JS, Lewis CM. Source: Arthritis and Rheumatism. 2003 May; 48(5): 1200-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12746892&dopt=Abstract
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Metacarpophalangeal joint arthroplasty in rheumatoid arthritis. Author(s): Kimball HL, Terrono AL, Feldon P, Zelouf DS. Source: Instr Course Lect. 2003; 52: 163-74. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12690846&dopt=Abstract
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Methotrexate pneumonitis in a patient with rheumatoid arthritis. Author(s): Hsu PC, Lan JL, Hsieh TY, Jan YJ, Huang WN. Source: J Microbiol Immunol Infect. 2003 June; 36(2): 137-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12886966&dopt=Abstract
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Mice transgenic for intracellular interleukin-1 receptor antagonist type 1 are protected from collagen-induced arthritis. Author(s): Palmer G, Talabot-Ayer D, Szalay-Quinodoz L, Maret M, Arend WP, Gabay C. Source: European Journal of Immunology. 2003 February; 33(2): 434-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12645941&dopt=Abstract
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Microsatellite instability and suppressed DNA repair enzyme expression in rheumatoid arthritis. Author(s): Lee SH, Chang DK, Goel A, Boland CR, Bugbee W, Boyle DL, Firestein GS. Source: Journal of Immunology (Baltimore, Md. : 1950). 2003 February 15; 170(4): 221420. Erratum In: J Immunol. 2003 May 1; 170(9): 4869. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12574395&dopt=Abstract
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Mitral valve surgery in a patient with rheumatoid arthritis being treated with methotrexate. Author(s): Takami Y, Ina H. Source: Jpn J Thorac Cardiovasc Surg. 2003 May; 51(5): 205-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12776953&dopt=Abstract
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Modified disease activity score versus radiologic progression as an indicator of rheumatoid arthritis disease status: comment on the article by Landewe et al. Author(s): McEntegart A, Madhok R. Source: Arthritis and Rheumatism. 2003 January; 48(1): 272; Author Reply 272-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12528133&dopt=Abstract
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Modified Larsen scoring of digitized radiographs in rheumatoid arthritis. Author(s): Young-Min SA, Shakhapur S, Marshall N, Griffiths I, Cawston T, Grainger A. Source: The Journal of Rheumatology. 2003 February; 30(2): 238-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12563674&dopt=Abstract
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Multifocal septic arthritis and osteomyelitis caused by group A Streptococcus in a patient receiving immunomodulating therapy with etanercept. Author(s): Elwood RL, Pelszynski MM, Corman LI. Source: The Pediatric Infectious Disease Journal. 2003 March; 22(3): 286-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12664882&dopt=Abstract
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Mycobacterium malmoense septic arthritis. Author(s): Whitehead SE, Allen KD, Abernethy VE, Feldberg L, Ridyard JB. Source: The Journal of Infection. 2003 January; 46(1): 60-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12504611&dopt=Abstract
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Myeloid related protein 8 and 14 secretion reflects phagocyte activation and correlates with disease activity in juvenile idiopathic arthritis treated with autologous stem cell transplantation. Author(s): Wulffraat NM, Haas PJ, Frosch M, De Kleer IM, Vogl T, Brinkman DM, Quartier P, Roth J, Kuis W. Source: Annals of the Rheumatic Diseases. 2003 March; 62(3): 236-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12594109&dopt=Abstract
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Natural killer cell dysfunction in patients with systemic-onset juvenile rheumatoid arthritis and macrophage activation syndrome. Author(s): Grom AA, Villanueva J, Lee S, Goldmuntz EA, Passo MH, Filipovich A. Source: The Journal of Pediatrics. 2003 March; 142(3): 292-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12640378&dopt=Abstract
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Natural killer cells in the synovial fluid of rheumatoid arthritis patients exhibit a CD56bright,CD94bright,CD158negative phenotype. Author(s): Pridgeon C, Lennon GP, Pazmany L, Thompson RN, Christmas SE, Moots RJ. Source: Rheumatology (Oxford, England). 2003 July; 42(7): 870-8. Epub 2003 April 16. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12730548&dopt=Abstract
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Nephrotic syndrome as a complication of anti-TNFalpha in a patient with rheumatoid arthritis. Author(s): den Broeder AA, Assmann KJ, van Riel PL, Wetzels JF. Source: The Netherlands Journal of Medicine. 2003 April; 61(4): 137-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12852723&dopt=Abstract
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Neutrophil migration and production of reactive oxygen species during treatment with a fully human anti-tumor necrosis factor-alpha monoclonal antibody in patients with rheumatoid arthritis. Author(s): den Broeder AA, Wanten GJ, Oyen WJ, Naber T, van Riel PL, Barrera P. Source: The Journal of Rheumatology. 2003 February; 30(2): 232-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12563673&dopt=Abstract
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New antibody approved for treatment of rheumatoid arthritis. Author(s): Piascik P. Source: Journal of the American Pharmaceutical Association (Washington,D.C. : 1996). 2003 March-April; 43(2): 327-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12688444&dopt=Abstract
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New concepts in the treatment of rheumatoid arthritis. Author(s): Goldbach-Mansky R, Lipsky PE. Source: Annual Review of Medicine. 2003; 54: 197-216. Epub 2001 December 03. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12359827&dopt=Abstract
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New developments in imaging in rheumatoid arthritis. Author(s): Peterfy CG. Source: Current Opinion in Rheumatology. 2003 May; 15(3): 288-95. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12707583&dopt=Abstract
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New evidence for vascular disease in patients with early rheumatoid arthritis. Author(s): Kaplan MJ, McCune WJ. Source: Lancet. 2003 March 29; 361(9363): 1068-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12672306&dopt=Abstract
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New radiographic bone erosions in the wrists of patients with rheumatoid arthritis are detectable with magnetic resonance imaging a median of two years earlier. Author(s): Ostergaard M, Hansen M, Stoltenberg M, Jensen KE, Szkudlarek M, Pedersen-Zbinden B, Lorenzen I. Source: Arthritis and Rheumatism. 2003 August; 48(8): 2128-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12905465&dopt=Abstract
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New role for an old friend: prednisone is a disease-modifying agent in early rheumatoid arthritis. Author(s): Conn DL, Lim SS. Source: Current Opinion in Rheumatology. 2003 May; 15(3): 193-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12707570&dopt=Abstract
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Newly available treatments for psoriatic arthritis and their impact on skin psoriasis. Author(s): Galadari H, Fuchs B, Lebwohl M. Source: International Journal of Dermatology. 2003 March; 42(3): 231-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12653923&dopt=Abstract
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NF-kappaB-dependent lymphocyte hyperadhesiveness to synovial fibroblasts by hypoxia and reoxygenation: potential role in rheumatoid arthritis. Author(s): Han MK, Kim JS, Park BH, Kim JR, Hwang BY, Lee HY, Song EK, Yoo WH. Source: Journal of Leukocyte Biology. 2003 April; 73(4): 525-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12660227&dopt=Abstract
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Non-contrast computed tomography-guided intra-articular corticosteroid injections of severe bilateral hip arthritis in a patient with ankylosing spondylitis. Author(s): Santos-Ocampo AS, Santos-Ocampo RS. Source: Clin Exp Rheumatol. 2003 March-April; 21(2): 239-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12747284&dopt=Abstract
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Non-inherited maternal HLA alleles are associated with rheumatoid arthritis. Author(s): Harney S, Newton J, Milicic A, Brown MA, Wordsworth BP. Source: Rheumatology (Oxford, England). 2003 January; 42(1): 171-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12509632&dopt=Abstract
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Novel autoantibodies to pituitary gland specific factor 1a in patients with rheumatoid arthritis. Author(s): Tanaka S, Tatsumi K, Tomita T, Kimura M, Takano T, Yoshikawa H, Amino N. Source: Rheumatology (Oxford, England). 2003 February; 42(2): 353-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12595635&dopt=Abstract
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Novel therapies for the treatment of juvenile rheumatoid arthritis (juvenile idiopathic arthritis). Author(s): Agle LM, Rosenkranz M, Lehman TJ. Source: Expert Opinion on Investigational Drugs. 2003 January; 12(1): 19-28. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12517251&dopt=Abstract
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Nutritional management of rheumatoid arthritis: a review of the evidence. Author(s): Rennie KL, Hughes J, Lang R, Jebb SA. Source: Journal of Human Nutrition and Dietetics : the Official Journal of the British Dietetic Association. 2003 April; 16(2): 97-109. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12662368&dopt=Abstract
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Occipitocervical fusion for rheumatoid arthritis using the inside-outside stabilization technique. Author(s): Sandhu FA, Pait TG, Benzel E, Henderson FC. Source: Spine. 2003 February 15; 28(4): 414-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12590220&dopt=Abstract
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Occurrence of chronic inflammatory rheumatic diseases among parents of multiple offspring affected by juvenile idiopathic arthritis. Author(s): Saila H, Savolainen A, Kauppi M, Alakulppi N, Tuomilehto-Wolf E, Tuomilehto J, Leirisalo-Repo M, Aho K. Source: Clin Exp Rheumatol. 2003 March-April; 21(2): 263-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12747288&dopt=Abstract
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OMERACT 6 Economics Working Group report: a proposal for a reference case for economic evaluation in rheumatoid arthritis. Author(s): Gabriel S, Drummond M, Maetzel A, Boers M, Coyle D, Welch V, Tugwell P; Patient Perspective Group. Source: The Journal of Rheumatology. 2003 April; 30(4): 886-90. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12672223&dopt=Abstract
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On call. I have arthritis of both knees. Prescription medicines didn't help and they irritated my stomach. I tried glucosamine, and it didn't do much good either. Finally my doctor sent me to a specialist, who washed out both knees with an arthroscope. My pain is nearly gone, but I read that doctors did a test that showed a fake operation was just as good as my surgery. It's an outrage. How can responsible doctors perform fake operations? Author(s): Simon HB. Source: Harvard Men's Health Watch. 2003 January; 7(6): 7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12543597&dopt=Abstract
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Oral contraceptives, rheumatoid arthritis, and androgens. Author(s): James WH. Source: Annals of the Rheumatic Diseases. 2003 March; 62(3): 279. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12594126&dopt=Abstract
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Orbital myositis in a rheumatoid arthritis patient during etanercept treatment. Author(s): Caramaschi P, Biasi D, Carletto A, Bambara LM. Source: Clin Exp Rheumatol. 2003 January-February; 21(1): 136-7. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12673906&dopt=Abstract
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Osteochondral grafting of the metacarpophalangeal joint in rheumatoid arthritis. Author(s): Lo CY, Chang YP. Source: Journal of Hand Surgery (Edinburgh, Lothian). 2003 February; 28(1): 94-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12531678&dopt=Abstract
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Osteoprotegerin expression in synovial tissue from patients with rheumatoid arthritis, spondyloarthropathies and osteoarthritis and normal controls. Author(s): Haynes DR, Barg E, Crotti TN, Holding C, Weedon H, Atkins GJ, Zannetino A, Ahern MJ, Coleman M, Roberts-Thomson PJ, Kraan M, Tak PP, Smith MD. Source: Rheumatology (Oxford, England). 2003 January; 42(1): 123-34. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12509625&dopt=Abstract
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Outcome after single technique ankle arthrodesis in patients with rheumatoid arthritis. Author(s): Kennedy JG, Harty JA, Casey K, Jan W, Quinlan WB. Source: Clinical Orthopaedics and Related Research. 2003 July; (412): 131-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12838063&dopt=Abstract
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Outcome in adults with juvenile idiopathic arthritis. Comparison of the DUTCHAIMS2 between JIA and RA. Author(s): Bruinooge LN, El Moussaoui R, Taal E, Dijkmans BA, Van Soesbergen RM. Source: Scandinavian Journal of Rheumatology. 2003; 32(2): 89-94. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12737327&dopt=Abstract
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Outcome in adults with juvenile idiopathic arthritis: a quality of life study. Author(s): Foster HE, Marshall N, Myers A, Dunkley P, Griffiths ID. Source: Arthritis and Rheumatism. 2003 March; 48(3): 767-75. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12632431&dopt=Abstract
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Overdiagnosed sciatica and stenosis, underdiagnosed hip arthritis. Author(s): Swezey RL. Source: Orthopedics. 2003 February; 26(2): 173-4; Discussion 174. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12597222&dopt=Abstract
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Overexpression of transcripts containing LINE-1 in the synovia of patients with rheumatoid arthritis. Author(s): Ali M, Veale DJ, Reece RJ, Quinn M, Henshaw K, Zanders ED, Markham AF, Emery P, Isaacs JD. Source: Annals of the Rheumatic Diseases. 2003 July; 62(7): 663-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12810431&dopt=Abstract
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p21waf1/cip1 is down-regulated in conjunction with up-regulation of c-Fos in the lymphocytes of rheumatoid arthritis patients. Author(s): Hikasa M, Yamamoto E, Kawasaki H, Komai K, Shiozawa K, Hashiramoto A, Miura Y, Shiozawa S. Source: Biochemical and Biophysical Research Communications. 2003 April 25; 304(1): 143-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12705898&dopt=Abstract
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Pain in children with arthritis: a review of the current literature. Author(s): Anthony KK, Schanberg LE. Source: Arthritis and Rheumatism. 2003 April 15; 49(2): 272-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12687523&dopt=Abstract
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Pantoea agglomerans as a cause of septic arthritis after palm tree thorn injury; case report and literature review. Author(s): Kratz A, Greenberg D, Barki Y, Cohen E, Lifshitz M. Source: Archives of Disease in Childhood. 2003 June; 88(6): 542-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12765929&dopt=Abstract
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Paraplegia in a patient receiving anti-tumor necrosis factor therapy for rheumatoid arthritis: comment on the article by Mohan et al. Author(s): van der Laken CJ, Lems WF, van Soesbergen RM, van der Sande JJ, Dijkmans BA. Source: Arthritis and Rheumatism. 2003 January; 48(1): 269-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12528130&dopt=Abstract
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Pathogenesis of bone and cartilage destruction in rheumatoid arthritis. Author(s): Goldring SR. Source: Rheumatology (Oxford, England). 2003 May; 42 Suppl 2: Ii11-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12817090&dopt=Abstract
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Patient compliance in rheumatoid arthritis, polymyalgia rheumatica, and gout. Author(s): de Klerk E, van der Heijde D, Landewe R, van der Tempel H, Urquhart J, van der Linden S. Source: The Journal of Rheumatology. 2003 January; 30(1): 44-54. Erratum In: J Rheumatol. 2003 February; 30(2): 423. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12508389&dopt=Abstract
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Patient education for adults with rheumatoid arthritis. Author(s): Riemsma RP, Kirwan JR, Taal E, Rasker JJ. Source: Cochrane Database Syst Rev. 2003; (2): Cd003688. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12804484&dopt=Abstract
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Patients and clinicians have different perspectives on outcomes in arthritis. Author(s): Hewlett SA. Source: The Journal of Rheumatology. 2003 April; 30(4): 877-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12672220&dopt=Abstract
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Patterns of disease modifying antirheumatic drug use in a Spanish cohort of patients with rheumatoid arthritis. Author(s): Gonzalez-Alvaro I, Carmona L, Balsa A, Sanmarti R, Belmonte MA, Tena X; EMECAR Study Group. Source: The Journal of Rheumatology. 2003 April; 30(4): 697-704. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12672186&dopt=Abstract
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Perceptions of control in patients with rheumatoid arthritis. Author(s): Ryan S, Hassell A, Dawes P, Kendall S. Source: Nurs Times. 2003 April 1-7; 99(13): 36-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12715557&dopt=Abstract
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Perinatal characteristics and risk of rheumatoid arthritis. Author(s): Jacobsson LT, Jacobsson ME, Askling J, Knowler WC. Source: Bmj (Clinical Research Ed.). 2003 May 17; 326(7398): 1068-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12750209&dopt=Abstract
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Peripheral-type benzodiazepine receptors in human mononuclear cells of patients affected by osteoarthritis, rheumatoid arthritis or psoriasic arthritis. Author(s): Bazzichi L, Betti L, Giannaccini G, Rossi A, Lucacchini A. Source: Clinical Biochemistry. 2003 February; 36(1): 57-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12554061&dopt=Abstract
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Physical activity levels among the general US adult population and in adults with and without arthritis. Author(s): Hootman JM, Macera CA, Ham SA, Helmick CG, Sniezek JE. Source: Arthritis and Rheumatism. 2003 February 15; 49(1): 129-35. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12579604&dopt=Abstract
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Physiotherapy in subtropic climate improves functional capacity and health-related quality of life in Swedish patients with rheumatoid arthritis and spondylarthropathies still after 6 months. Author(s): Hafstrom I, Hallengren M. Source: Scandinavian Journal of Rheumatology. 2003; 32(2): 108-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12737330&dopt=Abstract
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Pilot clinical trial of intravenous doxycycline versus placebo for rheumatoid arthritis. Author(s): Pillemer S, Gulko P, Ligier S, Yarboro C, Gourley M, Goldbach-Mansky R, Siegel R, Hirsch R, Pucino F, Tilley B, Wilder RL. Source: The Journal of Rheumatology. 2003 January; 30(1): 41-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12508388&dopt=Abstract
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Plasma pyridoxal 5'-phosphate concentration is correlated with functional vitamin B6 indices in patients with rheumatoid arthritis and marginal vitamin B-6 status. Author(s): Chiang EP, Bagley PJ, Roubenoff R, Nadeau M, Selhub J. Source: The Journal of Nutrition. 2003 April; 133(4): 1056-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12672918&dopt=Abstract
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Pneumococcal septic arthritis: review of 190 cases. Author(s): Ross JJ, Saltzman CL, Carling P, Shapiro DS. Source: Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America. 2003 February 1; 36(3): 319-27. Epub 2003 January 13. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12539074&dopt=Abstract
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Polyclonal activation as a consequence of infection of mice with Yersinia enterocolitica O:3 isolated from patients with or without arthritis. Author(s): Medeiros BM, Silva EE, Ramos OP, Falcao DP. Source: Advances in Experimental Medicine and Biology. 2003; 529: 151-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12756748&dopt=Abstract
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Polymicrobial septic arthritis in a patient with Wilson's disease. Author(s): Oliver AM, Baddley JW, Bridges SL Jr. Source: Annals of the Rheumatic Diseases. 2003 July; 62(7): 693-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12810447&dopt=Abstract
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Polymorphism at position -308 of the tumor necrosis factor alpha gene influences outcome of infliximab therapy in rheumatoid arthritis. Author(s): Mugnier B, Balandraud N, Darque A, Roudier C, Roudier J, Reviron D. Source: Arthritis and Rheumatism. 2003 July; 48(7): 1849-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12847678&dopt=Abstract
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Polymyositis with arthritis. Author(s): Handa R, Wali JP. Source: J Assoc Physicians India. 2003 February; 51: 192. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12725265&dopt=Abstract
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Population pharmacokinetic analysis of meloxicam in rheumatoid arthritis patients. Author(s): Meineke I, Turck D. Source: British Journal of Clinical Pharmacology. 2003 January; 55(1): 32-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12534638&dopt=Abstract
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Positional cloning of Ncf1--a piece in the puzzle of arthritis genetics. Author(s): Olofsson P, Holmdahl R. Source: Scandinavian Journal of Immunology. 2003 August; 58(2): 155-64. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12869136&dopt=Abstract
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Possible role of shared epitope status in the relationship between matrix metalloproteinase 3 genotype and radiographic progression of rheumatoid arthritis: comment on the article by Constantin et al. Author(s): de Vries N, Tak PP. Source: Arthritis and Rheumatism. 2003 April; 48(4): 1162-3; Author Reply 1163-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12687566&dopt=Abstract
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Posterior atlanto-axial fusion with the Olerud Cervical Fixation System for odontoid fractures and C1-C2 instability in rheumatoid arthritis. Author(s): Cornefjord M, Henriques T, Alemany M, Olerud C. Source: European Spine Journal : Official Publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society. 2003 February; 12(1): 91-6. Epub 2002 October 26. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12592552&dopt=Abstract
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Predicting mortality in patients with rheumatoid arthritis. Author(s): Wolfe F, Michaud K, Gefeller O, Choi HK. Source: Arthritis and Rheumatism. 2003 June; 48(6): 1530-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12794820&dopt=Abstract
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Predictors of radiological progression and changes in hand bone density in early rheumatoid arthritis. Author(s): Berglin E, Lorentzon R, Nordmark L, Nilsson-Sojka B, Rantapaa Dahlqvist S. Source: Rheumatology (Oxford, England). 2003 February; 42(2): 268-75. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12595621&dopt=Abstract
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Predominant cellular immune response to the cartilage autoantigenic G1 aggrecan in ankylosing spondylitis and rheumatoid arthritis. Author(s): Zou J, Zhang Y, Thiel A, Rudwaleit M, Shi SL, Radbruch A, Poole R, Braun J, Sieper J. Source: Rheumatology (Oxford, England). 2003 July; 42(7): 846-55. Epub 2003 February 28. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12730543&dopt=Abstract
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Presence of a 88 kDa Eales protein in uveitis, tuberculosis, leprosy and rheumatoid arthritis. Author(s): Rajesh M, Sulochana KN, Sundaram AL, Krishnakumar S, Biswas J, Ramakrishnan S. Source: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research. 2003 February; 9(2): Cr95-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12601295&dopt=Abstract
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Preseptal cellulitis in systemic onset juvenile idiopathic arthritis. Author(s): Coombes AG, Zaman A, Hall M, Cawley MI. Source: Eye (London, England). 2003 March; 17(2): 258-60. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12640422&dopt=Abstract
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Pretreatment cytokine profiles of peripheral blood mononuclear cells and serum from patients with rheumatoid arthritis in different american college of rheumatology response groups to methotrexate. Author(s): Seitz M, Zwicker M, Villiger PM. Source: The Journal of Rheumatology. 2003 January; 30(1): 28-35. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12508386&dopt=Abstract
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Prevalence and clinical significance of anti-cyclic citrullinated peptide and antikeratin antibodies in palindromic rheumatism. An abortive form of rheumatoid arthritis? Author(s): Salvador G, Gomez A, Vinas O, Ercilla G, Canete JD, Munoz-Gomez J, Sanmarti R. Source: Rheumatology (Oxford, England). 2003 August; 42(8): 972-5. Epub 2003 April 16. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12730510&dopt=Abstract
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Prevalence of arthritis and associated joint disorders in an employed population and the associated healthcare, sick leave, disability, and workers' compensation benefits cost and productivity loss of employers. Author(s): Muchmore L, Lynch WD, Gardner HH, Williamson T, Burke T. Source: Journal of Occupational and Environmental Medicine / American College of Occupational and Environmental Medicine. 2003 April; 45(4): 369-78. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12708140&dopt=Abstract
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Prevalence of dermatophytosis in patients with rheumatoid arthritis. Author(s): Bicer A, Tursen U, Cimen OB, Kaya TI, Ozisik S, Ikizoglu G, Erdogan C. Source: Rheumatology International. 2003 January; 23(1): 37-40. Epub 2002 August 29. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12548440&dopt=Abstract
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Prevalence of rheumatoid arthritis and hepatitis C in those age 60 and older in a US population based study. Author(s): Hsu FC, Starkebaum G, Boyko EJ, Dominitz JA. Source: The Journal of Rheumatology. 2003 March; 30(3): 455-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12610800&dopt=Abstract
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Prevalence of rheumatoid arthritis in persons 60 years of age and older in the United States: effect of different methods of case classification. Author(s): Rasch EK, Hirsch R, Paulose-Ram R, Hochberg MC. Source: Arthritis and Rheumatism. 2003 April; 48(4): 917-26. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12687533&dopt=Abstract
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Prevalence of rheumatoid arthritis. Author(s): Zauli D, Zucchini S, Manfredini E, Grassi A, Ballardini G, Fusconi M, Bianchi FB. Source: Rheumatology (Oxford, England). 2003 May; 42(5): 696-7; Author Reply 697. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12709551&dopt=Abstract
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Prevalence of Sindbis-related (Pogosta) virus infections in patients with arthritis. Author(s): Laine M, Vainionpaa R, Uksila J, Oksi J, Nissila M, Kaarela K, Luukkainen R, Toivanen A. Source: Clin Exp Rheumatol. 2003 March-April; 21(2): 213-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12747277&dopt=Abstract
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Primary bacterial pyomyositis associated with septic arthritis caused by Streptococcus pyogenes: a case report. Author(s): Lawrentschuk N, Falkenberg MP, Pirpiris M. Source: Am J Orthop. 2003 March; 32(3): 148-50. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12647881&dopt=Abstract
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Primary osteomyelitis and suppurative arthritis caused by coagulase-negative staphylococci in a preterm neonate. Author(s): Eggink BH, Rowen JL. Source: The Pediatric Infectious Disease Journal. 2003 June; 22(6): 572-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12828160&dopt=Abstract
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Prognostic factors in juvenile rheumatoid arthritis: a case-control study revealing early predictors and outcome after 14.9 years. Author(s): Flato B, Lien G, Smerdel A, Vinje O, Dale K, Johnston V, Sorskaar D, Moum T, Ploski R, Forre O. Source: The Journal of Rheumatology. 2003 February; 30(2): 386-93. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12563700&dopt=Abstract
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Progression of peripheral joint disease in psoriatic arthritis: a 5-yr prospective study. Author(s): McHugh NJ, Balachrishnan C, Jones SM. Source: Rheumatology (Oxford, England). 2003 June; 42(6): 778-83. Epub 2003 March 14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12730539&dopt=Abstract
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Prospective analysis of the impact of HLA-DR and -DQ on joint destruction in recentonset rheumatoid arthritis. Author(s): Wagner U, Kaltenhauser S, Pierer M, Seidel W, Troltzsch M, Hantzschel H, Kalden JR, Wassmuth R. Source: Rheumatology (Oxford, England). 2003 April; 42(4): 553-62. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12649403&dopt=Abstract
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Prospective comparative study of patients with culture proven and high suspicion of adult onset septic arthritis. Author(s): Gupta MN, Sturrock RD, Field M. Source: Annals of the Rheumatic Diseases. 2003 April; 62(4): 327-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12634231&dopt=Abstract
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Protein kinase signals activate interleukin 16 encoding transcripts in rheumatoid arthritis versus osteoarthritis synovial fibroblasts. Author(s): Schuler MK, Sell S, Aicher WK. Source: Annals of the Rheumatic Diseases. 2003 February; 62(2): 182-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12525392&dopt=Abstract
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Psoriasis vulgaris and arthritis psoriatica gravis mutilans. Author(s): Vrzogic P, Pasic A, Podobnik-Takac T. Source: Acta Dermatovenerol Croat. 2003; 11(1): 22-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12718792&dopt=Abstract
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Psoriatic arthritis as a mountain. Author(s): Berthelot JM. Source: Reumatismo. 2003; 55(1): 6-15. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12649695&dopt=Abstract
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Psoriatic arthritis: a guide for dermatology nurses. Author(s): Gottlieb AB. Source: Dermatology Nursing / Dermatology Nurses' Association. 2003 April; 15(2): 107-10, 113-8; Quiz 119. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12751345&dopt=Abstract
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Psychiatric adjustment in chronic fatigue syndrome of childhood and in juvenile idiopathic arthritis. Author(s): Rangel L, Garralda ME, Hall A, Woodham S. Source: Psychological Medicine. 2003 February; 33(2): 289-97. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12622307&dopt=Abstract
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Psychological adjustment of children and adolescents with chronic arthritis: a metaanalytic review. Author(s): LeBovidge JS, Lavigne JV, Donenberg GR, Miller ML. Source: Journal of Pediatric Psychology. 2003 January-February; 28(1): 29-39. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12490628&dopt=Abstract
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Psychometric properties of a Dutch short form of the Arthritis Impact Measurement Scales 2 (Dutch-AIMS2-SF). Author(s): Taal E, Rasker JJ, Riemsma RP. Source: Rheumatology (Oxford, England). 2003 March; 42(3): 427-34. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12626792&dopt=Abstract
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Quality of life, social support, and knowledge of disease in women with rheumatoid arthritis. Author(s): Minnock P, Fitzgerald O, Bresnihan B. Source: Arthritis and Rheumatism. 2003 April 15; 49(2): 221-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12687514&dopt=Abstract
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Radiographic damage associated with low bone mineral density and vertebral deformities in rheumatoid arthritis: the Oslo-Truro-Amsterdam (OSTRA) collaborative study. Author(s): Lodder MC, Haugeberg G, Lems WF, Uhlig T, Orstavik RE, Kostense PJ, Dijkmans BA, Kvien TK, Woolf AD; Oslo-Truro-Amsterdam (OSTRA) Collaborative Study. Source: Arthritis and Rheumatism. 2003 April 15; 49(2): 209-15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12687512&dopt=Abstract
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Radiographic data from recent randomized controlled trials in rheumatoid arthritis: what have we learned? Author(s): Strand V, Sharp JT. Source: Arthritis and Rheumatism. 2003 January; 48(1): 21-34. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12528100&dopt=Abstract
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Radiographic joint destruction in postmenopausal rheumatoid arthritis is strongly associated with generalised osteoporosis. Author(s): Forsblad D'Elia H, Larsen A, Waltbrand E, Kvist G, Mellstrom D, Saxne T, Ohlsson C, Nordborg E, Carlsten H. Source: Annals of the Rheumatic Diseases. 2003 July; 62(7): 617-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12810422&dopt=Abstract
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Radiologic features in juvenile idiopathic arthritis: a first step in the development of a standardized assessment method. Author(s): van Rossum MA, Zwinderman AH, Boers M, Dijkmans BA, van Soesbergen RM, Fiselier TJ, Franssen MJ, ten Cate R, van Suijlekom-Smit LW, Wulffraat NM, Kuis W, van Luijk WH, Oostveen JC, Dijkstra PF; Dutch Juvenile Idiopathic Arthritis Study Group. Source: Arthritis and Rheumatism. 2003 February; 48(2): 507-15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12571861&dopt=Abstract
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Radiologic findings of the lumbar spine in patients with rheumatoid arthritis, and a review of pathologic mechanisms. Author(s): Kawaguchi Y, Matsuno H, Kanamori M, Ishihara H, Ohmori K, Kimura T. Source: Journal of Spinal Disorders & Techniques. 2003 February; 16(1): 38-43. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12571483&dopt=Abstract
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Radiologic outcome and its relationship to functional disability in juvenile rheumatoid arthritis. Author(s): Oen K, Reed M, Malleson PN, Cabral DA, Petty RE, Rosenberg AM, Cheang M. Source: The Journal of Rheumatology. 2003 April; 30(4): 832-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12672208&dopt=Abstract
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RANKL and RANK as novel therapeutic targets for arthritis. Author(s): Nakashima T, Wada T, Penninger JM. Source: Current Opinion in Rheumatology. 2003 May; 15(3): 280-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12707582&dopt=Abstract
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Re: Silicone arthroplasty for trapeziometacarpal arthritis. Author(s): Dimri RK, Milling AW. Source: Journal of Hand Surgery (Edinburgh, Lothian). 2003 April; 28(2): 190-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12631498&dopt=Abstract
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Reactive arthritis and serum levels of mannose binding lectin -- lack of association. Author(s): Locht H, Christiansen M, Laursen I. Source: Clinical and Experimental Immunology. 2003 January; 131(1): 169-73. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12519401&dopt=Abstract
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Reactive arthritis, psoriasiform lesions and protein loosing enteropathy secondary to Strongyloidiasis. Author(s): Ghotekar LH, Jayanthi S, Mutha SM, Dutta TK, Thappa DM. Source: J Assoc Physicians India. 2003 April; 51: 395-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12723657&dopt=Abstract
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Reactive arthritis: newer developments. Author(s): Flores D, Marquez J, Garza M, Espinoza LR. Source: Rheumatic Diseases Clinics of North America. 2003 February; 29(1): 37-59, Vi. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12635499&dopt=Abstract
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Recombinant or peptide antigens in the serology of Lyme arthritis in children. Author(s): Heikkila T, Huppertz HI, Seppala I, Sillanpaa H, Saxen H, Lahdenne P. Source: The Journal of Infectious Diseases. 2003 June 15; 187(12): 1888-94. Epub 2003 Jun 04. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12792865&dopt=Abstract
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Reduced arterial elasticity in rheumatoid arthritis and the relationship to vascular disease risk factors and inflammation. Author(s): Wong M, Toh L, Wilson A, Rowley K, Karschimkus C, Prior D, Romas E, Clemens L, Dragicevic G, Harianto H, Wicks I, McColl G, Best J, Jenkins A. Source: Arthritis and Rheumatism. 2003 January; 48(1): 81-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12528107&dopt=Abstract
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Reduced chemokine and matrix metalloproteinase expression in patients with rheumatoid arthritis achieving remission. Author(s): Katrib A, Smith MD, Ahern MJ, Slavotinek J, Stafford L, Cuello C, Bertouch JV, McNeil HP, Youssef PP. Source: The Journal of Rheumatology. 2003 January; 30(1): 10-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12508384&dopt=Abstract
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Reduced perforin expression in systemic juvenile idiopathic arthritis is restored by autologous stem-cell transplantation. Author(s): Wulffraat NM, Rijkers GT, Elst E, Brooimans R, Kuis W. Source: Rheumatology (Oxford, England). 2003 February; 42(2): 375-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12595640&dopt=Abstract
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Reduction in plasma homocysteine level in patients with rheumatoid arthritis given pulsed glucocorticoid treatment. Author(s): Lazzerini PE, Capecchi PL, Bisogno S, Galeazzi M, Marcolongo R, Pasini FL. Source: Annals of the Rheumatic Diseases. 2003 July; 62(7): 694-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12810448&dopt=Abstract
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Regional differences in Finland in the prevalence of rheumatoid factor in the presence and absence of arthritis. Author(s): Korpilahde T, Heliovaara M, Kaipiainen-Seppanen O, Knekt P, Aho K. Source: Annals of the Rheumatic Diseases. 2003 April; 62(4): 353-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12634237&dopt=Abstract
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Regulation of CCR5 expression and MIP-1alpha production in CD4+ T cells from patients with rheumatoid arthritis. Author(s): Wang CR, Liu MF. Source: Clinical and Experimental Immunology. 2003 May; 132(2): 371-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12699431&dopt=Abstract
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Regulation of p53 by macrophage migration inhibitory factor in inflammatory arthritis. Author(s): Leech M, Lacey D, Xue JR, Santos L, Hutchinson P, Wolvetang E, David JR, Bucala R, Morand EF. Source: Arthritis and Rheumatism. 2003 July; 48(7): 1881-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12847682&dopt=Abstract
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Rehabilitation effects on compensatory gait mechanics in people with arthritis and strength impairment. Author(s): McGibbon CA, Krebs DE, Scarborough DM. Source: Arthritis and Rheumatism. 2003 April 15; 49(2): 248-54. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12687518&dopt=Abstract
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Relationship between functional ability and physical fitness in juvenile idiopathic arthritis patients. Author(s): Takken T, van der Net J, Helders PJ. Source: Scandinavian Journal of Rheumatology. 2003; 32(3): 174-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12892255&dopt=Abstract
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Relationship between human lymphocyte antigen-B27 and clinical features of psoriatic arthritis. Author(s): Tsai YG, Chang DM, Kuo SY, Wang WM, Chen YC, Lai JH. Source: J Microbiol Immunol Infect. 2003 June; 36(2): 101-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12886960&dopt=Abstract
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Relationship of social role quality to psychological well-being in women with rheumatoid arthritis. Author(s): Ann Intern Med. 2003 May 20;138(10):I39 Source: Research in Nursing & Health. 2003 June; 26(3): 190-202. /entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12755582
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Release of endogenous anti-inflammatory complement regulators FHL-1 and factor H protects synovial fibroblasts during rheumatoid arthritis. Author(s): Friese MA, Manuelian T, Junnikkala S, Hellwage J, Meri S, Peter HH, Gordon DL, Eibel H, Zipfel PF. Source: Clinical and Experimental Immunology. 2003 June; 132(3): 485-95. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12780697&dopt=Abstract
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Remission in juvenile chronic arthritis: a cohort study of 683 consecutive cases with a mean 10 year followup. Author(s): Fantini F, Gerloni V, Gattinara M, Cimaz R, Arnoldi C, Lupi E. Source: The Journal of Rheumatology. 2003 March; 30(3): 579-84. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12610820&dopt=Abstract
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Resolving arthritis, allergies, & immune compromising disorders with the JMT technique. Author(s): Mellor JM. Source: Beginnings. 2003 January-February; 23(1): 10-1. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12592973&dopt=Abstract
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Response to etanercept (Enbrel) in elderly patients with rheumatoid arthritis: a retrospective analysis of clinical trial results. Author(s): Fleischmann RM, Baumgartner SW, Tindall EA, Weaver AL, Moreland LW, Schiff MH, Martin RW, Spencer-Green GT. Source: The Journal of Rheumatology. 2003 April; 30(4): 691-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12672185&dopt=Abstract
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Retinoids and rexinoids for the 21st century: a brave new world for arthritis. Author(s): Brinckerhoff CE, Sporn MB. Source: The Journal of Rheumatology. 2003 February; 30(2): 211-3. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12563669&dopt=Abstract
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Reumacon (CPH82) showed similar x-ray progression and clinical effects as methotrexate in a two year comparative study on patients with early rheumatoid arthritis. Author(s): Svensson B, Pettersson H. Source: Scandinavian Journal of Rheumatology. 2003; 32(2): 83-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12737326&dopt=Abstract
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Rheumatoid arthritis and angiogenesis. Author(s): Yamanaka H. Source: Intern Med. 2003 March; 42(3): 297-9. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12705803&dopt=Abstract
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Rheumatoid arthritis and macrovascular disease. Author(s): Alkaabi JK, Ho M, Levison R, Pullar T, Belch JJ. Source: Rheumatology (Oxford, England). 2003 February; 42(2): 292-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12595625&dopt=Abstract
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Rheumatoid arthritis and the Arava (leflunomide) controversy. Author(s): Turkoski BB. Source: Orthopaedic Nursing / National Association of Orthopaedic Nurses. 2003 January-February; 22(1): 48-51. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12640952&dopt=Abstract
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Rheumatoid arthritis is a heterogeneous disease: evidence for differences in the activation of the STAT-1 pathway between rheumatoid tissues. Author(s): van der Pouw Kraan TC, van Gaalen FA, Kasperkovitz PV, Verbeet NL, Smeets TJ, Kraan MC, Fero M, Tak PP, Huizinga TW, Pieterman E, Breedveld FC, Alizadeh AA, Verweij CL. Source: Arthritis and Rheumatism. 2003 August; 48(8): 2132-45. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12905466&dopt=Abstract
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Rheumatoid arthritis of the shoulder. Author(s): Chen AL, Joseph TN, Zuckerman JD. Source: J Am Acad Orthop Surg. 2003 January-February; 11(1): 12-24. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12699368&dopt=Abstract
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Rheumatoid arthritis susceptibility and interleukin 10: a study of two ethnically diverse populations. Author(s): MacKay K, Milicic A, Lee D, Tikly M, Laval S, Shatford J, Wordsworth P. Source: Rheumatology (Oxford, England). 2003 January; 42(1): 149-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12509628&dopt=Abstract
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Rheumatoid arthritis: proposal for the use of anti-microbial therapy in early cases. Author(s): Ebringer A, Rashid T, Wilson C. Source: Scandinavian Journal of Rheumatology. 2003; 32(1): 2-11. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12635939&dopt=Abstract
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Rheumatoid factor is the strongest predictor of radiological progression of rheumatoid arthritis in a three-year prospective study in community-recruited patients. Author(s): Vittecoq O, Pouplin S, Krzanowska K, Jouen-Beades F, Menard JF, Gayet A, Daragon A, Tron F, Le Loet X. Source: Rheumatology (Oxford, England). 2003 August; 42(8): 939-46. Epub 2003 April 16. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12730503&dopt=Abstract
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Rheumatoid neutrophilic dermatitis, rheumatoid papules, and rheumatoid nodules in a patient with seronegative rheumatoid arthritis. Author(s): Yamamoto T, Matsunaga T, Nishioka K. Source: Journal of the American Academy of Dermatology. 2003 April; 48(4): 634-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12664038&dopt=Abstract
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Rheumatologists' opinions on the feasibility of a measurement feedback system in rheumatoid arthritis and the influence of motivation. Author(s): Fransen J, Daneel S, Langenegger T, Michel BA; Swiss Clinical Quality Management in rheumatoid arthritis. Source: Rheumatology (Oxford, England). 2003 August; 42(8): 924-8. Epub 2003 April 16. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12730552&dopt=Abstract
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Risk communication in rheumatoid arthritis. Author(s): Fraenkel L, Bogardus S, Concato J, Felson D. Source: The Journal of Rheumatology. 2003 March; 30(3): 443-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12610798&dopt=Abstract
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Risk of malignant lymphomas in patients with rheumatoid arthritis and in their firstdegree relatives. Author(s): Ekstrom K, Hjalgrim H, Brandt L, Baecklund E, Klareskog L, Ekbom A, Askling J. Source: Arthritis and Rheumatism. 2003 April; 48(4): 963-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12687538&dopt=Abstract
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Role of bacteria and HLA-B27 in the pathogenesis of reactive arthritis. Author(s): Yu D, Kuipers JG. Source: Rheumatic Diseases Clinics of North America. 2003 February; 29(1): 21-36, V-Vi. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12635498&dopt=Abstract
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Role of Crk-associated substrate lymphocyte type in the pathophysiology of rheumatoid arthritis in tax transgenic mice and in humans. Author(s): Miyake-Nishijima R, Iwata S, Saijo S, Kobayashi H, Kobayashi S, SoutaKuribara A, Hosono O, Kawasaki H, Tanaka H, Ikeda E, Okada Y, Iwakura Y, Morimoto C. Source: Arthritis and Rheumatism. 2003 July; 48(7): 1890-900. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12847683&dopt=Abstract
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Role of macrophage inflammatory protein-3alpha and its ligand CCR6 in rheumatoid arthritis. Author(s): Ruth JH, Shahrara S, Park CC, Morel JC, Kumar P, Qin S, Koch AE. Source: Laboratory Investigation; a Journal of Technical Methods and Pathology. 2003 April; 83(4): 579-88. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12695561&dopt=Abstract
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Role of metacarpophalangeal joint anatomic factors in the distribution of synovitis and bone erosion in early rheumatoid arthritis. Author(s): Tan AL, Tanner SF, Conaghan PG, Radjenovic A, O'Connor P, Brown AK, Emery P, McGonagle D. Source: Arthritis and Rheumatism. 2003 May; 48(5): 1214-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12746894&dopt=Abstract
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Salmonella septicemia in rheumatoid arthritis patients receiving anti-tumor necrosis factor therapy: association with decreased interferon-gamma production and Toll-like receptor 4 expression. Author(s): Netea MG, Radstake T, Joosten LA, van der Meer JW, Barrera P, Kullberg BJ. Source: Arthritis and Rheumatism. 2003 July; 48(7): 1853-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12847679&dopt=Abstract
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SAPHO syndrome presenting as septic arthritis in the hip. Author(s): O'Connor DA, Ridha H, Roche CJ, O'Sullivan M. Source: Ir Med J. 2003 February; 96(2): 41-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12674151&dopt=Abstract
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Screening for atherosclerosis in patients with rheumatoid arthritis: comparison of two in vivo tests of vascular function. Author(s): Van Doornum S, McColl G, Jenkins A, Green DJ, Wicks IP. Source: Arthritis and Rheumatism. 2003 January; 48(1): 72-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12528106&dopt=Abstract
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Screening for extensor tendon rupture in rheumatoid arthritis. Author(s): Williamson L, Burge P. Source: Rheumatology (Oxford, England). 2003 June; 42(6): 810. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12771447&dopt=Abstract
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Screening the genome for rheumatoid arthritis susceptibility genes: a replication study and combined analysis of 512 multicase families. Author(s): Jawaheer D, Seldin MF, Amos CI, Chen WV, Shigeta R, Etzel C, Damle A, Xiao X, Chen D, Lum RF, Monteiro J, Kern M, Criswell LA, Albani S, Nelson JL, Clegg DO, Pope R, Schroeder HW Jr, Bridges SL Jr, Pisetsky DS, Ward R, Kastner DL, Wilder RL, Pincus T, Callahan LF, Flemming D, Wener MH, Gregersen PK; North American Rheumatoid Arthritis Consortium. Source: Arthritis and Rheumatism. 2003 April; 48(4): 906-16. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12687532&dopt=Abstract
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Seasonal distribution of relapse onset in rheumatoid arthritis and spondyloarthropathy: the possible effect of the solar factor. Author(s): Rozin A, Balbir-Gurman A, Schapira D. Source: Clin Exp Rheumatol. 2003 March-April; 21(2): 161-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12747269&dopt=Abstract
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Selective elimination of synovial inflammatory macrophages in rheumatoid arthritis by an Fcgamma receptor I-directed immunotoxin. Author(s): van Roon JA, van Vuuren AJ, Wijngaarden S, Jacobs KM, Bijlsma JW, Lafeber FP, Thepen T, van de Winkel JG. Source: Arthritis and Rheumatism. 2003 May; 48(5): 1229-38. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12746896&dopt=Abstract
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Selective inhibition of cyclooxygenase 2-generated prostaglandin E2 synthesis in rheumatoid arthritis synoviocytes by taurine chloramine. Author(s): Kontny E, Rudnicka W, Kowalczewski J, Marcinkiewicz J, Maslinski W. Source: Arthritis and Rheumatism. 2003 June; 48(6): 1551-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12794822&dopt=Abstract
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Septic arthritis as a complication of allergic contact dermatitis. Author(s): Saunders H, Nixon R. Source: Contact Dermatitis. 2003 February; 48(2): 116-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12694219&dopt=Abstract
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Septic arthritis due to a toxigenic strain of Corynebacterium diphtheriae gravis. Author(s): Faraj S, French JG, McAuslan A. Source: N Z Med J. 2003 April 17; 116(1172): U404. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12740624&dopt=Abstract
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Septic arthritis in an infant with vesicoureteral reflux and urinary tract infection. Author(s): Nair S, Schoeneman MJ. Source: Pediatrics. 2003 February; 111(2): E195-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12563096&dopt=Abstract
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Septic arthritis in children: relationship of causative pathogens, complications, and outcome. Author(s): Wang CL, Wang SM, Yang YJ, Tsai CH, Liu CC. Source: J Microbiol Immunol Infect. 2003 March; 36(1): 41-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12741732&dopt=Abstract
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Septic arthritis of the hip in infancy: long-term follow-up. Author(s): Dobbs MB, Sheridan JJ, Gordon JE, Corley CL, Szymanski DA, Schoenecker PL. Source: Journal of Pediatric Orthopedics. 2003 March-April; 23(2): 162-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12604944&dopt=Abstract
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Septic arthritis. Author(s): Nade S. Source: Best Practice & Research. Clinical Rheumatology. 2003 April; 17(2): 183-200. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12787520&dopt=Abstract
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Serious bacterial infections in patients with rheumatoid arthritis under anti-TNFalpha therapy. Author(s): Kroesen S, Widmer AF, Tyndall A, Hasler P. Source: Rheumatology (Oxford, England). 2003 May; 42(5): 617-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12709536&dopt=Abstract
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Serologic changes following B lymphocyte depletion therapy for rheumatoid arthritis. Author(s): Cambridge G, Leandro MJ, Edwards JC, Ehrenstein MR, Salden M, BodmanSmith M, Webster AD. Source: Arthritis and Rheumatism. 2003 August; 48(8): 2146-54. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12905467&dopt=Abstract
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Serum levels of cartilage oligomeric matrix protein. A predicting factor and a valuable parameter for disease management in rheumatoid arthritis. Author(s): Skoumal M, Kolarz G, Klingler A. Source: Scandinavian Journal of Rheumatology. 2003; 32(3): 156-61. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12892252&dopt=Abstract
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Serum levels of pregnenolone and 17-hydroxypregnenolone in patients with rheumatoid arthritis and systemic lupus erythematosus: relation to other adrenal hormones. Author(s): Vogl D, Falk W, Dorner M, Scholmerich J, Straub RH. Source: The Journal of Rheumatology. 2003 February; 30(2): 269-75. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12563679&dopt=Abstract
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Serum MMP-3 and MMP-1 and progression of joint damage in early rheumatoid arthritis. Author(s): Green MJ, Gough AK, Devlin J, Smith J, Astin P, Taylor D, Emery P. Source: Rheumatology (Oxford, England). 2003 January; 42(1): 83-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12509618&dopt=Abstract
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Serum paraoxonase activity decreases in rheumatoid arthritis. Author(s): Tanimoto N, Kumon Y, Suehiro T, Ohkubo S, Ikeda Y, Nishiya K, Hashimoto K. Source: Life Sciences. 2003 May 9; 72(25): 2877-85. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12697270&dopt=Abstract
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Severe Parkinson's disease in rheumatoid arthritis patient treated with infliximab. Author(s): Hrycaj P, Korczowska I, Lacki JK. Source: Rheumatology (Oxford, England). 2003 May; 42(5): 702-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12709557&dopt=Abstract
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Short-term low-dose corticosteroids vs placebo and nonsteroidal antiinflammatory drugs in rheumatoid arthritis. Author(s): Gotzsche PC, Johansen HK. Source: Cochrane Database Syst Rev. 2003; (1): Cd000189. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12535392&dopt=Abstract
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Should infection still be considered as the most likely triggering factor for rheumatoid arthritis? Author(s): Carty SM, Snowden N, Silman AJ. Source: The Journal of Rheumatology. 2003 March; 30(3): 425-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12610794&dopt=Abstract
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Should rheumatoid arthritis be treated conservatively or aggressively? Author(s): Breedveld FC. Source: Rheumatology (Oxford, England). 2003 May; 42 Suppl 2: Ii41-3. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12817095&dopt=Abstract
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Shoulder arthroplasty for the treatment of postinfectious glenohumeral arthritis. Author(s): Mileti J, Sperling JW, Cofield RH. Source: The Journal of Bone and Joint Surgery. American Volume. 2003 April; 85-A(4): 609-14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12672834&dopt=Abstract
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Shoulder joint involvement in patients with newly diagnosed rheumatoid arthritis. Prevalence and associations. Author(s): Olofsson Y, Book C, Jacobsson LT. Source: Scandinavian Journal of Rheumatology. 2003; 32(1): 25-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12635942&dopt=Abstract
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Significance of laboratory and radiologic findings for differentiating between septic arthritis and transient synovitis of the hip. Author(s): Jung ST, Rowe SM, Moon ES, Song EK, Yoon TR, Seo HY. Source: Journal of Pediatric Orthopedics. 2003 May-June; 23(3): 368-72. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12724602&dopt=Abstract
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Silica-related rheumatoid arthritis without lung involvement. Author(s): Markovits D, Schapira D, Wiener A, Nahir AM. Source: Clinical Rheumatology. 2003 February; 22(1): 53-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12605320&dopt=Abstract
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Simultaneous occurrence of type I diabetes mellitus and juvenile rheumatoid arthritis. Author(s): Agrawal S, Desai MP. Source: Indian Pediatrics. 2003 June; 40(6): 568-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12824669&dopt=Abstract
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Sleep quality in children with juvenile rheumatoid arthritis. Author(s): Labyak SE, Bourguignon C, Docherty S. Source: Holistic Nursing Practice. 2003 July-August; 17(4): 193-200. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12889547&dopt=Abstract
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Smoking-gender interaction and risk for rheumatoid arthritis. Author(s): Krishnan E, Sokka T, Hannonen P. Source: Arthritis Research & Therapy. 2003; 5(3): R158-62. Epub 2003 March 24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12723987&dopt=Abstract
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Solar light effects on onset/relapses and circannual/circadian symptomatology in rheumatoid arthritis. Author(s): Cutolo M. Source: Clin Exp Rheumatol. 2003 March-April; 21(2): 148-50. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12747267&dopt=Abstract
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Somatostatin analogs in rheumatoid arthritis and other inflammatory and immunemediated conditions. Author(s): Paran D, Paran H. Source: Curr Opin Investig Drugs. 2003 May; 4(5): 578-82. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12833652&dopt=Abstract
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Splints/orthoses in the treatment of rheumatoid arthritis. Author(s): Egan M, Brosseau L, Farmer M, Ouimet MA, Rees S, Wells G, Tugwell P. Source: Cochrane Database Syst Rev. 2003; (1): Cd004018. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12535502&dopt=Abstract
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Sporadic enteric reactive arthritis and undifferentiated spondyloarthropathy: evidence for involvement of Salmonella typhimurium. Author(s): Sinha R, Aggarwal A, Prasad K, Misra R. Source: The Journal of Rheumatology. 2003 January; 30(1): 105-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12508398&dopt=Abstract
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Steroid myopathy in a child with juvenile rheumatoid arthritis. Case report. Author(s): Genel F, Arslanoglu S, Hizarcioglu M, Durmaz B, Uran N, Aktas S. Source: Panminerva Medica. 2003 March; 45(1): 75-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12682624&dopt=Abstract
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Stromal cell-derived factor-1 alpha in rheumatoid arthritis. Author(s): Mittal GA, Joshi VR, Deshpande A. Source: Rheumatology (Oxford, England). 2003 July; 42(7): 915-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12826719&dopt=Abstract
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Study of stromal cell-derived factor 1 alpha in synovial fluid in early rheumatoid arthritis: comment on the article by Kanbe et al. Author(s): Mittal G, Joshi VR. Source: Arthritis and Rheumatism. 2003 January; 48(1): 274-5; Author Reply 275-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12528136&dopt=Abstract
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Subcutaneous administration of polymerized-type I collagen for the treatment of patients with rheumatoid arthritis. An open-label pilot trial. Author(s): Furuzawa-Carballeda J, Cabral AR, Zapata-Zuniga M, Alcocer-Varela J. Source: The Journal of Rheumatology. 2003 February; 30(2): 256-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12563677&dopt=Abstract
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Sudden onset visual impairment and deafness in a patient with “long standing rheumatoid arthritis”. Author(s): Gaitonde S, Joshi VR. Source: J Assoc Physicians India. 2003 February; 51: 178-82. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12725263&dopt=Abstract
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Suicides in persons suffering from rheumatoid arthritis. Author(s): Timonen M, Viilo K, Hakko H, Sarkioja T, Ylikulju M, Meyer-Rochow VB, Vaisanen E, Rasanen P. Source: Rheumatology (Oxford, England). 2003 February; 42(2): 287-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12595624&dopt=Abstract
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Superior effect of arthroscopic lavage compared with needle aspiration in the treatment of inflammatory arthritis of the knee. Author(s): van Oosterhout M, Sont JK, van Laar JM. Source: Rheumatology (Oxford, England). 2003 January; 42(1): 102-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12509621&dopt=Abstract
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Surgical management of cataracts in children with juvenile rheumatoid arthritisassociated uveitis. Author(s): Lam LA, Lowder CY, Baerveldt G, Smith SD, Traboulsi EI. Source: American Journal of Ophthalmology. 2003 June; 135(6): 772-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12788115&dopt=Abstract
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Survival in fibrosing alveolitis associated with rheumatoid arthritis is better than cryptogenic fibrosing alveolitis. Author(s): Saravanan V, Kelly CA. Source: Rheumatology (Oxford, England). 2003 April; 42(4): 603-4; Author Reply 604-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12649414&dopt=Abstract
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Survival in rheumatoid arthritis: a population-based analysis of trends over 40 years. Author(s): Gabriel SE, Crowson CS, Kremers HM, Doran MF, Turesson C, O'Fallon WM, Matteson EL. Source: Arthritis and Rheumatism. 2003 January; 48(1): 54-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12528103&dopt=Abstract
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Sympathetic skin response and R-R interval variation in cases with rheumatoid arthritis. Author(s): Gozke E, Erdogan N, Akyuz G, Turan B, Akyuz E, Us O. Source: Electromyogr Clin Neurophysiol. 2003 March; 43(2): 81-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12661131&dopt=Abstract
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Synovial dendritic cells in juvenile idiopathic arthritis (JIA) express receptor activator of NF-kappaB (RANK). Author(s): Varsani H, Patel A, van Kooyk Y, Woo P, Wedderburn LR. Source: Rheumatology (Oxford, England). 2003 April; 42(4): 583-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12649407&dopt=Abstract
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Synovial fluid exoglycosidases are predictors of rheumatoid arthritis and are effective in cartilage glycosaminoglycan depletion. Author(s): Ortutay Z, Polgar A, Gomor B, Geher P, Lakatos T, Glant TT, Gay RE, Gay S, Pallinger E, Farkas C, Farkas E, Tothfalusi L, Kocsis K, Falus A, Buzas EI. Source: Arthritis and Rheumatism. 2003 August; 48(8): 2163-72. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12905469&dopt=Abstract
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Synoviocyte-derived CXCL12 is displayed on endothelium and induces angiogenesis in rheumatoid arthritis. Author(s): Pablos JL, Santiago B, Galindo M, Torres C, Brehmer MT, Blanco FJ, GarciaLazaro FJ. Source: Journal of Immunology (Baltimore, Md. : 1950). 2003 February 15; 170(4): 214752. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12574387&dopt=Abstract
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Systematic review of celecoxib for osteoarthritis and rheumatoid arthritis. Celecoxib's relative gastrointestinal safety is overstated. Author(s): Metcalfe S, Dougherty S, McNee W. Source: Bmj (Clinical Research Ed.). 2003 February 8; 326(7384): 334; Author Reply 334. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12575714&dopt=Abstract
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Systematic review of celecoxib for osteoarthritis and rheumatoid arthritis. Problems compromise review's validity. Author(s): Juni P, Sterchi R, Dieppe P. Source: Bmj (Clinical Research Ed.). 2003 February 8; 326(7384): 334; Author Reply 334. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12574052&dopt=Abstract
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Systemic and local expression of perforin in lymphocyte subsets in acute and chronic rheumatoid arthritis. Author(s): Gulan G, Ravlic-Gulan J, Strbo N, Sotosek V, Nemec B, Matovinovic D, Rubinic D, Podack ER, Rukavina D. Source: The Journal of Rheumatology. 2003 April; 30(4): 660-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12672182&dopt=Abstract
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Systemic juvenile idiopathic arthritis, Kikuchi's disease and haemophagocytic lymphohistiocytosis--is there a link? Case report and literature review. Author(s): Ramanan AV, Wynn RF, Kelsey A, Baildam EM. Source: Rheumatology (Oxford, England). 2003 April; 42(4): 596-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12649409&dopt=Abstract
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Systemic lupus erythematosus initially presenting as idiopathic juvenile arthritis with positive antinuclear antibodies. Author(s): Vuilleumier C, Sauvain MJ, Aebi C, Saurenmann T, Bianchetti MG. Source: Acta Paediatrica (Oslo, Norway : 1992). 2003 April; 92(4): 512-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12801125&dopt=Abstract
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T cell activation by soluble C1q-bearing immune complexes: implications for the pathogenesis of rheumatoid arthritis. Author(s): Jiang K, Chen Y, Xu CS, Jarvis JN. Source: Clinical and Experimental Immunology. 2003 January; 131(1): 61-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12519387&dopt=Abstract
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T(H)1/T(H)2 cytokine profile, metalloprotease-9 activity and hormonal status in pregnant rheumatoid arthritis and systemic lupus erythematosus patients. Author(s): Munoz-Valle JF, Vazquez-Del Mercado M, Garcia-Iglesias T, Orozco-Barocio G, Bernard-Medina G, Martinez-Bonilla G, Bastidas-Ramirez BE, Navarro AD, Bueno M, Martinez-Lopez E, Best-Aguilera CR, Kamachi M, Armendariz-Borunda J. Source: Clinical and Experimental Immunology. 2003 February; 131(2): 377-84. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12562402&dopt=Abstract
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Tackling ischaemic heart disease in rheumatoid arthritis. Author(s): Kitas GD, Erb N. Source: Rheumatology (Oxford, England). 2003 May; 42(5): 607-13. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12709534&dopt=Abstract
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Teasing apart the complex genetics of human autoimmunity: lessons from rheumatoid arthritis. Author(s): Gregersen PK. Source: Clinical Immunology (Orlando, Fla.). 2003 April; 107(1): 1-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12738244&dopt=Abstract
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The “X-Ray RheumaCoach” software: a novel tool for enhancing the efficacy and accelerating radiological quantification in rheumatoid arthritis. Author(s): Wick M, Peloschek P, Bogl K, Graninger W, Smolen JS, Kainberger F. Source: Annals of the Rheumatic Diseases. 2003 June; 62(6): 579-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12759300&dopt=Abstract
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The -308 polymorphism in the tumour necrosis factor (TNF) gene promoter region and ex vivo lipopolysaccharide-induced TNF expression and cytotoxic activity in Chilean patients with rheumatoid arthritis. Author(s): Cuenca J, Cuchacovich M, Perez C, Ferreira L, Aguirre A, Schiattino I, Soto L, Cruzat A, Salazar-Onfray F, Aguillon JC. Source: Rheumatology (Oxford, England). 2003 February; 42(2): 308-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12595628&dopt=Abstract
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The 5th Bristol unicompartmental arthritis meeting. Author(s): Beard D, Ashraf T. Source: The Knee. 2003 March; 10(1): 115-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12649038&dopt=Abstract
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The assessment of rheumatoid arthritis and the acceptability of self-report questionnaires in clinical practice. Author(s): Wolfe F, Pincus T, Thompson AK, Doyle J. Source: Arthritis and Rheumatism. 2003 February 15; 49(1): 59-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12579594&dopt=Abstract
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The benefits of early treatment in rheumatoid arthritis: confounding by indication, and the issue of timing. Author(s): Landewe RB. Source: Arthritis and Rheumatism. 2003 January; 48(1): 1-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12528097&dopt=Abstract
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The blossoming of evidence-based clinical rheumatology: The Arthritis Research Campaign's Clinical Trials Collaboration in association with the MRC Clinical Trials Unit, BSR and BOA. Author(s): Cooper C, Choy E; Arthritis Research Campaign's Clinical Trials Committee. Source: Rheumatology (Oxford, England). 2003 June; 42(6): 713-5. Epub 2003 March 14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12730530&dopt=Abstract
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The calcium-binding protein S100A12 induces neutrophil adhesion, migration, and release from bone marrow in mouse at concentrations similar to those found in human inflammatory arthritis. Author(s): Rouleau P, Vandal K, Ryckman C, Poubelle PE, Boivin A, Talbot M, Tessier PA. Source: Clinical Immunology (Orlando, Fla.). 2003 April; 107(1): 46-54. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12738249&dopt=Abstract
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The case against haste in the treatment of rheumatoid arthritis: comment on the editorial by Pincus et al. Author(s): Epstein WV. Source: Arthritis and Rheumatism. 2003 February; 48(2): 573-5; Author Reply 576-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12571870&dopt=Abstract
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The cost effectiveness of rofecoxib and celecoxib in patients with osteoarthritis or rheumatoid arthritis. Author(s): Maetzel A, Krahn M, Naglie G. Source: Arthritis and Rheumatism. 2003 June 15; 49(3): 283-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12794781&dopt=Abstract
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The cost-effectiveness of cyclooxygenase-2 selective inhibitors in the management of chronic arthritis. Author(s): Spiegel BM, Targownik L, Dulai GS, Gralnek IM. Source: Annals of Internal Medicine. 2003 May 20; 138(10): 795-806. Review. Summary for Patients In: http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12755551&dopt=Abstract
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The cost-effectiveness of infliximab (Remicade) in the treatment of rheumatoid arthritis in Sweden and the United Kingdom based on the ATTRACT study. Author(s): Kobelt G, Jonsson L, Young A, Eberhardt K. Source: Rheumatology (Oxford, England). 2003 February; 42(2): 326-35. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12595631&dopt=Abstract
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The costs of arthritis. Author(s): Dunlop DD, Manheim LM, Yelin EH, Song J, Chang RW. Source: Arthritis and Rheumatism. 2003 February 15; 49(1): 101-13. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12579600&dopt=Abstract
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The development and evaluation of a drug information leaflet for patients with rheumatoid arthritis. Author(s): Hill J, Bird H. Source: Rheumatology (Oxford, England). 2003 January; 42(1): 66-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12509615&dopt=Abstract
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The diagnosis and prognosis of early arthritis: comment on the editorial by Scott. Author(s): Visser H, Hazes JM. Source: Arthritis and Rheumatism. 2003 March; 48(3): 856-7; Author Reply 857-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12632444&dopt=Abstract
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The effect of HLA-DR on susceptibility to rheumatoid arthritis is influenced by the associated lymphotoxin alpha-tumor necrosis factor haplotype. Author(s): Newton J, Brown MA, Milicic A, Ackerman H, Darke C, Wilson JN, Wordsworth BP, Kwiatkowski D. Source: Arthritis and Rheumatism. 2003 January; 48(1): 90-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12528108&dopt=Abstract
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The effect of treatment on radiological progression in rheumatoid arthritis: a systematic review of randomized placebo-controlled trials. Author(s): Jones G, Halbert J, Crotty M, Shanahan EM, Batterham M, Ahern M. Source: Rheumatology (Oxford, England). 2003 January; 42(1): 6-13. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12509606&dopt=Abstract
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The efficacy and safety of leflunomide in patients with active rheumatoid arthritis: a five-year followup study. Author(s): Kalden JR, Schattenkirchner M, Sorensen H, Emery P, Deighton C, Rozman B, Breedveld F. Source: Arthritis and Rheumatism. 2003 June; 48(6): 1513-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12794818&dopt=Abstract
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The fate of the distal extensor retinaculum in dorsal wrist procedures for rheumatoid arthritis. Author(s): Skillman JM, Belcher HJ. Source: British Journal of Plastic Surgery. 2003 January; 56(1): 70-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12706161&dopt=Abstract
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The Influence of the HLA-DRB1 rheumatoid arthritis shared epitope on the clinical characteristics and radiological outcome of psoriatic arthritis. Author(s): Korendowych E, Dixey J, Cox B, Jones S, McHugh N. Source: The Journal of Rheumatology. 2003 January; 30(1): 96-101. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12508396&dopt=Abstract
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The JAK/STAT pathway in rheumatoid arthritis: pathogenic or protective? Author(s): Ivashkiv LB, Hu X. Source: Arthritis and Rheumatism. 2003 August; 48(8): 2092-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12905460&dopt=Abstract
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The mast cell in inflammatory arthritis. Author(s): Woolley DE. Source: The New England Journal of Medicine. 2003 April 24; 348(17): 1709-11. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12711748&dopt=Abstract
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The pivotal role of interleukin-1 in the clinical manifestations of rheumatoid arthritis. Author(s): Dayer JM. Source: Rheumatology (Oxford, England). 2003 May; 42 Suppl 2: Ii3-10. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12817089&dopt=Abstract
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The power of the third dimension: tissue architecture and autoimmunity in rheumatoid arthritis. Author(s): Weyand CM, Kang YM, Kurtin PJ, Goronzy JJ. Source: Current Opinion in Rheumatology. 2003 May; 15(3): 259-66. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12707579&dopt=Abstract
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The prevalence of patients with rheumatoid arthritis in the West Midlands fulfilling the BSR criteria for anti-tumour necrosis factor therapy: an out-patient study. Author(s): Yee CS, Filer A, Pace A, Douglas K, Situnayake D, Rowe IF; West Midlands Rheumatology Services and Training Committee. Source: Rheumatology (Oxford, England). 2003 July; 42(7): 856-9. Epub 2003 March 31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12730544&dopt=Abstract
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The relationship between basal joint arthritis and carpal tunnel syndrome: an MRI pilot study. Author(s): Goldfarb CA, Kiefhaber TR, Stern PJ, Bielecki DK. Source: The Journal of Hand Surgery. 2003 January; 28(1): 21-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12563633&dopt=Abstract
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The role of B cells in rheumatoid arthritis: mechanisms and therapeutic targets. Author(s): Dorner T, Burmester GR. Source: Current Opinion in Rheumatology. 2003 May; 15(3): 246-52. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12707577&dopt=Abstract
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The role of complementary and alternative therapies in managing rheumatoid arthritis. Author(s): Taibi DM, Bourguignon C. Source: Family & Community Health. 2003 January-March; 26(1): 41-52. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12802127&dopt=Abstract
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The role of COX-2 in angiogenesis and rheumatoid arthritis. Author(s): Woods JM, Mogollon A, Amin MA, Martinez RJ, Koch AE. Source: Experimental and Molecular Pathology. 2003 June; 74(3): 282-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12782016&dopt=Abstract
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The role of fish oils in the treatment of rheumatoid arthritis. Author(s): Cleland LG, James MJ, Proudman SM. Source: Drugs. 2003; 63(9): 845-53. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12678571&dopt=Abstract
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The role of free radicals in the pathogenesis of rheumatoid arthritis. Author(s): Hadjigogos K. Source: Panminerva Medica. 2003 March; 45(1): 7-13. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12682616&dopt=Abstract
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The role of HLA-DRB1*04 alleles and their association with HLA-DQB genes in genetic susceptibility to rheumatoid arthritis in Hungarian patients. Author(s): Varga E, Palkonyai E, Temesvari P, Toth F, Petri IB. Source: Acta Microbiol Immunol Hung. 2003; 50(1): 33-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12793199&dopt=Abstract
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The role of IL-17 and family members in the pathogenesis of arthritis. Author(s): Lubberts E. Source: Curr Opin Investig Drugs. 2003 May; 4(5): 572-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12833651&dopt=Abstract
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The role of the interleukin-6 family of cytokines in inflammatory arthritis and bone turnover. Author(s): Wong PK, Campbell IK, Egan PJ, Ernst M, Wicks IP. Source: Arthritis and Rheumatism. 2003 May; 48(5): 1177-89. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12746890&dopt=Abstract
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The short-term outcome of surgical treatment for painful varus arthritis in association with chronic ACL deficiency. Author(s): Williams RJ 3rd, Kelly BT, Wickiewicz TL, Altchek DW, Warren RF. Source: The Journal of Knee Surgery. 2003 January; 16(1): 9-16. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12568260&dopt=Abstract
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The spectrum of cutaneous lesions in rheumatoid arthritis: a clinical and pathological study of 43 patients. Author(s): Magro CM, Crowson AN. Source: Journal of Cutaneous Pathology. 2003 January; 30(1): 1-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12534797&dopt=Abstract
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The spontaneous remission of juvenile idiopathic arthritis is characterized by CD30+ T cells directed to human heat-shock protein 60 capable of producing the regulatory cytokine interleukin-10. Author(s): de Kleer IM, Kamphuis SM, Rijkers GT, Scholtens L, Gordon G, De Jager W, Hafner R, van de Zee R, van Eden W, Kuis W, Prakken BJ. Source: Arthritis and Rheumatism. 2003 July; 48(7): 2001-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12847694&dopt=Abstract
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The therapeutic potential of costimulatory blockade with CTLA4Ig in rheumatoid arthritis. Author(s): Emery P. Source: Expert Opinion on Investigational Drugs. 2003 April; 12(4): 673-81. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12665422&dopt=Abstract
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The therapeutic potential of TNF-alpha blockade in rheumatoid arthritis. Author(s): Paleolog E. Source: Expert Opinion on Investigational Drugs. 2003 July; 12(7): 1087-95. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12831345&dopt=Abstract
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The use of disease modifying antirheumatic drugs in women with rheumatoid arthritis of childbearing age: a survey of practice patterns and pregnancy outcomes. Author(s): Chakravarty EF, Sanchez-Yamamoto D, Bush TM. Source: The Journal of Rheumatology. 2003 February; 30(2): 241-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12563675&dopt=Abstract
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Therapeutic strategies for rheumatoid arthritis. Author(s): Smolen JS, Steiner G. Source: Nature Reviews. Drug Discovery. 2003 June; 2(6): 473-88. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12776222&dopt=Abstract
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Time trends in disability pensioning for rheumatoid arthritis, osteoarthritis and soft tissue rheumatism in Norway 1968-97. Author(s): Holte HH, Tambs K, Bjerkedal T. Source: Scandinavian Journal of Public Health. 2003; 31(1): 17-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12623520&dopt=Abstract
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Tips for easing arthritis symptoms in the workplace. Author(s): Sitzman K. Source: Aaohn Journal : Official Journal of the American Association of Occupational Health Nurses. 2003 August; 51(8): 360. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12934864&dopt=Abstract
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TNFR2 position 196 polymorphism in Japanese patients with rheumatoid arthritis: comment on the article by Dieude et al. Author(s): Kyogoku C, Tsuchiya N, Shibue T, Tokunaga K, Matsuta K. Source: Arthritis and Rheumatism. 2003 January; 48(1): 273-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12528135&dopt=Abstract
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Total knee arthroplasty in young patients with juvenile rheumatoid arthritis. Author(s): Parvizi J, Lajam CM, Trousdale RT, Shaughnessy WJ, Cabanela ME. Source: The Journal of Bone and Joint Surgery. American Volume. 2003 June; 85-A(6): 1090-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12784008&dopt=Abstract
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Toxicity profiles of traditional disease modifying antirheumatic drugs for rheumatoid arthritis. Author(s): Aletaha D, Kapral T, Smolen JS. Source: Annals of the Rheumatic Diseases. 2003 May; 62(5): 482-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12695166&dopt=Abstract
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Transoral approach using the mandibular osteotomy for atlantoaxial vertical subluxation in juvenile rheumatoid arthritis associated with mandibular micrognathia. Author(s): Kanamori Y, Miyamoto K, Hosoe H, Fujitsuka H, Tatematsu N, Shimizu K. Source: Journal of Spinal Disorders & Techniques. 2003 April; 16(2): 221-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12679681&dopt=Abstract
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Treatment of heart failure in older persons. Dilemmas with coexisting conditions: diabetes mellitus, chronic obstructive pulmonary disease, and arthritis. Author(s): Aronow WS. Source: Congestive Heart Failure (Greenwich, Conn.). 2003 May-June; 9(3): 142-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12826772&dopt=Abstract
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Treatment of leg length discrepancy with temporary epiphyseal stapling in children with juvenile idiopathic arthritis during 1957-99. Author(s): Skytta E, Savolainen A, Kautiainen H, Lehtinen J, Belt EA. Source: Journal of Pediatric Orthopedics. 2003 May-June; 23(3): 378-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12724604&dopt=Abstract
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Treatment of primary degenerative arthritis of the elbow by ulnohumeral arthroplasty. A long-term follow-up. Author(s): Phillips NJ, Ali A, Stanley D. Source: The Journal of Bone and Joint Surgery. British Volume. 2003 April; 85(3): 347-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12729106&dopt=Abstract
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Treatment of reactive arthritis with infliximab. Author(s): Oili KS, Niinisalo H, Korpilahde T, Virolainen J. Source: Scandinavian Journal of Rheumatology. 2003; 32(2): 122-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12737333&dopt=Abstract
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Treatment of rheumatoid arthritis with tumor necrosis factor inhibitors may predispose to significant increase in tuberculosis risk: a multicenter activesurveillance report. Author(s): Gomez-Reino JJ, Carmona L, Valverde VR, Mola EM, Montero MD; BIOBADASER Group. Source: Arthritis and Rheumatism. 2003 August; 48(8): 2122-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12905464&dopt=Abstract
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Treatment of the late sequelae of septic arthritis of the hip. Author(s): Manzotti A, Rovetta L, Pullen C, Catagni MA. Source: Clinical Orthopaedics and Related Research. 2003 May; (410): 203-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12771832&dopt=Abstract
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Tumor necrosis factor receptor 2 microsatellite and exon 6 polymorphisms in rheumatoid arthritis in Taiwan. Author(s): Yen JH, Tsai WC, Chen CJ, Ou TT, Lin CH, Hu CJ, Liu HW. Source: The Journal of Rheumatology. 2003 March; 30(3): 438-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12610797&dopt=Abstract
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Twenty eight joint count disease activity score in recent onset rheumatoid arthritis using C reactive protein instead of erythrocyte sedimentation rate. Author(s): Skogh T, Gustafsson D, Kjellberg M, Husberg M. Source: Annals of the Rheumatic Diseases. 2003 July; 62(7): 681-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12810437&dopt=Abstract
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Two year randomized controlled trial of etidronate in rheumatoid arthritis: changes in serum aminoterminal telopeptides correlate with radiographic progression of disease. Author(s): Valleala H, Laasonen L, Koivula MK, Mandelin J, Friman C, Risteli J, Konttinen YT. Source: The Journal of Rheumatology. 2003 March; 30(3): 468-73. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12610803&dopt=Abstract
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Two-year follow-up of a randomized controlled trial of a clinical nurse specialist intervention, inpatient, and day patient team care in rheumatoid arthritis. Author(s): Tijhuis GJ, Zwinderman AH, Hazes JM, Breedveld FC, Vlieland PM. Source: Journal of Advanced Nursing. 2003 January; 41(1): 34-43. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12519286&dopt=Abstract
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Type 1 autoimmune hepatitis revealed by a dysphonia related to cricoarytenoid arthritis. Author(s): Loukili NH, Pettorin C, Noel E, Andres E. Source: Qjm : Monthly Journal of the Association of Physicians. 2003 February; 96(2): 171-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12589015&dopt=Abstract
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Ultrasound guidance allows accurate needle placement and aspiration from small joints in patients with early inflammatory arthritis. Author(s): Raza K, Lee CY, Pilling D, Heaton S, Situnayake RD, Carruthers DM, Buckley CD, Gordon C, Salmon M. Source: Rheumatology (Oxford, England). 2003 August; 42(8): 976-9. Epub 2003 April 16. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12730511&dopt=Abstract
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Understanding the window of opportunity concept in early rheumatoid arthritis. Author(s): Boers M. Source: Arthritis and Rheumatism. 2003 July; 48(7): 1771-4. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12847667&dopt=Abstract
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Unicompartmental arthritis of the knee. Author(s): Iorio R, Healy WL. Source: The Journal of Bone and Joint Surgery. American Volume. 2003 July; 85-A(7): 1351-64. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12851363&dopt=Abstract
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US incidence of juvenile dermatomyositis, 1995-1998: results from the National Institute of Arthritis and Musculoskeletal and Skin Diseases Registry. Author(s): Mendez EP, Lipton R, Ramsey-Goldman R, Roettcher P, Bowyer S, Dyer A, Pachman LM; NIAMS Juvenile DM Registry Physician Referral Group. Source: Arthritis and Rheumatism. 2003 June 15; 49(3): 300-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12794783&dopt=Abstract
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Use of biologics for rheumatoid arthritis tempered by concerns over safety, cost. Author(s): Pressman Lovinger S. Source: Jama : the Journal of the American Medical Association. 2003 June 25; 289(24): 3229-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12824197&dopt=Abstract
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Use of methotrexate in juvenile idiopathic arthritis. Author(s): Ramanan AV, Whitworth P, Baildam EM. Source: Archives of Disease in Childhood. 2003 March; 88(3): 197-200. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12598376&dopt=Abstract
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Validation of a novel satisfaction questionnaire for patients with rheumatoid arthritis receiving outpatient clinical nurse specialist care, inpatient care, or day patient team care. Author(s): Tijhuis GJ, Kooiman KG, Zwinderman AH, Hazes JM, Breedveld FC, Vliet Vlieland TP. Source: Arthritis and Rheumatism. 2003 April 15; 49(2): 193-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12687510&dopt=Abstract
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Validation of the arthritis self-efficacy short-form scale in German fibromyalgia patients. Author(s): Mueller A, Hartmann M, Mueller K, Eich W. Source: European Journal of Pain (London, England). 2003; 7(2): 163-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12600798&dopt=Abstract
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Validity of the Nottingham Health Profile in a Finnish out-patient population with rheumatoid arthritis. Author(s): Uutela T, Hakala M, Kautiainen H. Source: Rheumatology (Oxford, England). 2003 July; 42(7): 841-5. Epub 2003 May 16. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12759465&dopt=Abstract
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Vertebral deformities in 229 female patients with rheumatoid arthritis: associations with clinical variables and bone mineral density. Author(s): Orstavik RE, Haugeberg G, Uhlig T, Falch JA, Halse JI, Hoiseth A, Lilleas F, Kvien TK. Source: Arthritis and Rheumatism. 2003 June 15; 49(3): 355-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12794791&dopt=Abstract
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Virus-associated arthritis. Author(s): Masuko-Hongo K, Kato T, Nishioka K. Source: Best Practice & Research. Clinical Rheumatology. 2003 April; 17(2): 309-18. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12787527&dopt=Abstract
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What employees with rheumatoid arthritis, diabetes mellitus and hearing loss need to cope at work. Author(s): Detaille SI, Haafkens JA, van Dijk FJ. Source: Scand J Work Environ Health. 2003 April; 29(2): 134-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12718499&dopt=Abstract
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Whipple arthritis: diagnosis by molecular analysis of synovial fluid--current status of diagnosis and therapy. Author(s): Lange U, Teichmann J. Source: Rheumatology (Oxford, England). 2003 March; 42(3): 473-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12626799&dopt=Abstract
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Will pharmacogenetics allow better prediction of methotrexate toxicity and efficacy in patients with rheumatoid arthritis? Author(s): Ranganathan P, Eisen S, Yokoyama WM, McLeod HL. Source: Annals of the Rheumatic Diseases. 2003 January; 62(1): 4-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12480661&dopt=Abstract
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Women with established rheumatoid arthritis perceive pain as the predominant impairment of health status. Author(s): Minnock P, FitzGerald O, Bresnihan B. Source: Rheumatology (Oxford, England). 2003 August; 42(8): 995-1000. Epub 2003 April 16. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12730516&dopt=Abstract
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CHAPTER 2. NUTRITION AND ARTHRITIS Overview In this chapter, we will show you how to find studies dedicated specifically to nutrition and arthritis.
Finding Nutrition Studies on Arthritis The National Institutes of Health’s Office of Dietary Supplements (ODS) offers a searchable bibliographic database called the IBIDS (International Bibliographic Information on Dietary Supplements; National Institutes of Health, Building 31, Room 1B29, 31 Center Drive, MSC 2086, Bethesda, Maryland 20892-2086, Tel: 301-435-2920, Fax: 301-480-1845, E-mail:
[email protected]). The IBIDS contains over 460,000 scientific citations and summaries about dietary supplements and nutrition as well as references to published international, scientific literature on dietary supplements such as vitamins, minerals, and botanicals.7 As a service of the ODS, access to the IBIDS database is available free of charge at the following Web address: http://ods.od.nih.gov/databases/ibids.html. After entering the search area, you have three choices: (1) IBIDS Consumer Database, (2) Full IBIDS Database, or (3) Peer Reviewed Citations Only. Now that you have selected a database, click on the “Advanced” tab. An advanced search allows you to retrieve up to 100 fully explained references in a comprehensive format. Type “arthritis” (or synonyms) into the search box, and click “Go.” To narrow the search, you can also select the “Title” field.
7 Adapted from http://ods.od.nih.gov. IBIDS is produced by the Office of Dietary Supplements (ODS) at the National Institutes of Health to assist the public, healthcare providers, educators, and researchers in locating credible, scientific information on dietary supplements. IBIDS was developed and will be maintained through an interagency partnership with the Food and Nutrition Information Center of the National Agricultural Library, U.S. Department of Agriculture.
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The following is a typical result when searching for recently indexed consumer information on arthritis: ·
Arthritis antidotes abound, but do any of them really work? Source: Forman, A. Environmental-nutrition (USA). (July 1998). volume 21(7) page 1, 4. arthritis diet fish oils polyunsaturated fatty acids linolenic acid antioxidants vitamins supplements 0893-4452 Summary: arthrite regime alimentaire huile de poisson acide gras polyinsature acide linolenique antioxydant vitamine complement alimentaire
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Fish oils may soothe arthritis pain, but don't depend on diet alone. Source: Klauser, A. Environmental-nutrition (USA). (February 1996). volume 19(2) page 1, 4. fish oils food intake arthritis fatty acids therapeutic diets antioxidants vegetarians diet food technology weight reduction physical activity 0893-4452 Summary: huile de poisson prise alimentaire homme arthrite acide gras regime alimentaire therapeutique antioxydant vegetarien regime alimentaire technologie alimentaire regime pour reduction de poids activite physique
Additional consumer oriented references include: ·
A friend recommended I take a dietary supplement for my arthritis that contains glucosamine and chondroitin. What are these made from? Do they help? Source: Anonymous Mayo-Clin-Health-Lett. 2003 January; 21(1): 8 0741-6245
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A friend recommends that I take something called glucosamine for my arthritis. What do you know about it? Source: Anonymous Mayo-Clin-Health-Lett. 1998 January; 16(1): 8 0741-6245
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A ray of dietary hope for arthritis sufferers. Source: Tufts-Univ-diet-nutr-lett. New York, N.Y. : Tufts University Diet and Nutrition Letter, 1983-c1997. February 1992. volume 9 (12) page 1-2. 0747-4105
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Agricultural practices affect arthritis. Source: Newnham, R E Nutr-Health. 1991; 7(2): 89-100 0260-1060
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Alternative arthritis remedies go mainstream; EN offers primer. Source: Solomons, N.W. Environ-nutr. New York : Environmental Nutrition, Inc.,. April 2000. volume 23 (4) page 1, 4-5. 0893-4452
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Arthritis guidelines emphasize exercise. Author(s): Arthritis Foundation, Atlanta, USA. Source: Klippel, J Health-News. 2000 November; 6(11): 3 1081-5880
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Arthritis relief: considering the alternatives. Source: Anonymous Harv-Health-Lett. 1999 July; 24(9): 7 1052-1577
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Arthritis supplements. Do natural dietary supplements for arthritis really work? Source: Anonymous Johns-Hopkins-Med-Lett-Health-After-50. 1999 October; 11(8): 8 1042-1882
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Breastfeeding-related onset, flare, and relapse of rheumatoid arthritis. Author(s): Department of Nutrition, Arizona State University, Mesa 85212, USA. Source: Hampl, J S Papa, D J Nutr-Revolume 2001 August; 59(8 Pt 1): 264-8 0029-6643
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By the way, doctor. Is MSM as good as it sounds? Can you tell me anything about the dietary supplement MSM? I've heard it's supposed to relieve arthritis pain. Source: Robb Nicholson, C Harv-Womens-Health-Watch. 2002 August; 9(12): 8 1070910X
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Can diet therapy offer relief for arthritis sufferers. Source: Environ-Nutr. New York, N.Y. : Environmental Nutrition, Inc. June 1990. volume 13 (6) page 1, 7. 0893-4452
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Dietary treatment of arthritis. Source: Nutr-M-D. Van Nuys, Calif. : The Journal. April 1987. volume 13 (4) page 4-5. 0732-0167
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Effects of diets containing fish oil and vitamin E on rheumatoid arthritis. Author(s): Loyola University Medical Center, Maywood, IL 60153, USA. Source: Tidow Kebritchi, S Mobarhan, S Nutr-Revolume 2001 October; 59(10): 335-8 0029-6643
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From arthritis to zeaxanthin, EN's A-to-Z guide meets the 21st century. Source: Welland, D. Environ-nutr. New York : Environmental Nutrition, Inc.,. December 2000. volume 23 (12) page 1, 4-5. 0893-4452
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NIH studying dietary supplements for arthritis. Source: Anonymous Mayo-Clin-Health-Lett. 2000 August; 18(8): 4 0741-6245
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Nutrition/arthritis link: so near and yet so far. Source: Volain, N. Environmental-nutrition (USA). (September 1993). volume 16(9) page 2. arthritis therapeutic diets 0893-4452
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On call. I am 46 years old and have arthritis of my knees. Ibuprofen helps, but I still have pain. Should I consider the new joint injections? Source: Simon, H B Harv-Mens-Health-Watch. 2000 September; 5(2): 8 1089-1102
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Vitamin D keeps a form of arthritis in check. Source: Tufts-University-diet-and-nutrition-letter (USA). (December 1996). volume 14(10) page 1. vitamin d joint diseases elderly recommended dietary allowances 07474105
The following information is typical of that found when using the “Full IBIDS Database” to search for “arthritis” (or a synonym): ·
A 7-day oral treatment of patients with active rheumatoid arthritis using the prostacyclin analog iloprost: cytokine modulation, safety, and clinical effects. Author(s): Rheumatology Practice, Dossenheimer Landstr. 100, 69121 Heidelberg, Germany.
[email protected] Source: Gao, I K Scholz, P Boehme, M W Norden, C Lemmel, E M Rheumatol-Int. 2002 June; 22(2): 45-51 0172-8172
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A friend recommended I take a dietary supplement for my arthritis that contains glucosamine and chondroitin. What are these made from? Do they help? Source: Anonymous Mayo-Clin-Health-Lett. 2003 January; 21(1): 8 0741-6245
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A look at glucosamine and chondroitin for easing arthritis pain. Source: Tufts-Univ-health-nutr-lett. New York, NY : Tufts University Health & Nutrition Letter, c1997-. January 2000. volume 17 (11) page 4-5.
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Acupuncture and other alternative therapies in rheumatoid arthritis. Author(s): Barnsley District General Hospital NHS Trust, Barnsley. Source: Hardware, Bernadette Lacey, Anne Prof-Nurse. 2002 March; 17(7): 437-9 02668130
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Acute iridocyclitis in antinuclear antibody-positive pauciarticular juvenile rheumatoid arthritis detected a decade earlier. Author(s): Alberto Moscona Department of Ophthalmology, Rambam Medical Center, Haifa, Israel. Source: Schaal, S Beiran, I Brik, R Miller, B J-Pediatr-Ophthalmol-Strabismus. 2002 NovDecember; 39(6): 365-6 0191-3913
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Advances in TCM symptomatology of rheumatoid arthritis. Author(s): Institute of Bioinformatics, Tsinghua University, Beijing 100084. Source: Li, S J-Tradit-Chin-Med. 2002 June; 22(2): 137-42 0254-6272
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Amelioration of rat adjuvant arthritis by therapeutic treatment with bindarit, an inhibitor of MCP-1 and TNF-alpha production. Author(s): Immunopharmacology Lab, ACRAF SpA - Angelini Ricerche, Rome, Italy.
[email protected] Source: Guglielmotti, A D'Onofrio, E Coletta, I Aquilini, L Milanese, C Pinza, M Inflamm-Res. 2002 May; 51(5): 252-8 1023-3830
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Analysis of cartilage-derived retinoic-acid-sensitive protein (CD-RAP) in synovial fluid from patients with osteoarthritis and rheumatoid arthritis. Author(s): Department of Surgery, Nagoya University School of Medicine, Japan. Source: Saito, S Kondo, S Mishima, S Ishiguro, N Hasegawa, Y Sandell, L J Iwata, H JBone-Joint-Surg-Br. 2002 September; 84(7): 1066-9 0301-620X
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Anti-inflammatory activity of a novel selective cyclooxygenase-2 inhibitor, FR140423, on type II collagen-induced arthritis in Lewis rats. Author(s): Department of Immunology and Inflammation, Medicinal Biology Research Laboratories, Fujisawa Pharmaceutical Co, Ltd, Osaka, Japan.
[email protected] Source: Ochi, T Goto, T Prostaglandins-Other-Lipid-Mediat. 2001 December; 66(4): 31727 1098-8823
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Arthritic diseases: melanocortin type 3 receptor agonists as potential therapeutics. Author(s): Department of Biochemical Pharmacology, St Bartholomew's and The Royal London School of Medicine and Dentistry, London, UK.
[email protected] Source: Getting, S J Perretti, M Curr-Opin-Investig-Drugs. 2001 August; 2(8): 1064-9 1472-4472
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Attained adult height in juvenile rheumatoid arthritis with or without corticosteroid treatment. Author(s): National Taiwan University Hospital, Taipei, Taiwan. Source: Wang, S J Yang, Y H Lin, Y T Yang, C M Chiang, B L Clin-Rheumatol. 2002 September; 21(5): 363-8 0770-3198
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Beating arthritis with the right food choices: eating right may even help you avoid the disease. Source: Tufts-Univ-health-nutr-lett. New York, NY : Tufts University Health & Nutrition Letter, c1997-. May 2002. volume 20 (3) 4 page
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By the way, doctor. Is MSM as good as it sounds? Can you tell me anything about the dietary supplement MSM? I've heard it's supposed to relieve arthritis pain. Source: Robb Nicholson, C Harv-Womens-Health-Watch. 2002 August; 9(12): 8 1070910X
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Complete Freund's adjuvant suppresses the development and progression of pristane-induced arthritis in rats. Author(s): Department of Microbiology, Saga Medical School, 5-1-1 Nabeshima, 8498501, Japan. Source: Zheng, Cong Long Hossain, Md Aslam Kukita, Akiko Ohki, Kazunori Satoh, Toshimi Kohashi, Osamu Clin-Immunol. 2002 May; 103(2): 204-9 1521-6616
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Differential function of nitric oxide in murine antigen-induced arthritis. Author(s): Department of Orthopaedics, Ludwig Maximilians University of Munich, Munich, Germany. Source: Veihelmann, A Hofbauer, A Krombach, F Dorger, M Maier, M Refior, H J Messmer, K Rheumatology-(Oxford). 2002 May; 41(5): 509-17 1462-0324
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Effects of alumina and zirconium dioxide particles on arachidonic acid metabolism and proinflammatory interleukin production in osteoarthritis and rheumatoid synovial cells. Source: Liagre, B Moalic, S Vergne, P Charissoux, J L Bernache Assollant, D Beneytout, J L J-Bone-Joint-Surg-Br. 2002 August; 84(6): 920-30 0301-620X
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Effects of synovial fluid on the respiratory burst of granulocytes in rheumatoid arthritis. Author(s): Center of Immunology, Institute of Virology St. S. Nicolau, Bucharest, Romania.
[email protected] Source: Bostan, M Brasoveanu, L I Livescu, A Manda, G Neagu, M Iordachescu, D JCell-Mol-Med. 2001 Apr-June; 5(2): 188-94 1582-1838
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Elk velvet antler in rheumatoid arthritis: phase II trial. Author(s): Faculty of Nursing, University of Alberta, Edmonton, Canada.
[email protected] Source: Allen, Marion Oberle, Kathleen Grace, Michael Russell, Anthony Biol-Res-Nurs. 2002 January; 3(3): 111-8 1099-8004
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Epidemiology of rheumatoid arthritis: determinants of onset, persistence and outcome. Author(s): University of Manchester Medical School, Oxford Road, Manchester, M13 9PT, UK. Source: Symmons, D P Best-Pract-Res-Clin-Rheumatol. 2002 December; 16(5): 707-22 1521-6942
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Evaluation of the cholesterol influence in type II collagen-induced arthritis in DBA/1J mice: an autoradiographic study. Author(s): Department of Biophysics and Biometrics, IBRAG, Universidade do Estado do Rio de Janeiro, Brasil.
[email protected] Source: Hamer, E R Apfel, M I Carvalho, J J Pereira, M J Levy, R A J-Cell-Mol-Med. 2002 Jul-September; 6(3): 407-14 1582-1838
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Facts and myths of neutraceuticals for canine arthritis. Source: Schulz, K.S. Proc-North-Am-Vet-Conf. [Gainesville, Fla.] : Eastern States Veterinary Association, 1992-. 2001. volume 15 page 465-467.
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Fibrin generated in the synovial fluid activates intimal cells from their apical surface: a sequential morphological study in antigen-induced arthritis. Author(s): Inflammation Research Unit, Division of Rheumatology, Fundacion Jimenez Diaz, Universidad Autonoma, Av. Reyes Catolicos 2, 28040 Madrid, Spain.
[email protected]
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Source: Sanchez Pernaute, O Lopez Armada, M J Calvo, E Diez Ortego, I Largo, R Egido, J Herrero Beaumont, G Rheumatology-(Oxford). 2003 January; 42(1): 19-25 1462-0324 ·
From arthritis to zeaxanthin, EN's A-to-Z guide meets the 21st century. Source: Welland, D. Environ-nutr. New York : Environmental Nutrition, Inc.,. December 2000. volume 23 (12) page 1, 4-5. 0893-4452
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Genotoxicity assessment using micronuclei assay in rheumatoid arthritis patients. Author(s): Department of Rheumatology, Centro Medico Nacional de Occidente del Instituto Mexicano del Seguro Social, Guadalajara.
[email protected] Source: Ramos Remus, C Dorazco Barragan, G Aceves Avila, F J Alcaraz Lopez, F Fuentes Ramirez, F Michel Diaz, J Torres Bugarin, O Ventura Aguilar, A Zuniga Gonzalez, G Clin-Exp-Rheumatol. 2002 Mar-April; 20(2): 208-12 0392-856X
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Glucocorticoid use in rheumatoid arthritis. Author(s): Division of Clinical Immunology and Rheumatology, Center for Education and Research on Therapeutics (CERTs) of Musculoskeletal Disorders, University of Alabama at Birmingham, MEB 625, 1813 Sixth Avenue South, Birmingham, AL 352943296, USA.
[email protected] Source: Saag, Kenneth G Curr-Rheumatol-Repage 2002 June; 4(3): 218-25 1523-3774
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Homocysteine and folate status in methotrexate-treated patients with rheumatoid arthritis. Author(s): Department of Rheumatology, University Medical Center St Radboud, Nijmegen, The Netherlands. Source: van Ede, A E Laan, R F J M Blom, H J Boers, G H J Haagsma, C J Thomas, C M G De Boo, T M van de Putte, L B A Rheumatology-(Oxford). 2002 June; 41(6): 658-65 14620324
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Inhibitory actions of glucosamine, a therapeutic agent for osteoarthritis, on the functions of neutrophils. Author(s): Department of Biochemistry, Juntendo University, School of Medicine, Tokyo, Japan. Source: Hua, Jian Sakamoto, Koji Nagaoka, Isao J-Leukoc-Biol. 2002 April; 71(4): 632-40 0741-5400
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Inhibitory effects of Spirulina in zymosan-induced arthritis in mice. Author(s): Ozone International Center, Havana, Cuba.
[email protected] Source: Remirez, D Gonzalez, R Merino, N Rodriguez, S Ancheta, O Mediators-Inflamm. 2002 April; 11(2): 75-9 0962-9351
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Leg ulceration in rheumatoid arthritis. Author(s): Royal National Hospital for Rheumatic Diseases NHS Trust, Bath. Source: Grange, M Henderson, C Nurs-Times. 2001 June 14-20; 97(24): 63 0954-7762
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Linear growth in children suffering from juvenile idiopathic arthritis requiring steroid therapy: natural history and effects of growth hormone treatment on linear growth. Author(s): Service d'Endocrinologie et de Diabetologie Pediatriques, Hjpital Robert Debre, Paris, France.
[email protected] Source: Simon, D Lucidarme, N Prieur, A M Ruiz, J C Czernichow, P J-PediatrEndocrinol-Metab. 2001; 14 Suppl 6: 1483-6
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Metabolism of kalopanaxsaponin K by human intestinal bacteria and antirheumatoid arthritis activity of their metabolites. Author(s): College of Pharmacy, Kyung-Hee University, Seoul, Korea.
[email protected]
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Source: Kim, Dong Hyun Bae, Eun Ah Han, Myung Joo Park, Hee Juhn Choi, Jong Won Biol-Pharm-Bull. 2002 January; 25(1): 68-71 0918-6158 ·
MRI of antigen-induced arthritis in rabbits: improved contrast and disease characterization with the blood pool agent MS-325. Author(s): Department of Radiology, University of California, San Francisco 94143-0628, USA. Source: Jiang, Y Zhao, J J Tang, H Wendland, M F Roberts, T P Lauffer, R B Genant, H K Acad-Radiol. 2002 August; 9 Suppl 2: S480 1076-6332
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Non-prescription complementary treatments used by rheumatoid arthritis patients attending a community-based rheumatology practice. Author(s): Department of Clinical Epidemiology, Cabrini Hospital, Melbourne, Victoria, Australia.
[email protected] Source: Buchbinder, R Gingold, M Hall, S Cohen, M Intern-Med-J. 2002 May-June; 32(56): 208-14 1444-0903
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Osteoclast formation and activity in the pathogenesis of osteoporosis in rheumatoid arthritis. Author(s): Nuffield Department of Orthopaedic Surgery, University of Oxford, Nuffield Orthopaedic Centre, Oxford OX3 7LD, UK. Source: Hirayama, T Danks, L Sabokbar, A Athanasou, N A Rheumatology-(Oxford). 2002 November; 41(11): 1232-9 1462-0324
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Osteoporosis in juvenile idiopathic arthritis. Author(s): Pediatric Rheumatology, Institute of Child Health, Birmingham Children's Hospital, Birmingham, United Kingdom.
[email protected] Source: McDonagh, J E Curr-Opin-Rheumatol. 2001 September; 13(5): 399-404 1040-8711
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Palmar fasciitis and arthritis: association with endometrial adenocarcinoma. Author(s): Department of Internal Medicine, Jolimont Hospital, Belgium. Source: Docquier, C h Majois, F Mitine, C Clin-Rheumatol. 2002 February; 21(1): 63-5 0770-3198
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Pharmacological characterisation of arthritis induced by Bothrops jararaca venom in rabbits: a positive cross talk between bradykinin, nitric oxide and prostaglandin E2. Author(s): Department of Internal Medicine, School of Medicine, University of Sao Paulo, SP, Brazil.
[email protected] Source: Mello, S B Guzzo, M L Lisboa, L F Farsky, S H Mediators-Inflamm. 2002 February; 11(1): 13-6 0962-9351
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PPA250 [3-(2,4-difluorophenyl)-6-[2-[4-(1H-imidazol-1-ylmethyl) phenoxy]ethoxy]-2phenylpyridine], a novel orally effective inhibitor of the dimerization of inducible nitric-oxide synthase, exhibits an anti-inflammatory effect in animal models of chronic arthritis. Author(s): Central Research Laboratories, SSP Co., Ltd., Chiba, Japan.
[email protected] Source: Ohtsuka, M Konno, F Honda, H Oikawa, T Ishikawa, M Iwase, N Isomae, K Ishii, F Hemmi, H Sato, S J-Pharmacol-Exp-Ther. 2002 October; 303(1): 52-7 0022-3565
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Preliminary evaluation of anti-inflammatory and anti-arthritic activity of S. lappa, A. speciosa and A. aspera. Author(s): Department of Pharmacology, Bombay College of Pharmacy, Kalina, Mumbai, India. Source: Gokhale, A B Damre, A S Kulkami, K R Saraf, M N Phytomedicine. 2002 July; 9(5): 433-7 0944-7113
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Radiographic outcome after three years of patients with early erosive rheumatoid arthritis treated with intramuscular methotrexate or parenteral gold. Extension of a one-year double-blind study in 174 patients. Author(s): Department of Rheumatology, Evangelisches Fachkrankenhaus, Ratingen, Germany. Source: Rau, R Herborn, G Menninger, H Sangha, O Rheumatology-(Oxford). 2002 February; 41(2): 196-204 1462-0324
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Resolving arthritis, allergies, & immune compromising disorders with the JMT technique. Source: Mellor, J M Beginnings. 2003 Jan-February; 23(1): 10-1 1071-2984
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Retrospective study of adverse events in patients with rheumatoid arthritis treated with second-line drugs. Author(s): Zhongshan Hospital, Fudan University, Shanghai 200032, China. Source: Jiang, L Zhao, N Ni, L Zhonghua-Liu-Xing-Bing-Xue-Za-Zhi. 2002 June; 23(3): 213-7 0254-6450
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Role of cholecystokinin-8 in nerve growth factor and nerve growth factor mRNA expression in carrageenan-induced joint inflammation in adult rats. Author(s): Institute of Neurobiology and Molecular Medicine, CNR, Viale Marx 15, 00137 Rome, Italy. Source: Manni, L Lundeberg, T Tirassa, P Aloe, L Rheumatology-(Oxford). 2002 July; 41(7): 787-92 1462-0324
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Second-line drugs used in recent-onset rheumatoid arthritis in Brittany (France). Author(s): Rheumatology department of Brest, hjpital de la Cavale-Blanche, France.
[email protected] Source: Saraux, Alain Berthelot, Jean Marie Chales, Gerard Le, Henaff Catherine Thorel, Jean Hoang, Sylvie Martin, Antoine Allain, Jerjme Nouy Trolle, Isabelle Devauchelle, Valerie Youinou, Pierre Le, Goff Paul Joint-Bone-Spine. 2002 January; 69(1): 37-42 1297319X
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Sex hormone adjuvanting therapy in rheumatoid arthritis. Author(s): Department of Internal Medicine, University
[email protected] Source: Cutolo, M Lupus. 2002; 11(10): 670-4 0961-2033
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The development and evaluation of a drug information leaflet for patients with rheumatoid arthritis. Author(s): Clinical Pharmacology Unit (Rheumatism Research, University of Leeds), Chapel Allerton Hospital, Chapeltown Road, Leeds, West Yorkshire LS7 4SA, UK.
[email protected] Source: Hill, J Bird, H Rheumatology-(Oxford). 2003 January; 42(1): 66-70 1462-0324
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The problem of empyematous pleural effusion in rheumatoid arthritis: report of two cases and review of the literature. Author(s): Department of Pulmonary Medicine, Rambam Medical Center and Faculty of Medicine, Technion-Israel Institute of Technology, Haifa.
[email protected] Source: Yigla, M Simsolo, C Goralnik, L Balabir German, A Nahir, A M Clin-Rheumatol. 2002 May; 21(2): 180-3 0770-3198
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Genova,
Italy.
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The rheumatoid arthritis patient in the clinic: comparing more than 1,300 consecutive DMARD courses. Author(s): Division of Rheumatology, Department of Internal Medicine III, University of Vienna, Vienna, Austria. Source: Aletaha, D Smolen, J S Rheumatology-(Oxford). 2002 December; 41(12): 1367-74 1462-0324
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The use of low-dose prednisone in the management of rheumatoid arthritis. Author(s): Emory University School of Medicine, Atlanta, GA, USA. Source: Lim, S S Conn, D L Bull-Rheum-Dis. 2001; 50(12): 1-4 0007-5248
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Trabecular bone density in premenopausal rheumatoid arthritis patients. Author(s): Department of Medicine, Rheumatic Diseases Unit, Groote Schuur Hospital, University of Cape Town. Source: Kalla, A A Bewerunge, L Langley, A Meyers, O L Fataar, A B S-Afr-Med-J. 2002 January; 92(1): 62-8 0038-2469
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Treatment of experimental adjuvant arthritis with the combination of methotrexate and lyophilized Enterococcus faecium enriched with organic selenium. Author(s): Institute of Rheumatic Diseases, 921 01 Piest'any, Slovakia.
[email protected] Source: Rovensky, J Svik, K Stancikova, M Istok, R Ebringer, L Ferencik, M FoliaMicrobiol-(Praha). 2002; 47(5): 573-8 0015-5632
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Treatment of rheumatic arthritis with Jiang Chen pian in 114 cases. Author(s): Rheumatism Department of Linyi TCM Hospital, Linyi 276002, Shandong Province. Source: Xia, J Zhu, X Feng, B Cao, Z Zhu, J J-Tradit-Chin-Med. 2002 September; 22(3): 178-9 0254-6272
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Two variables that can be used as pain indices in experimental animal models of arthritis. Author(s): Marine Biomedical Institute, University of Texas Medical Branch, Galveston, TX 77555-1069, USA. Source: Yu, Yun Cho Koo, Sung Tae Kim, Chang Hoon Lyu, Yeoungsu Grady, James J Chung, Jin Mo J-Neurosci-Methods. 2002 March 30; 115(1): 107-13 0165-0270
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Ulcerogenic influence of selective cyclooxygenase-2 inhibitors in the rat stomach with adjuvant-induced arthritis. Author(s): Department of Pharmacology and Experimental Therapeutics, Kyoto Pharmaceutical University, Misasagi, Yamashina, Kyoto 607-8414, Japan.
[email protected] Source: Kato, S Ogawa, Y Kanatsu, K Okayama, M Watanabe, T Arakawa, T Takeuchi, K J-Pharmacol-Exp-Ther. 2002 November; 303(2): 503-9 0022-3565
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Update on reactive arthritis. Author(s): Departments of Medicine, Pediatrics, and Molecular Genetics & Microbiology, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, New Brunswick, NJ, USA. Source: Sigal, L H Bull-Rheum-Dis. 2001; 50(4): 1-4 0007-5248
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Use of disease-modifying antirheumatic drugs in patients with psoriatic arthritis. Author(s): Service de Rhumatologie, Institut Calot, Berck sur mer, France. Source: Marguerie, L Flipo, R M Grardel, B Beaurain, D Duquesnoy, B Delcambre, B Joint-Bone-Spine. 2002 May; 69(3): 275-81 1297-319X
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Vitamin E and rheumatic diseases (osteoarthritis and rheumatoid arthritis). State of the art. Source: Biesalski, H. K. Frank, J. Bolten, W. Sangha, O. Nagel, E. Adam, O. AktuelleErnaehrungsmedizin (Germany). (1999). volume 24(1) page 29-36. 0341-0501
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Yellow nail syndrome associated with thiol compound therapy for rheumatoid arthritis. Two case reports. Author(s): Rheumatology department, CHU Jean-Minjoz, Besancon, France. Source: Lehuede, G Toussirot, E Despaux, J Michel, F Wendling, D Joint-Bone-Spine. 2002 June; 69(4): 406-8 1297-319X
Federal Resources on Nutrition In addition to the IBIDS, the United States Department of Health and Human Services (HHS) and the United States Department of Agriculture (USDA) provide many sources of information on general nutrition and health. Recommended resources include: ·
healthfinder®, HHS’s gateway to health information, including diet and nutrition: http://www.healthfinder.gov/scripts/SearchContext.asp?topic=238&page=0
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The United States Department of Agriculture’s Web site dedicated to nutrition information: www.nutrition.gov
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The Food and Drug Administration’s Web site for federal food safety information: www.foodsafety.gov
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The National Action Plan on Overweight and Obesity sponsored by the United States Surgeon General: http://www.surgeongeneral.gov/topics/obesity/
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The Center for Food Safety and Applied Nutrition has an Internet site sponsored by the Food and Drug Administration and the Department of Health and Human Services: http://vm.cfsan.fda.gov/
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Center for Nutrition Policy and Promotion sponsored by the United States Department of Agriculture: http://www.usda.gov/cnpp/
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Food and Nutrition Information Center, National Agricultural Library sponsored by the United States Department of Agriculture: http://www.nal.usda.gov/fnic/
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Food and Nutrition Service sponsored by the United States Department of Agriculture: http://www.fns.usda.gov/fns/
Additional Web Resources A number of additional Web sites offer encyclopedic information covering food and nutrition. The following is a representative sample: ·
AOL: http://search.aol.com/cat.adp?id=174&layer=&from=subcats
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Family Village: http://www.familyvillage.wisc.edu/med_nutrition.html
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Google: http://directory.google.com/Top/Health/Nutrition/
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Healthnotes: http://www.healthnotes.com/
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Open Directory Project: http://dmoz.org/Health/Nutrition/
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Yahoo.com: http://dir.yahoo.com/Health/Nutrition/
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WebMDÒHealth: http://my.webmd.com/nutrition
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WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,,00.html
The following is a specific Web list relating to arthritis; please note that any particular subject below may indicate either a therapeutic use, or a contraindication (potential danger), and does not reflect an official recommendation (some Web sites are subscription based): ·
Vitamins Ascorbic Acid Source: Integrative Medicine Communications; www.drkoop.com Folic Acid Source: Integrative Medicine Communications; www.drkoop.com Folic Acid Alternative names: Vitamin B9 (Folic Acid) Source: Integrative Medicine Communications; www.drkoop.com Niacin Source: Integrative Medicine Communications; www.drkoop.com Niacin Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,892,00.html Pantothenic Acid Source: Healthnotes, Inc. www.healthnotes.com Pantothenic Acid Source: Integrative Medicine Communications; www.drkoop.com Pantothenic Acid and Pantethine Source: Prima Communications, Inc.www.personalhealthzone.com Pyridoxine Source: Integrative Medicine Communications; www.drkoop.com Pyridoxine Alternative names: Vitamin B6 (Pyridoxine) Source: Integrative Medicine Communications; www.drkoop.com Riboflavin Source: Integrative Medicine Communications; www.drkoop.com Vitamin B2 (Riboflavin) Source: Integrative Medicine Communications; www.drkoop.com
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Vitamin B3 Source: Healthnotes, Inc. www.healthnotes.com Vitamin B3 Source: Prima Communications, Inc.www.personalhealthzone.com Vitamin B3 (Niacin) Source: Integrative Medicine Communications; www.drkoop.com Vitamin B5 (Pantothenic Acid) Source: Integrative Medicine Communications; www.drkoop.com Vitamin B6 Source: Prima Communications, Inc.www.personalhealthzone.com Vitamin B6 (Pyridoxine) Alternative names: Pyridoxine Source: Integrative Medicine Communications; www.drkoop.com Vitamin B6 (Pyridoxine) Source: Integrative Medicine Communications; www.drkoop.com Vitamin B9 (Folic Acid) Alternative names: Folate, Folic Acid Source: Integrative Medicine Communications; www.drkoop.com Vitamin B9 (Folic Acid) Alternative names: Folate Source: Integrative Medicine Communications; www.drkoop.com Vitamin C Source: Prima Communications, Inc.www.personalhealthzone.com Vitamin C (Ascorbic Acid) Source: Integrative Medicine Communications; www.drkoop.com Vitamin D Source: Healthnotes, Inc. www.healthnotes.com Vitamin D Alternative names: Calciferol, Calcitrol, Cholecalciferol, Erocalciferol Source: Integrative Medicine Communications; www.drkoop.com Vitamin D Source: Prima Communications, Inc.www.personalhealthzone.com Vitamin D Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,905,00.html
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Vitamin E Source: Healthnotes, Inc. www.healthnotes.com Vitamin E Alternative names: Alpha-Tocopherol, Beta-Tocopherol, D-Alpha-Tocopherol, Delta-Tocopherol, Gamma-Tocopherol Source: Integrative Medicine Communications; www.drkoop.com Vitamin E Source: Prima Communications, Inc.www.personalhealthzone.com ·
Minerals Alpha-Tocopherol Source: Integrative Medicine Communications; www.drkoop.com Betaine Hydrochloride Source: Healthnotes, Inc. www.healthnotes.com Betaine Hydrochloride Source: Prima Communications, Inc.www.personalhealthzone.com Beta-Tocopherol Source: Integrative Medicine Communications; www.drkoop.com Boron Source: Healthnotes, Inc. www.healthnotes.com Boron Source: Prima Communications, Inc.www.personalhealthzone.com Calcium Source: Prima Communications, Inc.www.personalhealthzone.com Chondroitin Source: Integrative Medicine Communications; www.drkoop.com Chondroitin Alternative names: chondroitin sulfate, sodium chondroitin sulfate Source: Integrative Medicine Communications; www.drkoop.com Chondroitin Source: Prima Communications, Inc.www.personalhealthzone.com Chondroitin Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10017,00.html Copper Source: Healthnotes, Inc. www.healthnotes.com
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Copper Source: Integrative Medicine Communications; www.drkoop.com Copper Source: Integrative Medicine Communications; www.drkoop.com Copper Source: Prima Communications, Inc.www.personalhealthzone.com Copper Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,886,00.html Creatine Monohydrate Source: Healthnotes, Inc. www.healthnotes.com D-Alpha-Tocopherol Source: Integrative Medicine Communications; www.drkoop.com Delta-Tocopherol Source: Integrative Medicine Communications; www.drkoop.com Folate Alternative names: Vitamin B9 (Folic Acid) Source: Integrative Medicine Communications; www.drkoop.com Folate Source: Integrative Medicine Communications; www.drkoop.com Folate Source: Prima Communications, Inc.www.personalhealthzone.com Gamma-Tocopherol Source: Integrative Medicine Communications; www.drkoop.com Glucosamine/Chondroitin Source: Healthnotes, Inc. www.healthnotes.com Iron Source: Healthnotes, Inc. www.healthnotes.com Magnesium Source: Integrative Medicine Communications; www.drkoop.com Magnesium Source: Integrative Medicine Communications; www.drkoop.com Magnesium Source: Prima Communications, Inc.www.personalhealthzone.com
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Manganese Source: Integrative Medicine Communications; www.drkoop.com Manganese Source: Prima Communications, Inc.www.personalhealthzone.com Naproxen/Naproxen Sodium Source: Healthnotes, Inc. www.healthnotes.com Quercetin Source: Integrative Medicine Communications; www.drkoop.com Retinol Source: Integrative Medicine Communications; www.drkoop.com Selenium Source: Healthnotes, Inc. www.healthnotes.com Selenium Source: Integrative Medicine Communications; www.drkoop.com Selenium Source: Prima Communications, Inc.www.personalhealthzone.com Selenium Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10055,00.html Stinging Nettle Alternative names: Urtica dioica, Urtica urens, Nettle Source: Integrative Medicine Communications; www.drkoop.com Stinging Nettle Alternative names: Nettle Source: Integrative Medicine Communications; www.drkoop.com Sulfur Source: Healthnotes, Inc. www.healthnotes.com Sulfur Source: Integrative Medicine Communications; www.drkoop.com Vitamin A (Retinol) Source: Integrative Medicine Communications; www.drkoop.com Zinc Source: Healthnotes, Inc. www.healthnotes.com Zinc Source: Integrative Medicine Communications; www.drkoop.com
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Zinc Source: Integrative Medicine Communications; www.drkoop.com Zinc Source: Prima Communications, Inc.www.personalhealthzone.com Zinc Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10071,00.html Zinc/copper Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,938,00.html ·
Food and Diet Barley Source: Healthnotes, Inc. www.healthnotes.com Burdock Alternative names: Arctium lappa Source: Healthnotes, Inc. www.healthnotes.com Burdock Source: Prima Communications, Inc.www.personalhealthzone.com Burdock Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/foods_view/0,1523,235,00.html Cartilage Alternative names: Shark Cartilage Source: Integrative Medicine Communications; www.drkoop.com Cartilage Source: Prima Communications, Inc.www.personalhealthzone.com Chondroitin Sulfate Source: Healthnotes, Inc. www.healthnotes.com Coffee Source: Healthnotes, Inc. www.healthnotes.com Eggplant Source: Healthnotes, Inc. www.healthnotes.com Fasting Diet Source: Healthnotes, Inc. www.healthnotes.com
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Fish, lean Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/foods_view/0,1523,93,00.html Gluten-Free Diet Source: Healthnotes, Inc. www.healthnotes.com Low-Purine Diet Source: Healthnotes, Inc. www.healthnotes.com Omega-3 Fatty Acids Source: Integrative Medicine Communications; www.drkoop.com Omega-3 fatty acids Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,992,00.html Omega-6 Fatty Acids Source: Integrative Medicine Communications; www.drkoop.com Omega-6 fatty acids Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,1037,00.html Pain Source: Healthnotes, Inc. www.healthnotes.com Polyunsaturated Fats Source: Healthnotes, Inc. www.healthnotes.com Potatoes Source: Healthnotes, Inc. www.healthnotes.com Rye Source: Healthnotes, Inc. www.healthnotes.com Salmon Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/foods_view/0,1523,102,00.html Sweet Peppers Source: Healthnotes, Inc. www.healthnotes.com Tendinitis Source: Healthnotes, Inc. www.healthnotes.com
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Tomatoes Source: Healthnotes, Inc. www.healthnotes.com Vegetarian Diet Source: Healthnotes, Inc. www.healthnotes.com Weight Loss and Obesity Source: Healthnotes, Inc. www.healthnotes.com Wheat Source: Healthnotes, Inc. www.healthnotes.com
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CHAPTER 3. ALTERNATIVE MEDICINE AND ARTHRITIS Overview In this chapter, we will begin by introducing you to official information sources on complementary and alternative medicine (CAM) relating to arthritis. At the conclusion of this chapter, we will provide additional sources.
The Combined Health Information Database The Combined Health Information Database (CHID) is a bibliographic database produced by health-related agencies of the U.S. federal government (mostly from the National Institutes of Health) that can offer concise information for a targeted search. The CHID database is updated four times a year at the end of January, April, July, and October. Check the titles, summaries, and availability of CAM-related information by using the “Simple Search” option at the following Web site: http://chid.nih.gov/simple/simple.html. In the drop box at the top, select “Complementary and Alternative Medicine.” Then type “arthritis” (or synonyms) in the second search box. We recommend that you select 100 “documents per page” and to check the “whole records” options. The following was extracted using this technique: ·
S-Adenosyl-L-Methionine for Treatment of Depression, Osteoarthritis, and Liver Disease Source: Rockville, MD: Agency for Healthcare Research and Quality. 2002. 6 p. Contact: Available from National Center for Complementary and Alternative Medicine Clearinghouse. P.O. Box 7923, Gaithersburg, MD 20898. (888) 644-6226; INTERNATIONAL PHONE: (301) 519-3153; TTY: (866) 464-3615; FAX: (866) 464-3616; EMAIL:
[email protected]. PRICE: Free. Publication Number: D175. Summary: This evidence report/technology assessment summary from the Agency for Healthcare Research and Quality (AHRQ) provides a review of the published literature on the use of S-adenosyl-L-methionine (SAMe) for the treatment of osteoarthritis, depression, and liver disease (cholestasis of pregnancy). The literature review is used to evaluate evidence for the efficacy of SAMe. The summary includes a description of the methodology, including the search strategy; selection criteria; and data collection and
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analysis. The findings are then discussed followed by an overview of future research on the topic. Information is also given on when and where the full report will be available. 1 reference.
National Center for Complementary and Alternative Medicine The National Center for Complementary and Alternative Medicine (NCCAM) of the National Institutes of Health (http://nccam.nih.gov/) has created a link to the National Library of Medicine’s databases to facilitate research for articles that specifically relate to arthritis and complementary medicine. To search the database, go to the following Web site: http://www.nlm.nih.gov/nccam/camonpubmed.html. Select “CAM on PubMed.” Enter “arthritis” (or synonyms) into the search box. Click “Go.” The following references provide information on particular aspects of complementary and alternative medicine that are related to arthritis: ·
A 57-year-old man with osteoarthritis of the knee. Author(s): Lonner JH. Source: Jama : the Journal of the American Medical Association. 2003 February 26; 289(8): 1016-25. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12597755&dopt=Abstract
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A phase I study of ethyl acetate extract of the chinese antirheumatic herb Tripterygium wilfordii hook F in rheumatoid arthritis. Author(s): Tao X, Cush JJ, Garret M, Lipsky PE. Source: The Journal of Rheumatology. 2001 October; 28(10): 2160-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11669150&dopt=Abstract
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A randomized controlled trial of homeopathy in rheumatoid arthritis. Author(s): Fisher P, Scott DL. Source: Rheumatology (Oxford, England). 2001 September; 40(9): 1052-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11561118&dopt=Abstract
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A randomized double blind, placebo controlled trial of topical Tripterygium wilfordii in rheumatoid arthritis: reanalysis using logistic regression analysis. Author(s): Cibere J, Deng Z, Lin Y, Ou R, He Y, Wang Z, Thorne A, Lehman AJ, Tsang IK, Esdaile JM. Source: The Journal of Rheumatology. 2003 March; 30(3): 465-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12610802&dopt=Abstract
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A randomized, double blind, placebo controlled trial of a topical cream containing glucosamine sulfate, chondroitin sulfate, and camphor for osteoarthritis of the knee. Author(s): Cohen M, Wolfe R, Mai T, Lewis D. Source: The Journal of Rheumatology. 2003 March; 30(3): 523-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12610812&dopt=Abstract
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A randomized, double-blind, placebo-controlled trial of glucosamine sulphate as an analgesic in osteoarthritis of the knee. Author(s): Hughes R, Carr A. Source: Rheumatology (Oxford, England). 2002 March; 41(3): 279-84. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11934964&dopt=Abstract
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A vegan diet free of gluten improves the signs and symptoms of rheumatoid arthritis: the effects on arthritis correlate with a reduction in antibodies to food antigens. Author(s): Hafstrom I, Ringertz B, Spangberg A, von Zweigbergk L, Brannemark S, Nylander I, Ronnelid J, Laasonen L, Klareskog L. Source: Rheumatology (Oxford, England). 2001 October; 40(10): 1175-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11600749&dopt=Abstract
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Acupuncture and other alternative therapies in rheumatoid arthritis. Author(s): Hardware B, Lacey A. Source: Prof Nurse. 2002 March; 17(7): 437-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11917436&dopt=Abstract
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Acupuncture-associated arthritis in a joint with an orthopaedic implant. Author(s): Laing AJ, Mullett H, Gilmore MF. Source: The Journal of Infection. 2002 January; 44(1): 43-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11972418&dopt=Abstract
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Advances in TCM symptomatology of rheumatoid arthritis. Author(s): Li S. Source: J Tradit Chin Med. 2002 June; 22(2): 137-42. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12125492&dopt=Abstract
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Alternative medicine and The Arthritis Foundation. Author(s): Marcus DM. Source: Arthritis and Rheumatism. 2002 February; 47(1): 5-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11932871&dopt=Abstract
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Alternative therapies for traditional disease states: osteoarthritis. Author(s): Morelli V, Naquin C, Weaver V. Source: American Family Physician. 2003 January 15; 67(2): 339-44. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12562155&dopt=Abstract
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Amelioration of rat adjuvant arthritis by therapeutic treatment with bindarit, an inhibitor of MCP-1 and TNF-alpha production. Author(s): Guglielmotti A, D'Onofrio E, Coletta I, Aquilini L, Milanese C, Pinza M.
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Source: Inflammation Research : Official Journal of the European Histamine Research Society. [et Al.]. 2002 May; 51(5): 252-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12056513&dopt=Abstract ·
An evaluation of the activity related to inflammation of four plants used in Thailand to treat arthritis. Author(s): Laupattarakasem P, Houghton PJ, Hoult JR, Itharat A. Source: Journal of Ethnopharmacology. 2003 April; 85(2-3): 207-15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12639742&dopt=Abstract
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An experimental study of a Mediterranean diet intervention for patients with rheumatoid arthritis. Author(s): Skoldstam L, Hagfors L, Johansson G. Source: Annals of the Rheumatic Diseases. 2003 March; 62(3): 208-14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12594104&dopt=Abstract
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An investigation of the effectiveness of exercise and manual therapy in treating symptoms of TMJ osteoarthritis. Author(s): Nicolakis P, Burak EC, Kollmitzer J, Kopf A, Piehslinger E, Wiesinger GF, Fialka-Moser V. Source: Cranio. 2001 January; 19(1): 26-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11842837&dopt=Abstract
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Anti-inflammatory effects of a low arachidonic acid diet and fish oil in patients with rheumatoid arthritis. Author(s): Adam O, Beringer C, Kless T, Lemmen C, Adam A, Wiseman M, Adam P, Klimmek R, Forth W. Source: Rheumatology International. 2003 January; 23(1): 27-36. Epub 2002 September 06. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12548439&dopt=Abstract
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Antioxidant intake, plasma antioxidants and oxidative stress in a randomized, controlled, parallel, Mediterranean dietary intervention study on patients with rheumatoid arthritis. Author(s): Hagfors L, Leanderson P, Skoldstam L, Andersson J, Johansson G. Source: Nutrition Journal [electronic Resource]. 2003 July 30; 2(1): 5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12952549&dopt=Abstract
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Archbishop Andreas Sunesson and his illness. Leprosy or arthritis? Author(s): Gejrot T. Source: Sydsven Medicinhist Sallsk Arsskr Suppl. 1992; 18: 23-8. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11623319&dopt=Abstract
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Arnica montana gel in osteoarthritis of the knee: an open, multicenter clinical trial. Author(s): Knuesel O, Weber M, Suter A. Source: Adv Ther. 2002 September-October; 19(5): 209-18. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12539881&dopt=Abstract
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Arthritis: taking control. Author(s): Hendrickson DG. Source: Home Care Provider. 2001 August; 6(4): 116-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11496261&dopt=Abstract
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Arthroscopic knee surgery. Daddy will make it better, even if it's arthritis. Author(s): Gillett G. Source: The Hastings Center Report. 2002 September-October; 32(5): 8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12360776&dopt=Abstract
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Association of low bone mass with vitamin d receptor gene and calcitonin receptor gene polymorphisms in juvenile idiopathic arthritis. Author(s): Masi L, Cimaz R, Simonini G, Bindi G, Stagi S, Gozzini A, Malentacchi C, Brandi ML, Falcini F. Source: The Journal of Rheumatology. 2002 October; 29(10): 2225-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12375338&dopt=Abstract
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Beneficial effect of climatic therapy on inflammatory arthritis at Tiberias Hot Springs. Author(s): Hashkes PJ. Source: Scandinavian Journal of Rheumatology. 2002; 31(3): 172-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12195633&dopt=Abstract
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Borage oil reduction of rheumatoid arthritis activity may be mediated by increased cAMP that suppresses tumor necrosis factor-alpha. Author(s): Kast RE. Source: International Immunopharmacology. 2001 November; 1(12): 2197-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11710548&dopt=Abstract
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Caring needs of patients with rheumatoid arthritis. Author(s): Nyman CS, Lutzen K. Source: Nursing Science Quarterly. 1999 April; 12(2): 164-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11847684&dopt=Abstract
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Clinical and immunomodulatory effects of fun-boi, an herbal medicine, on collageninduced arthritis in vivo. Author(s): Niizawa A, Kogure T, Hai LX, Fujinaga H, Takahashi K, Shimada Y, Terasawa K.
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Source: Clin Exp Rheumatol. 2003 January-February; 21(1): 57-62. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12673890&dopt=Abstract ·
Clinical effect of acupuncture treatment in 109 cases of knee osteoarthritis. Author(s): Jiang A, Zhang L, Zhao C, Yang F. Source: J Tradit Chin Med. 2001 December; 21(4): 282-5. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12014131&dopt=Abstract
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Clinical observation on treatment of rheumatoid arthritis with fengshi xiandan in 53 cases. Author(s): Shen Y, Qu Q, Wang D. Source: J Tradit Chin Med. 2003 March; 23(1): 21-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12747191&dopt=Abstract
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Comment on alternative medicine and The Arthritis Foundation. Author(s): Ernst E. Source: Arthritis and Rheumatism. 2002 October 15; 47(5): 566; Author Reply 566. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12382311&dopt=Abstract
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Comparison between the analgesic and therapeutic effects of a musically modulated electromagnetic field (TAMMEF) and those of a 100 Hz electromagnetic field: blind experiment on patients suffering from cervical spondylosis or shoulder periarthritis. Author(s): Rigato M, Battisti E, Fortunato M, Giordano N. Source: Journal of Medical Engineering & Technology. 2002 November-December; 26(6): 253-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12490031&dopt=Abstract
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Complementary and alternative drug therapy in arthritis. Author(s): Chandrashekara S, Anilkumar T, Jamuna S. Source: J Assoc Physicians India. 2002 February; 50: 225-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12038653&dopt=Abstract
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Computerized measurement of magnetic resonance imaging erosion volumes in patients with rheumatoid arthritis: a comparison with existing magnetic resonance imaging scoring systems and standard clinical outcome measures. Author(s): Bird P, Lassere M, Shnier R, Edmonds J. Source: Arthritis and Rheumatism. 2003 March; 48(3): 614-24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12632412&dopt=Abstract
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Concepts of arthritis in India's medical traditions: Ayurvedic and Unani perspectives. Author(s): Pugh JF.
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Source: Social Science & Medicine (1982). 2003 January; 56(2): 415-24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12473325&dopt=Abstract ·
Considerations in the selection of an appropriate conditioning regimen for the treatment of rheumatoid arthritis by autologous peripheral blood stem cell transplantation. Author(s): Kashyap A, Snowden J. Source: J Rheumatol Suppl. 2001 October; 64: 39-41. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11642503&dopt=Abstract
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Dietary glycine prevents peptidoglycan polysaccharide-induced reactive arthritis in the rat: role for glycine-gated chloride channel. Author(s): Li X, Bradford BU, Wheeler MD, Stimpson SA, Pink HM, Brodie TA, Schwab JH, Thurman RG. Source: Infection and Immunity. 2001 September; 69(9): 5883-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11500467&dopt=Abstract
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Different views of health care professionals on the treatment of osteoarthritis including low back pain. Author(s): Chrubasik S, Conradt C, Black A. Source: Rheumatology (Oxford, England). 2003 August; 42(8): 1020-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12869679&dopt=Abstract
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Differential effectiveness of psychological interventions for reducing osteoarthritis pain: a comparison of Erikson [correction of Erickson] hypnosis and Jacobson relaxation. Author(s): Gay MC, Philippot P, Luminet O. Source: European Journal of Pain (London, England). 2002; 6(1): 1-16. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11888223&dopt=Abstract
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Double-blind evaluation of implants of gold wire at acupuncture points in the dog as a treatment for osteoarthritis induced by hip dysplasia. Author(s): Hielm-Bjorkman A, Raekallio M, Kuusela E, Saarto E, Markkola A, Tulamo RM. Source: The Veterinary Record. 2001 October 13; 149(15): 452-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11688748&dopt=Abstract
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Dual inhibition of 5-lipoxygenase and cyclooxygenases 1 and 2 by ML3000 reduces joint destruction in adjuvant arthritis. Author(s): Gay RE, Neidhart M, Pataky F, Tries S, Laufer S, Gay S. Source: The Journal of Rheumatology. 2001 September; 28(9): 2060-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11550975&dopt=Abstract
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Education in the management of juvenile chronic arthritis. Changes in self-reported competencies among adolescents and parents of young children. Author(s): Andre M, Hagelberg S, Stenstrom CH. Source: Scandinavian Journal of Rheumatology. 2001; 30(6): 323-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11846049&dopt=Abstract
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Effect of acupuncture on knee function in advanced osteoarthritis of the knee: a prospective, non-randomised controlled study. Author(s): Tillu A, Tillu S, Vowler S. Source: Acupunct Med. 2002 March; 20(1): 19-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11926599&dopt=Abstract
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Effect of bioresonance therapy on antioxidant system in lymphocytes in patients with rheumatoid arthritis. Author(s): Islamov BI, Balabanova RM, Funtikov VA, Gotovskii YV, Meizerov EE. Source: Bulletin of Experimental Biology and Medicine. 2002 September; 134(3): 248-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12511993&dopt=Abstract
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Effect of cod liver oil on symptoms of rheumatoid arthritis. Author(s): Gruenwald J, Graubaum HJ, Harde A. Source: Adv Ther. 2002 March-April; 19(2): 101-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12069368&dopt=Abstract
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Effect of SKI 306X, a new herbal anti-arthritic agent, in patients with osteoarthritis of the knee: a double-blind placebo controlled study. Author(s): Jung YB, Roh KJ, Jung JA, Jung K, Yoo H, Cho YB, Kwak WJ, Kim DK, Kim KH, Han CK. Source: The American Journal of Chinese Medicine. 2001; 29(3-4): 485-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11789591&dopt=Abstract
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Effect of sulfur baths on antioxidative defense systems, peroxide concentrations and lipid levels in patients with degenerative osteoarthritis. Author(s): Ekmekcioglu C, Strauss-Blasche G, Holzer F, Marktl W. Source: Forschende Komplementarmedizin Und Klassische Naturheilkunde = Research in Complementary and Natural Classical Medicine. 2002 August; 9(4): 216-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12232493&dopt=Abstract
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Effect on osteoarthritis of spa therapy at Bourbonne-les-Bains. Author(s): Guillemin F, Virion JM, Escudier P, De Talance N, Weryha G. Source: Joint, Bone, Spine : Revue Du Rhumatisme. 2001 December; 68(6): 499-503. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11808987&dopt=Abstract
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Effectiveness of devil's claw for osteoarthritis. Author(s): Chrubasik S, Pollak S, Black A. Source: Rheumatology (Oxford, England). 2002 November; 41(11): 1332-3; Author Reply 1333. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12422011&dopt=Abstract
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Effects and mechanisms of glucosides of chaenomeles speciosa on collagen-induced arthritis in rats. Author(s): Chen Q, Wei W. Source: International Immunopharmacology. 2003 April; 3(4): 593-608. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12689663&dopt=Abstract
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Effects and mechanisms of melatonin on inflammatory and immune responses of adjuvant arthritis rat. Author(s): Chen Q, Wei W. Source: International Immunopharmacology. 2002 September; 2(10): 1443-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12400874&dopt=Abstract
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Effects of a ginger extract on knee pain in patients with osteoarthritis. Author(s): Altman RD, Marcussen KC. Source: Arthritis and Rheumatism. 2001 November; 44(11): 2531-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11710709&dopt=Abstract
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Effects of a milk-based bioactive micronutrient beverage on pain symptoms and activity of adults with osteoarthritis: a double-blind, placebo-controlled clinical evaluation. Author(s): Colker CM, Swain M, Lynch L, Gingerich DA. Source: Nutrition (Burbank, Los Angeles County, Calif.). 2002 May; 18(5): 388-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11985942&dopt=Abstract
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Effects of a very low-fat, vegan diet in subjects with rheumatoid arthritis. Author(s): McDougall J, Bruce B, Spiller G, Westerdahl J, McDougall M. Source: Journal of Alternative and Complementary Medicine (New York, N.Y.). 2002 February; 8(1): 71-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11890437&dopt=Abstract
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Effects of intranasal salmon calcitonin in juvenile idiopathic arthritis: an observational study. Author(s): Siamopoulou A, Challa A, Kapoglou P, Cholevas V, Mavridis AK, Lapatsanis PD. Source: Calcified Tissue International. 2001 July; 69(1): 25-30. Epub 2001 May 25. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11685430&dopt=Abstract
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Effects of long-term estrogen replacement therapy on osteoarthritis severity in cynomolgus monkeys. Author(s): Ham KD, Loeser RF, Lindgren BR, Carlson CS. Source: Arthritis and Rheumatism. 2002 July; 46(7): 1956-64. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12124881&dopt=Abstract
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Effects of oral administration of type II collagen on adjuvant arthritis in rats and its mechanisms. Author(s): Hu Y, Zhao W, Qian X, Zhang L. Source: Chin Med J (Engl). 2003 February; 116(2): 284-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12775248&dopt=Abstract
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Effects of paclitaxel on cultured synovial cells from patients with rheumatoid arthritis. Author(s): Kurose A, Yoshida W, Yoshida M, Sawai T. Source: Cytometry : the Journal of the Society for Analytical Cytology. 2001 August 1; 44(4): 349-54. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11500851&dopt=Abstract
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Effects of SKI 306X, a new herbal agent, on proteoglycan degradation in cartilage explant culture and collagenase-induced rabbit osteoarthritis model. Author(s): Choi JH, Choi JH, Kim DY, Yoon JH, Youn HY, Yi JB, Rhee HI, Ryu KH, Jung K, Han CK, Kwak WJ, Cho YB. Source: Osteoarthritis and Cartilage / Oars, Osteoarthritis Research Society. 2002 June; 10(6): 471-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12056850&dopt=Abstract
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Effects of tai chi exercise on pain, balance, muscle strength, and perceived difficulties in physical functioning in older women with osteoarthritis: a randomized clinical trial. Author(s): Song R, Lee EO, Lam P, Bae SC. Source: The Journal of Rheumatology. 2003 September; 30(9): 2039-44. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12966613&dopt=Abstract
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Efficacy and safety of freeze-dried cat's claw in osteoarthritis of the knee: mechanisms of action of the species Uncaria guianensis. Author(s): Piscoya J, Rodriguez Z, Bustamante SA, Okuhama NN, Miller MJ, Sandoval M. Source: Inflammation Research : Official Journal of the European Histamine Research Society. [et Al.]. 2001 September; 50(9): 442-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11603848&dopt=Abstract
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Efficacy and tolerability of Boswellia serrata extract in treatment of osteoarthritis of knee--a randomized double blind placebo controlled trial. Author(s): Kimmatkar N, Thawani V, Hingorani L, Khiyani R. Source: Phytomedicine : International Journal of Phytotherapy and Phytopharmacology. 2003 January; 10(1): 3-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12622457&dopt=Abstract
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Electrical stimulation for the treatment of rheumatoid arthritis. Author(s): Brosseau LU, Pelland LU, Casimiro LY, Robinson VI, Tugwell PE, Wells GE. Source: Cochrane Database Syst Rev. 2002; (2): Cd003687. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12076504&dopt=Abstract
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Elk velvet antler in rheumatoid arthritis: phase II trial. Author(s): Allen M, Oberle K, Grace M, Russell A. Source: Biological Research for Nursing. 2002 January; 3(3): 111-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12003439&dopt=Abstract
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Epigallocatechin-3-gallate selectively inhibits interleukin-1beta-induced activation of mitogen activated protein kinase subgroup c-Jun N-terminal kinase in human osteoarthritis chondrocytes. Author(s): Singh R, Ahmed S, Malemud CJ, Goldberg VM, Haqqi TM. Source: Journal of Orthopaedic Research : Official Publication of the Orthopaedic Research Society. 2003 January; 21(1): 102-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12507586&dopt=Abstract
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Erosive osteoarthritis: presentation, clinical pearls, and therapy. Author(s): Ehrlich GE. Source: Curr Rheumatol Rep. 2001 December; 3(6): 484-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11709110&dopt=Abstract
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Evaluation and treatment of the patient with osteoarthritis. Author(s): Easton BT. Source: The Journal of Family Practice. 2001 September; 50(9): 791-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11674913&dopt=Abstract
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Expression, modulation and signalling of IL-17 receptor in fibroblast-like synoviocytes of patients with rheumatoid arthritis. Author(s): Kehlen A, Thiele K, Riemann D, Langner J. Source: Clinical and Experimental Immunology. 2002 March; 127(3): 539-46. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11966773&dopt=Abstract
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First-line treatment for osteoarthritis. Part 2: Nonpharmacologic interventions and evaluation. Author(s): Baird CL. Source: Orthopaedic Nursing / National Association of Orthopaedic Nurses. 2001 November-December; 20(6): 13-8; Quiz 18-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12025798&dopt=Abstract
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Fish oils are beneficial to patients with established rheumatoid arthritis. Author(s): Harrison RA, Harrison BJ. Source: The Journal of Rheumatology. 2001 November; 28(11): 2563-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11708441&dopt=Abstract
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Folate-targeted imaging of activated macrophages in rats with adjuvant-induced arthritis. Author(s): Turk MJ, Breur GJ, Widmer WR, Paulos CM, Xu LC, Grote LA, Low PS. Source: Arthritis and Rheumatism. 2002 July; 46(7): 1947-55. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12124880&dopt=Abstract
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Folic acid and folinic acid supplementation during low-dose methotrexate therapy for rheumatoid arthritis: comment on the article by van Ede et al. Author(s): Morgan SL, Baggott JE, Alarcon GS, Koopman WJ. Source: Arthritis and Rheumatism. 2002 May; 46(5): 1413-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12115259&dopt=Abstract
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Glucosamine and chondroitin for osteoarthritis? Author(s): McAlindon T. Source: Bulletin on the Rheumatic Diseases. 2001 July; 50(7): 1-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11530541&dopt=Abstract
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Glucosamine and chondroitin sulfate are effective in the management of osteoarthritis. Author(s): Hungerford DS, Jones LC. Source: The Journal of Arthroplasty. 2003 April; 18(3 Suppl 1): 5-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12730919&dopt=Abstract
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Glucosamine for arthritis. Author(s): Keller L. Source: Adv Nurse Pract. 2003 June; 11(6): 19-21, 100. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12807050&dopt=Abstract
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Glucosamine sulfate use and delay of progression of knee osteoarthritis: a 3-year, randomized, placebo-controlled, double-blind study. Author(s): Pavelka K, Gatterova J, Olejarova M, Machacek S, Giacovelli G, Rovati LC.
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Source: Archives of Internal Medicine. 2002 October 14; 162(18): 2113-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12374520&dopt=Abstract ·
Gonarthritis in the course of Lyme disease in a one-and-a-half-year-old child. Author(s): Zajadacz B, Juszkiewicz A. Source: Wiad Lek. 2002; 55(3-4): 243-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12182012&dopt=Abstract
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Health-care use by rheumatoid arthritis patients compared with non-arthritic subjects. Author(s): Girard F, Guillemin F, Novella JL, Valckenaere I, Krzanowska K, Vitry F, Vittecoq O, Eschard JP, Blanchard F, Le Loet X. Source: Rheumatology (Oxford, England). 2002 February; 41(2): 167-75. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11886965&dopt=Abstract
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Herbal medicines for the treatment of rheumatoid arthritis: a systematic review. Author(s): Soeken KL, Miller SA, Ernst E. Source: Rheumatology (Oxford, England). 2003 May; 42(5): 652-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12709541&dopt=Abstract
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Home based exercise programme for knee pain and knee osteoarthritis: randomised controlled trial. Author(s): Thomas KS, Muir KR, Doherty M, Jones AC, O'Reilly SC, Bassey EJ. Source: Bmj (Clinical Research Ed.). 2002 October 5; 325(7367): 752. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12364304&dopt=Abstract
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How do adolescents with juvenile chronic arthritis consider their disease related knowledge, their unmet service needs, and the attractiveness of various services? Author(s): Ullrich G, Mattussek S, Dressler F, Thon A. Source: European Journal of Medical Research. 2002 January 29; 7(1): 8-18. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11827835&dopt=Abstract
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Human fetal adrenal transplant: a possible role in relieving intractable pain in advanced rheumatoid arthritis. Author(s): Bhattacharya N, Chhetri MK, Mukherjee KL, Das SP, Mukherjee A, Bhattacharya M, Bhattacharya S. Source: Clin Exp Obstet Gynecol. 2002; 29(3): 197-206. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12519043&dopt=Abstract
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Hyperhomocysteinemia in children with juvenile idiopathic arthritis is not influenced by methotrexate treatment and folic acid supplementation: a pilot study. Author(s): Huemer M, Fodinger M, Huemer C, Sailer-Hock M, Falger J, Rettenbacher A, Bernecker M, Artacker G, Kenzian H, Lang T, Stockler-Ipsiroglu S.
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Source: Clin Exp Rheumatol. 2003 March-April; 21(2): 249-55. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12747286&dopt=Abstract ·
Hyperhomocysteinemia in rheumatoid arthritis: influence of methotrexate treatment and folic acid supplementation. Author(s): Jensen OK, Rasmussen C, Mollerup F, Christensen PB, Hansen H, Ekelund S, Thulstrup AM. Source: The Journal of Rheumatology. 2002 August; 29(8): 1615-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12180718&dopt=Abstract
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Identification of the pharmaceutical care issues of rheumatoid arthritis patients in secondary care. Author(s): O'Hare R, Muir A, Chapman S, Watson A, Hudson SA. Source: Pharmacy World & Science : Pws. 2001 October; 23(5): 183-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11721675&dopt=Abstract
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Illness management strategies among Chinese immigrants living with arthritis. Author(s): Zhang J, Verhoef MJ. Source: Social Science & Medicine (1982). 2002 November; 55(10): 1795-802. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12383463&dopt=Abstract
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Immunomodulatory activity of the aqueous extract from rhizome of Smilax glabra in the later phase of adjuvant-induced arthritis in rats. Author(s): Jiang J, Xu Q. Source: Journal of Ethnopharmacology. 2003 March; 85(1): 53-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12576202&dopt=Abstract
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Improved sleep may reduce arthritis pain. Author(s): Davis GC. Source: Holistic Nursing Practice. 2003 May-June; 17(3): 128-35. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12784896&dopt=Abstract
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Improvement in hand grip strength in normal volunteers and rheumatoid arthritis patients following yoga training. Author(s): Dash M, Telles S. Source: Indian J Physiol Pharmacol. 2001 July; 45(3): 355-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11881576&dopt=Abstract
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Inhibition of adjuvant-induced arthritis by 16 alpha-fluoro-5-androsten-17-one. Author(s): Schwartz AG, Pashko LL.
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Source: Military Medicine. 2002 February; 167(2 Suppl): 60-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11873519&dopt=Abstract ·
Innovative therapies in osteoarthritis. Author(s): Polisson R. Source: Curr Rheumatol Rep. 2001 December; 3(6): 489-95. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11709111&dopt=Abstract
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Intercessory prayer and its effect on patients with rheumatoid arthritis. Author(s): Williams T. Source: Ky Nurse. 2002 January-March; 50(1): 16. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11859558&dopt=Abstract
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Is there a role for ginger in the treatment of osteoarthritis? Author(s): Marcus DM, Suarez-Almazor ME. Source: Arthritis and Rheumatism. 2001 November; 44(11): 2461-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11710700&dopt=Abstract
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Leech therapy for symptomatic treatment of knee osteoarthritis: results and implications of a pilot study. Author(s): Michalsen A, Moebus S, Spahn G, Esch T, Langhorst J, Dobos GJ. Source: Alternative Therapies in Health and Medicine. 2002 September-October; 8(5): 848. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12233807&dopt=Abstract
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Leg ulceration in rheumatoid arthritis. Author(s): Grange M, Henderson C. Source: Nurs Times. 2001 June 14-20; 97(24): 63. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11954493&dopt=Abstract
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Macrophage migration inhibitory factor in rheumatoid arthritis: clinical correlations. Author(s): Morand EF, Leech M, Weedon H, Metz C, Bucala R, Smith MD. Source: Rheumatology (Oxford, England). 2002 May; 41(5): 558-62. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12011381&dopt=Abstract
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Magnetic pulse treatment for knee osteoarthritis: a randomised, double-blind, placebo-controlled study. Author(s): Pipitone N, Scott DL. Source: Current Medical Research and Opinion. 2001; 17(3): 190-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11900312&dopt=Abstract
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Management of osteoarthritis. Author(s): Cote LG. Source: Journal of the American Academy of Nurse Practitioners. 2001 November; 13(11): 495-501. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11930514&dopt=Abstract
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Mediterranean diet intervention in rheumatoid arthritis. Author(s): Kjeldsen-Kragh J. Source: Annals of the Rheumatic Diseases. 2003 March; 62(3): 193-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12594101&dopt=Abstract
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Meeting the therapeutic challenge of the patient with osteoarthritis. Author(s): Todd C. Source: Journal of the American Pharmaceutical Association (Washington,D.C. : 1996). 2002 January-February; 42(1): 74-82. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11833521&dopt=Abstract
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Methodological differences in clinical trials evaluating nonpharmacological and pharmacological treatments of hip and knee osteoarthritis. Author(s): Boutron I, Tubach F, Giraudeau B, Ravaud P. Source: Jama : the Journal of the American Medical Association. 2003 August 27; 290(8): 1062-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12941679&dopt=Abstract
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Microsomal prostaglandin E synthase-1 is a major terminal synthase that is selectively up-regulated during cyclooxygenase-2-dependent prostaglandin E2 production in the rat adjuvant-induced arthritis model. Author(s): Claveau D, Sirinyan M, Guay J, Gordon R, Chan CC, Bureau Y, Riendeau D, Mancini JA. Source: Journal of Immunology (Baltimore, Md. : 1950). 2003 May 1; 170(9): 4738-44. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12707354&dopt=Abstract
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Moderation of iodoacetate-induced experimental osteoarthritis in rats by matrix metalloproteinase inhibitors. Author(s): Janusz MJ, Hookfin EB, Heitmeyer SA, Woessner JF, Freemont AJ, Hoyland JA, Brown KK, Hsieh LC, Almstead NG, De B, Natchus MG, Pikul S, Taiwo YO. Source: Osteoarthritis and Cartilage / Oars, Osteoarthritis Research Society. 2001 November; 9(8): 751-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11795995&dopt=Abstract
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MR imaging of murine arthritis using ultrasmall superparamagnetic iron oxide particles. Author(s): Dardzinski BJ, Schmithorst VJ, Holland SK, Boivin GP, Imagawa T, Watanabe S, Lewis JM, Hirsch R.
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Source: Magnetic Resonance Imaging. 2001 November; 19(9): 1209-16. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11755731&dopt=Abstract ·
Nonpharmacologic management of osteoarthritis. Author(s): Sharma L. Source: Current Opinion in Rheumatology. 2002 September; 14(5): 603-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12192263&dopt=Abstract
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Non-pharmacological approaches to managing arthritis. Author(s): March LM, Stenmark J. Source: The Medical Journal of Australia. 2001 November 19; 175 Suppl: S102-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11795555&dopt=Abstract
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Non-prescription complementary treatments used by rheumatoid arthritis patients attending a community-based rheumatology practice. Author(s): Buchbinder R, Gingold M, Hall S, Cohen M. Source: Internal Medicine Journal. 2002 May-June; 32(5-6): 208-14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12036218&dopt=Abstract
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Nutripharmaceuticals for osteoarthritis. Author(s): Hauselmann HJ. Source: Best Practice & Research. Clinical Rheumatology. 2001 October; 15(4): 595-607. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11567542&dopt=Abstract
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Nutritional management of rheumatoid arthritis: a review of the evidence. Author(s): Rennie KL, Hughes J, Lang R, Jebb SA. Source: Journal of Human Nutrition and Dietetics : the Official Journal of the British Dietetic Association. 2003 April; 16(2): 97-109. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12662368&dopt=Abstract
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Observation on the therapeutic effect of Shu Feng Huo Luo Pian for treatment of osseous arthritis. Author(s): Wu X, Zhou Y. Source: J Tradit Chin Med. 2002 March; 22(1): 12-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11977509&dopt=Abstract
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Osteoarthritis and MR imaging. Author(s): Ott K, Montes-Lucero J. Source: Radiol Technol. 2002 September-October; 74(1): 25-42; Quiz 43-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12362533&dopt=Abstract
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Osteoarthritis. Options for arthritis pain. Author(s): Shmerling R, Ulbricht C, Basch E. Source: Newsweek. 2002 December 2; 140(23): 53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12501510&dopt=Abstract
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Osteoarthritis: a review. Author(s): Sharma H. Source: J Indian Med Assoc. 2001 June; 99(6): 322-4. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11678620&dopt=Abstract
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Osteoarthritis: supplements and other alternative modalities. Author(s): Novey DW. Source: Primary Care. 2002 June; 29(2): 263-77. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12391711&dopt=Abstract
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Osteoporosis in juvenile idiopathic arthritis. Author(s): McDonagh JE. Source: Current Opinion in Rheumatology. 2001 September; 13(5): 399-404. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11604595&dopt=Abstract
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Oxidative stress in rheumatoid arthritis leukocytes: suppression by rutin and other antioxidants and chelators. Author(s): Ostrakhovitch EA, Afanas'ev IB. Source: Biochemical Pharmacology. 2001 September 15; 62(6): 743-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11551519&dopt=Abstract
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Pharmacologic therapy for osteoarthritis. Author(s): Goldberg SH, Von Feldt JM, Lonner JH. Source: Am J Orthop. 2002 December; 31(12): 673-80. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12498526&dopt=Abstract
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Potentiated Antibodies to Tumor Necrosis Factor-alpha in the Therapy of Patients with Rheumatoid Arthritis. Author(s): Kozlovskaya LV, Mukhin NA, Rameev VV, Sarkisova IA, Epstein OI. Source: Bulletin of Experimental Biology and Medicine. 2003; 135 Suppl 1: 152-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12949685&dopt=Abstract
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PPAR gamma ligands inhibit nitrotyrosine formation and inflammatory mediator expressions in adjuvant-induced rheumatoid arthritis mice. Author(s): Shiojiri T, Wada K, Nakajima A, Katayama K, Shibuya A, Kudo C, Kadowaki T, Mayumi T, Yura Y, Kamisaki Y.
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Source: European Journal of Pharmacology. 2002 July 19; 448(2-3): 231-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12144946&dopt=Abstract ·
Practice variation in the treatment of rheumatoid arthritis among German rheumatologists. Author(s): Zink A, Listing J, Ziemer S, Zeidler H; German Collaborative Arthritis Centres. Source: The Journal of Rheumatology. 2001 October; 28(10): 2201-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11669156&dopt=Abstract
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Principles of rheumatoid arthritis control. Author(s): Palferman TG. Source: J Rheumatol Suppl. 2003 August; 67: 10-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12926645&dopt=Abstract
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Principles of rheumatoid arthritis control. Author(s): Palferman TG. Source: The Journal of Rheumatology. 2003 August; 30(8): 10-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12913895&dopt=Abstract
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Promoting self-help strategies by sharing the lived experience of arthritis. Author(s): Taylor B. Source: Contemp Nurse. 2001 March; 10(1-2): 117-25. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11855014&dopt=Abstract
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Psychological interventions for rheumatoid arthritis: a meta-analysis of randomized controlled trials. Author(s): Astin JA, Beckner W, Soeken K, Hochberg MC, Berman B. Source: Arthritis and Rheumatism. 2002 June 15; 47(3): 291-302. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12115160&dopt=Abstract
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Pulsed magnetic field therapy for osteoarthritis of the knee--a double-blind shamcontrolled trial. Author(s): Mullner M. Source: Wiener Klinische Wochenschrift. 2002 November 30; 114(21-22): 953; Author Reply 953. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12528331&dopt=Abstract
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Randomised, double-blind, placebo-controlled parallel group study of P54FP for the treatment of dogs with osteoarthritis. Author(s): Innes JF, Fuller CJ, Grover ER, Kelly AL, Burn JF.
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Source: The Veterinary Record. 2003 April 12; 152(15): 457-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12723628&dopt=Abstract ·
Randomized double blind trial of an extract from the pentacyclic alkaloid-chemotype of uncaria tomentosa for the treatment of rheumatoid arthritis. Author(s): Mur E, Hartig F, Eibl G, Schirmer M. Source: The Journal of Rheumatology. 2002 April; 29(4): 678-81. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11950006&dopt=Abstract
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Rapid improvement of osteomalacia by treatment in a case with Sjogren's syndrome, rheumatoid arthritis and renal tubular acidosis type 1. Author(s): Okada M, Suzuki K, Hidaka T, Shinohara T, Kataharada K, Matsumoto M, Takada K, Ohsuzu F. Source: Intern Med. 2001 August; 40(8): 829-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11518137&dopt=Abstract
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Resolving arthritis, allergies, & immune compromising disorders with the JMT technique. Author(s): Mellor JM. Source: Beginnings. 2003 January-February; 23(1): 10-1. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12592973&dopt=Abstract
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Retrospective study of adverse events in patients with rheumatoid arthritis treated with second-line drugs. Author(s): Jiang L, Zhao N, Ni L. Source: Zhonghua Liu Xing Bing Xue Za Zhi. 2002 June; 23(3): 213-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12411093&dopt=Abstract
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Rheumatoid arthritis: proposal for the use of anti-microbial therapy in early cases. Author(s): Ebringer A, Rashid T, Wilson C. Source: Scandinavian Journal of Rheumatology. 2003; 32(1): 2-11. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12635939&dopt=Abstract
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Role of macrophages in experimental group B streptococcal arthritis. Author(s): Puliti M, von Hunolstein C, Bistoni F, Castronari R, Orefici G, Tissi L. Source: Cellular Microbiology. 2002 October; 4(10): 691-700. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12366405&dopt=Abstract
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Role of protein tyrosine kinase in IL-1 beta induced activation of mitogen-activated protein kinase in fibroblast-like synoviocytes of rheumatoid arthritis. Author(s): Lu H, Sun T, Yao L, Zhang Y.
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Source: Chin Med J (Engl). 2000 October; 113(10): 872-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11775830&dopt=Abstract ·
Safety and efficacy of S-adenosylmethionine (SAMe) for osteoarthritis. Author(s): Soeken KL, Lee WL, Bausell RB, Agelli M, Berman BM. Source: The Journal of Family Practice. 2002 May; 51(5): 425-30. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12019049&dopt=Abstract
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Selenium supplementation in rheumatoid arthritis investigated in a double blind, placebo-controlled trial. Author(s): Peretz A, Siderova V, Neve J. Source: Scandinavian Journal of Rheumatology. 2001; 30(4): 208-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11578015&dopt=Abstract
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Sleep quality in children with juvenile rheumatoid arthritis. Author(s): Labyak SE, Bourguignon C, Docherty S. Source: Holistic Nursing Practice. 2003 July-August; 17(4): 193-200. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12889547&dopt=Abstract
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Spirituality, resourcefulness, and arthritis impact on health perception of elders with rheumatoid arthritis. Author(s): Potter ML, Zauszniewski JA. Source: Journal of Holistic Nursing : Official Journal of the American Holistic Nurses' Association. 2000 December; 18(4): 311-31; Discussions 332-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11847790&dopt=Abstract
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Structural and symptomatic efficacy of glucosamine and chondroitin in knee osteoarthritis: a comprehensive meta-analysis. Author(s): Richy F, Bruyere O, Ethgen O, Cucherat M, Henrotin Y, Reginster JY. Source: Archives of Internal Medicine. 2003 July 14; 163(13): 1514-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12860572&dopt=Abstract
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Structural effect of avocado/soybean unsaponifiables on joint space loss in osteoarthritis of the hip. Author(s): Lequesne M, Maheu E, Cadet C, Dreiser RL. Source: Arthritis and Rheumatism. 2002 February; 47(1): 50-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11932878&dopt=Abstract
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Subacute toxicity evaluation of a hydroalcoholic extract of Pterodon pubescens seeds in mice with collagen-induced arthritis. Author(s): Pinto Coelho MG, Marques PR, Gayer CR, Vaz LC, Neto JF, Sabino KC.
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Source: Journal of Ethnopharmacology. 2001 October; 77(2-3): 159-64. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11535359&dopt=Abstract ·
Supplementary vitamin E does not affect the loss of cartilage volume in knee osteoarthritis: a 2 year double blind randomized placebo controlled study. Author(s): Wluka AE, Stuckey S, Brand C, Cicuttini FM. Source: The Journal of Rheumatology. 2002 December; 29(12): 2585-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12465157&dopt=Abstract
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Suppression of chronic streptococcal cell wall-induced arthritis in Lewis rats by liposomal clodronate. Author(s): Richards PJ, Williams BD, Williams AS. Source: Rheumatology (Oxford, England). 2001 September; 40(9): 978-87. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11561107&dopt=Abstract
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Suppression of collagen-induced arthritis in rats by continuous administration of dae-bang-poong-tang (da-fang-feng-tang). Author(s): Joe SM, Lee IS, Lee YT, Lee JH, Choi BT. Source: The American Journal of Chinese Medicine. 2001; 29(2): 355-65. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11527077&dopt=Abstract
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Suppressive effect of hochu-ekki-to on collagen induced arthritis in DBA1J mice. Author(s): Hai le X, Kogure T, Niizawa A, Fujinaga H, Sakakibara I, Shimada Y, Watanabe H, Terasawa K. Source: The Journal of Rheumatology. 2002 August; 29(8): 1601-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12180716&dopt=Abstract
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Suppressive effects of PG201, an ethanol extract from herbs, on collagen-induced arthritis in mice. Author(s): Shin SS, Jin M, Jung HJ, Kim B, Jeon H, Choi JJ, Kim JM, Cho BW, Chung SH, Lee YW, Song YW, Kim S. Source: Rheumatology (Oxford, England). 2003 May; 42(5): 665-72. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12709543&dopt=Abstract
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Symptoms modifying effect of avocado/soybean unsaponifiables (ASU) in knee osteoarthritis. A double blind, prospective, placebo-controlled study. Author(s): Appelboom T, Schuermans J, Verbruggen G, Henrotin Y, Reginster JY. Source: Scandinavian Journal of Rheumatology. 2001; 30(4): 242-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11578021&dopt=Abstract
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Syngeneic fibroblasts transfected with a plasmid encoding interleukin-4 as non-viral vectors for anti-inflammatory gene therapy in collagen-induced arthritis.
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Author(s): Bessis N, Cottard V, Saidenberg-Kermanach N, Lemeiter D, Fournier C, Boissier MC. Source: The Journal of Gene Medicine. 2002 May-June; 4(3): 300-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12112647&dopt=Abstract ·
Synthesis and inhibitory effect of threo-DL-phenyl-serine derivatives in rat experimental adjuvant arthritis model. Author(s): Dirvianskyte N, Leonaviciene L, Butkus E. Source: Pharmazie. 2002 September; 57(9): 650-1. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12369458&dopt=Abstract
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The age of arthritis. Author(s): Gorman C, Park A. Source: Time. 2002 December 9; 160(24): 70, 72-6, 79. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12500506&dopt=Abstract
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The analgesic efficacy of bee venom acupuncture for knee osteoarthritis: a comparative study with needle acupuncture. Author(s): Kwon YB, Kim JH, Yoon JH, Lee JD, Han HJ, Mar WC, Beitz AJ, Lee JH. Source: The American Journal of Chinese Medicine. 2001; 29(2): 187-99. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11527062&dopt=Abstract
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The antinociceptive and anti-inflammatory effect of ethylacetate extracts from BangPoong (Radix ledebouriellae) on the Freund's adjuvant-induced arthritis in rats. Author(s): Kim HW, Kwon YB, Ham TW, Roh DH, Yoon SY, Han HJ, Kang SK, Lee HJ, Mar WC, Yang IS, Beitz AJ, Lee JH. Source: J Vet Sci. 2002 December; 3(4): 343-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12819385&dopt=Abstract
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The case for nonpharmacologic therapy of osteoarthritis. Author(s): Chard J, Dieppe P. Source: Curr Rheumatol Rep. 2001 June; 3(3): 251-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11794136&dopt=Abstract
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The effect of whole bee venom on arthritis. Author(s): Kang SS, Pak SC, Choi SH. Source: The American Journal of Chinese Medicine. 2002; 30(1): 73-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12067099&dopt=Abstract
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The effectiveness of Commiphora mukul for osteoarthritis of the knee: an outcomes study. Author(s): Singh BB, Mishra LC, Vinjamury SP, Aquilina N, Singh VJ, Shepard N.
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Source: Alternative Therapies in Health and Medicine. 2003 May-June; 9(3): 74-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12776478&dopt=Abstract ·
The efficacy of acupuncture for osteoarthritis. Author(s): Cebuliak E. Source: Aust Vet J. 2002 March; 80(3): 128. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12019689&dopt=Abstract
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The role of B cells in rheumatoid arthritis: mechanisms and therapeutic targets. Author(s): Dorner T, Burmester GR. Source: Current Opinion in Rheumatology. 2003 May; 15(3): 246-52. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12707577&dopt=Abstract
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The role of complementary and alternative therapies in managing rheumatoid arthritis. Author(s): Taibi DM, Bourguignon C. Source: Family & Community Health. 2003 January-March; 26(1): 41-52. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12802127&dopt=Abstract
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The role of fish oils in the treatment of rheumatoid arthritis. Author(s): Cleland LG, James MJ, Proudman SM. Source: Drugs. 2003; 63(9): 845-53. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12678571&dopt=Abstract
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The role of self-help education for patients with arthritis. Author(s): Weber D. Source: Tenn Med. 2002 January; 95(1): 33-4. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11797568&dopt=Abstract
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The therapeutic effects of Cserkeszolo thermal water in osteoarthritis of the knee: a double blind, controlled, follow-up study. Author(s): Kovacs I, Bender T. Source: Rheumatology International. 2002 April; 21(6): 218-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12036207&dopt=Abstract
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The use of homeopathic preparation vozraston in the therapy of patients with rheumatoid arthritis. Author(s): Noskov SM, Snigireva AV, Dolgova LN, Somova MA, Polyakov DP. Source: Bulletin of Experimental Biology and Medicine. 2003; 135 Suppl 1: 94-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12949664&dopt=Abstract
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Thermotherapy for treating rheumatoid arthritis. Author(s): Robinson V, Brosseau L, Casimiro L, Judd M, Shea B, Wells G, Tugwell P. Source: Cochrane Database Syst Rev. 2002; (2): Cd002826. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12076454&dopt=Abstract
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Thermotherapy for treating rheumatoid arthritis. Author(s): Robinson V, Brosseau L, Casimiro L, Judd M, Shea B, Wells G, Tugwell P. Source: Cochrane Database Syst Rev. 2002; (1): Cd002826. Review. Update In: http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11869637&dopt=Abstract
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Total abrogation of collagen II-induced arthritis and the B cell response to type II collagen using suboptimal doses of a topoisomerase II antagonist. Author(s): Verdrengh M, Jonsson IM, Zaether O, Bajtner E, Holmdahl R, Tarkowski A. Source: Annals of the Rheumatic Diseases. 2002 September; 61(9): 829-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12176810&dopt=Abstract
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Toward optimal health: the experts discuss osteoarthritis in women [interviewed by Jodi Godfrey Meisler] Author(s): Loeser RF Jr, Lachmann EA. Source: Journal of Women's Health (2002). 2002 November; 11(9): 759-65. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12626077&dopt=Abstract
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Transcutaneous electrical nerve stimulation (TENS) for the treatment of rheumatoid arthritis in the hand. Author(s): Brosseau L, Yonge KA, Robinson V, Marchand S, Judd M, Wells G, Tugwell P. Source: Cochrane Database Syst Rev. 2003; (3): Cd004287. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12918009&dopt=Abstract
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Treatment of experimental adjuvant arthritis with the combination of methotrexate and lyophilized Enterococcus faecium enriched with organic selenium. Author(s): Rovensky J, Svik K, Stancikova M, Istok R, Ebringer L, Ferencik M. Source: Folia Microbiol (Praha). 2002; 47(5): 573-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12503406&dopt=Abstract
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Treatment of rheumatic arthritis with Jiang Chen pian in 114 cases. Author(s): Xia J, Zhu X, Feng B, Cao Z, Zhu J. Source: J Tradit Chin Med. 2002 September; 22(3): 178-9. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12400419&dopt=Abstract
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Treatment of rheumatoid arthritis with electromagnetic millimeter waves applied to acupuncture points--a randomized double blind clinical study. Author(s): Usichenko TI, Ivashkivsky OI, Gizhko VV.
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Source: Acupuncture & Electro-Therapeutics Research. 2003; 28(1-2): 11-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12934956&dopt=Abstract ·
Two configurations of static magnetic fields for treating rheumatoid arthritis of the knee: a double-blind clinical trial. Author(s): Segal NA, Toda Y, Huston J, Saeki Y, Shimizu M, Fuchs H, Shimaoka Y, Holcomb R, McLean MJ. Source: Archives of Physical Medicine and Rehabilitation. 2001 October; 82(10): 1453-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11588753&dopt=Abstract
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Update of ACR guidelines for osteoarthritis: role of the coxibs. Author(s): Schnitzer TJ; American College of Rheumatology. Source: Journal of Pain and Symptom Management. 2002 April; 23(4 Suppl): S24-30; Discussion S31-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11992747&dopt=Abstract
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Use of complementary and alternative medicine by arthritis patients in a university hospital clinic serving rheumatology patients in Korea. Author(s): Kim HA, Seo YI. Source: Rheumatology International. 2003 March 27 [epub Ahead of Print] http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12679879&dopt=Abstract
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Use of complementary and alternative medicine by older patients with arthritis: a population-based study. Author(s): Kaboli PJ, Doebbeling BN, Saag KG, Rosenthal GE. Source: Arthritis and Rheumatism. 2001 August; 45(4): 398-403. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11501729&dopt=Abstract
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Use of sand bathing for the treatment of arthritis and other conditions. Author(s): Dilixat Y, Aytulun S, Mayiram S, Arkin S, Ibadet R, Sekine M, Kagamimori S. Source: Alternative Therapies in Health and Medicine. 2001 November-December; 7(6): 24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11712469&dopt=Abstract
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Variation in perceptions of treatment and self-care practices in elderly with osteoarthritis: a comparison between African American and white patients. Author(s): Ibrahim SA, Siminoff LA, Burant CJ, Kwoh CK. Source: Arthritis and Rheumatism. 2001 August; 45(4): 340-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11501721&dopt=Abstract
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Vascular endothelial dysfunction associated with elevated serum homocysteine levels in rat adjuvant arthritis: effect of vitamin E administration. Author(s): Can C, Cinar MG, Kosay S, Evinc A.
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Source: Life Sciences. 2002 June 14; 71(4): 401-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12044840&dopt=Abstract ·
What a difference a year makes: reflections on the ACR recommendations for the medical management of osteoarthritis. Author(s): Hochberg MC. Source: Curr Rheumatol Rep. 2001 December; 3(6): 473-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11709108&dopt=Abstract
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Willow bark extract, a useful alternative for the treatment of osteoarthritis: comment on the editorial by Marcus and Suarez-Almazor. Author(s): Chrubasik S, Pollak S, Black A. Source: Arthritis and Rheumatism. 2003 January; 48(1): 278-80; Author Reply 280. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12528142&dopt=Abstract
Additional Web Resources A number of additional Web sites offer encyclopedic information covering CAM and related topics. The following is a representative sample: ·
Alternative Medicine Foundation, Inc.: http://www.herbmed.org/
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AOL: http://search.aol.com/cat.adp?id=169&layer=&from=subcats
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Chinese Medicine: http://www.newcenturynutrition.com/
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drkoop.comÒ: http://www.drkoop.com/InteractiveMedicine/IndexC.html
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Family Village: http://www.familyvillage.wisc.edu/med_altn.htm
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Google: http://directory.google.com/Top/Health/Alternative/
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Healthnotes: http://www.healthnotes.com/
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MedWebPlus: http://medwebplus.com/subject/Alternative_and_Complementary_Medicine
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Open Directory Project: http://dmoz.org/Health/Alternative/
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HealthGate: http://www.tnp.com/
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WebMDÒHealth: http://my.webmd.com/drugs_and_herbs
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WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,,00.html
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Yahoo.com: http://dir.yahoo.com/Health/Alternative_Medicine/
The following is a specific Web list relating to arthritis; please note that any particular subject below may indicate either a therapeutic use, or a contraindication (potential danger), and does not reflect an official recommendation (some Web sites are subscription based):
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General Overview Arthritis Source: Integrative Medicine Communications; www.drkoop.com Arthritis, OsteoSource: Integrative Medicine Communications; www.drkoop.com Arthritis, Rheumatoid Source: Integrative Medicine Communications; www.drkoop.com Osteoarthritis Source: Healthnotes, Inc. www.healthnotes.com Osteoarthritis Source: Integrative Medicine Communications; www.drkoop.com Osteoarthritis Source: Prima Communications, Inc.www.personalhealthzone.com Reiter's Syndrome Source: Integrative Medicine Communications; www.drkoop.com Rheumatoid Arthritis Source: Healthnotes, Inc. www.healthnotes.com Rheumatoid Arthritis Source: Integrative Medicine Communications; www.drkoop.com Rheumatoid Arthritis Source: Prima Communications, Inc.www.personalhealthzone.com
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Alternative Therapy Acupuncture Source: Integrative Medicine Communications; www.drkoop.com Acupuncture Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,663,00.html Alexander technique Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,665,00.html Apitherapy Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,669,00.html
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Aromatherapy Source: Healthnotes, Inc. www.healthnotes.com Ayurveda Source: Integrative Medicine Communications; www.drkoop.com Ayurveda Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,672,00.html Bach flower remedies Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,673,00.html Cell Therapy Source: Healthnotes, Inc. www.healthnotes.com Chelation Therapy Source: Healthnotes, Inc. www.healthnotes.com Chiropractic Source: Healthnotes, Inc. www.healthnotes.com Chiropractic Source: Integrative Medicine Communications; www.drkoop.com Chiropractic Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,681,00.html Dance therapy Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,687,00.html Detoxification Therapy Source: Healthnotes, Inc. www.healthnotes.com Detoxification therapy Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10119,00.html Fasting Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,694,00.html
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Feldenkrais Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,695,00.html Hellerwork Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,700,00.html Homeopathy Source: Integrative Medicine Communications; www.drkoop.com Homeopathy Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,703,00.html Homeovitics Alternative names: homoeovitics Source: The Canoe version of A Dictionary of Alternative-Medicine Methods, by Priorities for Health editor Jack Raso, M.S., R.D. Hyperlink: http://www.canoe.ca/AltmedDictionary/h.html Hydrotherapy Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,705,00.html Hypnotherapy Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,706,00.html Light therapy Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,713,00.html Macrobiotics Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,714,00.html Magnet therapy Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,715,00.html Massage Source: Integrative Medicine Communications; www.drkoop.com
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Massage therapy Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,716,00.html Myotherapy Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,931,00.html Naturopathy Source: Integrative Medicine Communications; www.drkoop.com Nutrition Source: Integrative Medicine Communications; www.drkoop.com Osteopathy Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,724,00.html Polarity therapy Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,727,00.html Qigong Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,729,00.html Reflexology Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,730,00.html Reiki Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,731,00.html Rolfing Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,732,00.html Shiatsu Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,733,00.html
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Tai Chi Source: Integrative Medicine Communications; www.drkoop.com Tai chi Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,737,00.html Therapeutic touch Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,739,00.html Traditional Chinese medicine Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10085,00.html Trager approach Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,741,00.html Writing therapy Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,745,00.html Yoga Source: Integrative Medicine Communications; www.drkoop.com Yoga Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,746,00.html ·
Chinese Medicine Baixianpi Alternative names: Densefruit Pittany Root-bark; Cortex Dictamni Source: Chinese Materia Medica Cang'erzi Alternative names: Siberian Cocklebur Fruit; Fructus Xanthii Source: Chinese Materia Medica Chixiaodou Alternative names: Rice Bean; Semen Phaseoli Source: Chinese Materia Medica
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Chuanwu Alternative names: Common Monkshood Mother Root; Radix Aconiti Source: Chinese Materia Medica Danshen Alternative names: Danshen Root; Radix Salviae Miltiorrhizae Source: Chinese Materia Medica Duhuo Alternative names: Doubleteeth Pubescent Angelica Root; Radix Angelicae Pubescentis Source: Chinese Materia Medica Duyi wei Pian Alternative names: Duyiwei Tablets; Duyi wei Pian (Du Yi Wei Pian) Source: Pharmacopoeia Commission of the Ministry of Health, People's Republic of China
Fangji Alternative names: Fourstamen Stephania Root; Radix Stephaniae Tetrandrae Source: Chinese Materia Medica Fengliaoxing Fengshi Dieda Yaojiu Alternative names: Fengliaoxing Fengshi Dieda Wine Source: Pharmacopoeia Commission of the Ministry of Health, People's Republic of China Fuzi Alternative names: Beivedere Fruit; Difuzi; Fructus Kochiae Source: Chinese Materia Medica Goupi Gao Alternative names: Goupi Plaster Source: Pharmacopoeia Commission of the Ministry of Health, People's Republic of China Guanmutong Alternative names: Manchurian Dutchmanspipe Stem; Caulis Aristolochiae Manshuriensis Source: Chinese Materia Medica Guogong Jiu Alternative names: Guogong Wine Source: Pharmacopoeia Commission of the Ministry of Health, People's Republic of China Haifengteng Alternative names: Kadsura Pepper Stem; Caulis Piperis Kadsurae Source: Chinese Materia Medica
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Hufeng Jiu Alternative names: Hufeng Wine Source: Pharmacopoeia Commission of the Ministry of Health, People's Republic of China Jinqian Baihuashe Alternative names: Coin-like White-banded Snake; Jinqian Baihuashe (Jin Qian Bai Hua She); Bungarus Parvus Source: Chinese Materia Medica Liangtoujian Alternative names: Radde Anemone Rhizome; Rhizoma Ahemones Daddeanae Source: Chinese Materia Medica Loulu Alternative names: Globethistle Root; Yuzhou loulu; Radix Echinopsis Source: Chinese Materia Medica Luoshiteng Alternative names: Chinese Starjasmine Stem; Caulis Trachelospermi Source: Chinese Materia Medica Maqianzi Alternative names: Nux Vomica; Semen Strychni Source: Chinese Materia Medica Mugua Alternative names: Common Floweringquince Fruit; Fructus Chaenomelis Source: Chinese Materia Medica Mugua Wan Alternative names: Mugua Pills Source: Pharmacopoeia Commission of the Ministry of Health, People's Republic of China Qiannianjian Alternative names: Obscured Homalomena Rhizome; Rhizoma Homalomenae Source: Chinese Materia Medica Qishe Alternative names: Long-noded Pit Viper; Qishe (Qi She); Agkistrodon Source: Chinese Materia Medica Quanxie Alternative names: Scorpion; Scorpio Source: Chinese Materia Medica Hyperlink: http://www.newcenturynutrition.com/
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Qufeng Shujin Wan Alternative names: Qufeng Shujin Pills Source: Pharmacopoeia Commission of the Ministry of Health, People's Republic of China Qufeng Zhitong Pian Alternative names: Qufeng Zhitong Tablets; Qufeng Zhitong Pian(Qu Feng Zhi Tong Pi An) Source: Pharmacopoeia Commission of the Ministry of Health, People's Republic of China Rendongteng Alternative names: Honeysuckle Stem; Caulis Lonicerae Source: Chinese Materia Medica Shexiang Alternative names: Musk; Moschus Source: Chinese Materia Medica Shufeng Dingtong Wan Alternative names: Shufeng Dingtong Pills; Shufeng Dingtong Wan(Shu Feng Ding Tong Wan) Source: Pharmacopoeia Commission of the Ministry of Health, People's Republic of China Shujin Huoluo Jiu Alternative names: Shujin Huoluo Wine; Shujin Huoluo Jiu(Shu Jin Huo Luo Jiu) Source: Pharmacopoeia Commission of the Ministry of Health, People's Republic of China Shujin Wan Alternative names: Qufeng Shujin Pills; Qufeng Shujin Wan Source: Pharmacopoeia Commission of the Ministry of Health, People's Republic of China Wushaoshe Alternative names: Black-tail Snake; Zaocys Source: Chinese Materia Medica Xiangjiapi Alternative names: Chinese Silkvine Root-bark; Cortex Periplocae Source: Chinese Materia Medica Xiatianwu Alternative names: Decumbent Corydalis Rhizome; Rhizoma Corydalis Decumbentis Source: Chinese Materia Medica Yiyiren Alternative names: Coix Seed; Semen Coicis Source: Chinese Materia Medica
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Homeopathy Aconitum napellus Source: Healthnotes, Inc. www.healthnotes.com Actaea racemosa Source: Healthnotes, Inc. www.healthnotes.com Apis mellifica Source: Healthnotes, Inc. www.healthnotes.com Arnica Source: Healthnotes, Inc. www.healthnotes.com Aurum metallicum Source: Healthnotes, Inc. www.healthnotes.com Belladonna Source: Healthnotes, Inc. www.healthnotes.com Bryonia Source: Healthnotes, Inc. www.healthnotes.com Calcarea carbonica Source: Healthnotes, Inc. www.healthnotes.com Calcarea fluorica Source: Healthnotes, Inc. www.healthnotes.com Calcarea phosphorica Source: Healthnotes, Inc. www.healthnotes.com Causticum Source: Healthnotes, Inc. www.healthnotes.com Cimicifuga Source: Healthnotes, Inc. www.healthnotes.com Dulcamara Source: Healthnotes, Inc. www.healthnotes.com Kali bichromicum Source: Healthnotes, Inc. www.healthnotes.com Kali carbonicum Source: Healthnotes, Inc. www.healthnotes.com Kalmia latifolia Source: Healthnotes, Inc. www.healthnotes.com
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Ledum palustre Source: Healthnotes, Inc. www.healthnotes.com Pulsatilla Source: Healthnotes, Inc. www.healthnotes.com Rhododendron Source: Healthnotes, Inc. www.healthnotes.com Rhus toxicodendron Source: Healthnotes, Inc. www.healthnotes.com Ruta graveolens Source: Healthnotes, Inc. www.healthnotes.com ·
Herbs and Supplements Acetaminophen Alternative names: Acephen, Aceta, Amaphen, Anoquan, Apacet, Arthritis Foundation Aspirin Free, Arthritis Foundation Nighttime, Aspirin Free Anacin, Aspirin Free Excedrin, Bayer Select, Dapacin, Dynafed, Endolor, Esgic, Excedrin P.M., Fem-Etts, Femcet, Feverall, Fioricet, Fiorpap, Genapap, Genebs, Halenol, Isocet, Liquiprin, Mapap, Maranox, Meda, Medigesic, Midol, Multi-Symptom Pamprin, Neopap, Nighttime Pamprin, Oraphen-PD, Panadol, Phrenilin, Repan, Ridenol, Sedapap, Silapap, Sominex Pain Relief, Tapanol, Tempra, Tylenol, Uni-Ace, Unisom with Pain Relief Source: Prima Communications, Inc.www.personalhealthzone.com Adrenal Extract Source: Healthnotes, Inc. www.healthnotes.com ALA Source: Integrative Medicine Communications; www.drkoop.com Alfalfa Alternative names: Medicago sativa Source: Healthnotes, Inc. www.healthnotes.com Alpha-Linolenic Acid (ALA) Source: Integrative Medicine Communications; www.drkoop.com Amino Acids Overview Source: Healthnotes, Inc. www.healthnotes.com Ananas comosus Source: Integrative Medicine Communications; www.drkoop.com Antimalarial Drugs Source: Healthnotes, Inc. www.healthnotes.com
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Antioxidants Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10004,00.html Apium graveolens Source: Integrative Medicine Communications; www.drkoop.com Arginine Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10005,00.html Arnica Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,753,00.html Ashwagandha Alternative names: Withania somniferum Source: Healthnotes, Inc. www.healthnotes.com Aspirin Source: Healthnotes, Inc. www.healthnotes.com Azathioprine Source: Healthnotes, Inc. www.healthnotes.com Barberry Alternative names: Berberis vulgaris, Berberry Source: Integrative Medicine Communications; www.drkoop.com Berberis Alternative names: Barberry; Berberis sp. Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Hyperlink: http://www.herbmed.org/ Berberis vulgaris Source: Integrative Medicine Communications; www.drkoop.com Berberry Source: Integrative Medicine Communications; www.drkoop.com Beta-Carotene Source: Prima Communications, Inc.www.personalhealthzone.com Black Cohosh Alternative names: Cimicifuga racemosa Source: Healthnotes, Inc. www.healthnotes.com
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Black Cohosh Source: Prima Communications, Inc.www.personalhealthzone.com BLACK COHOSH Source: The Canadian Internet Directory for Holistic Help, WellNet, Health and Wellness Network; www.wellnet.ca BLADDERWRACK Source: The Canadian Internet Directory for Holistic Help, WellNet, Health and Wellness Network; www.wellnet.ca Blue Cohosh Alternative names: Caulophyllum thalictroides Source: Healthnotes, Inc. www.healthnotes.com Boswellia Alternative names: Frankincense; Boswellia serrata Roxb. Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Hyperlink: http://www.herbmed.org/ Boswellia Alternative names: Boswellia serrata Source: Healthnotes, Inc. www.healthnotes.com Boswellia Source: Prima Communications, Inc.www.personalhealthzone.com Boswellia Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,759,00.html Bromelain Source: Healthnotes, Inc. www.healthnotes.com Bromelain Alternative names: Ananas comosus, Bromelainum Source: Integrative Medicine Communications; www.drkoop.com Bromelain Source: Prima Communications, Inc.www.personalhealthzone.com Bromelain Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,760,00.html Bromelainum Source: Integrative Medicine Communications; www.drkoop.com
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Bryonia Bryony Alternative names: Bryony; Bryonia sp. Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Hyperlink: http://www.herbmed.org/ Calciferol Source: Integrative Medicine Communications; www.drkoop.com Calcitrol Source: Integrative Medicine Communications; www.drkoop.com Capsaicin Source: Integrative Medicine Communications; www.drkoop.com Capsicum frutescens Source: Integrative Medicine Communications; www.drkoop.com Cartilage (Bovine and Shark) Source: Healthnotes, Inc. www.healthnotes.com Cat’s Claw Alternative names: Uncaria tomentosa Source: Healthnotes, Inc. www.healthnotes.com Cat's Claw Alternative names: Uncaria tomentosa Source: Integrative Medicine Communications; www.drkoop.com Cat's Claw Source: Prima Communications, Inc.www.personalhealthzone.com Cayenne Alternative names: Capsicum annuum, Capsicum frutescens Source: Healthnotes, Inc. www.healthnotes.com Cayenne Alternative names: Capsicum frutescens, Capsicum spp., Capsaicin, Chili Pepper, Red Pepper Source: Integrative Medicine Communications; www.drkoop.com Cayenne Source: Prima Communications, Inc.www.personalhealthzone.com Cayenne Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,765,00.html Celecoxib Source: Healthnotes, Inc. www.healthnotes.com
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Celery extract Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10014,00.html Celery Seed Alternative names: Apium graveolens Source: Integrative Medicine Communications; www.drkoop.com CELERY SEED Source: The Canadian Internet Directory for Holistic Help, WellNet, Health and Wellness Network; www.wellnet.ca Cetyl Myristoleate Source: Healthnotes, Inc. www.healthnotes.com Chamomile Source: Prima Communications, Inc.www.personalhealthzone.com Chaparral Alternative names: Larrea tridentata Source: Healthnotes, Inc. www.healthnotes.com Chemotherapy Source: Healthnotes, Inc. www.healthnotes.com Cherry fruit extract Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10015,00.html Chili Pepper Source: Integrative Medicine Communications; www.drkoop.com Chitosan Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10016,00.html Cholecalciferol Source: Integrative Medicine Communications; www.drkoop.com Chrysanthemum parthenium Source: Integrative Medicine Communications; www.drkoop.com Corticosteroids Source: Prima Communications, Inc.www.personalhealthzone.com Crataegus Alternative names: Hawthorn; Crataegus oxyacantha L. Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Hyperlink: http://www.herbmed.org/
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Curcuma Alternative names: Turmeric; Curcuma longa L. Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Hyperlink: http://www.herbmed.org/ Curcuma longa Source: Integrative Medicine Communications; www.drkoop.com Dandelion Source: Prima Communications, Inc.www.personalhealthzone.com Dehydroepiandrosterone (DHEA) Source: Healthnotes, Inc. www.healthnotes.com Dehydroepiandrosterone (DHEA) Source: Integrative Medicine Communications; www.drkoop.com Devil’s Claw Alternative names: Harpagophytum procumbens Source: Healthnotes, Inc. www.healthnotes.com Devil's Claw Alternative names: Harpagophytum procumbens, Harpagophytum zeyheri Source: Integrative Medicine Communications; www.drkoop.com Devil's Claw Source: Prima Communications, Inc.www.personalhealthzone.com DEVIL'S CLAW Source: The Canadian Internet Directory for Holistic Help, WellNet, Health and Wellness Network; www.wellnet.ca Devil's claw Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,970,00.html DHEA Source: Integrative Medicine Communications; www.drkoop.com DHEA (Dehydroepiandrosterone) Source: Prima Communications, Inc.www.personalhealthzone.com Diclofenac Source: Healthnotes, Inc. www.healthnotes.com Dioscorea villosa Source: Integrative Medicine Communications; www.drkoop.com
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DMSO Source: Healthnotes, Inc. www.healthnotes.com Docosahexaenoic Acid Source: Healthnotes, Inc. www.healthnotes.com Echinacea Alternative names: Echinacea angustifolia, Echinacea pallida, Echinacea purpurea, Purple Coneflower Source: Integrative Medicine Communications; www.drkoop.com Echinacea Source: Prima Communications, Inc.www.personalhealthzone.com Echinacea Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,775,00.html Echinacea angustifolia Source: Integrative Medicine Communications; www.drkoop.com Echinacea pallida Source: Integrative Medicine Communications; www.drkoop.com Echinacea purpurea Source: Integrative Medicine Communications; www.drkoop.com EDTA Source: Integrative Medicine Communications; www.drkoop.com Eicosapentaenoic Acid (EPA) Source: Integrative Medicine Communications; www.drkoop.com Elderberry Source: Prima Communications, Inc.www.personalhealthzone.com EPA Source: Integrative Medicine Communications; www.drkoop.com Equisetum arvense Source: Integrative Medicine Communications; www.drkoop.com Erocalciferol Source: Integrative Medicine Communications; www.drkoop.com Ethylenediaminetetraacetic Acid (EDTA) Source: Integrative Medicine Communications; www.drkoop.com Etodolac Source: Healthnotes, Inc. www.healthnotes.com
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Eucalyptus Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,778,00.html Evening Primrose Alternative names: Oenothera biennis, Sun Drop Source: Integrative Medicine Communications; www.drkoop.com Fenugreek Alternative names: Trigonella foenum-graecum Source: Healthnotes, Inc. www.healthnotes.com Feverfew Alternative names: Tanacetum parthenium, Chrysanthemum parthenium Source: Integrative Medicine Communications; www.drkoop.com Feverfew Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,780,00.html Flavonoids Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,782,00.html Flurbiprofen Source: Healthnotes, Inc. www.healthnotes.com Gamma-Linolenic Acid (GLA) Source: Integrative Medicine Communications; www.drkoop.com Ginger Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,787,00.html GLA (Gamma-Linolenic Acid) Source: Prima Communications, Inc.www.personalhealthzone.com Glucosamine Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,790,00.html Glutamine Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10030,00.html
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Glutathione Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,854,00.html Glycyrrhiza glabra Source: Integrative Medicine Communications; www.drkoop.com Goldenrod Alternative names: Solidago virgaurea Source: Integrative Medicine Communications; www.drkoop.com Green tea Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10032,00.html Green-Lipped Mussel Source: Healthnotes, Inc. www.healthnotes.com Guaraná Alternative names: Paullinia cupana Source: Healthnotes, Inc. www.healthnotes.com Guggul Source: Prima Communications, Inc.www.personalhealthzone.com Gugulipid Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10033,00.html Gymnema Alternative names: Gurmar; Gymnema sylvestre Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Hyperlink: http://www.herbmed.org/ Harpagophytum procumbens Source: Integrative Medicine Communications; www.drkoop.com Harpagophytum zeyheri Source: Integrative Medicine Communications; www.drkoop.com Herbal digestive formula Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10104,00.html Histidine Source: Healthnotes, Inc. www.healthnotes.com Histidine
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Source: Prima Communications, Inc.www.personalhealthzone.com Horse Chestnut Alternative names: Aesculus hippocastanum Source: Healthnotes, Inc. www.healthnotes.com Horseradish Alternative names: Cochlearia armoracia Source: Healthnotes, Inc. www.healthnotes.com Horsetail Alternative names: Equisetum arvense, Scouring Rush, Shave Grass Source: Integrative Medicine Communications; www.drkoop.com Hydroxychloroquine Source: Healthnotes, Inc. www.healthnotes.com Ibuprofen Source: Healthnotes, Inc. www.healthnotes.com Indomethacin Source: Healthnotes, Inc. www.healthnotes.com Inhalant, Systemic, and Topical Corticosteroids Source: Integrative Medicine Communications; www.drkoop.com Ivy Leaf Alternative names: Hedera helix Source: Healthnotes, Inc. www.healthnotes.com Juniper Berry Source: Prima Communications, Inc.www.personalhealthzone.com Kava Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,798,00.html Ketoprofen Source: Healthnotes, Inc. www.healthnotes.com Licorice Alternative names: Glycyrrhiza glabra, Spanish Licorice Source: Integrative Medicine Communications; www.drkoop.com Lipase Source: Integrative Medicine Communications; www.drkoop.com Lobelia Alternative names: Lobelia inflata L. Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Hyperlink: http://www.herbmed.org/
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Meadowsweet Alternative names: Filipendula ulmaria Source: Healthnotes, Inc. www.healthnotes.com Melatonin Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,804,00.html Methotrexate Alternative names: Rheumatrex Source: Prima Communications, Inc.www.personalhealthzone.com Methylsulfonylmethane Source: Healthnotes, Inc. www.healthnotes.com MSM Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,807,00.html Nabumetone Source: Healthnotes, Inc. www.healthnotes.com N-Acetyl-Glucosamine Source: Healthnotes, Inc. www.healthnotes.com Nettle Alternative names: Urtica dioica Source: Healthnotes, Inc. www.healthnotes.com Nettle Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10048,00.html Nonsteroidal Anti-inflammatory Drugs (NSAIDs) Source: Integrative Medicine Communications; www.drkoop.com Oenothera biennis Source: Integrative Medicine Communications; www.drkoop.com Oral Corticosteroids Source: Healthnotes, Inc. www.healthnotes.com Oregon Grape Alternative names: Berberis aquifolium Source: Healthnotes, Inc. www.healthnotes.com
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Oxaprozin Source: Healthnotes, Inc. www.healthnotes.com PABA Source: Healthnotes, Inc. www.healthnotes.com Penicillamine Alternative names: Cuprimine, Depen Source: Prima Communications, Inc.www.personalhealthzone.com Phenylalanine Source: Prima Communications, Inc.www.personalhealthzone.com Phosphorus Source: Integrative Medicine Communications; www.drkoop.com Phytolacca Alternative names: Poke root, Endod; Phytolacca dodecandra L. Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Hyperlink: http://www.herbmed.org/ Picrorhiza Alternative names: Picrorhiza kurroa Source: Healthnotes, Inc. www.healthnotes.com Piroxicam Source: Healthnotes, Inc. www.healthnotes.com Pollen Source: Healthnotes, Inc. www.healthnotes.com Pregnenolone Source: Prima Communications, Inc.www.personalhealthzone.com Proteolytic Enzymes Source: Prima Communications, Inc.www.personalhealthzone.com Purple Coneflower Source: Integrative Medicine Communications; www.drkoop.com Red Pepper Source: Integrative Medicine Communications; www.drkoop.com Ribes Alternative names: Black Currant; Ribes nigrum L. Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Hyperlink: http://www.herbmed.org/ Rofecoxib Source: Healthnotes, Inc. www.healthnotes.com
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Rosemary Alternative names: Rosmarinus officinalis Source: Healthnotes, Inc. www.healthnotes.com S-Adenosylmethionine (SAMe) Source: Integrative Medicine Communications; www.drkoop.com Salicylates Source: Integrative Medicine Communications; www.drkoop.com Salsalate Source: Healthnotes, Inc. www.healthnotes.com SAMe (S-adenosylmethionine) Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,818,00.html Sarsaparilla Source: The Canadian Internet Directory for Holistic Help, WellNet, Health and Wellness Network; www.wellnet.ca Scouring Rush Source: Integrative Medicine Communications; www.drkoop.com Shark Cartilage Source: Integrative Medicine Communications; www.drkoop.com Shave Grass Source: Integrative Medicine Communications; www.drkoop.com Siberian ginseng Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,821,00.html Solidago virgaurea Source: Integrative Medicine Communications; www.drkoop.com Spanish Licorice Source: Integrative Medicine Communications; www.drkoop.com Spirulina and kelp Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10058,00.html Sulfasalazine Source: Healthnotes, Inc. www.healthnotes.com
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Sulindac Source: Healthnotes, Inc. www.healthnotes.com Sun Drop Source: Integrative Medicine Communications; www.drkoop.com Symphytum Alternative names: Comfrey; Symphytum officinale L. Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Hyperlink: http://www.herbmed.org/ Tanacetum Alternative names: Feverfew; Tanacetum parthenium (L.) Schultz-Bip. Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Hyperlink: http://www.herbmed.org/ Tanacetum parthenium Source: Integrative Medicine Communications; www.drkoop.com Terminalia Alternative names: Myrobalans; Terminalia arjuna Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Hyperlink: http://www.herbmed.org/ Trigonella Alternative names: Fenugreek; Trigonella foenum graecum L. Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Hyperlink: http://www.herbmed.org/ Turmeric Alternative names: Curcuma longa Source: Integrative Medicine Communications; www.drkoop.com Turmeric Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10062,00.html Uncaria tomentosa Source: Integrative Medicine Communications; www.drkoop.com Urtica dioica Alternative names: Stinging Nettle Source: Integrative Medicine Communications; www.drkoop.com Urtica urens Alternative names: Stinging Nettle Source: Integrative Medicine Communications; www.drkoop.com
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Verbascum Alternative names: Mullein; Verbascum thapsus L. Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Hyperlink: http://www.herbmed.org/ White Willow Source: Prima Communications, Inc.www.personalhealthzone.com White willow bark Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10069,00.html Wild yam Alternative names: Dioscorea villosa Source: Integrative Medicine Communications; www.drkoop.com Willow Alternative names: Salix alba Source: Healthnotes, Inc. www.healthnotes.com Willow Bark Alternative names: There are several species of willow includingSalix alba, Salix nigra, Salix fragilis, Salix purpurea, Salix babylonica, White Willow, European Willow, Black Willow, Pussy Willow, Crack Willow, Purple Willow, Weeping Willow, Liu-zhi Source: Integrative Medicine Communications; www.drkoop.com Withania Ashwagandha Alternative names: Ashwagandha; Withania somnifera L. Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Hyperlink: http://www.herbmed.org/ Yucca Alternative names: Yucca schidigera , Yucca spp. Source: Healthnotes, Inc. www.healthnotes.com Zanthoxylum Alternative names: Prickly Ash; Zanthoxylum sp. Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Hyperlink: http://www.herbmed.org/ Zingiber Alternative names: Ginger; Zingiber officinale Roscoe Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Hyperlink: http://www.herbmed.org/
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Zingiber officinale Source: Integrative Medicine Communications; www.drkoop.com
General References A good place to find general background information on CAM is the National Library of Medicine. It has prepared within the MEDLINEplus system an information topic page dedicated to complementary and alternative medicine. To access this page, go to the MEDLINEplus site at http://www.nlm.nih.gov/medlineplus/alternativemedicine.html. This Web site provides a general overview of various topics and can lead to a number of general sources.
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CHAPTER 4. DISSERTATIONS ON ARTHRITIS Overview In this chapter, we will give you a bibliography on recent dissertations relating to arthritis. We will also provide you with information on how to use the Internet to stay current on dissertations. IMPORTANT NOTE: When following the search strategy described below, you may discover non-medical dissertations that use the generic term “arthritis” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on arthritis, we have not necessarily excluded non-medical dissertations in this bibliography.
Dissertations on Arthritis ProQuest Digital Dissertations, the largest archive of academic dissertations available, is located at the following Web address: http://wwwlib.umi.com/dissertations. From this archive, we have compiled the following list covering dissertations devoted to arthritis. You will see that the information provided includes the dissertation’s title, its author, and the institution with which the author is associated. The following covers recent dissertations found when using this search procedure: ·
A Comparison of the Effects of Isometric and Isokinetic Training on Muscle Fibre Size and Strength in Women with Rheumatoid Arthritis by Wessel, Jean; Phd from University of Alberta (canada), 1983 http://wwwlib.umi.com/dissertations/fullcit/NK63989
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A Cross-cultural Comparison of Pain Description in Children with Polyarticular Juvenile Rheumatoid Arthritis in the United States and in Egypt by Von Weiss, Renee Terese; Phd from University of Kansas, 2002, 140 pages http://wwwlib.umi.com/dissertations/fullcit/3083203
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A Psychosocial Model for the Impact of Rheumatoid Arthritis on Well-being by Wilkins, Kendra E. Phd from Wayne State University, 1999, 162 pages http://wwwlib.umi.com/dissertations/fullcit/9954575
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A Vocational Outcome Study of Vocational Rehabilitation Clients with Arthritis by Cusick, Gary Matthew, Phd from The University of Wisconsin - Madison, 1990, 116 pages http://wwwlib.umi.com/dissertations/fullcit/9025708
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An Investigation of Oral History Narrative and Content Analysis Technique for Community Field Work in Rehabilitation Focusing upon Females with Rheumatoid Arthritis by Sirmons, Martha Ruddon, Edd from Auburn University, 1985, 166 pages http://wwwlib.umi.com/dissertations/fullcit/8518414
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Appraisal and Coping in Older Persons with Osteoarthritis by Regan, Catherine A., Phd from Stanford University, 1990, 178 pages http://wwwlib.umi.com/dissertations/fullcit/9017917
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Arthritis Patients Information Needs and Barriers: Analysis of Psycho-social Factors Affecting Flow of Medical Information to Patients (psychosocial Factors) by Molaparast Vali, Firoozeh, Phd from University of Pittsburgh, 1990, 270 pages http://wwwlib.umi.com/dissertations/fullcit/9120476
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Arthritis Self-care Strategies of Older African-americans: a Qualitative Study by Gershanok, Deborah E. Valins, Phd from University of Pittsburgh, 1996, 145 pages http://wwwlib.umi.com/dissertations/fullcit/9718652
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Arthritis Self-management: a Joint Venture. a Multiple Outcome Patient Education Evaluation by Lorig, Kate R., Drph from University of California, Berkeley, 1980, 485 pages http://wwwlib.umi.com/dissertations/fullcit/8112934
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Chemistry of Gold Complexes Related to Anti-arthritis Drugs by Turner, Mary Alice; Phd from Mcmaster University (canada), 1988 http://wwwlib.umi.com/dissertations/fullcit/NL50273
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Comparison of the Walking Performance at Two Different Speeds in Adolescents with and without Juvenile Arthritis Using a Dual-task Method by Stiskal-galisewski, Doreen Marie; Phd from Seton Hall University, College of Education and Human Services, 2003, 141 pages http://wwwlib.umi.com/dissertations/fullcit/3081031
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Connective Tissue Adaptation and Changes in Functional Ability of Individuals with Osteoarthritis of the Knee in Response to an Exercise Program by Bautch, Judith Catherine, Phd from The University of Wisconsin - Madison, 1992, 126 pages http://wwwlib.umi.com/dissertations/fullcit/9224140
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Coping with Arthritis: a Descriptive Study of Adaptation to Chronic Illness (roleadjustment, Qualitative Research, Decision-making, Social Identity, Disability) by Shea, Carole A., Phd from Rutgers the State University of New Jersey - New Brunswick, 1986, 436 pages http://wwwlib.umi.com/dissertations/fullcit/8620079
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Correlates of Health Perceptions among Individuals with Rheumatoid Arthritis by Guccione, Andrew Anthony, Phd from Boston University, 1988, 174 pages http://wwwlib.umi.com/dissertations/fullcit/8813637
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Determinants of Participation in an Arthritis Self-management Program by Rankin, James Alexander, Phd from University of Calgary (canada), 1998, 194 pages http://wwwlib.umi.com/dissertations/fullcit/NQ34696
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Determinants of Physical Activity in Older Women with Rheumatoid Arthritis by Semanik, Pamela A. Phd from University of Illinois at Chicago, Health Sciences Center, 2002, 204 pages http://wwwlib.umi.com/dissertations/fullcit/3058240
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Development of a Measure of Investigativeness, and Its Role in Women's Adaptation to Rheumatoid Arthritis by Vagi, Anne Barbara; Phd from University of Waterloo (canada), 1984 http://wwwlib.umi.com/dissertations/fullcit/NK66425
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Development of an Instrument to Measure Barriers to Arthritis Pain Management in Older Adults by Hiemenz, Melinda Lee; Phd from Texas Woman's University, 2002, 302 pages http://wwwlib.umi.com/dissertations/fullcit/3046308
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Economic Approaches to the Problem of Acceptable Clinical Risks: the Case of Prescription Drugs and Chronic Rheumatic Disease (clinical Risk, Rheumatoid Arthritis) by O'brien, Bernie J., Phd from Brunel University (united Kingdom), 1990, 385 pages http://wwwlib.umi.com/dissertations/fullcit/DX92575
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Evaluation of the People with Arthritis Can Exercise Program (pace) Using Three Approaches: Physiological, Clinical, and Subjective (arthritis, Exercise) by Ober, Kathleen Mary, Phd from University of Oregon, 1992, 161 pages http://wwwlib.umi.com/dissertations/fullcit/9238947
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Exercise Maintenance Behavior of Subjects with Arthritis Following Participation in a Supervised Exercise Program by Minor, Marian A., Phd from University of Missouri Columbia, 1989, 214 pages http://wwwlib.umi.com/dissertations/fullcit/8925308
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Exploring the Lived Experience of Female Adolescents with Juvenile Rheumatoid Arthritis: a Model of Human Occupation Perspective by Tommasulo, Jeanmarie F. Ms from D'youville College, 2002, 109 pages http://wwwlib.umi.com/dissertations/fullcit/1409942
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Exploring the Lived Experience of Women with Rheumatoid Arthritis: a Model of Human Occupation Perspective by Gee, Bryan Mark; Ms from D'youville College, 2002, 168 pages http://wwwlib.umi.com/dissertations/fullcit/1409937
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Family Adaptability, Cohesion and Conflict in Families with Rheumatoid Arthritis, Chronic Pain and Depression by Caldwell, Karen Leigh, Phd from Virginia Polytechnic Institute and State University, 1988, 106 pages http://wwwlib.umi.com/dissertations/fullcit/8910943
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From Social Theory to Social Policy: Social Class and the Epidemiology of Disability: a Case Study among Persons with Rheumatoid Arthritis. by Yelin, Edward Harris, Phd from University of California, Berkeley, 1979, 280 pages http://wwwlib.umi.com/dissertations/fullcit/8000583
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Gender Differences in Health Care Utilization by Individuals with Self-reported Arthritis or Rheumatism: Analysis of the 1990 Ontario Health Survey by Kasman, Naomi Michelle; Msc from University of Toronto (canada), 2002, 105 pages http://wwwlib.umi.com/dissertations/fullcit/MQ68671
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Gender, Class and the Illness Experience of Rheumatoid Arthritis by Fifield, Judith Anne, Phd from The University of Connecticut, 1990, 158 pages http://wwwlib.umi.com/dissertations/fullcit/9110414
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Gold in Rheumatoid Arthritis : Its Effect on Plasma Cortisol and Its Deposition in Skin by Jeffery, Dorothy A; Phd from University of Alberta (canada), 1974 http://wwwlib.umi.com/dissertations/fullcit/NK21856
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Holistic Fatherhood: a Grounded Theory Approach to Understanding Fathers of Children with Juvenile Rheumatoid Arthritis (jra) by Mcneill, Harold Edwin (ted); Phd from University of Toronto (canada), 2001, 312 pages http://wwwlib.umi.com/dissertations/fullcit/NQ63799
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Illness Management and Maintenance of Self-concept among Older Adults with Arthritis by Brown, Jane Amanda; Phd from Case Western Reserve University, 2003, 373 pages http://wwwlib.umi.com/dissertations/fullcit/3086235
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Immunity to Homologous Collagens and Cartilage Proteoglycans in Rabbits with Experimental Arthritis by Champion, Brian Robert; Phd from Mcgill University (canada), 1981 http://wwwlib.umi.com/dissertations/fullcit/NK58053
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Impact of a Supervised Walking and Education Program on Functional Status: Results from a Randomized Controlled Trial in Patients with Osteoarthritis of the Knee by Kovar, Pamela Ann, Edd from Columbia University Teachers College, 1991, 229 pages http://wwwlib.umi.com/dissertations/fullcit/9136404
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Impact of Anti-inflammatory Medications, Methotrexate, and Steroidal Medications on Psychosocial Functioning and Medical Status in Juvenile Rheumatoid Arthritis Patients by Ryser, Christina Nicole; Phd from The University of Texas Southwestern Medical Center at Dallas, 2002 http://wwwlib.umi.com/dissertations/fullcit/f774577
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Interpersonal Expectations and Psychosocial Adjustment to Chronic Illness: Reducing Discrepancies among Persons with Rheumatoid Arthritis by Thompson, Shawn Norvell; Phd from State University of New York at Stony Brook, 2002, 87 pages http://wwwlib.umi.com/dissertations/fullcit/3067559
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Juvenile Rheumatoid Arthritis: a Psychosocial Assessment of Adolescent Females and Their Mothers (pediatric Chronic Illness, Coping Models, Family Systems) by Baird, Sally Felgenhauer, Phd from University of Washington, 1986, 141 pages http://wwwlib.umi.com/dissertations/fullcit/8613135
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Juvenile Rheumatoid Arthritis: Implications for Nursing Education (childhood Illness) by Dressler, Mary Buckley, Edd from Temple University, 1992, 158 pages http://wwwlib.umi.com/dissertations/fullcit/9227454
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Life Stress and Emotional Regulation Strategies during a Personal Disclosure Task: Health Implications for Patients with Rheumatoid Arthritis by Meyer, Tina Marie; Phd from Wayne State University, 2003, 139 pages http://wwwlib.umi.com/dissertations/fullcit/3086453
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Locus of Control Beliefs, Controllability and Adjustment to Chronic Illness Arthritis and Diabetes by Ryan, David Patrick; Phd from York University (canada), 1986 http://wwwlib.umi.com/dissertations/fullcit/NL30945
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·
Lymphocytes and Rheumatoid Arthritis by Mandeville, Robert Parnell; Phd from Memorial University of Newfoundland (canada), 1979 http://wwwlib.umi.com/dissertations/fullcit/NK46760
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Measuring Subjective Well-being in Daily Life in Arthritis, Heart Disease, and Chronic Pain (health, Quality of Life) by Marnell, Margaret Esther, Phd from Stanford University, 1987, 277 pages http://wwwlib.umi.com/dissertations/fullcit/8707699
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Measuring the Family Helper Costs of Disabling Osteoarthritis of the Hip or Knee in Older Persons (arthritis, Cost Analysis) by Werkner, Janet Elaine, Phd from Case Western Reserve University, 1990, 287 pages http://wwwlib.umi.com/dissertations/fullcit/9035315
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More Than Medicine: the Meaning of Arthritis among Middle Class Americans by Mckenna, Margaret Ann, Phd from University of Washington, 1989, 389 pages http://wwwlib.umi.com/dissertations/fullcit/9000279
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Negative Mood Regulation Expectancies, Depression, Coping, and Self-efficacy in Arthritis Patients by Vernoy, Katharine Thomas; Ms from California State University, Fullerton, 2003, 66 pages http://wwwlib.umi.com/dissertations/fullcit/1411676
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Nutritional Status of Postmenopausal Women with and without Rheumatoid Arthritis by Woolf, Kathleen; Phd from Arizona State University, 2002, 158 pages http://wwwlib.umi.com/dissertations/fullcit/3057423
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Pain Measurement in Rheumatoid Arthritis: Applications of a Behavioral Approach (arthritis) by Buescher, Keith Lee, Phd from University of Missouri - Columbia, 1989, 178 pages http://wwwlib.umi.com/dissertations/fullcit/9010541
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Part I: Hexosaminidase Inhibitors As New Drug Candidates for the Therapy of Osteoarthritis. Part Ii: Dera-catalyzed Asymmetric Synthesis of Novel Pyranose Synthons As a New Entry to Heterocycles and Epothilones by Liu, Junjie; Phd from The Scripps Research Institute, 2002, 228 pages http://wwwlib.umi.com/dissertations/fullcit/3045858
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Piroxicam in Healthy Adults and Rheumatoid Arthritis Patients Disposition Kinetics and Clinical Effects by Richardson, Corrie Jane; Phd from The University of Saskatchewan (canada), 1986 http://wwwlib.umi.com/dissertations/fullcit/NL29256
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Predictive Relationships among Perceived Stress, Possible Selves, and Physical Activity in Elderly Individuals with Knee Osteoarthritis by Guinan, Diane Marie, Phd from The University of North Carolina at Greensboro, 1997, 171 pages http://wwwlib.umi.com/dissertations/fullcit/9730000
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Relationships between Coping Beliefs, Coping Practices, and Coping Resources and the Quality of Life in Rheumatoid Arthritis Patients (arthritis) by Strong, Thomas Irvin, Phd from University of Alberta (canada), 1990, 243 pages http://wwwlib.umi.com/dissertations/fullcit/NN64859
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Shaping the Illness: Living with Osteoarthritis by Grabowski, Regina Marie; Dnsc from Rush University, College of Nursing, 2002, 123 pages http://wwwlib.umi.com/dissertations/fullcit/3068074
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Social and Psychological Well-being, Pain, Functional Ability, and Choice of Coping Strategies in Patients with Rheumatoid Arthritis (counseling, Health) by Morgan, Cynthia Gray, Phd from University of California, Los Angeles, 1985, 362 pages http://wwwlib.umi.com/dissertations/fullcit/8603974
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Sociocultural Aspects of Arthritis from the Mississippi Choctaw Perspective by Sepulvado, Donald Lester, Phd from The Catholic University of America, 1983, 207 pages http://wwwlib.umi.com/dissertations/fullcit/8314882
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Sociocultural Determinants of Illness Behavior: the Treatment Strategies of Arthritis Sufferers (australia) by Gray, Dennis Arthur, Phd from University of Hawaii, 1982, 368 pages http://wwwlib.umi.com/dissertations/fullcit/8313526
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Socioeconomic Influences on the Disease Experience, Medical Care, and Preventive Behaviors of Elderly Persons with Osteoarthritis by Dexter, Phyllis A., Phd from Indiana University, 1991, 196 pages http://wwwlib.umi.com/dissertations/fullcit/9134802
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Socio-psychological Factors in Rheumatoid Arthritis by Steffenhagen, Ronald Albert, Phd from State University of New York at Buffalo, 1966, 142 pages http://wwwlib.umi.com/dissertations/fullcit/6607988
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Systematic Procedures for Parents of Children with Arthritis: a Guide to Emotional Growth. by Ziebell, Elizabeth Anne, Phd from The University of Arizona, 1976, 180 pages http://wwwlib.umi.com/dissertations/fullcit/7619727
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The Effect of an Individualized Instruction Program on the Education of Outpatients with Rheumatoid Arthritis by Neuberger, Geri Budesheim, Edd from University of Kansas, 1983, 108 pages http://wwwlib.umi.com/dissertations/fullcit/8403597
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The Effect of Arthritis on Work Behavior (disability, Labor Supply, Diseases, Costs of Poor Health) by Mitchell, Jean Marie, Phd from Vanderbilt University, 1986, 160 pages http://wwwlib.umi.com/dissertations/fullcit/8616366
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The Effect of Yoga and Relaxation Techniques on Outcome Variables Associated with Osteoarthritis of the Hands and Finger Joints (pain Control, Arthritis Therapy) by Garfinkel, Marian S., Edd from Temple University, 1992, 173 pages http://wwwlib.umi.com/dissertations/fullcit/9227466
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The Effects of Expressive Release Therapy upon the Physical and Psychological Wellbeing of Rheumatoid Arthritis Patients by Engle, David Eugene, Phd from The University of Arizona, 1985, 178 pages http://wwwlib.umi.com/dissertations/fullcit/8517495
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The Effects of Music and Music Vibration Using the Mvt(tm) on the Relief of Rheumatoid Arthritis Pain by Chesky, Kris S., Phd from University of North Texas, 1992, 142 pages http://wwwlib.umi.com/dissertations/fullcit/9300593
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The Effects of Neuromuscular Electrical Stimulation on Chronic Knee Pain and Functional Performance in Older Adults with Osteoarthritis of the Knee by Gaines, Jean M. Phd from The Johns Hopkins University, 2002, 269 pages http://wwwlib.umi.com/dissertations/fullcit/3028271
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The Experience of Rheumatoid Arthritis by Hovanec, Margret Anne, Phd from University of Toronto (canada), 1981 http://wwwlib.umi.com/dissertations/fullcit/f468806
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The Experience of Rheumatoid Arthritis by Hovanec, Margret; Phd from University of Toronto (canada), 1981 http://wwwlib.umi.com/dissertations/fullcit/NK50276
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The Functional Characterization of in Vivo Activated Interleukin-2 Responsive T Cells in Rheumatoid Arthritis by Cell Cloning Techniques by Ofosu-appiah, William A; Phd from The University of Manitoba (canada), 1988 http://wwwlib.umi.com/dissertations/fullcit/NL47924
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The Relationship between Antibody Response to Caprine Arthritis-encephalitis Virus Surface Protein and the Development of Viral-induced Arthritis by Snekvik, Kevin Roy; Phd from Washington State University, 2002, 64 pages http://wwwlib.umi.com/dissertations/fullcit/3086317
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The Relationship between Pain Responsiveness and Disease Activity in Fibrositis and Rheumatoid Arthritis by Scudds, Roger A; Phd from The University of Western Ontario (canada), 1990 http://wwwlib.umi.com/dissertations/fullcit/NL55283
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The Role of Inflammatory Cytokines in Rheumatoid Arthritis: Comparison to Allergic Diseases by Schuerwegh, Annemie Johanna; Phd from Universitaire Instelling Antwerpen (belgium), 2002, 214 pages http://wwwlib.umi.com/dissertations/fullcit/3066152
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Toward an Understanding of the Experience of Members of a Self-help Group (arthritis, Group Interaction) by Parker, Elizabeth, Edd from University of Toronto (canada), 1991, 172 pages http://wwwlib.umi.com/dissertations/fullcit/NN69386
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Tumor Necrosis Factor Receptor Gene Therapy Influences Humoral and Cellular Immune Responses in Collagen Induced Arthritis by Mukherjee, Paramita; Phd from Wayne State University, 2003, 177 pages http://wwwlib.umi.com/dissertations/fullcit/3086457
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Variations in Compliance with Medical Regimens and Utilization of Medical Services among Patients with Rheumatoid Arthritis by Kasteler, Josephine Mix, Phd from The University of Utah, 1970, 140 pages http://wwwlib.umi.com/dissertations/fullcit/7023079
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Vulnerability and Resilience As Predictors of Pain and Affect in Women with Arthritis by Smith, Bruce Walter; Phd from Arizona State University, 2002, 126 pages http://wwwlib.umi.com/dissertations/fullcit/3045667
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Why Does Formal Education Predict Mortality? an Evaluation of Mediational Processes (rheumatoid Arthritis, Education Level, Learned Helplessness) by Callahan, Leigh Fleming, Phd from Vanderbilt University, 1992, 150 pages http://wwwlib.umi.com/dissertations/fullcit/9315805
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Women with Rheumatoid Arthritis: a Qualitative Investigation of Personality and Coping Methods (arthritis) by Thompson, Linda V., Phd from Arizona State University, 1993, 245 pages http://wwwlib.umi.com/dissertations/fullcit/9320665
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Keeping Current Ask the medical librarian at your library if it has full and unlimited access to the ProQuest Digital Dissertations database. From the library, you should be able to do more complete searches via http://wwwlib.umi.com/dissertations.
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CHAPTER 5. CLINICAL TRIALS AND ARTHRITIS Overview In this chapter, we will show you how to keep informed of the latest clinical trials concerning arthritis.
Recent Trials on Arthritis The following is a list of recent trials dedicated to arthritis.8 Further information on a trial is available at the Web site indicated. ·
A Multicenter Study of the Safety of Human Anti-TNF Monoclonal Antibody D2E7 in Subjects with Active Rheumatoid Arthritis Condition(s): Rheumatoid Arthritis Study Status: This study is currently recruiting patients. Sponsor(s): Abbott Laboratories Purpose - Excerpt: Purpose of the study is to evaluate safety by collecting serious adverse events in subjects with moderately to severely active rheumatoid arthritis who are unable to obtain etanercept and who have failed one or more prior DMARDs. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00049751
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A Multicenter, Randomized, Double-Blind, Placebo-Controlled Study of the Safety, Efficacy, and Pharmacokinetics of the Human Anti-TNF Monoclonal Antibody Adalimumab in Children With Polyarticular Juvenile Rheumatoid Arthritis Condition(s): Arthritis, Juvenile Rheumatoid Study Status: This study is currently recruiting patients. Sponsor(s): Abbott Laboratories
8
These are listed at www.ClinicalTrials.gov.
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Purpose - Excerpt: This is a multicenter, Phase III randomized, placebo-controlled study in which polyarticular JRA subjects who are either MTX treated or non-MTX treated will initially receive Adalimumab by subcutaneous injection every other week for a fourmonth open-label lead-in period. Subjects who respond to the open-label therapy will then be rolled over into the double-blind portion of the study and will be randomized to receive either adalimumab or placebo for an additional 32 weeks or until flare of disease, whichever is earlier. Subjects who experience disease flare during the doubleblind portion of the study or subjects who complete 48 weeks of the study will be given the option to receive open-label treatment with adalimumab for an additional 44 weeks. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00048542 ·
A Phase 2 open-label clinical study using intravenous Paxceed(tm) to treat patients with rheumatoid arthritis Condition(s): Rheumatoid Arthritis Study Status: This study is currently recruiting patients. Sponsor(s): Angiotech Pharmaceuticals Purpose - Excerpt: Paxceed(tm) is being developed by Angiotech Pharmaceuticals, Inc. for the treatment of Rheumatoid arthritis (RA). The main objective of this study is to determine the effectiveness of treatment with Paxceed(tm) in patients with RA. In RA, there is an increase in cell growth and changes in cell function. The active substance in Paxceed(tm), paclitaxel, has undergone clinical studies as a cancer chemotherapeutic agent and has demonstrated its usefulness as an agent that stops growth of cells and blocks certain types of cell function associated with RA. Because of these effects, it is thought that Paxceed(tm) might alter the destructive course of RA. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00055133
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Clinically Important Changes in Rheumatoid Arthritis Condition(s): Rheumatoid Arthritis Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Purpose - Excerpt: This study will explore how patients with rheumatoid arthritis evaluate, or rate, symptom improvements. Physicians generally evaluate patients' health and treatment benefits based on laboratory measures, such as the number of tender or swollen joints, duration of morning stiffness, grip strength, pain severity and others. Less attention is given to whether these treatment results are meaningful to patients. This study will examine how much of an improvement in pain, stiffness, function, and other symptoms is needed before patients consider the change an important improvement. Patients 18 years of age or older who were diagnosed with rheumatoid
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arthritis after age 16 and who have active arthritis (6 or more tender joints) may be eligible for this study. Of particular interest are patients beginning treatment with prednisone, methotrexate, leflunomide, infliximab, or etanercept, although patients receiving any type of treatment may be included. Participants will be evaluated twice at the NIH Clinical Center, once at the start of the study and again at either 1 month or 4 months later, depending on the individual's treatment regimen. Permission will also be requested to review patients' medical records for results of previous blood tests and xrays. At each NIH visit, patients will undergo the following tests and procedures: Medical history and physical examination, including evaluation of joint swelling and tenderness; - Questionnaires about rheumatoid arthritis symptoms; - Computer-based exercise to assess preferences for various state-of-health choices; - Grip strength test; Walking test on level ground, with or without the use of a cane or walker; - Blood test to measure inflammation. At the second visit, in addition to the above procedures, participants will complete a questionnaire to rate the importance of changes, if any, in pain, morning stiffness, fatigue, joint swelling, functioning, worry, depression, and overall impressions, since the first visit. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00056602 ·
Coping Skills Training for Early Rheumatoid Arthritis Condition(s): Rheumatoid Arthritis Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Purpose - Excerpt: Rheumatoid arthritis (RA) is the most common inflammatory arthritis and a major health problem. Medical treatments are now being used much earlier in the course of RA, but these treatments do not address the challenges of coping with the early stages of this disease. This study will determine whether a comprehensive coping skills training program can decrease pain, psychological disability, and physical disability in patients with early RA. Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00056394
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Efficacy & Safety of an Investigational Drug + Methotrexate Compared to Methotrexate Alone in Patients with Rheumatoid Arthritis Condition(s): Rheumatoid Arthritis Study Status: This study is currently recruiting patients. Sponsor(s): (Sponsor Name Pending) Purpose - Excerpt: The purpose of this study is to help researchers confirm that an investigational drug given subcutaneously (injection given under the skin), once every 4 weeks, is an effective and safe treatment for rheumatoid arthritis in patients who are already taking methotrexate. Patients will be in this study for approximately 6 months and will need to attend the doctor's clinic on up to 12 occasions during that time. They will have a 50% chance of receiving the investigational drug and a 50% chance of
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receiving placebo in addition to their methotrexate. Prior to entry into this study patients will need to undergo chest x-ray and ECG (heart trace). Blood and urine tests, as well as arthritis assessments will be carried out regularly throughout the study, and patients will be required to complete health questionnaires at most clinic visits. Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00048178 ·
ENBREL(R) (etanercept) as Treatment for Children with Systemic Onset Juvenile Rheumatoid Arthritis Condition(s): Juvenile Rheumatoid Arthritis Study Status: This study is currently recruiting patients. Sponsor(s): Immunex Corporation Purpose - Excerpt: Rationale: etanercept inhibits the effects of tumor necrosis factor, which plays an important role in the progression of rheumatoid arthritis. A study of children with polyarticular course juvenile rheumatoid arthritis showed that Enbrel had efficacy and was generally well tolerated in children ages 4-17 who had moderately to severely active disease and who failed treatment with one or more disease modifying antiarthritic drugs. The children in the study may have had arthritis onset of pauciarticular, polyarticular, or systemic nature. Systemic onset juvenile rheumatoid arthritis (SOJRA) may result in approximately one-third of patients having significant long-term disability. Purpose: the Phase 4 study is designed to further define the safety and efficacy of etanercept in those children with SOJRA. Phase(s): Phase IV Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00039949
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ENBREL(R) (Etanercept) Safety Study in Children with Juvenile Rheumatoid Arthritis Condition(s): Arthritis, Juvenile Rheumatoid Study Status: This study is currently recruiting patients. Sponsor(s): Immunex Corporation Purpose - Excerpt: This Phase 4 open-label, nonrandomized multicenter registry study is being conducted to evaluate the long-term safety of ENBREL(R) (etanercept) compared to methotrexate in patients aged 2 to 18 years with polyarticular-course or systemiconset juvenile rheumatoid arthritis (JRA). Patients will be evaluated for a total of 3 years. The registry will include patients who have recently started and are currently receiving ENBREL alone, ENBREL in combination with methotrexate or other diseasemodifying antirheumatic drugs (DMARDs), methotrexate alone, or methotrexate in combination with other DMARDs. Approximately 600 patients will be enrolled at sites in the United States and Canada, with 400 patients receiving ENBREL and 200 receiving methotrexate without ENBREL. One group of patients will receive ENBREL by subcutaneous (SC) injection twice a week for up to 3 years and may continue taking other medicines such as prednisone or methotrexate. Another group will continue to receive methotrexate, either alone or in combination with DMARDs other than ENBREL. Candidates will be screened with a medical history and physical examination,
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including height, weight, and Tanner scores. A behavioral assessment, quality of life assessment, and physician's global assessment of disease activity will be performed. A blood test and joint evaluation will also be done. Both treatment groups will have onstudy evaluations at baseline and months 3, 6, 9, 12, 18, 24, 30, and 36. Each follow-up visit will include a repeat of the screening assessments and an evaluation of adverse events or toxicity, including psychiatric and behavioral effects and new symptoms of autoimmune disorders. The two groups will be compared for safety, including effects on growth and development parameters. Patients will need to purchase or arrange the purchase of commercially available ENBREL. Patients entering the study during the period when ENBREL is in short supply will be able to obtain ENBREL after enrolling in the ENBREL Enrollment Program. Patients will receive ENBREL enrollment information at the time of registration into the study. Phase(s): Phase IV Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00016575 ·
Identification of Genes Associated with Lung Disease in Patients with Rheumatoid Arthritis Condition(s): Healthy; Pulmonary Fibrosis; Rheumatoid Arthritis Study Status: This study is currently recruiting patients. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: Pulmonary fibrosis (PF) is a condition in which the lungs of a patient become scarred and fibrous. It has been known to occur in as many as 40% of patients diagnosed with rheumatoid arthritis (RA). The cause of the pulmonary fibrosis in patients with RA is unknown. Data gathered from previous research studies suggest that genetics may play a role in the development of PF in patients with rheumatoid arthritis. However, the actual genetic factors involved in the disease process have not been identified. The goal of this study is to identify the genetic markers in patients with pulmonary fibrosis and rheumatoid arthritis. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00001885
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Infliximab for the Treatment of Early Rheumatoid Arthritis Condition(s): Rheumatoid Arthritis Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Purpose - Excerpt: This study will test whether the drug combination of methotrexate and infliximab (anti-TNF-alpha antibody) is more effective than methotrexate alone for treating rheumatoid arthritis early in the disease. (The Food and Drug Administration has approved both treatment regimens for patients with long-standing rheumatoid arthritis.) The study will also evaluate how effectively magnetic resonance imaging (MRI) can detect differences in the development of bone damage in the two treatment groups by as early as 6 months. Patients 18 years of age and older who have had
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rheumatoid arthritis for less than 2 years and who have four or more affected joints may be eligible for this 1-year study. Patients must have received methotrexate treatment in the past without complete success, and must not have been treated previously with Anti-Thymocyte therapy. All participants will receive 20 Mg./week of methotrexate. In addition, patients will be randomly assigned to receive a monthly infusion of infliximab or placebo (a fluid that contains no active drug). After 6 months, all patients will receive active infliximab for the remaining half year of the study. Patients will also receive folic acid (1mg/day), Vitamin D (400 IU/day), and calcium supplements. They may continue to take prednisone (no more than 10 Mg./day) and non-steroidal anti-inflammatory drugs (NSAIDS). Medication dosages will be adjusted as needed if pain and joint swelling worsen. Over the course of the study, patients will come to NIH for 15 visits and undergo the following tests and procedures: 1. Joint examination-at every visit. 2. Drug side effects evaluation-at every visit during the study and after the study at 24 and 36 months by questionnaires to be filled out and returned. 3. Hand and feet X-rays at the first visit, at 6 months and at 12 months. 4. MRIs of the wrist to examine damage in the bone and synovial tissue (tissue lining the joint)-before treatment begins and at weeks 15, 27 and 54. For this study, the patient lies still in a narrow cylinder (the scanner) with a strong magnetic field. A contrast material (gadolinium) is injected into the blood to enhance the images of the synovium. The MRI takes about 45 minutes. 5. DEXA scans (dual emission X-ray absorptiometry) of the lower spine, one hip and one wrist to measure bone density and assess bone loss-before treatment begins and at weeks 27 and 54. This X-ray test takes about 5 to 10 minutes. 6. CTs (computed tomography) of one hand to assess joint damage in the wrist-before treatment begins and at weeks 27 and 54. Only half the patients in the study will have this X-ray study, which produces 3dimensional images of the hand. It will be done to compare the location, size and change of damage in the wrist seen on CT with the information obtained on MRI. The procedure takes about 5 to 10 minutes to complete. 7. Blood tests-at every visit to evaluate treatment response and side effects. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00006292 ·
Infliximab to Treat Children with Juvenile Rheumatoid Arthritis Condition(s): Juvenile Rheumatoid Arthritis Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Purpose - Excerpt: This study will determine whether a stepwise increase of the drug infliximab (Remicade(r) (Registered Trademark)) controls juvenile rheumatoid arthritis more effectively than a fixed dose. It will look at the safety and effectiveness of increasing the dose to a maximum of 15mg/kg body weight per dose, examining the drug's effect on bone and cartilage, and whether it can improve abnormal growth, metabolism and hormones. Infliximab is approved for treating adults with rheumatoid arthritis and Crohn's disease. Children between 4 and 17 years of age with active juvenile rheumatoid arthritis who do not respond adequately to standard therapy may be eligible for this study. Participants will receive nine infusions of infliximab during this 62-week study. The drug is given intravenously (IV, into a vein) over 2 hours. The
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first three infusions will be at a dose of 5 mg/kg of body weight. Children who improve on this regimen will receive another 6 infusions at the same dose. Children who do not significantly improve on 5 mg/kg at the end of 6 weeks (the third infusion) may continue with phase 2 of the study, in which they will be randomly assigned to receive either: 1) 6 additional doses of the drug at 5 mg/kg per dose, or 2) a gradually increased dose to a maximum of 15 mg/kg. In addition, all children will continue to take methotrexate at the same dose as when they entered the study. Participants will visit the NIH Clinical Center 12 times (about every 8 weeks) during the study for the following tests and procedures: - History and physical examination, including a complete joint exam - Puberty assessment - breast development in girls, testicle size in boys, and pubic hair - Height and weight measurements Children will have imaging studies (x-rays, MRI and Dexa scan) at the beginning and end of the study and will collect a 24-hour urine sample before each infliximab infusion. Patients may elect to have an endocrine evaluation. This involves Clinical Center hospitalizations for 1-1/2 days on visits 1, 4 and 12. Small amounts of blood will be drawn every 20 minutes (through an indwelling catheter to avoid multiple needle sticks) for 8 hours while the child sleeps. The blood will be examined for the normal rhythm of growth hormone and other substances in the body and how they are affected by arthritis. Participants will complete a questionnaire once a year for 2 years to provide information on their health status and any problems that might be related to the study drug. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00029042 ·
ISIS 104838, an Inhibitor of Tumor Necrosis Factor, for Active Rheumatoid Arthritis Condition(s): Rheumatoid Arthritis Study Status: This study is currently recruiting patients. Sponsor(s): Isis Pharmaceuticals Purpose - Excerpt: ISIS 104838 is an antisense oligonucleotide drug that reduces the production of a specific protein called tumor necrosis factor (TNF-alpha), a substance that contributes to joint pain and swelling in rheumatoid arthritis. ISIS 104838 works by blocking TNF-alpha messenger RNA, the "instruction" molecule that is required for the production of TNF-alpha protein. This trial will assess the safety and efficacy of ISIS 1048383 by subcutaneous injection, administered by 3 different dosing regimens for 3 months, versus placebo. Approximately 160 TNF-alpha inhibitor-naïve rheumatoid arthritis patients will be evaluated at 32 sites in the U.S. and Canada. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00048321
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Literacy in Arthritis Management Condition(s): Rheumatoid Arthritis; Psoriatic Arthritis Study Status: This study is currently recruiting patients.
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Sponsor(s): National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Purpose - Excerpt: This study will test a new patient education program designed for people who do not read well. It will also look at how poor reading skills affect a person's health and how people who do not read well learn best. We will randomly assign patients who have a rheumatic condition (arthritis) that causes inflammation throughout the body (rheumatoid arthritis, psoriatic arthritis, and seronegative polyarthritis) to three groups that will receive different types of educational materials. We will use the new, experimental patient education program in one of these groups. Each group will have a similar percentage of people from each of three reading level categories: 8th grade or lower, 9th to 11th grade, and 12th grade and higher readers. We will follow patients for one year after the education program to look for changes in health status, disease activity, communication with the doctor, belief that they can manage their own disease (known as self-efficacy), understanding and continued use of prescribed treatments, satisfaction, and health care use. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00023205 ·
Lung Disease Associated with Rheumatoid Arthritis Condition(s): Pulmonary Fibrosis; Rheumatoid Arthritis Study Status: This study is currently recruiting patients. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: Pulmonary fibrosis (PF) is a condition in which the lungs of a patient become scarred and fibrous. It has been known to occur in as many as 40% of patients diagnosed with rheumatoid arthritis (RA). The cause of the pulmonary fibrosis in patients with RA is unknown. Patients participating in this study will undergo a series of tests and examinations before and throughout the study. The tests include blood and urine tests, electrical measures of heart function (ECG), chest x-rays, CAT scans, nuclear medicine scans, breathing tests, exercise tests, and fiberoptic bronchoscopy. The goals of this study are to: 1. Estimate how common pulmonary fibrosis is in patients with rheumatoid arthritis, 2. Describe the natural course of pulmonary fibrosis in patients with rheumatoid arthritis, 3. Estimate the survival rate of patients with pulmonary fibrosis and rheumatoid arthritis, and 4. Learn more about the factors that contribute to the development or progression fibrotic lung disease. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00001876
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Phase I Study of High-Dose Cyclophosphamide, Anti-Thymocyte Globulin, and Total Body Irradiation With T-Cell-Depleted Autologous Bone Marrow Rescue in Patients With High-Risk Rheumatoid Arthritis Condition(s): Rheumatoid Arthritis; Juvenile Rheumatoid Arthritis Study Status: This study is currently recruiting patients. Sponsor(s): Northwestern Memorial Hospital
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Purpose - Excerpt: Objectives: I. Determine the toxicity of high-dose cyclophosphamide, anti-thymocyte globulin, and total body irradiation with T-cell-depleted autologous bone marrow rescue in patients with high-risk rheumatoid arthritis. II. Determine the safety and efficacy of this regimen in this patient population. Phase(s): Phase I Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00017615 ·
Relaxation Response Training for the Treatment of Rheumatoid Arthritis Condition(s): Rheumatoid Arthritis Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Purpose - Excerpt: This study will evaluate the relative effectiveness of Relaxation Response (RR) training for the treatment of rheumatoid arthritis (RA). The study will compare RR training to RR training with cognitive behavioral therapy and to a standard RA education program. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00056667
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Safety and efficacy of a monoclonal antibody for treatment of rheumatoid arthritis. Condition(s): Rheumatoid Arthritis Study Status: This study is currently recruiting patients. Sponsor(s): XOMA Purpose - Excerpt: The purpose of this study is to determine whether a humanized monoclonal antibody (efalizumab) is safe and effective in the treatment of rheumatoid arthritis. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00034203
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Shared Epitope Peptides in Rheumatoid Arthritis Condition(s): Rheumatoid Arthritis Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Purpose - Excerpt: This study will test whether a small protein, or peptide (dnaJ peptide) can help people with rheumatoid arthritis (RA) by preventing their immune
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system cells from abnormally reacting against the body's own tissues. This study will look at whether taking small amounts of dnaJ peptide by mouth can "re-educate" immune cells in some people with RA so that the cells become tolerant to, or get used to, this substance and stop attacking joint tissues. The study involves a screening, treatment, and follow-up phase. If the person qualifies for the study, he or she will be assigned to one of two groups. One group will receive the placebo (an inactive substance) and the other group will receive the study drug (dnaJ peptide). We will examine study participants, collect their blood and urine for testing, and ask them to answer a questionnaire about their arthritis once every 4 weeks over a period of 24 weeks of treatment and at a follow-up visit one month after the end of the treatment period. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00000435 ·
Specimen Collection for Individuals with Lung Disease Associated with Rheumatoid Arthritis Condition(s): Pulmonary Fibrosis; Rheumatoid Arthritis Study Status: This study is currently recruiting patients. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: Pulmonary fibrosis (PF) is a condition in which the lungs of a patient become scarred and fibrous. It has been known to occur in as many as 40% of patients diagnosed with rheumatoid arthritis (RA). The cause of the pulmonary fibrosis in patients with RA is unknown. Researchers hope to improve their understanding of the disease process involved in PF and RA by analyzing specimens collected by bronchoscopy, lung biopsy, lung transplantation, or autopsy from patients with these conditions. The purpose of this study is to collect specimens from rheumatoid arthritis patients with and without pulmonary fibrosis as well as patients with pulmonary fibrosis without associated diseases or cause (idiopathic pulmonary fibrosis). Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00001884
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Study of Arthritis and Related Conditions Condition(s): Arthritis; Synovitis Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Purpose - Excerpt: The purpose of this study is to learn more about the causes of rheumatoid arthritis, juvenile rheumatoid arthritis and related conditions and the course of these diseases. Patients in this study will not receive treatment, but may be offered participation in a treatment protocol if an appropriate study is available. Children and adults of all ages with known or suspected arthritis are eligible for this study. Participants will undergo the following tests and procedures: -Medical history and physical examination - Measurements of weight and height - Blood sample
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collections for clinical and research purposes - X-rays of hand, feet or other affected joints, if x-rays have not been taken in the past 3 months and are medically indicated Magnetic resonance imaging (in some patients) to assess disease or study the usefulness of this diagnostic method for arthritis patients - Quality of life questionnaires - Stride analyzer test (children only) - computer system analysis of walking speed and pattern Hand functional test (children only) - detailed study of hand function - Walk/run time (children only) - measurement of distance the child can walk or run in 9 minutes (heart rate and blood pressure are taken before and after the test) -Synovial biopsy (in some patients) - removal of a sample of tissue from the synovium (lining of the joint) for evaluation under the microscope. The procedure is done under local anesthetic. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00006333 ·
Study of Psoriatic Arthritis Condition(s): Psoriasis; Psoriatic Arthritis Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Purpose - Excerpt: This study will examine the genetic and immune factors involved in the cause and development of psoriatic arthritis-a disease of both the skin and joints. It will describe the medical features and natural course of the disease and determine participants' eligibility for experimental treatment protocols. Patients with known or suspected psoriatic arthritis 5 years of age and older and their relatives may enroll in this study. Patients will be evaluated with a medical history and physical examination, electrocardiogram, blood tests and X-rays. Additional procedures may include: 1. Leukapheresis-Collection of white blood cells for genetic analysis. Whole blood is collected through a needle placed in an arm vein. The blood circulates through a machine that separates it into its components. The plasma is removed and the cells are returned to the body through a second needle placed in the other arm. 2. Skin biopsyRemoval of a small skin sample for microscopic analysis. An area of skin is numbed with an anesthetic and one to three small circular portions (about 1/4 inch in diameter) are cut and removed. 3. Joint aspiration-Removal of a small sample of synovial fluid (lubricating joint fluid). An area of skin around the biopsy site is numbed with an anesthetic, and a needle is inserted into the joint to pull out a small fluid sample. 4. Synovial needle biopsy-Removal of a small sample of synovial tissue (tissue lining the joint). An area of skin around the biopsy site is numbed with an anesthetic and a large needle is inserted into the joint. A smaller needle attached to a syringe is then placed inside the larger needle and small pieces of synovial tissue are removed. 5. Genetic studies-Saliva and blood samples will be collected for gene testing. Saliva is collected by rinsing the mouth with a tablespoon of salt water and spitting into a test tube. Patients will be followed once or twice a year and may be evaluated for participation in an experimental treatment study. Participating relatives of patients will fill out a brief medical history questionnaire and provide a DNA sample (blood sample or tissue swab from the inside of the cheek). Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00001420
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The Role of Cytokines on Growth Hormone Suppression in Premenopausal Women with Rheumatoid Arthritis and the Effect of Treatment with Etanercept Condition(s): Rheumatoid Arthritis; Healthy Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Purpose - Excerpt: This study has two phases. Phase 1 will examine the role of inflammatory mediators called cytokines on growth hormone levels in women with rheumatoid arthritis (RA). Phase 2 will evaluate the effect of etanercept on these growth hormone levels. Etanercept is approved for the treatment of RA. It lowers the levels of a key inflammatory mediator called tumor necrosis factor-alpha and is very effective in reducing arthritis symptoms. Growth hormone promotes bone and muscle growth. With aging, people lose muscle mass and bone strength, possibly because of decreased levels of growth hormone. People with RA have bone and muscle changes similar to those in older people, perhaps also due to decreased levels of growth hormone. The first part of this study will see if the inflammatory mediators responsible for joint inflammation (warmth, redness, pain, and swelling) in RA are related to the lowered growth hormone levels in this disease. The second part will evaluate the effect of etanercept treatment on muscle mass and bone density, in addition to growth hormone levels. Premenopausal women between 18 and 55 years of age with a recent diagnosis of rheumatoid arthritis (less than 3 years) are eligible for this study. Healthy volunteers will also be enrolled in the first phase of the study as control subjects. This study is conducted at two sites, the NIH and the Johns Hopkins Medical Center in Baltimore. Healthy volunteers enrolled in this study will be interviewed about their health status and will fill out questionnaires on diet and general physical function, including fatigue, energy and well being. In addition, they will be hospitalized once at the NIH Clinical Center for 24-hour blood sampling and will visit to Johns Hopkins Medical Center in Baltimore for a brachial artery reactivity study, as follows: - 24-hour blood sampling for growth hormone levels. Blood samples (1/2 teaspoon each) will be collected every 20 minutes from 8 AM one day until 8 AM the following day through a plastic tube in an arm vein. - Dual energy X-ray absorptiometry (DEXA) scan on a small area of the spine, hip and wrist to assess bone density and a total body DEXA scan to assess the amount and distribution of muscle and body fat. - Blood vessel (brachial artery reactivity) study to measure the ability of the brachial artery to dilate and increase its blood flow. For this procedure, the subject lies on a table with electrocardiogram leads attached to the chest. A blood pressure cuff is inflated for several minutes and a drop of nasal spray of nitroglycerin is given that may cause a headache. Blood pressure and headache are monitored and treated as needed. Patients with rheumatoid arthritis will be seen at the NIH clinic on six separate visits (weeks 0, 1, 6, 12, 18, and 26) over 26 weeks. Week 0 is a screening visit. At weeks 1 and 26, patients will be admitted to the hospital for 24-hour blood sampling, DEXA scans, and brachial artery reactivity tests, as described above, plus X-rays of the hand and feet. After the first visit, they will start taking etanercept, given by self-injection under the skin (like insulin shots) twice a week. Follow-up visits at weeks 6, 12, and 18 will involve evaluations of disease activity and drug side effects through joint examination, blood tests, and questionnaires. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00034060
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Treating Rheumatoid Arthritis with Tripterygium Wilfordi Hook F or Sulfasalazine Condition(s): Rheumatoid Arthritis Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Purpose - Excerpt: Various forms of the plant extract Tripterygium wilfordi Hook F (TwHF) have been used in China as a remedy for inflammatory diseases, including rheumatoid arthritis. The purpose of this study is to investigate how tolerable, safe, and effective TwHF is for patients with rheumatoid arthritis. Investigators will compare the therapeutic effects of TwHF with Sulfasalazine, an FDA-approved drug for arthritis. Participants in this 24-week study must have had active rheumatoid arthritis for at least six months. Approximately 120 patients will participate. Participants will be assigned to one of two drug-treatment groups, TwHF or Sulfasalazine. They will be given the study drug at each of six clinic visits and will be asked to take two capsules three times each day with meals and water. During the clinic visits, investigators will obtain multiple blood samples; give physical exams; assess swollen, tender, and painful joints; and administer x-rays. Study participants will be compensated up to $260 for their involvement in this study. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00062465
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A multi-center trial to compare the efficacy and safety of three doses of Meloxicam and placebo in patients with Rheumatoid Arthritis. Condition(s): Rheumatoid Arthritis Study Status: This study is no longer recruiting patients. Sponsor(s): Boehringer Ingelheim Pharmaceuticals Purpose - Excerpt: A 12-week trial consisting of 5 visits (6 if follow up is needed) to find out how effective and safe three different doses of meloxicam are compared with placebo in Rheumatoid Arthritis. Patient will take one dose of study medication daily. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00042068
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Arthritis Patient Education for Urban African Americans Condition(s): Arthritis Study Status: This study is no longer recruiting patients. Sponsor(s): National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Purpose - Excerpt: Research has shown that people with arthritis can improve their ability to cope with arthritis pain with the help of patient education programs, which teach people things they can do to help manage their disease. However, we do not know
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much about the effects of arthritis patient education programs on minorities, such as urban African Americans. We will gather participants for this project through a faithbased community network. The project is made up of four studies that will provide information about culturally relevant ways of reaching urban African Americans with arthritis and providing patient education that addresses arthritis care needs of the African American community. This project will also provide information on the effectiveness of an arthritis self-help course for urban African Americans. We hope to better understand the differences among cultural groups and how these differences should affect the design of culturally appropriate patient education. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00000396 ·
Calcium Supplements for Bone Health in Juvenile Rheumatoid Arthritis Condition(s): Juvenile Rheumatoid Arthritis Study Status: This study is no longer recruiting patients. Sponsor(s): National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Purpose - Excerpt: This study looks at the effects of taking calcium pills on bone health in young people with juvenile rheumatoid arthritis (JRA). In this 2-year study, children aged 6-18 who have JRA will take either a calcium supplement or a matching placebo (inactive or "dummy" pill) containing no calcium. During the study, researchers and patients will not know if a patient is taking calcium or placebo. We believe that patients who take calcium supplements will have at least a 10 percent greater increase in total body bone mineral density compared to patients who take the placebo. We will evaluate patients at Children's Hospital Medical Center every 6 months for 2 years. During this 2year period, participants in the study will take one multivitamin containing 400 IU (international units) of vitamin D and either 1,000 mg of calcium carbonate (Tums tablets) by mouth or a matching placebo once a day. We will check patients 6 and 18 months after the 2-year treatment period to find out if people in the Tums-treated group maintain any increases in bone formation that occurred during the 2-year treatment period. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00000429
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Evaluation of the Efficacy of Combination Treatment with Anakinra and Pegsunercept in Improving Rheumatoid Arthritis Condition(s): Rheumatoid Arthritis Study Status: This study is no longer recruiting patients. Sponsor(s): Amgen Purpose - Excerpt: The purpose of this study is to evaluate the effect of anakinra (IL-1 ra) and pegsunercept (PEG sTNF-RI) when they are used together in improving the
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signs and symptoms of rheumatoid arthritis. The study will also evaluate the safety of the combination treatment and its effect on slowing down bone and joint destruction due to rheumatoid arthritis. The results will be compared to the effect when only 1 single medication (anakinra or pegsunercept) is used. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00037700 ·
Genetics of Rheumatoid Arthritis Condition(s): Rheumatoid Arthritis Study Status: This study is no longer recruiting patients. Sponsor(s): National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Purpose - Excerpt: This study attempts to identify the genes responsible for rheumatoid arthritis (RA), or inflammation of the joints. It is known that genes play an important role in RA, but their number and significance have not been determined. RA tends to run in families. This study will examine the DNA (hereditary material) of patients with RA and their family members to try to determine which chromosomes(s) contain the genes responsible for the disease. Patients with rheumatoid arthritis and their family members may be eligible for this study. Participants with RA who have a brother or sister with RA will undergo the following procedures: -Review of their medical records Medical history -Examination of the joints -Hand X-rays -Blood tests Participants who 1) do not have RA but who have a relative with the disease, or 2) have RA and a relative other than a brother or sister who has the disease will provide a blood sample or a buccal (cheek) cell sample. Cheek cells are obtained by swishing a small amount of mouthwash in the mouth or by lightly bushing the inside of the cheek with a swab or brush. The samples will be tested for rheumatoid factor, DNA studies, and HLA type (a blood type found on white blood cells). Certain HLA types have been associated with an increased risk or severity of RA. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00001678
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Juvenile Rheumatoid Arthritis Condition(s): Juvenile Chronic Arthritis Study Status: This study is no longer recruiting patients. Sponsor(s): Amgen Purpose - Excerpt: The purpose of this study is to determine the safety and effectiveness of anakinra in patients with Polyarticular-Course Juvenile Rheumatoid arthritis, a form of rheumatoid arthritis affecting children. Phase(s): Phase II; Phase III Study Type: Interventional Contact(s): see Web site below
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Web Site: http://clinicaltrials.gov/ct/show/NCT00037648 ·
Oral Collagen for Rheumatoid Arthritis Condition(s): Rheumatoid Arthritis Study Status: This study is no longer recruiting patients. Sponsor(s): National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Purpose - Excerpt: This protocol allows us to determine whether doses of CII from 30130ug/day will induce oral tolerance to CII in RA patients. This will be a 2 year MultiCenter Clinical Trial (CT) with the University of Tennessee, Memphis as the Lead Center to determine whether oral administration of 6 different doses of bovine type II collagen (CII) to patients with rheumatoid arthritis (RA) will induce immune tolerance defined as a >30% reduction in IFN gamma/PBMC alpha 1(II)/PBS stimulation index. Patients will be enrolled with stable RA, without stopping DMARDs, NSAIDs or prednisone (equal to or less than 7 1/2 mg daily) and the study will not be restricted to patients with early disease. Patients taking NSAIDS will take misoprostol 100ug bid. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00000401
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Safety Study for Remicade Condition(s): Rheumatoid Arthritis Study Status: This study is no longer recruiting patients. Sponsor(s): Centocor Purpose - Excerpt: To assess the relative risk for serious infection in infliximab-treated patients within the first 22 weeks after initiation of therapy in a population of patients with rheumatoid arthritis (RA) reflective of the demographics (severity of RA, background disease-modifying anti-rheumatic drugs, concomitant diseases) seen in clinical practice. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00036387
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Study to Assess Efficacy of Tacrolimus + Methotrexate Vs. Placebo + Methotrexate in Treatment of Rheumatoid Arthritis Condition(s): Rheumatoid Arthritis Study Status: This study is no longer recruiting patients. Sponsor(s): Fujisawa Healthcare, Inc. Purpose - Excerpt: The purpose of this study is to evaluate the efficacy of the combination of tacrolimus + methotrexate compared to methotrexate alone in the
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treatment of the signs and symptoms of rheumatoid arthritis over 6 months in patients with partial response to methotrexate. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00036153 ·
Trial with HuMax-CD4 in Patients with Rheumatoid Arthritis failing treatment with Methotrexate and a TNF-alpha blocker. Condition(s): Rheumatoid Arthritis Study Status: This study is no longer recruiting patients. Sponsor(s): Genmab Purpose - Excerpt: The purpose of this study is to determine whether HuMax-CD4 is effective in the treatment of active rheumatoid arthritis in patients who have failed treatment with Methotrexate and at least one TNF-alpha blocking agent. Phase(s): Phase II; Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00042406
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A Controlled Trial of Intermittent Fludarabine for Psoriatic Arthritis Condition(s): Arthritis, Psoriatic; Psoriasis Study Status: This study is completed. Sponsor(s): National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Purpose - Excerpt: This is a placebo controlled study evaluating the role of fludarabine (a nucleoside analog targeting both resting and proliferating lymphocytes) in the treatment of moderate to severe psoriotic arthritis. Patients should have failed at least one disease modifying antirheumatic drug. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00001422
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Antifolate Effectiveness in Arthritis Condition(s): Rheumatoid Arthritis; Adjuvant Arthritis Study Status: This study is completed. Sponsor(s): National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS); Office of Dietary Supplements (ODS) Purpose - Excerpt: This study looks at how the arthritis drug methotrexate works in low doses to treat rheumatoid arthritis. (High doses of methotrexate are used to treat some types of cancer.) Methotrexate blocks the action of the B-vitamin known as folic acid. We
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are studying the biochemical reactions affected by this vitamin because we think that blocking many of these reactions may be necessary for methotrexate to work in treating rheumatoid arthritis. Through these studies, we hope to gain a better understanding of how this drug and related drugs work as treatments for arthritis. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00000395 ·
Genetic and Immune Studies of Rheumatoid Arthritis and Related Conditions Condition(s): Arthritis, Psoriatic; Autoimmune Diseases; Joint Diseases; Osteoarthritis; Rheumatoid Arthritis Study Status: This study is completed. Sponsor(s): National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Purpose - Excerpt: This protocol will examine blood, synovial fluid and synovial tissue from patients with rheumatoid arthritis and other chronic inflammatory joint diseases to study genetic and immunologic factors involved in the cause, development and progression of these conditions. Synovial fluid is the lubricating fluid in joints. The synovial membrane is a delicate tissue lining the inner surface of joints, which, in arthritic conditions, thickens and becomes infiltrated with various types of cells. Patients with rheumatoid arthritis and certain patients with other forms of arthritis may be eligible for this study. Those enrolled will be followed periodically for follow-up and disease evaluation. They may undergo the following procedures: 1. Synovial fluid aspiration, when medically indicated (for example, for joint swelling and inflammation). For this procedure, an area of skin around the joint is numbed with an anesthetic, and a needle is inserted into the joint to withdraw a small fluid sample. 2. Periodic blood sampling, not to exceed 450 milliliters (15 ounces) during any 6-week period, for genetic studies of rheumatoid arthritis. The samples are usually taken at the same times that synovial fluid is withdrawn. 3. Synovial tissues, collected by needle biopsy or during surgical procedures for arthroscopy (examination of the interior of the joint and repair of the joint) or total joint replacement. For the needle biopsy, the skin over the biopsy site is washed and anesthetized. A needle is inserted and fluid is aspirated. The biopsy needle is then inserted through the outer needle and a tissue sample is suctioned. Patients who qualify for other research studies may be invited to participate. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00001291
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Improving Vocational Outcomes in Arthritis Condition(s): Arthritis; Musculoskeletal Diseases; Rheumatic Diseases Study Status: This study is completed. Sponsor(s): National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Purpose - Excerpt: The long-term objectives of this research project are to enhance program participation and improve the employment prospects of people with work
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disability due to arthritis and related musculoskeletal disorders (ARMD) who are actively seeking vocational (job-related) rehabilitation (VR) services. This study is designed to compare the employment situations of a group of people receiving a twopart intervention and a group that is not receiving the intervention. The intervention consists of training sessions to help prospective VR clients with ARMD successfully enter and complete the VR program, and training sessions for a randomly selected group of VR professionals to help them serve VR clients with ARMD more effectively. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00000407 ·
Methotrexate Alone Versus Combination of Methotrexate and Subcutaneous Fludarabine for Severe Rheumatoid Arthritis: Safety, Tolerance and Efficacy Condition(s): Arthritis, Rheumatoid; Synovitis Study Status: This study is completed. Sponsor(s): National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Purpose - Excerpt: The safety profile and efficacy of combination therapy will be evaluated using methotrexate (MTX) and the nucleoside analog fludarabine in 40 patients with severe refractory rheumatoid arthritis. The patients enrolled will be those who have experienced inadequate disease control with MTX alone or in combination with other immunosuppressive drugs such as sulfasalazine (SSZ), cyclosporin A (CsA), or hydroxychloroquine (HCQ). In this randomized, double-blind, placebo controlled trial, patients will be maintained on oral MTX at 17.5 mg/week to which either placebo or subcutaneous fludarabine at 30 mg/m(2) daily for three consecutive days per month will be added for four months. The fludarabine (or placebo) treatment period will be followed by two months of follow-up, at which time patients will be evaluated for response. Patients will be monitored for adverse effects/tolerability, disease activity, and changes in synovial volume as measured by magnetic resonance imaging (MRI). Additionally synovial biopsies will be obtained before and after treatment for investigation of infiltrating cell numbers and phenotypes, cytokine profiles, Th1 versus Th2 responses, and angiogenesis. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00001677
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Patient Education in Rheumatoid Arthritis and Osteoarthritis Condition(s): Rheumatoid Arthritis; Osteoarthritis Study Status: This study is completed. Sponsor(s): National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Purpose - Excerpt: This project will evaluate the effectiveness and general usefulness of two arthritis patient education programs. The first, the arthritis Self-Management
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Program, is a 6-week, community-based program taught in small groups by peer leaders. The second, the Self-Managed arthritis Relief Therapy (SMART) Program, is a computer-driven program delivered through the mail. Participants in this project are people with rheumatoid arthritis or osteoarthritis who are taking part in the larger longterm studies being conducted by ARAMIS (the arthritis, Rheumatism and Aging Medical Information System). Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00000414 ·
Positron Emission Tomography and Magnetic Resonance Imaging to Evaluate Synovial Blood Flow in Rheumatoid Arthritis Patients Condition(s): Rheumatoid Arthritis Study Status: This study is completed. Sponsor(s): National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Purpose - Excerpt: This study will test whether positron emission tomography (PET) imaging can be used to measure blood flow to joints in patients with rheumatoid arthritis (RA). It will also compare blood flow measurements using PET with measurements obtained with magnetic resonance imaging (MRI) to determine how useful MRI is in measuring blood flow to joints. Much of the joint damage in RA is caused by the synovium-the lining of the joint. In RA, the synovium increases in size and destroys bone and cartilage. The synovium maintains its growth by forming many new small blood vessels to nourish it. New drug treatments are being developed to stop the growth of these new blood vessels. The effect of these treatments on the synovium is usually measured by performing a biopsy-removing a small piece of synovium for examination under a microscope. The biopsy requires inserting a needle into the joint to withdraw the synovial tissue. This study will see if changes in blood flow can be assessed accurately using noninvasive imaging procedures, such as PET scanning, instead of a biopsy. Patients 18 years of age and older with rheumatoid arthritis who have at least one tender and swollen knee due to synovitis may be eligible for this study. Candidates will be screened with a medical history and physical examination. Participants will have a mold made of the knee to be studied and will have routine blood tests. Women who are able to become pregnant will have a pregnancy test. All participants will then undergo PET and MRI scanning as described below: PET - A needle is used to insert a catheter (small plastic tube) into an arm vein for injection of the radioactive substance H215O. The patient lies in a doughnut-shaped machine (the PET scanner) and a quick scan is done to measure body thickness. Then, a separate scan is taken following each of six or fewer injections of H215O. Each scan lasts about 13 minutes. MRI - The patient lies on a stretcher that is moved into a cylinder containing a magnetic field (the MRI scanner). A special coil is placed over the knee to improve the quality of the images. Earplugs are worn to muffle the loud thumping sound produced by electrical switching of the magnetic fields during the imaging. A contrast agent called gadolinium is injected through a catheter into a vein to improve the quality of the images. An intercom system permits the patient to communicate with the technician at all times during the procedure. Phase(s): Phase I
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Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00014794 ·
Prevention of Arthritis-Related Work Disability Condition(s): Rheumatoid Arthritis; Systemic Lupus Erythematosus; Osteoarthritis, Knee; Ankylosing Spondylitis Study Status: This study is completed. Sponsor(s): National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Purpose - Excerpt: People with rheumatic disorders (arthritis) often have trouble keeping their jobs. This study will look at whether vocational rehabilitation (VR) will improve the ability of employed people with arthritis to keep their jobs. Job retention VR services target key factors that increase the risk of job loss. They aim to modify jobs to reduce barriers caused by functional limitations and disease symptoms, future career planning, and establish a partnership with a VR counselor for ongoing help. We will conduct the study among patients with rheumatic disorders recruited in eastern Massachusetts. We will give 120 study participants job retention services provided by VR counselors. We will give another 120 participants literature about employmentrelated resources. We will compare the outcomes of the two groups to evaluate the usefulness of job retention services in preventing job loss in people with rheumatic disorders. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00000416
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Prognostic Indicators and Determinants of the 2-5 Year Outcome in a Cohort of Early Synovitis Patients Condition(s): Arthritis, Reactive; Arthritis, Rheumatoid; Synovitis Study Status: This study is completed. Sponsor(s): National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Purpose - Excerpt: This study will evaluate the 2-5 year outcome of a cohort of 250 patients with early synovitis, who were recruited into protocol 94-AR-0194 (The Pathogenesis of Inflammatory Synovitis: A Study of Early Arthritis). Clinical, radiographic, and functional outcome parameters, particularly those relating to articular damage and functional loss, will be evaluated and related back to clinical, serologic, immunogenetic, and pathologic variables identified at the onset of the arthropathy. A model will be generated which incorporates and weighs the variables in order to determine diagnostic and prognostic markers in the early stages of arthritis. Synovial tissue samples have been obtained from the entire cohort at the initial visit of protocol 94-AR-0194. Studies of these biopsies have so far demonstrated evidence for the presence of infectious agents in a proportion of the samples, and have generated information regarding the cytokine profiles in the early stages of synovitis. In an attempt to further define the pathogenetic mechanisms of synovitis longitudinally,
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biopsies will be repeated on selected subsets of the cohort. Specific questions to be answered relate to the persistence of microbial agents in the synovium, and to the evolution of cellular and molecular mechanisms which mediate the invasive, destructive potential of the synovial lesion. It is anticipated that these studies should prove valuable to clinicians who are attempting to stratify patients for therapeutic strategies, early in their disease course. They should also prove valuable in enhancing the understanding of the pathogenetic mechanisms of synovitis. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00001679 ·
Safety, Efficacy and Pharmacokinetics of an Antibody for Psoriatic Arthritis Condition(s): Psoriatic Arthritis Study Status: This study is not yet open for patient recruitment. Sponsor(s): XOMA Purpose - Excerpt: The purpose of this study is to determine whether a humanized monoclonal antibody (efalizumab) is safe and effective in the treatment of psoriatic arthritis (PsA) Phase(s): Phase I Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00051662
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Steroid Hormones, TH1/TH2 Cytokines and Reproductive Status Condition(s): Arthritis, Rheumatoid; Healthy; Pregnancy Study Status: This study is completed. Sponsor(s): National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Purpose - Excerpt: This study is designed to evaluate blood Th1 and Th2 immunoregulatory cytokine production and hormonal levels associated with the third trimester of pregnancy and the postpartum state. Cytokine and hormone levels will be assessed in blood specimens obtained from healthy pregnant and postpartum females and compared to levels from premenopausal non-pregnant and non-postpartum females. Blood samples obtained at 30-36 weeks of gestation and 2-6 weeks postpartum will be the primary study points. Samples will also be obtained from pregnant, postpartum, and non-pregnant, non-postpartum, premenopausal female patients with rheumatoid arthritis. Additional data will be generated from samples from normal males, which will be compared with data from females. We expect to find that pregnancy is associated with enhanced Th2 cytokine expression and that the postpartum state is associated with enhanced Th1 cytokine expression. We expect to see differences in cytokine expression between males and females as well. We seek to gather data supporting the view that distinct hormonal environments regulate these contrasting immunological states. Study Type: Observational Contact(s): see Web site below
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Web Site: http://clinicaltrials.gov/ct/show/NCT00001376 ·
Study of Gammalinolenic Acid for Juvenile Rheumatoid Arthritis Condition(s): Juvenile Rheumatoid Arthritis Study Status: This study is completed. Sponsor(s): FDA Office of Orphan Products Development; University of Massachusetts Medical Center Purpose - Excerpt: Objectives: I. Determine the efficacy and safety of gammalinolenic acid in the treatment of childhood arthritis. Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00004420
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Study of infliximab in combination with methotrexate for the treatment of patients with polyarticular juvenile rheumatoid arthritis Condition(s): Juvenile Rheumatoid Arthritis Study Status: This study is completed. Sponsor(s): Centocor Purpose - Excerpt: Research study to evaluate the safety and effectiveness of an investigational drug is currently being conducted in children diagnosed with polyarticular juvenile rheumatoid arthritis with active disease while receiving methotrexate therapy. Aim of the international study is to evaluate the efficacy and safety of the drug in patients with active JRA/JIA who are receiving methotrexate therapy. Study is being conducted in Belgium, Canada, Finland, France, Germany, Italy, the Netherlands, Spain, Sweden, Switzerland, United Kingdom, and USA. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00036374
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Study of Remicade (Infliximab) in Psoriatic Arthritis Condition(s): Psoriatic Arthritis Study Status: This study is completed. Sponsor(s): Centocor Purpose - Excerpt: To assess the effectiveness and safety of infliximab for use in active Psoriatic Arthritis Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00051623
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The Pathogenesis of Inflammatory Synovitis: A Study of Early Arthritis Condition(s): Arthritis; Arthritis, Reactive; Arthritis, Rheumatoid; Reiter's Disease; Synovitis Study Status: This study is completed. Sponsor(s): National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Purpose - Excerpt: This study will evaluate patients with inflammatory forms of arthritis within the first year of onset. The study will attempt to clarify factors that may predict disease course such as evolution into rheumatoid arthritis (RA) or other chronic inflammatory arthropathies. Synovial biopsies and synovial fluid will be obtained to search for microbial agents and other initiating and modulating factors that may be most readily distinguished early in the disease and to determine the stage of disease at which certain immunologic and hormonal changes become evident. The study will also search for genetic and other features that may be associated with specific forms of inflammatory arthropathies that might predict the subsequent clinical disease course or response to different agents used in treatment of RA, Reiter’s syndrome and other types of chronic inflammatory arthropathies. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00001375
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The Safety and Efficacy of Chicken Type II Collagen on Uveitis Associated with Juvenile Rheumatoid Arthritis Condition(s): Arthritis, Juvenile Rheumatoid; Uveitis Study Status: This study is completed. Sponsor(s): National Eye Institute (NEI) Purpose - Excerpt: Current treatment modalities for uveitis associated with juvenile rheumatoid arthritis have not been beneficial in the juvenile population. A new approach for treating patients with presumed autoimmune disorders is oral tolerance therapy. Chicken type II collagen (Colloral) is being developed as an oral tolerance therapy for the treatment of rheumatoid arthritis. This open label pilot study will describe the safety of chicken type II collagen added to current anti-inflammatory medications as treatment for patients with uveitis associated with juvenile rheumatoid arthritis. The primary ophthalmic outcomes of this study will be a change from baseline in the number of anterior chamber cells and the number and dosage of antiinflammatory medications. Secondary outcomes for JRA will include change in physician's global assessment, parent/patient assessment of overall well-being, functional assessment, number of joints with active arthritis, number of joints with limited range of motion, and erythrocyte sedimentation rate (ESR). Secondary outcomes for uveitis will include change in visual acuity, vitreous haze, and anterior chamber flare. Phase(s): Phase I Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00001614
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TNRF:Fc to Treat Eye Inflammation in Juvenile Rheumatoid Arthritis Condition(s): Juvenile Rheumatoid Arthritis; Uveitis Study Status: This study is completed. Sponsor(s): National Eye Institute (NEI) Purpose - Excerpt: This study will investigate the safety and effectiveness of the drug TNFR:Fc to treat uveitis (eye inflammation) in patients with juvenile rheumatoid arthritis. In other studies, TNFR:Fc significantly reduced joint pain and swelling in adult patients with rheumatoid arthritis, and the Food and Drug Administration has approved the drug for that use. Because medicines for arthritis often help patients with eye inflammation, this study will examine whether TNFR:Fc can help patients with uveitis. Patients with uveitis who are not responding well to standard treatment, such as steroids, and patients who have side effects from other medicines used to treat their uveitis or have refused treatment because of possible side effects may be eligible for this study. Candidates will be screened with a medical history, physical examination, and eye examination. The eye exam includes a check of vision and eye pressure, examination of the back of the eye (retina), and front of the eye, including measurements of protein and inflammation. Candidates will also undergo fluorescein angiography-a procedure in which photographs are taken of the retina to see if there is any leakage in the eye's blood vessels. A blood test and joint evaluation will also be done. Study participants will be given a shot of TNFR:Fc twice a week for up to 12 months and may continue other medicines they may be taking, such as prednisone or methotrexate. They will have follow-up examinations at week two and months one, two, three and four. Those who wish to continue treatment after the fourth month can receive the drug for another eight months and will have follow-up exams at months six, nine and 12, and one month after treatment ends. Each follow-up visit will include a repeat of the screening exams and an evaluation of side effects or discomfort from the medicine. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00001862
Keeping Current on Clinical Trials The U.S. National Institutes of Health, through the National Library of Medicine, has developed ClinicalTrials.gov to provide current information about clinical research across the broadest number of diseases and conditions. The site was launched in February 2000 and currently contains approximately 5,700 clinical studies in over 59,000 locations worldwide, with most studies being conducted in the United States. ClinicalTrials.gov receives about 2 million hits per month and hosts approximately 5,400 visitors daily. To access this database, simply go to the Web site at http://www.clinicaltrials.gov/ and search by “arthritis” (or synonyms). While ClinicalTrials.gov is the most comprehensive listing of NIH-supported clinical trials available, not all trials are in the database. The database is updated regularly, so clinical trials are continually being added. The following is a list of specialty databases affiliated with the National Institutes of Health that offer additional information on trials:
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For clinical studies at the Warren Grant Magnuson Clinical Center located in Bethesda, Maryland, visit their Web site: http://clinicalstudies.info.nih.gov/
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For clinical studies conducted at the Bayview Campus in Baltimore, Maryland, visit their Web site: http://www.jhbmc.jhu.edu/studies/index.html
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For cancer trials, visit the National Cancer Institute: http://cancertrials.nci.nih.gov/
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For eye-related trials, visit and search the Web page of the National Eye Institute: http://www.nei.nih.gov/neitrials/index.htm
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For heart, lung and blood trials, visit the Web page of the National Heart, Lung and Blood Institute: http://www.nhlbi.nih.gov/studies/index.htm
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For trials on aging, visit and search the Web site of the National Institute on Aging: http://www.grc.nia.nih.gov/studies/index.htm
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For rare diseases, visit and search the Web site sponsored by the Office of Rare Diseases: http://ord.aspensys.com/asp/resources/rsch_trials.asp
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For alcoholism, visit the National Institute on Alcohol Abuse and Alcoholism: http://www.niaaa.nih.gov/intramural/Web_dicbr_hp/particip.htm
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For trials on infectious, immune, and allergic diseases, visit the site of the National Institute of Allergy and Infectious Diseases: http://www.niaid.nih.gov/clintrials/
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For trials on arthritis, musculoskeletal and skin diseases, visit newly revised site of the National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health: http://www.niams.nih.gov/hi/studies/index.htm
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For hearing-related trials, visit the National Institute on Deafness and Other Communication Disorders: http://www.nidcd.nih.gov/health/clinical/index.htm
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For trials on diseases of the digestive system and kidneys, and diabetes, visit the National Institute of Diabetes and Digestive and Kidney Diseases: http://www.niddk.nih.gov/patient/patient.htm
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For drug abuse trials, visit and search the Web site sponsored by the National Institute on Drug Abuse: http://www.nida.nih.gov/CTN/Index.htm
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For trials on mental disorders, visit and search the Web site of the National Institute of Mental Health: http://www.nimh.nih.gov/studies/index.cfm
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For trials on neurological disorders and stroke, visit and search the Web site sponsored by the National Institute of Neurological Disorders and Stroke of the NIH: http://www.ninds.nih.gov/funding/funding_opportunities.htm#Clinical_Trials
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CHAPTER 6. PATENTS ON ARTHRITIS Overview Patents can be physical innovations (e.g. chemicals, pharmaceuticals, medical equipment) or processes (e.g. treatments or diagnostic procedures). The United States Patent and Trademark Office defines a patent as a grant of a property right to the inventor, issued by the Patent and Trademark Office.9 Patents, therefore, are intellectual property. For the United States, the term of a new patent is 20 years from the date when the patent application was filed. If the inventor wishes to receive economic benefits, it is likely that the invention will become commercially available within 20 years of the initial filing. It is important to understand, therefore, that an inventor’s patent does not indicate that a product or service is or will be commercially available. The patent implies only that the inventor has “the right to exclude others from making, using, offering for sale, or selling” the invention in the United States. While this relates to U.S. patents, similar rules govern foreign patents. In this chapter, we show you how to locate information on patents and their inventors. If you find a patent that is particularly interesting to you, contact the inventor or the assignee for further information. IMPORTANT NOTE: When following the search strategy described below, you may discover non-medical patents that use the generic term “arthritis” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on arthritis, we have not necessarily excluded non-medical patents in this bibliography.
Patents on Arthritis By performing a patent search focusing on arthritis, you can obtain information such as the title of the invention, the names of the inventor(s), the assignee(s) or the company that owns or controls the patent, a short abstract that summarizes the patent, and a few excerpts from the description of the patent. The abstract of a patent tends to be more technical in nature, while the description is often written for the public. Full patent descriptions contain much more information than is presented here (e.g. claims, references, figures, diagrams, etc.). We
9Adapted
from the United States Patent and Trademark Office: http://www.uspto.gov/web/offices/pac/doc/general/whatis.htm.
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will tell you how to obtain this information later in the chapter. The following is an example of the type of information that you can expect to obtain from a patent search on arthritis: ·
1-[4-(4-Sulfanilyl)phenyl] urea and derivatives in compositions and methods of treating rheumatoid arthritis and immune complex diseases Inventor(s): Jensen; Norman P. (New Providence, NJ), Jacobus; David P. (Princeton, NJ), Jones; Howard (Holmdel, NJ) Assignee(s): Merck & Co., Inc. (Rahway, NJ) Patent Number: 4,338,334 Date filed: February 29, 1980 Abstract: The invention relates to 1-[4-(4-sulfanilyl)phenyl] urea and derivatives thereof in pharmaceutical compositions and in methods of treating rheumatoid arthritis and immune complex diseases such as dermatitis herpetiformis. Excerpt(s): The present invention is concerned with pharmaceutical compositions containing as an active ingredient the known compound 1-[4-(4-sulfanilyl)phenyl]urea and known derivatives thereof, and the use of these compositions, or the compounds themselves, in treating rheumatoid arthritis, muscular dystrophy, immune complex diseases, including dermatitis herpetiformis, celiac disease, and certain forms of leukemia, and autoimmune endocrine diseases such as juvenile diabetes. ... Dapsone (4,4'-diaminodiphenylsulfone) is an established antimalarial and antileprotic agent. It has been found to be effective in treating rheumatoid arthritis; see McConkey et al., Rheumatology and Rehabilitation, 1976, 15, 230-234. It has also been employed in clinical treatment of dermatitis herpetiformis; see Lorincz and Pearson, "Sulfapyridine and Sulfone Type Drugs in Dermatology", Arch. Derm. 85: 42-56 (1962). Derivatives of diaminodiphenyl sulfone have been described in the literature for many years; see E. H. Northey, "Sulfonamides", A.C.S. monograph No. 106 (1948). The compound 1-[4-(4sulfanilyl)phenyl]urea, as well as a variety of substituted diphenyl sulfones have been found useful in reducing mortality and decreasing lesion incidence of poultry exposed to Marek's disease. See U.S. Pat. Nos. 3,689,671; 3,702,362; 3,715,375; 3,775,403; 3,775,444; and 3,786,050. However, none of these patents suggests the use of the substituted diphenyl sulfones disclosed therein as agents for treating rheumatoid arthritis, muscular dystrophy, or immune complex diseases. ... The compound 1-[4-(4sulfanilyl)phenyl]urea, and several substituted diphenyl sulfones have been found to inhibit the incorporation of chloline in chick peritoneal macrophages, an activity associated with the ability of such compounds to suppress growth or function of Marek's disease virus. See Shigeura et al., "Metabolic Studies on Diphenylsulfone Derivatives in Chick Macrophages", Biochemical Pharmacology, Vol. 24, pp. 687-691 (1975). Web site: http://www.delphion.com/details?pn=US04338334__
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10-deazaaminopterin: a new arthritis remittive drug Inventor(s): Krumdieck; Carlos L. (3408 Welford Cir., Birmingham, AL 35226), Castaneda; Oswaldo (Apartment 2713, Clinica Anglo Americana, Lima, PE), Alarcon; Graciela (1221 Rumson Dr., Birmingham, AL 35226), Koopman; William J. (452-H Wildwood La., Helena, AL 35080), Nair; Madhavan G. (7005 Charleston Oaks Dr., Mobile, AL 36695) Assignee(s): none reported Patent Number: 5,030,634 Date filed: March 29, 1990 Abstract: A double blind clinical trial of 10-deazaaminopterin versus the antirheumatoid drug methotrexate (MTX) established that 10-deazaaminopterin, in addition to being at least equally effective as methotrexate in all respects in ameliorating rheumatoid arthritis in humans, it is superior to methotrexate in controlling pain and joint stiffness and in improving grip strength. In accordance with this invention 10-deazaaminopterin is claimed as a more effective disease modifying arthritis remittive drug for the treatment of rheumatoid arthritis in humans. Excerpt(s): Methotrexate is the only effective drug currently available in the classical antifolate series for the treatment of rheumatoid arthritis and related inflammatory diseases such as asthma in humans. Methotrexate is a very toxic drug and the use of methotrexate in rheumatoid arthritis is limited by its toxicity. Many rheumatologists have concluded that toxicity is the major factor limiting prolonged MTX therapy. Toxic manifestations such as nausea, stomatitis, elevated liver function tests, cytopenias, and pulmonary toxicity have generally been reported in 30-60% of patients receiving the drug. A recent two year study documented that 93% of patients experienced an adverse drug reaction during treatment. ... 10-deazaaminopterin is a more powerful antiproliferative agent than methotrexate; yet in clinical trials it was found to be remarkably less toxic to humans. In clinical trials as an anti-rheumatoid drug 10-deazaaminopterin was found to be superior to methotrexate. 10-deazaaminopterin used for this study was prepared by the procedure of Nair as described in the Journal of Organic Chemistry (50:1875, 1985) as opposed to the more elaborate and expensive procedures using unstable intermediates for the preparation of methotrexate. Therefore, 10deazaaminopterin can be considered as less toxic, more effective and an inexpensive anti-rheumatoid drug compared to methotrexate. ... Rheumatoid arthritis is a chronic systemic disease believed to be of auto-immune origin. Common to all auto-immune diseases is the failure of the body's immune system to distinguish between self and nonself and to attack its own tissues as if belonging to a foreign organism. Severe articular pain and tissue destruction, leading to crippling joint deformities, as well as systemic manifestations such as vasculitis, heart disease, anemia, subcutaneous nodule formation, eye involvement, and others, are characteristic of this disease. There is no cure for rheumatoid arthritis. Drug therapy is aimed at reducing chronic inflammation and pain and at preventing progression of the disease. Aside from anti-inflammatory steroids, two classes of drugs are currently available for the treatment of this disease. One is made up by the non-steroidal anti-inflammatory drugs (NSAIDs) that help control inflammation and alleviate the pain and swelling of affected joints, but that have limited if any effect on the progression of the disease. Examples are aspirin, and a number of newer inhibitors of prostaglandin synthesis such as ibuprofen, naproxen, indomenthacin, fenoprofen, sulindac, meclofenamate, and other related compounds. The second class is referred to as the disease modifying arthritis remittive drugs (DMARDs). Compounds in this class appear to arrest progression of the disease by
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mechanisms that remain largely unknown. Examples are gold salts, hydroxychloroquine, D-pencillamine, levamisol and cytotoxic agents, particularly cyclophosphamide and azathioprine. Antifolates, such as methotrexate and sulfasalazine belong in this latter group. Web site: http://www.delphion.com/details?pn=US05030634__ ·
2,4,5-Triaryl pyrimidines and a method of treating pain, fever, thrombosis, inflammation and arthritis Inventor(s): Matsumoto; Ken (Indianapolis, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 4,500,533 Date filed: June 22, 1983 Abstract: This invention provides for certain novel 2,4,5-triaryl pyrimidine derivatives, their pharmaceutical formulations, and a method of treating pain, fever, thrombosis, inflammation, and arthritis. Excerpt(s): It is an object of this invention to provide novel 2-phenyl-4,5-bis(4methoxyphenyl)pyrimidine derivatives. These compounds are active as prostaglandin synthetase inhibitors, analgesic agents, anti-inflammatory agents, anti-arthritic agents, anti-pyretic agents, and antithrombotic agents. ... Certain 2-arylthio-4,5-bis(4methoxyphenyl)-pyrimidines are taught in the art to be less active as anti-inflammatory agents than the corresponding imidazole compounds. See J. Het. Chem., 19, 1162 (1982). ... Further provided by this invention are pharmaceutical formulations for these compounds and a method for treating pain, fever, thrombosis, inflammation, and arthritis in mammals using compounds of Formula I or their pharmaceutical formulations. Web site: http://www.delphion.com/details?pn=US04500533__
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2-guanidino-4-(2-methyl-4-imidazolyl)thiazoles in the treatment of rheumatoid arthritis Inventor(s): Larson; David L. (East Lyme, CT) Assignee(s): Pfizer Inc. (New York, NY) Patent Number: 4,591,595 Date filed: August 9, 1985 Abstract: 2-Guanidino-4-(2-methyl-4-imidazolyl)thiazole and 2-(N-pentyl-N'guanidino)-4-(2-methyl-4-imidazolyl)thiazole, histamine-H.sub.2 antagonist useful as a gastric acid antisecretory and antiulcer agents, are also useful per se in the treatment of rheumatoid arthritis. Excerpt(s): The present invention is directed to the use of 2-guanidino-4-(2-methyl-4imidazolyl)thiazole, 2-(N-pentyl-N'-guanidiano)-4-(2-methyl-4-imidazolyl)thiazole and analogs (or pharmaceutically acceptable salts thereof) in the treatment of rheumatoid arthritis. In spite of the wide use of steroidal and nonsteroidal antiinflammatory agents, rheumatoid arthritis remains an inadequately treated disease. For example, in many individuals, the gastrointestinal side effects associated with said antiinflammatory
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agents effectively prevents their use. Thus, present use of 2-guanidino-4-(2-methyl-4imidazolyl)thiazole and its N-pentyl analog, lacking such gastrointestinal side effects, represents a valuable addition to the physician's aramentarium of agents for the treatment of rheumatoid arthritis. ... 2-Guanidino-4-(2-methyl-4-imidazolyl)thiazole, analogs, and pharmaceutically acceptable salts thereof have been previously reported as histamine-H.sub.2 antagonists, and so are useful as gastric acid antisecretory and antiulcer agents; LaMattina and Lipinski, U.S. Pat. No. 4,374,843 (1983). An improved method for the preparation of 2-guanidino-4-(2-methyl-4-imidazolyl)-thiazole and its salts, in particular the dihydrochloride preferred for use in the present invention, is also disclosed hereinafter in specific examples below. ... 2-(N-Pentyl-N'-guanidino)-4-(2methyl-4-imidazolyl)-thiazole is the subject of copending U S. application of Reiter, Ser. No. 605,510, filed April 30, 1984, for "2-(N-Substituted guanidino)-4-heteroarylthiazole Antiulcer Agents." The method of preparing said N-pentylguanidino compound and employing same as an antiulcer and/or as a gastric antisecretory agent is also detailed hereinafter. Web site: http://www.delphion.com/details?pn=US04591595__ ·
2-halo-2'-deoxyadenosines in the treatment of rheumatoid arthritis Inventor(s): Carson; Dennis A. (Del Mar, CA), Carrera; Carlos J. (San Digeo, CA) Assignee(s): The Scripps Research Institute (La Jolla, CA) Patent Number: 5,310,732 Date filed: February 19, 1992 Abstract: Novel adenine derivatives whose structures are represented by Formula I, are disclosed, as are methods of using those compounds and others of Formula II to treat monocyte-mediated disorders such as rheumatoid arthritis and multiple sclerosis. Excerpt(s): This invention relates to agents that are useful in the treatment of chronic inflammatory diseases, infection, and autoimmune disorders. More particularly, this invention relates to a compound and a method of treatment for monocyte-mediated diseases or disease states (disorders). In one specific aspect, this invention pertains to a method for treating diseases in which a pathogen resides in monocytes. In a second specific aspect, this invention pertains to the treatment of monocyte-mediated autoimmune disorders, or other chronic inflammatory diseases in which monocyte activation contributes to and thus mediates the pathology of the disease. ... Chan et al. (1982) J. Cell Physiol., 111:28-32 studied the pathways of pyrimidine nucleotide metabolism in murine peritoneal macrophages and monocytes, and reported undetectable levels of deoxycytidine kinase or thymidine kinase in these cells. High levels of adenosine kinase were found, however. ... Similar high levels of adenosine kinase have been found in human monocytes and human monocyte-derived macrophages (MDM) in work carried out in the inventors' laboratory. In the preliminary work, MDM were found to exhibit about one-tenth to about one-fourth the nucleoside kinase activity of GEM T lymphoblasts (e.g. ATCC CCL 119) toward uridine, deoxycytidine and thymidine, and about two-thirds the adenosine kinase activity of GEM cells. In addition, that adenosine kinase activity of MDM cells was at least about 10-fold higher than any of the other kinase activities. Those studies also indicated relatively low levels of nucleoside phosphorylation using AZT, dideoxycytidine (ddC) and 2',3'-dideoxyadenosine (ddA) in intact GEM T lymphoblasts and still lower levels with the MDM.
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Web site: http://www.delphion.com/details?pn=US05310732__ ·
Acyl cyanoguanidines for treating rheumatoid arthritis Inventor(s): Shen; Tsung-Ying (Westfield, NJ), Jones; Howard (Holmdel, NJ) Assignee(s): Merck & Co., Inc. (Rahway, NJ) Patent Number: 4,202,903 Date filed: September 30, 1975 Abstract: Certain novel acyl cyanoguanidines, their preparation, pharmaceutical compositions and novel methods of treating inflammation and autoimmune diseases such as rheumatoid arthritis are disclosed. Excerpt(s): In spite of the extensive antiinflammatory research in the past two decades there is still an obvious need for an effective and well-tolerated agent for the treatment of rheumatoid arthritis. Conventional antiinflammatory-analgesic-antipyretic agents, such as aspirin, and many experimental new drugs under clinical evaluation, are mostly effective in providing symptomatic relief of the acute syndrome only. As a consequence, the antirheumatic actions of two other remedies, gold and particularly D-penicillamine, have received renewed interest in the past few years. The clinical efficiancy of both drugs has been confirmed by well-controlled multi-center clinical studies. Impressed by these findings, a growing population of rheumatologists have expressed the opinion that compounds possessing properties similar to D-penicillamine should be a valuable contribution to medicine in this important field. Thus it is an important discovery that acyl cyanoguanidines possess immunological properties similar to that of Dpenicillamine, being of value in the treatment of rheumatoid arthritis and related inflammatory disorders, as well as antiinflammatory properties. ... 1-[3'-(4'methylthionicotinoyl)]-3-cyanoguanidine. ... Another aspect of this invention relates to the novel pharmaceutical compositions for treating inflammation and autoimmune diseases, such as rheumatoid arthritis, comprising a non-toxic pharmaceutically acceptable carrier and a compound of the formula I, supra, wherein R is as defined above. Web site: http://www.delphion.com/details?pn=US04202903__
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Analgesic composition useful in providing a temporary relief from symptoms of arthritis Inventor(s): Beck; Fred (P.O. Box 693, 999 Old Town Rd., Coram, NY 11727) Assignee(s): none reported Patent Number: 5,073,366 Date filed: May 30, 1989 Abstract: An analgesic composition useful in providing temporary relief from the symptoms of arthritis is disclosedng having the following components in approximately the stated weight-percentages ranges: Excerpt(s): The present invention relates, generally, to an analgesic composition useful in temporarily relieving the effects of arthritis. More particularly, the present invention relates to an analgesic composition, preferably in the form of a gel, which is to be applied externally by a patient to areas of arthritic pain. ... It is, therefore, an object of the
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present invention to provide an analgesic composition useful in providing temporary relief from the symptoms of arthritis that is both safe and effective. ... It is a further object of the present invention to provide an analgesic gel preparation, useful in the temporary relief of arthritic pain, which is economical to manufacture and which may be dispensed without a prescription. Web site: http://www.delphion.com/details?pn=US05073366__ ·
Anti immune complex antibody for determining SLE, rheumatoid arthritis or tetanus Inventor(s): Soma; Kazunori (Tokyo, JP), Kasahara; Yasushi (Tokyo, JP) Assignee(s): Fujizoki Pharmaceutical Co., Ltd. (Tokyo, JP) Patent Number: 4,544,640 Date filed: April 7, 1983 Abstract: An antibody is obtained by using as an antigen a complex of an antigen and the F(ab').sub.2 fragment of the human antibody of this antigen or an aggregate of the F(ab').sub.2 fragment of human immunoglobulin. This antibody reacts with an immune complex in a blood serum of a patient of systemic lupus erythematosus and with an immune complex in a blood serum of a patient of rheumatoid arthritis, and it does not react with an aggregated IgG. The amount of immune complex in a blood serum is easily and exactly determined by using this antibody. Excerpt(s): This invention related to a novel antibody capable of detecting an immune complex and relates to its preparation method and use. ... Immune complex is the combined product of an antigen, an antibody and a complement. When this immune complex is formed in a human body, the immune complex is usually rendered harmless by a leucocyte or a macrophage. However, when a large quantity of antigen exists in a human body, or when an antigen the antibody of which forms with difficulty, exists in a human body, the amount of immune complex increases, and it causes various diseases such as acute glomerulonephritis, angitis, chronic urticaria, and thrombocytopenia. ... Various measuring methods of this immune complex are known such as the method utilizing a reaction of complement or rheumatoid factor with the immune complex, the method utilizing a reaction of the Fc receptor with the immune complex, and various physicochemical methods such as the gel filtration method, the sucrose density gradient centrifuge and precipitation with polyethyleneglycol. However, the method using the complement or rheumatoid factor and the method using Fc receptor have a fatal defect in that these methods cannot distinguish between aggregated IgG and the immune complex. The physicochemical methods are complicated and they are insufficient in specificity. Web site: http://www.delphion.com/details?pn=US04544640__
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Antiangiogenic drug to treat cancer, arthritis and retinopathy Inventor(s): Henkin; Jack (Highland Park, IL), Bouck; Noel P. (Oak Park, IL), Dawson; David W. (Chicago, IL), Schneider; Andrew J. (Gurnee, IL) Assignee(s): Abbott Laboratories (Abbott Park, IL) Patent Number: 5,932,545 Date filed: March 16, 1998
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Abstract: Peptides having the formula:T-Gly-Val-D-Ile-Thr-Arg-Ile-U,V-Gly-D-Val-IleD-Thr-D-Arg-D-Ile-W,X-D-Arg-D-Ile-D-Arg-D-Thr-lle-D-Val-Y, andZ-Gly-Val-Ile-ThrArg-Ile-Uwherein T is absent or is selected from N-protecting group and a polypeptide of up to 12 amino acid residues optionally terminated with a N-protecting group; U is selected from Arg and Arg-NR.sup.1 R.sup.2 wherein R.sup.1 and R.sup.2 are independently selected from hydrogen and alkyl of one to four carbon atoms; V is absent or a N-protecting group; W is selected from D-Arg and D-Arg-NR.sup.1 R.sup.2 ; X is absent or a N-protecting group; Y is selected from Gly and Gly-NR.sup.1 R.sup.2 ; and Z is 1-12 amino acid residues optionally terminated with a N-protecting group wherein at least one of the amino acid residues is a D-amino acid residue inhibit angiogenesis and are useful in the treatment of disease states such as cancer, arthritis, macular degeneration and diabetic retinopathyin which angiogenesis plays a role. Excerpt(s): The present invention relates to compounds useful for treating pathological states which arise or are exacerbated by angiogenesis. More particularly, the invention relates to certain peptides which inhibit angiogenesis, to pharmaceutical compositions comprising these compounds and to a method inhibiting angiogenesis. ... Angiogenesis is the fundamental process by which new blood vessels are formed and is essential to a variety of normal body activities (such as reproduction, development and wound repair). Although the process is not completely understood, it is believed to involve a complex interplay of molecules which both stimulate and inhibit the growth of endothelial cells, the primary cells of the capillary blood vessels. Under normal conditions, these molecules appear to maintain the microvasculature in a quiescent state (i.e. one of no capillary growth) for prolonged periods which may last for as long as weeks or in some cases, decades. When necessary however (such as during wound repair), these same cells can undergo rapid proliferation and turnover within a 5 day period. (Folkman, J. and Shing, Y., The Journal of Biological Chemistry, 267(16): 1093110934, and Folkman, J. and Klagsbrun, M., Science, 235: 442-447 (1987)). ... Although angiogenesis is a highly regulated process under normal conditions, many diseases (characterized as "angiogenic diseases") are driven by persistent unregulated angiogenesis. Otherwise stated, unregulated angiogenesis may either cause a particular disease directly or exascerbate an existing pathological condition. For example, ocular neovacularization has been implicated as the most common cause of blindness and dominates approximately 20 eye diseases. In certain existing conditions such as arthritis, newly formed capillary blood vessels invade the joints and destroy cartilage. In diabetes, new capillaries formed in the retina invade the vitreous, bleed, and cause blindness. Growth and metastasis of solid tumors are also angiogenesis-dependent (Folkman, J., Cancer Research, 46: 467-473 (1986), Folkman, J., Journal of the National Cancer Institute, 82: 4-6 (1989)). It has been shown for example that tumors which enlarge to greater than 2 mm, must obtain their own blood supply and do so by inducing the growth of new capillary blood vessels. Once these new blood vessels become embedded in the tumor, they provide a means for tumor cells to enter the circulation and metastasize to distant sites, such as liver, lung or bone (Weidner, N., et al., The New England Journal of Medicine, 324(1): 1-8 (1991)). Web site: http://www.delphion.com/details?pn=US05932545__
Patents 301
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Antibody against rheumatoid arthritis specific protein Inventor(s): Yamanaka; Naoki (Nagoya, JP), Yoshida; Makoto (Kawasaki, JP) Assignee(s): Asahi Medical Co., Ltd. (Tokyo, JP), Medecs Co., Ltd. (Nagoya, JP) Patent Number: 4,950,741 Date filed: February 16, 1988 Abstract: A substantially pure rheumatoid arthritis specific protein (RASP) and an antibody against the rheumatoid arthritis specific protein (anti-RASP antibody) are disclosed. The RASP is found specifically in the serum or plasma of a patient suffering from rheumatoid arthritis, and may be detected using an anti-RASP antibody easily and effectively. Therefore, the anti-RASP antibody of the present invention is useful for the diagnosis of rheumatoid arthritis by the criterion of the presence of RASP. Excerpt(s): (3) an electrophoretic mobility of about 0.30 to 0.45 in terms of a value as measured by a two-dimensional electrophoresis method as defined herein. ... and which antibody has a molecular weight of about 150,000 to 160,000 in terms of a value as measured by an SDS-polyacrylamide gel electrophoresis method as defined herein. ... Now, a substantially pure rheumatoid arthritis specific protein of the present invention will be explained below. Web site: http://www.delphion.com/details?pn=US04950741__
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Antigens recognized by antibodies to rheumatoid arthritis, their preparation and their applications Inventor(s): Serre; Guy (Toulouse, FR), Somme; Gerard (Bures Sur Yvette, FR), Vincent; Christian (Lauzerville, FR) Assignee(s): Biomerieux S.A. (Marcy L'Etoile, FR) Patent Number: 5,888,833 Date filed: June 3, 1994 Abstract: The present invention relates to antigens extracted from mammalian malpighian epithelia, in particular rat esophageal epithelium or human epidermis, which are specifically recognized by the autoantibodies present in patients suffering form rheumatoid arthritis in respect of antigenic determinants in common with filaggrin and human profilaggrin, as well as to the antigenic proteins of which said antigens are composed and to the peptide fragments derived therefrom. The invention relates to the use of these antigens, proteins and peptide fragments, and that of filaggrin and human profilaggrin, for the preparation of antigenic compositions, and to their applications, in particular for the diagnosis of rheumatoid arthritis. The invention also relates to the preparation of antibodies directed towards these antigens, and to their applications. Excerpt(s): The present invention relates to the use of human filaggrin and antigens related thereto for the diagnosis or treatment of rheumatoid arthritis (RA). ... The presence of autoantibodies directed towards cellular components is the general feature of autoimmune diseases such as RA, systemic lupus erythematosus, scleroderma or polymyositis. Among the many types of autoantibodies identified in these diseases, those specifically present in patients suffering from RA and reacting with an esophageal epithelial antigen were described for the first time by B. J. J. Young et al. in Br. Med. J. 2:97-99, (1979). These autoantibodies were named at the time "antikeratin antibodies". Hitherto, it was commonly accepted that they were directed towards cytokeratins. ...
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These autoantibodies specific to RA are at the present time detected and titrated by indirect immuno-fluorescence (IIF) on transverse cryosections of rat esophagus. Web site: http://www.delphion.com/details?pn=US05888833__ ·
Anti-human stromelysin monoclonal antibody and method for diagnosis of rheumatoid arthritis by enzyme immunoassay Inventor(s): Okada; Yasunori (32, Wakamiya 2-chome, Matto-shi, Ishikawa-ken, 924, JP), Shinmei; Masayoshi (4-4, Nakaaral 4-chome, Tokorozawa-shi, Saitama-ken, 359, JP), Hayakawa; Taro (406, Mukaigaoka 3-chome, Tenpaku-ku, Nagoya-shi, Aichi-ken, 468, JP), Iwata; Kazushi (190 Ikarihigashimachi, Takaoka-shi, Toyama-ken, 933, JP), Korin; Yumi (Fu-134, Takamatsucho, Kahoku-gun, Ishikawa-ken, 929-12, JP), Kodama; Shuji (603, Takaokasukaihaitsu, 1868, Nagae, Takaoka-shi, Toyama-ken, 933, JP), Yoshida; Shinichi (13-16, Nakajima 4-chome, Toyama-shi, Toyama-ken, 930, JP) Assignee(s): none reported Patent Number: 5,834,212 Date filed: April 6, 1995 Abstract: Anti-human stromelysin monoclonal antibodies reactive with latent and active forms of stromelysin without discrimination between the two, each being immunoreactive with only one of the antigenic determinants of human stromelysin, are provided. The use of a combination of two such monoclonal antibodies which specifically react with different antigenic determinants of human stromelysin renders it possible to accurately determine the amount of human stromelysin in human body fluids, and thus to carry out the diagnosis of rheumatoid arthritis.There are thus provided said monoclonal antibodies per se, a sandwich enzyme immunoassay for the determination of the amount of human stromelysin in human body fluid samples using a combination of two such monoclonal antibodies, and a method for the diagnosis of rheumatoid arthritis using said immunoassay. Excerpt(s): The present invention relates to anti-human stromelysin monoclonal antibodies, an enzyme immunoassay using such monoclonal antibodies, and a method for the diagnosis of rheumatoid arthritis by determination, on the basis of said immunoassay, of the amount of human stromelysin present in samples as the sum of the amount of latent stromelysin and that of active stromelysin. ... Stromelysin, also called proteoglycanase or MMP-3 (matrix metalloproteinase-3), is a substance produced in fibroblasts or tumor cells stimulated by different cytokines, growth factors, etc. In the live body, it is present in blood or synovial fluids, besides being produced locally in joints of patients with rheumatoid arthritis. ... Stromelysin has been considered to play an important role in the intraarticular cartilage destruction in patients with rheumatoid arthritis since it decomposes gelatin, laminin, type IV collagen, fibronectin etc. in addition to proteoglycan and type IX collagen, both being important extracellular matrices for articular cartilage. Web site: http://www.delphion.com/details?pn=US05834212__
Patents 303
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Anti-TNF antibodies and methotrexate in the treatment of arthritis and crohn's disease Inventor(s): Feldman; Marc (Highgate, GB), Maini; Ravinder N. (London, GB) Assignee(s): The Kennedy Institute of Rheumatology (London, GB) Patent Number: 6,270,766 Date filed: August 1, 1996 Abstract: Methods for treating and/or preventing a TNF-mediated disease in an individual are disclosed. Also disclosed is a composition comprising methotrexate and an anti-tumor necrosis factor antibody. TNF-mediated diseases include rheumatoid arthritis, Crohn's disease, and acute and chronic immune diseases associated with transplantation. Excerpt(s): Monocytes and macrophages secrete cytokines known as tumor necrosis factor alpha (TNF.alpha.) and tumor necrosis factor beta (TNF.beta.) in response to endotoxin or other stimuli. TNF.alpha. is a soluble homotrimer of 17 kD protein subunits (Smith et al., J. Biol. Chem. 262:6951-6954 (1987)). A membrane-bound 26 kD precursor form of TNF also exists (Kriegler et al., Cell 53:45-53 (1988)). For reviews of TNF, see Beutler et al., Nature 320:584 (1986); Old, Science 230:630 (1986); and Le et al., Lab. Invest. 56:234 (1987). ... Cells other than monocytes or macrophages also produce TNF.alpha.. For example, human non-monocytic tumor cell lines produce tumor necrosis factor (TNF) (Rubin et al., J. Exp. Med. 164:1350 (1986); Spriggs et al., Proc. Natl. Acad. Sci. USA 84:6563 (1987)). CD4+ and CD8+ peripheral blood T lymphocytes and some cultured T and B cell lines (Cuturi et al., J. Exp. Med. 165:1581 (1987); Sung et al., J. Exp. Med. 168:1539 (1988); Turner et al., Eur. J. Immunol. 17:1807-1814 (1987)) also produce TNF.alpha.. ... Recent evidence associates TNF with infections (Cerami et al., Immunol. Today 9:28 (1988)), immune disorders, neoplastic pathologies (Oliff et al., Cell 50:555 (1987)), autoimmune pathologies and graft-versus-host pathologies (Piguet et al., J. Exp. Med. 166:1280 (1987)). The association of TNF with cancer and infectious pathologies is often related to the host's catabolic state. Cancer patients suffer from weight loss, usually associated with anorexia. Web site: http://www.delphion.com/details?pn=US06270766__
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Apparatus and method for treating rheumatoid and psoriatic arthritis Inventor(s): Diamond; Donald A. (5416 Harbor Rd., Bradenton, FL 34209-1832) Assignee(s): none reported Patent Number: 5,511,563 Date filed: February 18, 1994 Abstract: An apparatus and method for irradiating an inflamed joint of a patient having rheumatoid or psoriatic arthritis are presented. A noncoherent source of radiation having a predetermined wavelength range is utilized to transilluminate affected tissues of the subject for a predetermined duration. The radiation source has sufficient intensity and is applied for sufficient duration to reducing inflammation and substantially halt disease progression. Excerpt(s): This invention relates to apparatus and methods for therapeutic intervention of the complex immune response in rheumatoid and psoriatic arthritis. ... Arthritis is a general term that encompasses several distinguishable joint disorders, such as
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osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, and psoriatic arthritis. ... Osteoarthritis, also known as degenerative joint disease, is caused by long-term wear and tear on the protective cartilage that lines the inner surfaces of joints. Although typically a disorder of old age, certain predisposing conditions can hasten the degenerative process in younger persons. Symptoms may include joint aching and stiffness, with x rays showing a narrowing of the joint space and new bone formation adjacent to the joint. Treatment includes anti-inflammatory medication, heat, and physical therapy; in severe cases refractory to conservative treatment surgery, including joint replacement, may be necessary. Web site: http://www.delphion.com/details?pn=US05511563__ ·
Arthritis treatment Inventor(s): Lysaght; Wallace (9 Coniston Ave., Te Atatu South, Auckland, NZ) Assignee(s): none reported Patent Number: 4,387,093 Date filed: December 18, 1981 Abstract: This invention relates to the treatment of arthritis by administering cobalts in a form acceptable to the body. The dosage typically comprises measured amounts of cyanocobalamin, potassium iodide, magnesium sulphate and ferrous sulphate. Excerpt(s): This invention relates to a dietary supplement suitable for restoring the body chemistry to deal with various disorders such as arthritis, and to a method of treating such disorders. ... Arthritis is a very common disease for which orthodox medical treatment is generally ineffective. It is an object of the present invention to provide a means whereby arthritis may be effectively treated. ... In a first aspect the present invention consists in a method of treating a bodily disorder, the method comprising administering a non-lethal dose of a cobalt compound. Web site: http://www.delphion.com/details?pn=US04387093__
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Arthritis treatment with hypoxanthine Inventor(s): Livingston; William S. (1080 Triunfo Canyon Rd., West Lake Village, CA 91361) Assignee(s): none reported Patent Number: 4,931,431 Date filed: June 2, 1988 Abstract: The complex mixture of substances in the product made from human placentae according to the procedure described in U.S. Pat. Nos. 3,526,697 and 4,335,040 includes hypoxanthine. Hypoxanthine is effective in treating arthritis, particularly if administered intradermally at low (e.g., not more than about 0.1 mg. of hypoxanthine per does) dose. Preferably, the dose level is not more than about 0.00002 mg. active material per dose, e.g., 0.1 cc of a dilution not stronger than about 1 mg. of active material per 5,000 ml of diluent. Excerpt(s): This invention relates to the treatment of arthritis and more particularly, to such treatment by intradermal administration of low doses of hypoxanthine. ... U.S. Pat.
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Nos. 3,526,697 and 4,335,040 disclose producing a therapeutic product by a process of autolysis of animal tissue in which a quantity of material comprising animal tissue is placed in a pressure vessel, the vessel is enclosed, sealed, and maintained at a temperature in the range of about 5 to about 65 degrees centigrade and a pressure in the range of about 15 to 45 psig for a period of not less than about two weeks, and the liquid portion of the semi-liquid thereby produced is recovered and sterilized. As discussed in such patents, the material thus produced is useful in the treatment of rheumatoid arthritis and osteoarthritis. The patents state that treatment is by intravenous or intercutaneous injection, preferably intercutaneous, and that mice have been treated intraperitonically. ... Livingston Placental Autolyste ("LPA") is a complex mixture of substances derived from the autolysis of human placentae under the conditions defined in the patents, and in the California veterinarian industry is known as "Scott A-510". The use of LPA in the treatment of cancer tumors and arthritis has been reported in e.g., Livingston, W. S., "The Treatment of Spontaneous Tumors of the Dog and Cat With a Filtrate From a Tissue Lysate", J. Nat. Cancer Inst., 1958, 20:245-306; Livingston, W. S., "Growth Inhibition of Transplantable Mouse Lyphosarcoma by a Filtrate from Placental Lysate", J. Nat. Cancer Inst., 1959, 23:597-603; Bender, W. M. "Nontraditional Treatment of Mycosis Fungoides in a Dog", J. Am. Vet. Med. Assn. 1984, 185:900-901; and Maxson, T. R. and Compton, E. L., "Controlled Study of a New Anti-Arthritic Substance", Ann. Allergy, 1969, 21:54-64. Web site: http://www.delphion.com/details?pn=US04931431__ ·
Arthritis, muscle pain, and dry skin remedy Inventor(s): Merich, deceased; Nick (late of Daytona Beach, FL) Assignee(s): none reported Patent Number: 6,146,639 Date filed: July 26, 1999 Abstract: An arthritis, muscle pain, and dry skin remedy is provided containing rubbing alcohol, witch hazel, and olive oil. In the preferred embodiment, the remedy contains sixteen parts rubbing alcohol, sixteen parts witch hazel, and four parts olive oil. An alternate embodiment arthritis, muscle pain, and dry skin remedy is also disclosed which relieves symptoms of muscle pain, arthritis, and dry, scaly skin in horses. This alternate remedy uses castor oil instead of olive oil. Excerpt(s): This invention relates to arthritis remedies, and in particular to an arthritis and muscle pain remedy which also treats dry or scaly skin. ... Arthritis is a term which refers to a group of diseases which affect the joint. Symptoms of arthritis include pain, stiffness and swelling of the affected joints. The disease is a serious problem in that it is very widely spread. For example, in the United States alone more than 31 million individuals suffer from arthritis. The two main types of arthritis are osteoarthritis and rheumatoid arthritis. ... Osteoarthritis is also referred to as degenerative joint disease, and occurs where the joint itself wears out. This strain of arthritis is common in elderly people, and it may also occur where a joint has been injured repeatedly. The most commonly affected joints are in the hands, knees, lower back and neck. Web site: http://www.delphion.com/details?pn=US06146639__
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Azabenzimidazoles in the treatment of asthma, arthritis and related diseases Inventor(s): Marfat; Anthony (Mystic, CT), Eggler; James F. (Stonington, CT), Fray; Michael J. (Wingham, GB), Cooper; Kelvin (Noank, CT) Assignee(s): Pfizer Inc. (New York, NY) Patent Number: 5,322,847 Date filed: November 5, 1992 Abstract: A series of imidazo[4,5-c]pyridines which inhibit platelet activating factor (PAF) and also block leukotriene D4 receptors are useful in treating asthma, arthritis, psoriasis, gastrointestinal distress, myocardial infarction, stroke and shock. Excerpt(s): This application is a continuation of International Application PCT/US91/02997, filed 01 May 1991, entitled "Azabenzimidazoles in the Treatment of Asthma, Arthritis and Related Diseases," which is a continuation-in-part of U.S. Ser. No. 07/521,199, filed 09 May 1990, entitled "Azabenzimidazoles in the Treatment of Asthma, Arthritis and Related Diseases" (now abandoned). ... The present invention is directed to azabenzimidazoles of formula I, which as inhibitors of platelet activating factor (PAF) and of LTD.sub.4 receptor binding sites are useful in the treatment or prevention to of asthma, arthritis, psoriasis and a wide range of inflammatory disorders. ... More recently, International Application PCT/US89/00975, Publication No. WO 89/08653, describes the preparation of 1-carbamylbenzvlimidazo[4,5-c]pyridines useful as PAF antagonists. Web site: http://www.delphion.com/details?pn=US05322847__
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Benzoylecgonine or benzoylnorecgonine as active agents for the treatment of rheumatoid arthritis Inventor(s): Somers; Lowell (16630 Mountain View Rd., Desert Hot Springs, CA 92240) Assignee(s): none reported Patent Number: 4,512,996 Date filed: February 29, 1984 Abstract: Pharmaceutical formulation containing benzoylecgonine and/or benzoylnorecgonine and their use in the treatment of rheumatoid arthritis are disclosed. Excerpt(s): This invention relates to pharmaceutical compositions and dosage forms and their use in the treatment of chronic disease. More particularly, it concerns pharmaceutical compositions and dosage forms and their use in the treatment of the pain and locomotor dysfunction of rheumatoid arthritis. ... Rheumatoid arthritis is a serious, often crippling, disease characterized by pain and locomotor dysfunction. As pointed out by Nickander et al in their article "Nonsteroidal Antiinflammatory Agents" which appeared at Ann. Rev. Pharmacol. Toxical., 1979, 19:469-90, this sort of pain and locomotor dysfunction are among man's most common and frustrating afflictions. The gravity of this disease has led to the investigation and/or adoption of a wide range of drugs for its alleviation. Aspirin has been commonly used since the turn of this century. Other major drugs for arthritis have historically included indomethacin, other salicylates, phenylbutazone, steroids and gold. While more recently, fenoprofen, ibuprofen, naproxen, sulindac and tolmetin have been approved for use in the United States. ... While these compounds can offer antiinflammatory, antipyretic and analgesic effects and have proven helpful in the management of rheumatoid arthritis in many
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patients, when combined with other modalities such as proper rest, exercise, physical therapy and surgery, they are less than ideal. Many exhibit serious side-effects with many patients, particularly gastrointestinal damage and renal toxicity. Each of these materials have the failing of being far from universal--some patients will respond to one material while others respond favorably only to others. Web site: http://www.delphion.com/details?pn=US04512996__ ·
Benzoylecgonine, benzoylnorecgonine and ecgonine as active agents for the treatment of rheumatoid arthritis and osteoarthritis Inventor(s): Somers; Lowell M. (46861 Madison, Indio, CA 92201) Assignee(s): none reported Patent Number: 4,556,663 Date filed: August 31, 1984 Abstract: Pharmaceutical preparations containing benzoylecgonine, benzoylnorecgonine, and ecgonine are disclosed for treatment of rheumatoid arthritis, and in case of benzoylecgonine and benzoylnorecgonine for the treatment of osteoarthritis as well. The pharmaceutical preparations containing the active compounds are administered to human patients in effective amounts orally, through inhalation, transdermally or through the mucosal membranes. Excerpt(s): This invention relates to pharmaceutical compositions, dosage forms and their use in the treatment of chronic disease. More particularly, it concerns pharmaceutical compositions and dosage forms and their use in the treatment of the pain and locomotor dysfunction of rheumatoid arthritis, and osteoarthritis. ... Rheumatoid arthritis is a serious, often crippling, disease characterized by pain and locomotor dysfunction. As pointed out by Nickander et al in their article "Nonsteroidal Antiinflammatory Agents" which appeared at Ann. Rev. Pharmacol. Toxicol., 1979, 19:469-90, this sort of pain and locomotor dysfunction are among man's most common and frustrating afflictions. The gravity of this disease has led to the investigation and/or adoption of a wide range of drugs for its alleviation. Aspirin has been commonly used since the turn of this century. Other major drugs for arthritis have historically included indomethacin, other salicylates, phenylbutazone, steroids and gold. While more recently, fenoprofen, ibuprofen, naproxen, sulindac and tolmetin have been approved for use in the United States. ... While these compounds can offer antiinflammatory, antipyretic and analgesic effects and have proven helpful in the management of rheumatoid arthritis in many patients, when combined with other modalities such as proper rest, exercise, physical therapy and surgery, they are less than ideal. Many exhibit serious side effects with many patients, particularly gastrointestinal damage and renal toxicity. Each of these materials have the failing of being far from universal--some patients will respond to one material while others respond favorably only to others. Web site: http://www.delphion.com/details?pn=US04556663__
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Biological treatment for rheumatoid arthritis Inventor(s): Fort; John G. (Philadelphia, PA), Smith; J. Bruce (Philadelphia, PA) Assignee(s): Thomas Jefferson University (Philadelphia, PA) Patent Number: 5,723,503 Date filed: September 28, 1994 Abstract: A method of treating rheumatoid arthritis is provided which involves administering an effective amount of allogeneic mononuclear cells or a molecule derived from these cells to an individual having rheumatoid arthritis. Also provided are compositions for the treatment of rheumatoid arthritis. Excerpt(s): Tens of millions of people in the United States suffer from rheumatoid arthritis (RA) or a related disease. While arthritis results in significantly fewer deaths as compared to cancer and cardiovascular diseases, there is no other group of diseases that causes so much suffering in so many people for such a prolonged period of time. Because of the tendency to disable and even permanently cripple individuals suffering from arthritis, this group of diseases is extremely important both socially and economically. There is presently no satisfactory cure for rheumatoid arthritis because its cause is unknown. In addition, many of the therapeutic agents administered to alleviate pain and inflammation associated with the disease, such as disease-modifying antirheumatic drugs (DMARDs) and non-steroidal anti-inflammatory agents (NSAIDs), produce intolerable side effects. ... The understanding of the RA disease process has been considerably enhanced by the application of molecular immunology techniques. It is now generally accepted that rheumatoid arthritis represents a multifactorial disease with environmental factors (infectious agents or toxins), genetic susceptibility, and immune or autoimmune responses playing inter-connected roles. After initiation of the disease process, it is believed that activated T cells and their products are responsible for the progressive destruction of articular cartilage and sub-chondral bone that is characteristic of rheumatoid arthritis. ... Advances in the understanding of the immunopathogenesis of rheumatoid arthritis have been coupled with immunologic strategies for treatment. Immunologic approaches to the treatment of rheumatoid arthritis are important and desirable given the potential toxicities associated with most remittive therapy in use today and the continued poor prognosis of rheumatoid arthritis despite aggressive drug treatment. Web site: http://www.delphion.com/details?pn=US05723503__
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Biphenyl hydroxy imino butyric acids and their derivatives for treating arthritis Inventor(s): Purchase, Jr.; Claude Forsey (Ann Arbor, MI), Roth; Bruce David (Plymouth, MI), Schielke; Gerald Paul (Ann Arbor, MI), Walker; Lary Craswell (Ann Arbor, MI), White; Andrew David (Pinckney, MI) Assignee(s): Warner-Lambert Company (Morris Plains, NJ) Patent Number: 6,239,288 Date filed: March 2, 1999 Abstract: Biphenyl butyric acid compounds and derivatives are described as well as acid methods for the preparation and pharmaceutical compositions of same, which are useful as inhibitors of matrix metalloproteinases, particularly gelatinase A (72 kD gelatinase) and stromelysin-1 and for the treatment of multiple sclerosis, atherosclerotic plaque
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rupture, aortic aneurism, heart failure, restenosis, periodontal disease, corneal ulceration, treatment of bums, decubital ulcers, wound healing, cancer, inflammation, pain, arthritis, or other autoimmune or inflammatory disorders dependent upon tissue invasion by leukocytes or other activated migrating cells, acute and chronic neurodegenerative disorders including stroke, head trauma, spinal cord injury, Alzheimer's disease, amyotrophic lateral sclerosis, cerebral amyloid angiopathy, AIDS, Parkinson's disease, Huntington's disease, prion diseases, myasthenia gravis, and Duchenne's muscular dystrophy. Excerpt(s): The present invention relates to novel biphenyl butyric acid compounds and their derivatives useful as pharmaceutical agents, to methods for their production, to pharmaceutical compositions which include these compounds and a pharmaceutically acceptable carrier, and to pharmaceutical methods of treatment. The novel compounds of the present invention are inhibitors of matrix metalloproteinases, e.g., gelatinase A (72 kDa gelatinase) and stromelysin-1. More particularly, the novel compounds of the present invention are useful in the treatment of atherosclerotic plaque rupture, aortic aneurism, heart failure, restenosis, periodontal disease, corneal ulceration, treatment of burns, decubital ulcers, wound repair, cancer, inflammation, pain, arthritis, multiple sclerosis, and other autoimmune or inflammatory disorders dependent on the tissue invasion of leukocytes or other activated migrating cells. Additionally, the compounds of the present invention are useful in the treatment of acute and chronic neurodegenerative disorders including stroke, head trauma, spinal cord injury, Alzheimer's disease, amyotrophic lateral sclerosis, cerebral amyloid angiopathy, AIDS, Parkinson's disease, Huntington's disease, prion diseases, myasthenia gravis, and Duchenne's muscular dystrophy. ... Gelatinase A and stromelysin-1 are members of the matrix metalloproteinase (MMP) family (Woessner J. F., FASEB J., 1991;5:2145-2154). Other members include fibroblast collagenase, neutrophil collagenase, gelatinase B (92 kDa gelatinase), stromelysin-2, stromelysin-3, matrilysin, collagenase 3 (Freije J. M., Diez-Itza I., Balbin M., Sanchez L. M., Blasco R., Tolivia J., and Lopez-Otin C., J. Biol. Chem., 1994;269:16766-16773), and the membrane-associated matrix metalloproteinases (Sato H., Takino T., Okada Y., Cao J., Shinagawa A., Yamamoto E., and Seiki M., Nature, 1994;370:61-65). ... The catalytic zinc in matrix metalloproteinases is a focal point for inhibitor design. The modification of substrates by introducing chelating groups has generated potent inhibitors such as peptide hydroxymates and thiol-containing peptides. Peptide hydroxamates and the natural endogenous inhibitors of MMPs (TIMPs) have been used successfully to treat animal models of cancer and inflammation. Web site: http://www.delphion.com/details?pn=US06239288__ ·
Chronic rheumatoid arthritis therapy containing IL-6 antagonist as effective component Inventor(s): Kishimoto; Tadamitsu (Tondabayashi, JP), Mihara; Masahiko (Gotenba, JP), Moriya; Yoichiro (Gotenba, JP), Ohsugi; Yoshiyuki (Gotenba, JP) Assignee(s): Chugai Seiyaku Kabushiki Kaisha (Tokyo, JP), Tadamitsu Kishimoto (Tondabayashi, JP) Patent Number: 5,888,510 Date filed: April 7, 1997 Abstract: Methods for inhibiting synovial cell growth and treating chronic rheumatoid arthritis are provided. The methods comprise administering a pharmaceutical
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composition comprising an interleukin-6 antagonist, such as an anti-IL-6 receptor antibody, and a physiologically acceptable carrier. Excerpt(s): The present invention relates to a chronic rheumatoid arthritis therapy or synovial cell growth inhibitor comprising an interleukin-6 antagonist as an effective component. ... Chronic rheumatoid arthritis is a systemic chronic inflammatory disease in which abnormal growth of connective tissue, including synovial tissue, occurs in the joints (Melnyk et al., Arthritis Rheum. 33: 493-500, 1990). The joints of chronic rheumatoid arthritis patients have been shown to have marked growth of synovial cells, formation of a multilayer structure due to abnormal growth of the synovial cells (pannus formation), invasion of the synovial cells into cartilage tissue and bone tissue, vascularization toward the synovial tissue, and infiltration of inflammatory cells such as lymphocytes and macrophages. Mechanisms of onset of chronic rheumatoid arthritis have been reported to be based on such factors as heredity, bacterial infection and the contribution of various cytokines and growth factors, but the overall mechanism of onset has remained unclear. ... In recent years, cytokines and growth factors including interleukin-1 (IL-1), interleukin-8 (IL-8), tumor necrosis factor .alpha. (TNF.alpha.), transforming growth factor .beta. (TGF.beta.), fibroblast growth factor (FGF) and platelet-derived growth factor (PDGF) have been detected in the synovial membrane and synovial fluid of chronic rheumatoid arthritis patients (Nouri et al., Clin. Exp. Immunol. 55:295-302, 1984; Thornton et al., Clin. Exp. Immunol. 86:79-86, 1991; Saxne, et al., Arthritis Rheum. 31:1041-1045, 1988; Seitz et al., J. Clin. Invest. 87:463-469, 1991; Lafyatis et al., J. Immunol. 143:1142-1148, 1989; Melnyk et al., Arthritis Rheum. 33:493500, 1990). Web site: http://www.delphion.com/details?pn=US05888510__ ·
Collagen mimetic and method of treating rheumatoid arthritis using same Inventor(s): Braswell; A. Glenn (6100 Lake Forest Dr., NE., Suite 400, Atlanta, GA 30328), Ahmed; Aftab J. (Marina Del Ray, CA) Assignee(s): Braswell; A. Glenn (Atlanta, GA) Patent Number: 5,849,323 Date filed: June 12, 1997 Abstract: A collagen mimetic peptide having the nine amino acid sequence glycineproline-hydroxyproline-glycine -proline-glutamine-glycine-methionine-glycine, and analogs thereof is described. The collagen mimetic peptide may be included within a pharmaceutical composition also containing a pharmaceutically acceptable carrier and/or animal tissue. The collagen mimetic peptide is used in a treatment of rheumatoid arthritis by orally administering the collagen mimetic in an amount effective to reduce or alleviate one or more symptoms associated with rheumatoid arthritis. Excerpt(s): This invention relates to a specific collagen mimetic peptide, pharmaceutical compositions containing the peptide, and a method of treating rheumatoid arthritis through the oral administration of the peptide and/or pharmaceutical composition. ... Rheumatoid arthritis is an autoimmune disease wherein the immune system of the body mistakenly perceives the body's own collagen as foreign and mounts an abnormal immune response against it. Rheumatoid arthritis is characterized by persistent swollen and inflamed joints, and progresses into the destruction of cartilage and the erosion of bone, ultimately leading to destruction of joints. Collagen, in particular Type II collagen,
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is a major component of cartilage that is particularly affected. ... Known treatments for arthritis have involved the use of nonspecific immunosuppressive drugs which suppress the entire immune system and are incapable of selectively suppressing the abnormal autoimmune response. This restraint of the immune system also increases the risk of infection. In addition, prolonged use of such drugs can entail severe toxic side effects. Moreover, such immunosuppressive drugs are only partially effective in mitigating symptoms of rheumatoid arthritis, and this partial effectiveness greatly decreases even more over time. Web site: http://www.delphion.com/details?pn=US05849323__ ·
Collagen-based methods and formulations for the treatment of arthritis Inventor(s): Neff; Thomas (Laguna Beach, CA), Martin; George (Bethesda, MD), Piez; Karl A. (Chevy Chase, MD), Pihlajaniemi; Taina (Oulunsalo, FI), Kivirikko; Kari I. (Oulu, FI) Assignee(s): FibroGen, Inc. (South San Francisco, CA) Patent Number: 5,925,736 Date filed: May 27, 1998 Abstract: The invention provides novel methods and compositions for the treatment of immune system-mediated arthritis, including rheumatoid arthritis. The subject compositions comprise one or more different types of collagen or collagen derivatives and a mucosa binding structure. Specific combinations of collagen and/or collagen derivatives may be used to treat specific types of arthritis. The collagen(s) and/or collagen(s) derivatives used in the subject compositions may be either obtained from natural sources or produced by recombinant genetic engineering techniques by chemical modification. Another aspect of the invention is to provide methods for treating various types of arthritis by administering an effective amount of the subject collagen-containing compositions. The methods of the invention involve the oral administration of a collagen or collagens found in a specific tissue, e.g., cartilage, so as to induce the suppression (immunological tolerance) of inflammation against the tissue from which the collagen is found to occur in nature. The methods of the invention include the administration of the subject collagen(s) and/or collagen derivative(s) containing compositions into the intestines so as to induce immune tolerance, e.g., oral administration. Excerpt(s): The invention is in the field of autoimmune disease, in particular arthritis, and treatments thereof employing collagen and/or derivatives. ... While the immune system is essential for fighting off infections, the immune response to infections (foreign antigens) and the immune response to molecules produced in the body (autologous antigens) may result in numerous diseases, i.e., immune system-mediated diseases. Immune system-mediated diseases may be either B cell-mediated (i.e., antibodymediated) or T cell-mediated. Additionally, immune system-mediated diseases may be caused by immune complexes formed between antibodies and antigens (either foreign or autologous). Many immune system-mediated diseases involve an undesirable inflammatory response, e.g., diseases which include rheumatoid arthritis, chronic hepatitis, Crohn's Disease, psoriasis, vasculitis, and the like. ... Existing therapies for immune system-mediated diseases, particularly immune system-mediated diseases resulting in an undesirable inflammatory response, such as rheumatoid arthritis, are inadequate. Most immune system-mediated diseases are chronic conditions which require the prolonged administration of drugs. Accordingly, it is important to employ
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relatively non-toxic drugs. However, many compounds used for the treatment of autoimmune diseases, e.g., steroids and non-steroidal anti-inflammatory compounds, have significant toxic side effects that become apparent after long-term use. Additionally, immunosuppressive drugs have been used to treat autoimmune responses. Such immunosuppressive drugs, e.g., cyclosporin A and azathioprine, are relatively non-specific and have the adverse effect of weakening the entire immune system, thereby leaving a patient susceptible to infectious disease. Web site: http://www.delphion.com/details?pn=US05925736__ ·
Combination therapy for rheumatoid arthritis Inventor(s): Ridolfo; Anthony S. (Zionsville, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 4,355,029 Date filed: June 1, 1981 Abstract: A therapeutic method for treating rheumatoid arthritis in which benoxaprofen plus aspirin are administered once a day and aspirin alone three times a day, all dosages being given at six hour intervals. Excerpt(s): This invention provides a novel treatment method for rheumatoid arthritis and other related inflammatory conditions, utilizing combination drug therapy in part, such as a combination of benoxaprofen, a lipoxygenase inhibitor, and a cyclo-oxygenase inhibitor such as aspirin. According to my invention, patients suffering from rheumatoid arthritis are administered from 200 to 800 milligrams of benoxaprofen and from 325 to 1170 of aspirin once a day and then at 6 hour intervals during the remainder of the 24 hour period from 325 to 1170 milligrams of aspirin alone. Preferably, the rheumatoid arthritis patient is given 600 mg. of benoxaprofen plus 975 milligrams (15 grains) of aspirin once a day and 975 milligrams of aspirin alone at 6 hour intervals. The regimen is then repeated on a daily basis. ... The basis for the enhanced therapeutic effect from my novel process is the use of drugs acting at different sites of the inflammatory process. Improvement occurs even though blood levels of benoxaprofen are decreased with the concomitant addition of aspirin. It is an advantage of this invention that in the combination of a lipoxygenase inhibitor such as benoxaprofen and a cyclo-oxygenase inhibitor, each drug can be employed at dose levels lower than the commonly accepted effective dose for the individual drug. ... Benoxaprofen, 2-(2-pchlorophenyl-5-benzoxazolyl)propionic acid, is disclosed in Example 2 of U.S. Pat. Re No. 29,608 reissued April 11, 1978. Web site: http://www.delphion.com/details?pn=US04355029__
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Composition and method for the treatment of arthritis Inventor(s): Burger; John A. (220 10th St., Huntington Beach, CA 92648) Assignee(s): none reported Patent Number: 5,843,919 Date filed: October 22, 1997 Abstract: A composition and method for the treatment of arthritis in animals, such as mammals, and a method for making the composition, is disclosed. The composition
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comprises one or more glucosamines and one or more omega-3-fatty acids and is made by combining an omega-3-fatty acid with a glucosamine. Excerpt(s): This application claims the benefit of the priority of pending Provisional Application 60/032,001, filed Nov. 25, 1996. ... The invention pertains to the field of therapeutic agents to control the symptoms of arthritis, such as osteoarthritis. ... Arthritis is a serious medical condition affecting the joints of humans and domestic animals, such as dogs, cats, horses, and cattle. Osteoarthritis, a chronic degenerative arthritis in which the cartilage of the joint breaks down, is often a sequela of chronic or acute injury to a joint due to any cause such as, for example, trauma, infection, autoimmune disease such as lupus or rheumatoid arthritis, or as a result of wear due to aging. Clinical signs of osteoarthritis can range from mild pain on extension and flexion of a joint to severe pain and disability, up to complete loss of use of the joint or inability to bear weight on an affected limb. Web site: http://www.delphion.com/details?pn=US05843919__ ·
Composition and method for treating arthritis Inventor(s): Malachowski; Henry (Wilton, CT) Assignee(s): Robert Daniels & Company, Inc. (Moonachie, NJ) Patent Number: 3,995,030 Date filed: January 6, 1971 Abstract: This invention relates to usage of the ignition residue of anthracite coal to treat arthritis. Excerpt(s): This invention relates to the treatment of arthritis, and in particular to a mineral composition which is of value in the treatment of arthritis, (including osteoarthritis, osteoarthrosis, and polyarthritis of unknown etiology). ... Briefly stated, the therepeutic composition of the present invention consists of the ignition residue of anthracite coal. ... This residue, in finely divided form, can be administered orally at dosage rates of up to 100 milligrams per kilogram of body weight. Web site: http://www.delphion.com/details?pn=US03995030__
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Composition and method of treatment of arthritis and related diseases with holmium-166 radionuclides Inventor(s): Lieberman; Ephraim (Suffern, NY), Bordoni; Maurice E. (Westtown, NY), Thornton; Alfred K. (New Hampton, NY) Assignee(s): Cadema Medical Products, Inc. (Middletown, NY) Patent Number: 5,061,475 Date filed: June 28, 1989 Abstract: An aggregate suspension containing holmium-166 hydroxide and a carrier (such as a particulate ferric hydroxide) is injected into a patient's anesthetized joint (such as a knee joint or hip joint) for the treatment of inflamed synovial tissues such as present in arthritis, especially rheumatoid arthritis. The aggregate suspension is in a range of particle sizes from 1 to 40 microns. The holmium-166-containing suspension treats the synovial tissues, whereby radiation synovectomy takes place.
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Excerpt(s): The present invention relates to radioactive compounds, methods for the preparation thereof and a method for the treatment of arthritis and related diseases, including rheumatoid arthritis, and osteoarthritis. ... Inflammatory diseases, which include inflammatory synovitis, arthritis generally, rheumatoid arthritis more specifically, and other diseases including osteoarthritis are leading causes of losses in time and earnings in the United States. More specifically, approximately six million of all arthritis sufferers are afflicted with rheumatoid arthritis. Of these, if past trends continue, over fifty percent (50%) ultimately will have involvement of the knee joint; over eighty percent (80%) will have involvement with the hand joint; and somewhat smaller percentages will have involvement of other joints such as the ankle, elbow, shoulder, hip and wrist. ... Rheumatoid arthritis and other forms of inflammatory disease are believed to be autoimmune diseases wherein parts of the body are attacked by antibodies manufactured in the body. These antibodies may be produced in response to viruses present in the body. While the mechanism for rheumatoid arthritis is not defined, it is a systemic disease. When the disease is active, the erythrocyte sedimentation rate (ESR) is elevated and the blood tests positive for rheumatoid factor. Web site: http://www.delphion.com/details?pn=US05061475__ ·
Composition for relief of arthritis-induced symptoms Inventor(s): Hersh; Theodore (Atlanta, GA) Assignee(s): Thione International, Inc. (Atlanta, GA) Patent Number: 5,827,886 Date filed: May 7, 1997 Abstract: A composition and method of using it for ameliorating inflammatory reactions and painful and other symptoms of the diseases of arthritis, lumbago, low back pain, myalgias and neuralgias. The composition includes reduced glutathione, a selenoamino acid and an anesthetic, such as capsaicin, in a suitable carrier for topical application. Excerpt(s): The present invention deals with the combinations of several synergistic antioxidants, including enzymatic co-factors with analgesics such as capsaicin or the local caine anesthetics and anti-inflammatory agents in appropriate delivery vehicles employed in topical carriers as a means of ameliorating the inflammatory reactions and painful symptoms of a variety of arthritis syndromes, spinal pain, lumbago, myalgias and neuralgias and exercise and sport injuries. These clinical entities result primarily or secondarily from free radical damage to particular surfaces (joints and associated musculo-skeletal structures) resulting from a variety of inflammatory pathologies. A classic example is the process of "hypoxic-reperfusion injury" of rheumatoid arthritis where the etiologic factor is unknown but the free radical species and other products derived from the neutrophils "oxygen burst reaction" contribute to the joint's injury. All of these etiologies engender free radicals in joint spaces and contiguous cutaneous and musculo-skeletal tissues, requiring additional local antioxidant compositions to the therapeutic armamentarium of each disease state to aid in the amelioration of signs and symptoms and repair of the affected tissues. The synergistic locally applied antioxidants plus capsaicin as a depletor of substance P which is the major neuronal chemomediator of painful stimuli are thus adjuncts in the management of inflammation and pain in these clinical entities. ... There are a number of rheumatologic and neurologic disorders as well as clinical musculo-skeletal syndromes where free radicals play a primary or secondary role in the clinical signs and symptoms of these distinct entities. Exercise, whether as calisthenics, weight lifting, swimming, running or jogging, generates free
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radical species. Exercise may be followed by muscle strain and aches or sprains, or result in painful sport injuries. The most common diseases affecting joints are rheumatoid arthritis and osteoarthritis. The former is an autoimmune disease where the articular inflammation in part leads to the generation of free radicals causing further inflammation and damage to the lining (synovium) of the affected joints. Free radicals also arise in rheumatoid arthritis and the other autoimmune related diseases, as periarteritis, lupus and scleroderma, through the mechanism of ischemia-reperfusion, similar to that in myocardial damage from coronary artery disease. The common syndromes of low back pain, fibrositis, and other neuro-muscular entities cause chronic pain from local inflammation. Thus, locally administered synergistic antioxidants play a role as adjuvant therapy alone or in combination with anti-inflammatory and analgesic medications, including topical capsaicin. ... To follow first are some definitions of free radicals, the clinical conditions and the antioxidant defense system which the body utilizes to scavenge and neutralize the deleterious free radicals. The present invention utilizes the synergistic and complementary antioxidants most similar to those endogenous human defense mechanisms. Web site: http://www.delphion.com/details?pn=US05827886__ ·
Compositions comprising tetramic acid analogs of pulvinic acid and methods of combating arthritis Inventor(s): Weinstock; Joseph (Phoenixville, PA) Assignee(s): SmithKline Corporation (Philadelphia, PA) Patent Number: 3,984,559 Date filed: October 17, 1975 Abstract: Pharmaceutical compositions comprising tetramic acid analogs of pulvinic acid and methods of combating arthritis by administration of these compositions are disclosed. Excerpt(s): This invention relates to novel tetramic acid analogs of pulvinic acid which have useful pharmacological activity. More specifically, the compounds of this invention have anti-arthritic activity as measured by their ability to inhibit adjuvantinduced polyarthritis in rats. In addition, these compounds exhibit anti-bacterial activity. ... R.sup.6 is hydrogen, phenyl optionally substituted with methyl, halogen or trifluoromethyl or a five or six membered heterocycle containing carbon and one or two atoms of nitrogen, sulfur or oxygen and optionally substituted with methyl, halogen or trifluoromethyl. ... As used herein, halogen refers to fluoro, chloro and bromo; lower alkyl and lower alkoxy may be straight or branched chain moieties; and fluoroalkyl is preferably trifluoromethyl. Web site: http://www.delphion.com/details?pn=US03984559__
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Compositions, methods and kits for treating rheumatoid arthritis Inventor(s): Albert; Daniel A. (Philadelphia, PA) Assignee(s): Super Gen, Inc. (Dublin, CA) Patent Number: 6,362,176 Date filed: July 20, 2000
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Abstract: Disclosed are methods of treating rheumatoid arthritis by coadministering synergistic effective amounts of pentostatin and methotrexate to a host in need thereof, and kits and compositions that include pentostatin and methotrexate. Excerpt(s): This invention relates to treatment of rheumatoid arthritis through coadministration of pentostatin and methotrexate and analogs and derivatives thereof. ... Rheumatoid arthritis (RA) is a systematic inflammatory condition that results in swelling, pain, loss of motion, and tenderness of target joints throughout the body. RA is characterized by chronically inflamed synovium that is densely crowded with lymphocytes. The synovial membrane, which is typically one cell layer thick, becomes intensely cellular and assumes a form similar to lymphoid tissue, thus including vessels, dendritic cells, T, B, and NK cells, macrophages, and clusters of plasma cells. Additionally, there is often a plethora of immunopathological mechanisms at work, including antigen-antibody complexes, polymorphonuclear neutrophils, inflammatory T cells, and activated macrophages. Eventually, these processes result in destruction of the integrity of the joint, resulting in deformity and permanent loss of function. A more detailed description of the etiology and physiology of RA can be found in Zvaifler, N., "Etiology and Pathogenesis of Rheumatoid Arthritis in Arthritis and Allied Conditions" 659-73 (ed. D. M. McCarty). This document, and all other documents or references, cited to herein are incorporated by reference as if reproduced completely herein. ... Rheumatoid arthritis is a common disease affecting 1 to 2% of the world's population with a female to male predominance of 3-4:1. The peak incidence is in the third to fourth decade. Once acquired the disorder is chronic; therefore the prevalence of the disease increases as one examines increasing age groups. The disease is of unknown cause, although genetics may impact the risk of developing rheumatoid arthritis. Although it is not certain, some common infection or infections might trigger the autoimmune process in susceptible individuals. Environmental influences are not thought to play a major role in the development of the disease. Interestingly, exogenous estrogens in the form of BCPS appear to reduce the risk. Web site: http://www.delphion.com/details?pn=US06362176__ ·
Constant order release aspirin composition and method of treating arthritis Inventor(s): Dunn; James M. (Englewood, CO) Assignee(s): Verex Laboratories, Inc. (Englewood, CO) Patent Number: 4,375,468 Date filed: April 8, 1982 Abstract: A constant order release aspirin tablet comprising aspirin, from 0.5 to 10 weight percent of a hydrogenated vegetable oil and from 0.5 to 7 weight percent of a saccharide selected from the group consisting of lactose, sucrose, dextrose fructose and maltose. The aspirin tablet is administered once or twice a day for the chronic treatment of arthritis, and has substantially lessened gastrointestinal side effects. Excerpt(s): The number of people who have arthritis is increasing. It is currently estimated that between 35-40 million people in the United States alone, or one out of every seven individuals, has arthritic symptoms which require medical treatment. There will be one person every thirty three seconds who will develop symptomatic arthritis and need medical treatment. ... One problem with aspirin, as usually formulated for typical, commercial formulations is that it has to be administered four to six times a day to produce satisfactory pain relief and suppression of inflammation. When drugs or
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medications have to be administered more than twice daily, patient compliance is approximately forty five (45%) percent. When the therapeutic agent is given once or twice daily, compliance by the patient increases to about seventy five (75%) percent. Further, standard aspirin formulations can produce a high incidence, seventy (70) percent, of gastrointestinal side effects including nausea, heartburn, vomiting, gastric erosion, gastro-duodenal ulcers as well as bleeding from the gastrointestinal tract. Approximately twenty-five (25) percent of patients taking regular aspirin tablets complain of ringing in the ears and other central nervous system side effects. ... Because of the side effects of this valuable, therapeutic agent, there has been a long standing need for an aspirin product which can be taken once or twice daily and which provides a slow, steady release of aspirin to decrease side effects without loss of efficacy. The present invention provides one such product. Web site: http://www.delphion.com/details?pn=US04375468__ ·
Device and method for treating arthritis of knee Inventor(s): Toda; Yoshitaka (14 -1 Toyotsu-cho, Suita, Osaka, JP 564-0051) Assignee(s): none reported Patent Number: 6,585,674 Date filed: March 28, 2001 Abstract: The present invention relates generally to a therapeutic device and related methods for treating arthritis of the knee. The therapeutic device includes a stretchable band having a predetermined length, a flexible and resilient body installed in the longitudinal middle of the stretchable band with a substantially triangular cross-section whose height is greater at one side of the stretchable band than at the other, such that the higher portion of the flexible and resilient body is applied to the sole at a position nearer to the inner or outer side thereof, and the stretchable band may be used to wrap and fix the ankle. Excerpt(s): The present invention relates to a therapeutic device for treating arthritis of the knee, including osteoarthritis of the knee. ... Osteoarthritis of the knee commonly begins with cartilage degeneration secondary to varus deformity that is multifactorial and often age-related. Varus deformity, whether or not age related, disturbs the positional relationship between the femur and tibia, resulting in partial wear and gradual loss of elasticity of the cartilage between the femur and the tibia. This causes local pressure directly on the bone and consequent bony proliferation at the joint edge and deformity. Overwork may wear or partly wear the joint due to its inherent disorder and similar proliferative change at the joint edge and the induction of osteoarthritis. ... Osteoarthritis has been treated with an insole known as a sole plate. For an insole to function as a therapeutic device, the right or left side is higher than the opposite side. Web site: http://www.delphion.com/details?pn=US06585674__
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Diagnosing autoimmune rheumatoid arthritis by measuring proteolytic activity of .alpha..sub.2 -macroglobulin Inventor(s): Teodorescu; Marius C. (Westchester, IL), Gaspar; Alexander M. (Chicago, IL), Spear; Gregory T. (Forest Park, IL), Ganea; Doina (Elmhurst, IL), Skosey; John L. (Chicago, IL) Assignee(s): University of Illinois, Board of Trustees (Urbana, IL) Patent Number: 4,499,186 Date filed: December 30, 1982 Abstract: A method for diagnosis of rheumatoid arthritis and related autoimmune diseases comprises blocking calcium ions contained in a blood sample, effecting hydrolysis of a selected substrate in the presence of .alpha..sub.2 -macroglobulin (.alpha..sub.2 M) from the blood sample, and determining the extent of hydrolysis of the substrate. Preferably, .alpha..sub.2 M in plasma is incubated with a hydrolyzable chromogenic substrate and the liberated chromogen is determined spectrophotometrically. A diagnostic kit is also provided. Excerpt(s): The invention described herein was made in the course of work supported in part by NCI Grant CA 21399 and in part by NIH Grant AM 28469. ... It is well-known that some diseases have an autoimmune pathogenetic mechanism. Among these are rheumatoid arthritis, systemic lupus erythematosus, and chronic active hepatitis. A general increase in the level of gammaglobulins (antibodies) often accompanies an increase in the level of a particular antibody or antibodies in patient serum. These observations have led to the suggestion that polyclonal (general) activation of Blymphocytes is involved in the disease process and might even precede the emergence of a particular antibody. For example, in rheumatoid arthritis the symptoms may appear before the characteristic antibody, i.e., the rheumatoid factor, develops. ... On the other hand, other arthritides are known to have no systemic autoimmune basis and are commonly described as "sero-negative". These include Reiter's syndrome, ankylosing spondylitis, psoriatic arthritis, osteo-arthritis, and gout. Web site: http://www.delphion.com/details?pn=US04499186__
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Diagnosis of rheumatoid arthritis in vivo using a novel spectroscopic approach Inventor(s): Jackson; Michael (435 Elliece Avenue, Winnipeg, Manitoba, CA), Sowa; Michael G. (435 Elliece Avenue, Winnipeg, Manitoba, CA), Mansfield; James R. (435 Elliece Avenue, Winnipeg, Manitoba, CA), Eysel; Hans H. (435 Elliece Avenue, Winnipeg, Manitoba, CA), Mantsch; Henry H. (435 Elliece Avenue, Winnipeg, Manitoba, CA), El-Gabalawy; Hani (c/o University of Manitoba, Department of Medicine, Section of, Winnipeg, Manitoba, CA), Canvin; Jan M. (c/o University of Manitoba, Department of Medicine, Section of, Winnipeg, Manitoba, CA) Assignee(s): none reported Patent Number: 6,424,859 Date filed: June 17, 1999 Abstract: A novel near infrared spectroscopic technique was used to characterize the joints in arthritis with comparison against normal joints. A beam of near infrared light was passed to joints through a fibre optic cable. Scattered light was collected by the same fibre bundle and a spectrum of the joint computed. Multivariate pattern
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recognition techniques identified regions of the spectrum which allowed discrimination between healthy and affected joints. Linear discriminant analysis resulted in correct classification of 74% of the joints. The high degree of similarity between mean spectra representing the early, late and control groups along with the significant between-subject variability in the data make diagnosis based on visual assessment of the spectra impossible. Linear discriminant analysis was therefore applied to spectra to determine if spectra could be classified by statistical methods as arising from early or late RA. Application of LDA resulted in correct classification of 74% of the joints. Interestingly, the spectral regions in which diagnostic differences were found by the multivariate analysis contain absorption bands related to tissue oxygenation status (oxy and deoxyhaemoglobin) and oxygen utilisation (cytochrome aa.sub.3), suggesting that ischaemic changes within the joint are being detected. Excerpt(s): The present invention relates generally to the fields of diagnostic devices and methods of use thereof. More specifically, the present invention relates to a device for diagnosing rheumatoid arthritis. ... There are almost 100 disorders that fall under the umbrella classification of arthritis. The most prevalent are osteoarthritis and rheumatoid arthritis. Osteoarthritis (OA) is a disease of wear and tear commonly affecting the elderly. Rheumatoid arthritis (RA) is a systemic auto-immune disorder causing a symmetric inflammatory polyarthritis. Once the inflammatory process is activated, there can be rapid destruction of joints that can, in some cases, be very aggressive. It has been shown that erosive damage occurs within weeks of the onset of the clinical symptoms. Typically, RA involves the small joints of the hands and feet leading to the clinical signs of joint tenderness and swelling. ... Despite its prevalence, arthritis can often be a difficult disease to diagnose. Clinical history and physical examination by a specialised medical practitioner are of key importance in diagnosis. However, any diagnosis based upon the personal skills and experience of the examining physician must of necessity contain an element of subjectivity. Among the more objective tests are X-ray investigation and magnetic resonance imaging of the affected joints and serological and immunological analysis of synovial fluid and blood. Web site: http://www.delphion.com/details?pn=US06424859__ ·
Diagnostic assay for latent matrix metallo-proteinase No. 9 and use thereof in the diagnosis of rheumatoid and inflammatory arthritis and inflammatory bowel disease Inventor(s): Ahrens; Diane (Beacon Falls, CT), Niedbala; Michael J. (Oxford, CT) Assignee(s): Bayer Corporation (Tarrytown, NY) Patent Number: 5,674,754 Date filed: April 27, 1995 Abstract: Elevated plasma levels of proMMP-9 and proMMP-9/TIMP-1 complex have been shown to correlate with and are useful in aiding the diagnosis of rheumatoid arthritis and inflammatory bowel disease; a hybridoma which produces a monoclonal antibody which specifically binds to and recognizes proMMP-9 and proMMP-9/TIMP-1 complex is disclosed and is designated mAb 277.13. Excerpt(s): The present invention relates to assay methods for detecting levels of specific enzymes in biological samples. More particularly, the present invention relates to methods for the detection of Matrix Metallo-Proteinase No. 9 (hereinafter "MMP" when referring to the class of matrix metallo-proteinases and "MMP-9" when referring to matrix metallo-proteinase No. 9 in particular). The inventive assay method is useful to
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diagnose rheumatoid arthritis, inflammatory arthritis (including psoriatic, gout, systemic lupus erythematous, and spondyl arthritis) and inflammatory bowel disease (hereinafter "IBD"). ... Physiological variances in MMP levels are known. For instance, significant increases in plasma 72 kDa gelatinase (MMP-2 levels have been observed in women during the second half of pregnancy as compared to early pregnancy and nonpregnant women (Zucker et al., 1992, J. Immunol. Methods, 148: 189). ... Pathologically, MMPs have been identified as associated with several disease states. For example, anomalous MMP-2 levels have been detected in lung cancer patients, where it was observed that serum MMP-2 levels were significantly elevated in stage IV disease and in those patients with distant metastases as compared to normal sera values (Garbisa et al., 1992, Cancer Res., 53: 4548). Also, using an ELISA methodology, it was observed that plasma levels of MMP-9 were elevated in patients with colon and breast cancer (Zucker et al., 1993, Cancer Res. 53: 140). However, these researchers did not investigate potential relationships among MMP-9 plasma levels in arthritis and IBD. Web site: http://www.delphion.com/details?pn=US05674754__ ·
Diagnostic probe for rheumatoid arthritis predisposition Inventor(s): Nepom; Gerald T. (Bainbridge Island, WA) Assignee(s): Virginia Mason Research Center (Seattle, WA) Patent Number: 4,971,902 Date filed: October 30, 1987 Abstract: Oligonucleotide probes for diagnosing predisposition to rheumatoid arthritis, capable of specifically hybridizing with5'-TACGGGGTTGR.sub.1 GAGAGCTT-3'or3'AR.sub.2 GCCCCAACR.sub.3 CR.sub.2 CR.sub.2 CGAA-5'wherein A is adenine, C is cytosine, G is guanine, T is thymine, R.sub.1 is GT or TG, R.sub.2 is T or uracil, and R.sub.3 is CA or AC. Or, capable of specifically hybridizing with5'-GGAGCAGAR.sub.2 GCGGGCCGCGG-3'or3'-CCR.sub.2 CGR.sub.2 CR.sub.2 R.sub.3 CGCCCGGCGCC5'wherein R.sub.1 is A or G, R.sub.2 is T or uracil, and R.sub.3 is R.sub.2 or C. Excerpt(s): This invention relates generally to genetic engineering and more particularly to DNA and RNA probes useful for diagnosing predisposition to disease states, specifically rheumatoid arthritis. ... Genetic screening for inherited diseases based on the use of specific gene probes is a promising technology that will augment both the breadth and the precision of genetic diagnostic testing. There are an estimated 3,000 genetic disorders known which result from a single gene mutation, for which the application of specific gene probes is of direct value. In addition, however, there are a number of common disorders, such as rheumatoid arthritis (RA) and type I diabetes, which result not from a single gene mutation but from a combination of genetic and possibly environmental factors. In such cases, genetic inheritance determines the predisposition, or disease risk, associated with a large proportion of clinical disease. Thus, genetic testing for rheumatoid arthritis should be viewed as the identification of genetic predisposition, distinct from the more conventional notion of a single gene defect resulting in a specific inherited disease. ... The identification of a particular gene associated with predisposition to rheumatoid arthritis can be viewed from two different perspectives. On the one hand, the gene being detected may be linked on the chromosome to other genes which actually confer disease susceptibility, in which case the gene being tested would function as a marker gene. On the other hand, the gene being identified may itself contribute directly to disease, but only if other genetic
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elements or appropriate environmental agents are present. Both of these concepts are important for understanding the genetic predisposition to rheumatoid arthritis. Web site: http://www.delphion.com/details?pn=US04971902__ ·
Diagnostic technique for rheumatoid arthritis Inventor(s): Teodorescu; Marius C. (10547 Essex, Westchester, IL 60153), Skosey; John L. (4932 S. Kimbark, Chicago, IL 60615), Chang; Jin-Lai (1648 Gilberto Dr., Glendale Heights, IL 60137) Assignee(s): none reported Patent Number: 4,402,934 Date filed: October 30, 1980 Abstract: A method for diagnosis of rheumatoid arthritis and related diseases comprises determination of polyclonal lymphocyte activation in B-cells cultured in the presence of patient serum. A diagnostic kit is also provided. Excerpt(s): Rheumatic diseases affect a significant proportion of the population, crippling many people and having only a palliative treatment at best. Diagnosis of rheumatic diseases is difficult and uncertain, and many patients escape classification until the disease has progressed to a stage where serious damage is evident. The classification of the different rheumatic diseases, including rheumatoid arthritis, is based on both clinical and laboratory data, and the same criteria are used to determine the efficiency of any selected treatment. In all of the rheumatic diseases, the common denominator is an abnormal function of the immune system. This abnormal function is suggested by the appearance of antibodies against a patient's own structures and also by the beneficial effect of immunosuppressive or cytotoxic drugs which destroy cells involved in the immune mechanisms. ... It has been shown that in some of these diseases the B-cells that produce antibodies are overactive, and produce antibodies against a variety of antigens, including some to which they may not have been previously exposed. Another relatively common feature is the increase in the serum immunoglobulin with polyclonal character. From such observations, it has been ascertained that B-cells programmed to produce antibodies against self antigens are present in normal individuals. It has likewise been suggested that polyclonal B-cell activation may be the cause of some autoimmune diseases. ... Despite such studies of rheumatic diseases, there remains a critical need for a diagnostic technique capable of providing, with suitable certainty, an early diagnosis of the incidence of such diseases. This is especially true of the crippling diseases, such as, particularly, rheumatoid arthritis. Web site: http://www.delphion.com/details?pn=US04402934__
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Dietary regimen of nutritional supplements for relief of symptoms of arthritis Inventor(s): Florio; Vito V. (Tamarac, FL) Assignee(s): Omni Nutraceuticals, Inc (Los Angeles, CA) Patent Number: 6,136,795 Date filed: November 18, 1998
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Abstract: This invention is directed to a dietary regimen and a unique combination of nutritional supplements and a method. More specifically, this invention is directed to a unique combination of nutritional supplements which provides symptomatic relief from arthritis. The unique combination of nutritional supplements of this invention is believed to function by both increasing the available (effective blood level) of antiinflammatory agents and promotion of the healing/regenerative process in the effected joints, thus, producing unexpected and lasting symptomatic relief from the debilitating effects of both osteoarthritis and rheumatoid arthritis. The essential nutritional supplements of the dietary regimen of this invention are as follows:(a) gamma linolenic acid (unrefined), hereinafter "GLA"(b) a mixture of eicosapentaenoic acid and docosahexaneoic acid, hereinafter collectively "EPA"(c) a mixture of chondroitin sulfate, N-acetyl glucosamine sulfate, glucosamine sulfate and manganese aspartate, hereinafter collectively "CHONDROX"The regimen is adjusted based upon the weight of the individual, and once symptomatic relief is achieved, the individual remains essentially free from the debilitating effects of arthritis so as long the daily regimen is faithfully followed. Excerpt(s): This invention is directed to a unique combination of nutritional supplements and a method. More specifically, this invention is directed to a unique combination of nutritional supplements which provides symptomatic relief from arthritis. The unique combination of nutritional supplements of this invention is believed to function by increasing the available (effective blood level) of antiinflammatory agents and, thus, unexpected and lasting symptomatic relief from the debilitating effects of both osteoarthritis and rheumatoid arthritis. ... Osteoarthritis or degenerative joint disease is the most common form of arthritis. It is seen primarily, but not exclusively, in the elderly; surveys have indicated that 80% of persons over the age of 50 have osteoarthritis. Under the age of 45, osteoarthritis is much more common in men; after age 45 it is ten times more common in women than men. ... The weightbearing joints and joints of the hands are the joints principally affected by the degenerative changes associated with osteoarthritis. Specifically, there is much cartilage destruction, followed by hardening, and the formation of large bone spurs (Calcified osteophytes) in the joint margins. Pain, deformity and limitation of motion in the joint results. Inflammation is usually minimal. Web site: http://www.delphion.com/details?pn=US06136795__ ·
Drug for the treatment of rheumatoid arthritis Inventor(s): Nishida; Tadashi (Osaka, JP), Miyake; Sachiko (Tokyo, JP), Yagita; Hideo (Tokyo, JP), Okumura; Ko (Chiba, JP) Assignee(s): Kanebo, Ltd. (Tokyo, JP) Patent Number: 5,855,888 Date filed: October 17, 1996 Abstract: A drug for the treatment of rheumatoid arthritis, which comprises as an active ingredient a monoclonal antibody which recognizes specifically extracellular region of human VLA-2. Preferable drug for the treatment of rheumatoid arthritis comprises as an active ingredient a monoclonal antibody which recognizes specifically extracellular region of human VLA-2, .alpha. chain. The above drug for the treatment of rheumatoid arthritis can suppress swelling due to arthritis in rheumatoid arthritis with low toxicity and hence is useful for the treatment of rheumatoid arthritis.
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Excerpt(s): This application is a 371 of PCT/JP95/00527 filed Mar. 22, 1995. ... This invention relates to a drug for the treatment of rheumatoid arthritis which comprises as an active ingredient a monoclonal antibody which can specifically recognize extracellular region of human VLA-2. ... Rheumatoid arthritis (hereinafter, abbrebiated as "RA") is a chronic inflammatory disease which shows an inflammatory symptom mainly in the articular synovial membrane, where various inflammatory cells permeate into synovial fluid through hemangioendotheliocytes of synovial membrane. It is assumed that the pathological symptoms may be participated by immunological mechanism, and the symptoms may become a trigger of immuno-response, but it is still difficult to specify the mechanism. It is also important to make clear the reason why the inflammatory symptoms are maintained at the synovial membrane even after the cause of the disease has been removed. A series of processes of these inflammation symptoms, particularly chronicity and duration thereof, will be deeply participated by lymphocytes which take charge of immunization. Web site: http://www.delphion.com/details?pn=US05855888__ ·
Epidermal growth factor receptor targeted molecules for treatment of inflammatory arthritis Inventor(s): Bacha; Patricia A. (Hollis, NH) Assignee(s): Seragen, Inc. (Hopkinton, MA) Patent Number: 5,906,820 Date filed: May 5, 1997 Abstract: The invention features a method for treating a patient having inflammatory arthritis, the method includes administering to the patient a molecule which is capable of specifically binding to an epidermal growth factor receptor expressed on a cell of the patient which contributes to the inflammatory arthritis of the patient, the molecule being capable of decreasing the viability of the cell. Excerpt(s): The field of the invention is treatment of inflammatory arthritis. ... Inflammatory arthritis is a family of arthritic diseases characterized by lymphokinemediated inflammation of the joints. Inflammatory arthritis is often autoimmune in origin; examples include rheumatoid arthritis, psoriatic arthritis, and lupus-associated arthritis. The most common form of inflammatory arthritis is rheumatoid arthritis which occurs in approximately 1 percent of the population. Rheumatoid arthritis is characterized by persistent inflammation of the joints. Inflammation can eventually lead to cartilage destruction and bone erosion. ... Stukel et al. (Immunology 64:683, 1988) report that a monoclonal antibody directed against the interleukin-2 receptor inhibits passively transferred adjuvant arthritis in rats (i.e., adjuvant arthritis induced by transfer of spleen cells from rats having adjuvant arthritis to naive rats), but is not effective in suppressing the development of adjuvant arthritis in rats. Web site: http://www.delphion.com/details?pn=US05906820__
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Formulation for alleviating symptoms associated with arthritis Inventor(s): Chavali; Sambasiva R. (Boston, MA), Forse; R. Armour (Brookline, MA) Assignee(s): New England Deaconess Hospital (Boston, MA) Patent Number: 5,683,698 Date filed: August 2, 1996 Abstract: The invention describes an herbal formulation and its use for reducing/alleviating symptoms associated with rheumatoid arthritis, osteoarthritis and reactive arthritis and for reducing the production of proinflammatory cytokines. Foods and beverages containing the herbal formulation are also described. Excerpt(s): The manifestation of rheumatoid arthritis (RA) in humans is a consequence of a complex interplay of genetic and environmental factors. The disease is initiated following activation of T cells which is perpetuated when autoantigen reactive T cells and antigen presenting cells are generated. Consequently, autoantibodies (rheumatoid factors) which are directed against host's own immunoglobulins are produced. These processes are further complicated when proinflammatory mediators (such as IL-1, IL-6 and TNF-.alpha.) are produced in response to signals received from auto reactive T cells. As a result of these factors, the host loses the ability to control immune functions which results in final manifestation of the disease. The important role of TNF-.alpha., IL-1.beta. and IFN-.gamma. in exacerbating the disease process has been demonstrated in several animal models, and many investigators have aimed at regulating the production and synthesis of these proinflammatory mediators to control the disease. Thus, therapeutic approaches are targeted towards modifying the disease process. ... Therapy for rheumatoid arthritis is focused around alleviating symptoms associated with the disease, such as relief of pain, reduction of inflammation and increasing range of motion. Aspirin, non-steroidal anti-inflammatory drugs (NSAIDs) (e.g., ibuprofen, naproxen, methotrexate) and glucocorticoids have been used to manage RA. However, these therapeutic agents have a variety of toxic side effects, such as gastric erosion and adverse effects on kidneys and liver, and may inadequately regulate the cellular immune functions and secretions of various cytokines. More recent therapeutic approach include the treatment of patients with multiple drugs has been proven to be more effective. There still remains a need for alternative therapies for the medical management of RA which can eliminate the need for traditional drugs and their associated side effects, particularly over prolonged daily use. ... This invention describes a formulation and use of the formulation to reduce and alleviate symptoms associated with arthritis, such as rheumatoid arthritis, osteoarthritis and reactive arthritis. The formulation can also reduce the production of proinflammatory cytokines such as tumor necrosis factor, IL-1 and IL-6. The formulation comprises an herbal extract from the roots, rhizomes and/or vegetation of six herbal plant varieties. In particular, the herbs are a combination of species of Alpinia, Smilax, Tinospora, Tribulus, Withania and Zingiber. A preferred formulation comprises Alpinia galanga, Smilax glabra, Tinospora cordifolia, Tribulus terrestris, Withania somnifera and Zingiber officinale, each present in a physiologically acceptable amount. Web site: http://www.delphion.com/details?pn=US05683698__
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Free fatty acids for treatment or propyhlaxis of rheumatoid arthritis arthritis Inventor(s): Rubin; David (San Diego, CA) Assignee(s): Century Laboratories, Inc. (Port Washington, NY) Patent Number: 4,843,095 Date filed: August 7, 1987 Abstract: Free fatty acids form fish oil, DHA and EPA, are useful in treating rheumatoid arthritis. The free fatty acids were an order of magnitude more effective in treating arthritis than unhydrolyzed fatty acids derived from fish oil. Excerpt(s): The present invention relates to the use of free fatty acids which can be used to treat or provide effective prophylaxis against rheumatoid arthritis. ... Rheumatoid arthritis is a serious, often crippling, disease characterized by pain and locomotor dysfunction. This sort of pain and dysfunction are among the most common and frustrating afflictions. The gravity of this disease has led to the investigation and/or adoption of a wide range of drugs for its alleviation. Aspirin has been commonly used since the turn of this century. Other major drugs used to treat arthritis include indomethacin, other salicylates, phenylbutazone, steroids, and gold. Other compounds which have been used to treat arthritis are fenoprofen, ibuprofen, naproxen, sulindac, and tolmetin. ... While the known compounds can offer anti-inflammatory, antipyretic, and analgesic effects, and have proven helpful in the management of rheumatoid arthritis in many patients, when combined with other modalities such as proper rest, exercise, physical therapy, and surgery, they are less than ideal. Many of these medications exhibit serious side effects with many patients, particularly gastrointestinal damage and renal toxicity. None of these materials is universally useful in treating rheumatoid arthritis, as some patients will respond to one material while others respond favorably only to others. Web site: http://www.delphion.com/details?pn=US04843095__
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Gold coated carbon implant and method of treating arthritis therewith Inventor(s): Jacob; Ezekiel J. (25 Monroe Pl., Brooklyn, NY 11201) Assignee(s): none reported Patent Number: 4,606,354 Date filed: May 21, 1985 Abstract: An implant for the treatment of the pain of arthritis which comprises a carbon fiber which has a discontinuous coating of gold thereon, exposing the carbon in patches. The carbon and gold form a galvanic couple which is implanted in an arthritic joint and in the presence of body fluids acts like a battery and released gold ions continuously, thus relieving pain. Excerpt(s): U.S. Pat. No. 4,405,311 "METHOD AND APPARATUS FOR DIRECT ELECTRICAL INJECTION OF GOLD IONS INTO TISSUE SUCH AS BONE" Sept. 20, 1983. ... The Arthritis Foundation estimates (1985) the number of persons afflicted with arthritis in the U.S. is 37 Million. About 2 to 10 billion dollars are spent in "cures" in each year. ... Gold, however, is a valid answer. Web site: http://www.delphion.com/details?pn=US04606354__
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Herbal compositions and their use as anti-inflammatory agents for alleviation of arthritis and gout Inventor(s): Tomer; Onkar S. (Watchung, NJ), Glomski; Peter (South Amboy, NJ), Borah; Kripanath (Morris Plains, NJ) Assignee(s): Chromak Research, Inc. (Somerset, NJ) Patent Number: 6,274,176 Date filed: July 1, 1999 Abstract: An edible composition for use as an anti-inflammatory agent for alleviation of arthritis and gout in mammals. The edible composition is a mixture of at least three, preferably at least seven, herbs selected from the group consisting of Tanacetum parthenium, Zingibar officinale, Curcuma longa, Coriandrum sativum, Centella asiatica, Oenothera biennis, Valeriana officinalis, Tabebuia impetiginosa, Thymus vulgaris and Sambucus nigra. A preferred composition will contain at least Tanacetum parthenium, Zingibar officinale and Curcuma longa. The composition preferably contains the herbs in approximately equal amounts. Excerpt(s): The present invention is directed to an edible composition for use as an antiinflammatory agent for alleviation of arthritis and gout in mammals. The composition comprises a synergistic mixture of at least three herbs selected from a group of ten herbs identified below. ... The prior art is replete with references to herbal medicines for treatment of a variety of ailments in mammals. Typically, such herbal medicines are obtained as the active compound(s) by extraction from plant tissues. Although the use of various herbs have been described in related areas, the synergistic combination of the herbs in the edible composition of the invention has never previously been described. ... Japanese Patent Publication No. 4,005,237 discloses a combination of Cinnamomum sieboldii and Allium sativum for superoxide scavenging in the treatment of inflammatory disorders. German patent Publication No. 3,724,341 discloses a combination of Cinnamomum zeylanicum, Pumica granitum cortex, Cardamon zingiberaceie fruit and Piper longum fruit. Web site: http://www.delphion.com/details?pn=US06274176__
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Heteroaroyl 10-deazaamino-pterine compounds and use for rheumatoid arthritis Inventor(s): DeGraw; Joseph I. (Sunnyvale, CA), Colwell; William T. (Menlo Park, CA), Sirotnak; Francis M. (New York, NY), Smith; R. Lane (Palo Alto, CA), Piper; James R. (Birmingham, AL) Assignee(s): SRI International (Menlo Park, CA) Patent Number: 5,354,751 Date filed: July 12, 1993 Abstract: There is disclosed certain heteroaroyl 10-deazaaminopterin and 5, 10 and 8, 10 di deazaminopterin compounds and their use for treatment of rheumatoid arthritis and related diseases and preparative process.Also disclosed are 10 alkenyl-(and alkynyl) 10deazaminopterins also disclosed for treatment of rheumatoid arthritis and for leukemia and ascites tumors and preparative process. Excerpt(s): The current invention concerns novel antiinflammatory and antineoplastic 10-deazaaminopterin compounds. In particular, the invention concerns heteroaroyl-10deazaaminopterins and 10-alkenyl or 10-alkynyl-10-deazaaminopterins having
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pronounced antiinflammatory activity, antileukemic and antitumorigenic activity, as well as a method for treatment of inflammatory diseases, leukemia and tumors. Pharmaceutical compositions containing these heteroaroyl-10-deazaaminopterin compounds are also disclosed. The invention further concerns a process for preparation of these compounds. ... Rheumatoid arthritis, malignant tumors and leukemia are severely debilitating diseases which are often fatal, as in cases of leukemia and malignant growths. Drugs which are currently available and used for treatment of these diseases typically have unpleasant secondary symptoms or are highly toxic. ... Rheumatoid arthritis is one of a number of forms of proliferative disease, and the development of drugs for amelioration or curing the disease has occupied the attention of research organizations for many years, until most recently without appreciable success. Web site: http://www.delphion.com/details?pn=US05354751__ ·
HLA-DRBI peptides with specific binding affinity for HLA-DQ molecules: prevention and treatment of rheumatoid arthritis Inventor(s): Luthra; Harvinder S. (Rochester, MN), David; Chella S. (Rochester, MN), Zanelli; Eric (Rochester, MN) Assignee(s): Mayo Foundation for Medical Education and Research (Rochester, MN) Patent Number: 5,965,787 Date filed: August 31, 1995 Abstract: Disclosed are transgenic mice carrying a human HLA-DQ sgene. The transgenic mice are deficient in mouse H-2 class II molecules. Such mice provide animal model systems to identify peptides useful for preventing or treating rheumatoid arthritis. Also disclosed are methods and materials for treating rheumatoid arthritis, including administration of peptides having specific binding affinity for HLA-DQ molecules expressed in a rheumatoid arthritis patient. Excerpt(s): Rheumatoid arthritis (RA) is a chronic inflammatory polyarthritis leading to destruction of joints and, sometimes, to severe systemic complications such as vasculitis, amyloidosis or Felty's syndrome. It is widely accepted that a strong genetic component contributes to the susceptibility or resistance to certain human autoimmune diseases such as RA. Attempts to identify the particular genes involved in these disorders has been an area of major focus for many laboratories. Among the numerous genes studied, those encoding the class I and class II molecules of the human leukocyte antigen (HLA) complex have garnered particular attention. The primary function of HLA-class I and class II molecules is binding and presentation of processed antigenic peptides to T cells bearing receptors specific for particular HLA-peptide complexes. The presentation event plays a pivotal role in shaping the cellular immune repertoire and in shaping the nature and scope of the immune response against a given antigen. ... In Caucasians, genetic studies initially showed a high prevalence of certain HLA DR subtypes among RA patients. Specifically, predisposition to RA has been linked to the class 30 II HLA-DRB1 locus, and in particular to the DR4 specificity. Within the HLA-DR4 specificity, the Dw4 (DRB1*0401), Dw14 (DRB1*0404/0408), and Dw15 (DRB1*0405) subtypes confer genetic predisposition to RA, while the Dw10 (DRB1*0402) subtype does not confer such genetic predisposition. Nepom et al., Ann. Rev. Immunol. 9: 493-525 (1991); Wordsworth et al., Proc. Natl. Acad. Sci. USA 86: 10049-53 (1989); Ollier et al., Rheum. Dis. Clin. North. Am. 18: 741-59 (1992). Several studies have also shown that the incidence of RA is significantly decreased in patients expressing HLA-DR2 alleles compared with normal
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controls. Jaraquemada et al., Ann. Rheum. Dis. 45: 627-36 (1986); Deighton et al., Br. J. Rheumatol. 32: 893-98 (1993); Ollier et al., cited supra. Indeed, the DR2Dw12 subtype is associated with a low incidence of RA in the Japanese population. Ohta et al., Human Immunol. 5: 123-32 (1982). For a general review of HLA nomenclature, see Bodmer et al., Tissue Antigens 44: 1-18 (1994), incorporated herein by reference. ... A further caveat regarding studies aimed at identifying the precise HLA-D region gene responsible for susceptibility to RA is the presence of certain DQB alleles in linkage disequilibrium with particular HLA-DR genes. Such linkages further constrain any conclusions concerning the relative impact of particular HLA-D region genes on RA susceptibility. For example, two allelic forms of DQB, HLA-DQ7 and HLA-DQ8, are associated with the HLA-DR4 genotype in RA susceptibility. Gregersen et al., cited supra; Singal et al., Lancet 2: 111820 (1987); Lanchbury et al., Human Immunol. 26: 59-71 (1989). Moreover, an interesting, albeit small, study analyzing Indian patients with RA showed that 100% possessed the HLA-DQ8 allele, versus 33.3% for the normal subjects. Taneja, Rheumatol. Int. 11: 251-55 (1992). Thus, despite an association of the "Shared Epitope" with RA susceptibility, prior studies have also pointed to a possible role for HLA-DQ alleles in this disease. Web site: http://www.delphion.com/details?pn=US05965787__ ·
Human phospholipase activating protein and methods for diagnosis of rheumatoid arthritis Inventor(s): Bomalaski; John S. (11 Chestnut La., Wayne, PA 19087), Clark; Mike A. (15 Wetmore Dr., Denville, NJ 07835), Shorr; Robert (36 Overbrook Pkwy., Wynnewood, PA 19096) Assignee(s): none reported Patent Number: 5,786,154 Date filed: June 5, 1995 Abstract: The invention provides methods for detecting elevated levels of phospholipase A.sub.2 activating protein in persons suspected of having rheumatoid arthritis to thereby indicate the presence of rheumatoid arthritis in the person comprising the steps of providing a sample of body fluid or tissue from said person; contacting the sample with an antibody specific for phospholipase A.sub.2 activating protein such that the antibody binds with phospholipase A.sub.2 activating protein in the sample; detecting the antibody thereby indicating the presence of phospholipase A.sub.2 activating protein, whereby elevated levels of phospholipase A.sub.2 activating protein in the sample as compared with levels found in persons not having rheumatoid arthritis indicates the presence of rheumatoid arthritis in the person. Kits and reagents for detecting rheumatoid arthritis are also provided. Excerpt(s): The present invention relates to the field of methods for diagnosing rheumatoid arthritis. More particularly the present invention relates to methods for diagnosing rheumatoid arthritis using immunoassays. ... Rheumatoid arthritis is the best known form of arthritic disease, affecting millions of patients worldwide. It is characterized by a progressive inflammation of joints and internal organs by immunocompetent cells and destructin of articular cartilage resulting in progressive morbidity and death. Prostaglandins and related eicosanoids are thought to be important mediators of these immune and inflammatory responses. Increased quantities of eicosanoids are produced by rheumatoid synovium in both organ and cell culture and are found in elevated levels in rheumatoid synovial fluid and from peripheral blood cells of affected patients. Clinical evidence suggests that early diagnosis and
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intervention with cytotoxic and immunomodulatory agents is essential to altering the course of the disease. ... Phospholipase A.sub.2 (PLA.sub.2) is a lipolytic enzyme which hydrolyzes the 2-acyl fatty acid ester of glycerophospholipids, thus releasing arachidonic acid. Arachidonic acid has been shown to be converted into a number of biologically active compounds known as eicosanoids. PLA.sub.2 activity has been shown to be ubiquitous and to reside in several different gene products. Both membrane bound and soluble forms of the enzyme have been described. Extracellular secretion of soluble PLA.sub.2 was first described in 1980. Circulating PLA.sub.2 was implicated in endotoxin shock and has since been implicated in acute and chronic inflammatory reactions. Web site: http://www.delphion.com/details?pn=US05786154__ ·
Human phospholipase activating protein and methods for diagnosis of rheumatoid arthritis Inventor(s): Bomalaski; John S. (11 Chestnut La., Wayne, PA 19087), Clark; Mike A. (15 Westmore Dr., Denville, NJ 07835), Shorr; Robert (36 Overbrook Pky., Wynnewood, PA 19096) Assignee(s): none reported Patent Number: 5,367,063 Date filed: November 4, 1993 Abstract: The invention provides methods for detecting elevated levels of phospholipase A.sub.2 activating protein in persons suspected of having rheumatiod arthritis to thereby indicate the presence of rheumatoid arthritis in the person comprising the steps of providing a sample of body fluid or tissue from said person; contacting the sample with an antibody specific for phospholipase A.sub.2 activating protein such that the antibody binds with phospholipase A.sub.2 activating protein in the sample; detecting the antibody thereby indicating the presence of phospholipase A.sub.2 activating protein, whereby elevated levels of phospholipase A.sub.2 activating protein in the sample as compared with levels found in persons not having rheumatoid arthritis indicates the presence of rheumatoid arthritis in the person. Kits and reagents for detecting rheumatoid arthritis are also provided. Excerpt(s): The present invention relates to the field of methods for diagnosing rheumatoid arthritis. More particularly the present invention relates to methods for diagnosing rheumatoid arthritis using immunoassays. ... Rheumatoid arthritis is the best known form of arthritic disease, affecting millions of patients worldwide. It is characterized by a progressive inflammation of joints and internal organs by immunocompetent cells and destructin of articular cartilage resulting in progressive morbidity and death. Prostaglandins and related eicosanoids are thought to be important mediators of these immune and inflammatory responses. Increased quantities of eicosanoids are produced by rheumatoid synovium in both organ and cell culture and are found in elevated levels in rheumatoid synovial fluid and from peripheral blood cells of affected patients. Clinical evidence suggests that early diagnosis and intervention with cytotoxic and immunomodulatory agents is essential to altering the course of the disease. ... Phospholipase A.sub.2 (PLA.sub.2) is a lipolytic enzyme which hydrolyzes the 2-acyl fatty acid ester of glycerophospholipids, thus releasing arachidonic acid. Arachidonic acid has been shown to be converted into a number of biologically active compounds known as eicosanoids. PLA.sub.2 activity has been shown to be ubiquitous and to reside in several different gene products. Both membrane
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bound and soluble forms of the enzyme have been described. Extracellular secretion of soluble PLA.sub.2 was first described in 1980. Circulating PLA.sub.2 was implicated in endotoxin shock and has since been implicated in acute and chronic inflammatory reactions. Web site: http://www.delphion.com/details?pn=US05367063__ ·
Immunoassays for measuring the avidity of rheumatoid factor in rheumatoid arthritis Inventor(s): Newkirk; Marianna M. (Pierrefonds, CA) Assignee(s): McGill University (Montreal, CA) Patent Number: 5,679,537 Date filed: October 26, 1994 Abstract: The present invention relates to a novel immunoassay for measurement of rheumatoid factors (RFs) avidity for correlation with rheumatoid arthritis disease activity and for the presence of the different glycoforms of IgG. Excerpt(s): The invention relates to a novel ELISA immunoassay for measurement of rheumatoid factors (RFs) avidity for possible correlation with rheumatoid arthritis disease activity and for the presence of the different glycoforms of IgG. ... Rheumatoid factors (RF) have long been suspected to play a role in the pathogenesis of rheumatoid arthritis (RA), as they are detected in up to 70% of RA patients and are sustained at high titers for years. Their association with the pathogenic changes have been controversial, and indeed they are found in normal individuals generally in low titers and in patients with mixed cryoglobulinemia frequently in high titers, who lack the synovitis characteristic of RA. ... In the past decade, since the discovery of an imbalance of the different glycoforms of IgG in patients with RA, much research has focused on the possible consequences of one of the glycoforms of IgG, namely the Gal(0) form. Since the oligosaccharide chain on IgG resides in between the two gamma-2 domains, it has been postulated that changes in the structure such as the absence of the terminal sialic acid and galactose ›gal(0)! could affect the binding of RFs since it is thought that they bind in the cleft between the gamma-2 and gamma-3 domains. It has been found that, whereas some purified monoclonal RFs bound maximally to IgG when the oligosaccharide chain was intact (Newkirk, M. M. et al., 1993, J. Rheumatol., 20:776), other RFs bound even when the oligosaccharide was altered or removed (Newkirk, M. M. et al., 1990, Arthritis Rheum., 33:800). These previous studies have all had the short coming that it was not known, which, if any, of the monoclonal antibodies studied, could be correlated with any pathogenic role. Web site: http://www.delphion.com/details?pn=US05679537__
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Immunodiagnostic assay for rheumatoid arthritis Inventor(s): Stanworth; Dennis Raymond (Birmingham, GB2), Lewin; Ian Victor (Tamworth, GB2), Nayyar; Sarita (Penn, GB2) Assignee(s): Peptide Therapeutics Limited (Cambridgeshire, GB2) Patent Number: 5,827,668 Date filed: August 10, 1995
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Abstract: The assay of rheumatoid arthritis by reference to IgA-.alpha..sub.1 antitrypsin complex present in analytes is facilitated by certain novel antibody reagents. These are ligands comprising an antibody domain specific for an antigenic determinant of a complex of human IgA and .alpha..sub.1 -antitrypsin, this antibody domain being substantially non reactive with free human IgA and free human .alpha..sub.1 antitrypsin. Monoclonal antibodies to the naturally occurring IgA-.alpha..sub.1 AT complex and monoclonal or polyclonal antibodies to a synthetic peptide are preferred. The synthetic peptide in itself part of the invention and preferably has an amino acid sequence: Val-Ser-Val-Val-Met-Ala-Glu-Val-Asp-Gly-Thr-Cys-Tyr (SEQ ID NO:2) Excerpt(s): The present invention is directed to a method of assay of rheumatoid arthritis (RA). More particularly, the present invention is directed to the assay of human immunoglobulin A-.alpha..sub.1 -antitrypsin complex (IgA-.alpha..sub.1 AT) in patients who are suspected of having or are being treated for RA. ... Rheumatoid arthritis has been described as an unresolved systemic inflammation in which immune dysfunction and genetic susceptibility play roles. In earlier stages, it is often characterised by fluctuating remissions and exacerbations, and in later stages by a chronic granulatamous response (pannus formation) leading to tissue destruction notably of bone and cartilage. The synovial membrane in RA has many of the characteristics of a hyperactive immunologically stimulated lymphoid organ and the ratio of T suppressor to T helper lymphocytes has been shown to be significantly reduced. ... wherein diagnosis of 3 or 4 of these factors is considered representative of probable RA and diagnosis of 5 or more of the factors is considered representative of definite RA. Web site: http://www.delphion.com/details?pn=US05827668__ ·
Implements usable by persons afflicted with arthritis Inventor(s): McRae; Lucy Theresa (28059 Kendallwood Road, Farmington Hills, MI 48024), McRae; Brian Joseph (28059 Kendallwood Road, Farmington Hills, MI 48024) Assignee(s): none reported Patent Number: 4,035,865 Date filed: January 19, 1976 Abstract: Implements of the hand-manipulated type are equipped with spherical handles that can be easily grasped by persons afflicted with arthritis. The spherical handle has a diameter that permits the sphere to be retained against the person's palm between the thumb and a finger without bending internal joints. Excerpt(s): Persons afflicted with arthritis often have difficulty in moving certain joints, particularly joints in the fingers. Such persons therefore cannot easily grasp small implements such as writing pens or pencils, table knives or other cutlery, toothbrushes, combs, or medicine bottle covers. The present invention contemplates handle modification of, or addition to, such implements whereby the person afflicted with arthritis can position a thumb and finger on widely spaced surface areas of the handle without bending internal joints. An aim of the invention is to provide improved implements that a person afflected with arthritis can grasp and use effectively without excessive pain or sense of uncertainty. ... Arthritis adversely affects primarily the joint cartilage and tendons associated with phalanges 26. The joints at the ends of the metacarpals are not affected to as great an extent, presumably because they are in a fleshy area having relatively great blood circulation. A hand afflicted with arthritis is more or less precluded from bending movements at the fingers and thumb phalanges. It
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is thought that the hinging movement of the thumb metacarpal (designated by letter A) usually is largely unimpaired. The present invention recognizes the retained ability of the thumb metacarpal to move toward and away from the immobilized fingers. ... It is contemplated that spherical element 30 will be positioned against the palm area, and that the thumb metacarpal 24 will be moved in the direction designated by letter B to enable the person to exert gripping pressure on element 30. The present invention involves the employment of spherical element 30 as a handle for various manipulatable devices, such as writing pens or pencils, eating implements, etc. The aim is to concern ourselves with the types of implements normally used on a daily or regular basis by elderly persons that might be afflicted with arthritis. Web site: http://www.delphion.com/details?pn=US04035865__ ·
Inhibition of arthritis by L-type calcium channel antagonists nimodipine, nisoldipine and nifedipine Inventor(s): Aune; Thomas M. (Hamden, CT) Assignee(s): Bayer Corporation (Pittsburgh, PA) Patent Number: 5,478,848 Date filed: January 26, 1994 Abstract: The present invention comprises new methods for treating rheumatoid arthritis. It has been found that the L-type calcium channel antagonists are effective in treating arthritis. Nimodipine, nisoldipine, and nifedipine, are examples of specific compounds useful in the present invention. Excerpt(s): This invention relates to methods of using L-type calcium channel antagonists to treat arthritis. ... Rheumatoid arthritis is a debilitating disease of the connective tissue. It most often manifests itself through inflammation and thickening of the synovial membranes, the sacs that hold the fluid (synovial fluid) that lubricates the joints. It generally causes irreversible damage to the joint capsule and the articular cartilage. There is evidence that suggests that an autoimmune mechanism may play a role in the disease. ... Synovium is composed of two cell types termed type A synoviocytes and type B synoviocytes. (Gay and Gay, Rheumatol Int. 9, 105-113 (1989); Kouri et al., Scand. J. Immunol 19, 359-364 (1984); Burmester et al., Scand. J. Immunol. 17, 68-82 (1983)). Type A synoviocytes resemble tissue macrophages and type B synoviocytes resemble fibroblasts. Certain examples of tissue macrophage-like cells and fibroblasts possess calcium channels that resemble L-type calcium channels. Baumgarten and Villereal, J. Biol. Chem. 267, 10524-10530 (1992); Bernini et al., J. Cardiovasc. Pharmacol. 18, 42-45 (1991); Hijioka et al., Mol. Pharmacol. 41, 435-440 (1992); Kong et al., Second Messenger Phosphoproteins 13, 117-130 (1991); Olsen et at. Biochem. Biophys. Res. Commun. 162, 448-455 (1989). The evidence that suggests that certain macrophage- or fibroblast-like cells have L-type calcium channels includes: 1 ) electrophysiologic studies, 2) inhibition of calcium currents by selective L-type calcium channel antagonists, and 3 ) activation of calcium currents by selective L-type calcium channel agonists. In rheumatoid arthritis, type A cells and type B cells participate in the inflammatory process. Web site: http://www.delphion.com/details?pn=US05478848__
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Isolated nucleotide sequences associated with multiple sclerosis or rheumatoid arthritis and a process of detecting Inventor(s): Perron; Herve (Lyons, FR), Beseme; Frederic (Villefontaine, FR), Bedin; Frederic (Lyons, FR), Paranhos-Baccala; Glaucia (Lyons, FR), Komurian-Pradel; Florence (Saint Cyr au Mont d'Or, FR), Jolivet-Reynaud; Colette (Bron, FR), Mandrand; Bernard (Villeurbanne, FR) Assignee(s): Bio Merieux (Marcy l'Etoile, FR) Patent Number: 6,582,703 Date filed: November 26, 1997 Abstract: The invention provides viral material and nucleotide fragments associated with multiple sclerosis and/or rheumatoid arthritis for use in methods of diagnosis, prophylaxis, and therapy. Excerpt(s): Multiple sclerosis (MS) is a demyelinating disease of the central nervous system (CNS), the cause of which remains as yet unknown. ... Many studies have supported the hypothesis of a viral aetiology of the disease, but none of the known viruses tested has proved to be the causal agent sought: a review of the viruses sought for several years in MS has been compiled by E. Norrby (1) and R. T. Johnson (2). ... The discovery of pathogenic retroviruses in man (HTLVs and HIVs) was followed by great interest in their ability to impair the immune system and to provoke central nervous system inflammation and/or degeneration. In the case of HTLV-1, its association with a chronic inflammatory demyelinating disease in man (48) led to extensive investigations to search for an HTLV1-like retrovirus in MS patients. However, despite initial claims, the presence of HTLV-1 or HTLV-like retroviruses was not confirmed. Web site: http://www.delphion.com/details?pn=US06582703__
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Magnetic thermal vibrational device for the treatment of arthritis and the like Inventor(s): Franco-Vila; Jose J. (730 E. 6th Pl., Hialeah, FL 33010) Assignee(s): none reported Patent Number: 4,177,796 Date filed: August 22, 1977 Abstract: A device for simultaneously applying electromagnetic alternating directional energy, thermal, and vibrational energy to various areas of the body which has been found to reduce or even eliminate the pains and symptoms caused from arthritis, bursitis and other bone joint maladies. The device includes a housing, an electromagnet disposed in said housing, an elastic band having a pair of permanent magnets coupled magnetically on each side of the band to each other with the elastic band being suspended at each end to the housing and positioned within the alternating magnetic field of the electromagnet. The electromagnet has a shaped steel core which acts to concentrate the magnetic flux lines through the suspended permanent magnets and is driven by low frequency alternating current causing the suspended magnets to vibrate. The electromagnet core is contructed in such a way to contribute heat for thermal application to the body simultaneously in conjunction with the concentrated magnetic field and vibration. The resulting simultaneous effects of the low frequency alternating (in direction) magnetic field, the vibrating elastic band and thermal concentration of
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energy is found to be extremely effective for the reduction or elimination of pain and other body disorders caused by arthritis, bursitis and other related bone joint diseases. Excerpt(s): This invention relates generally to a therapeutic device for reducing periodically or eliminating the deleterious effects caused from bone joint diseases such as arthritis, bursitis and the like, and specifically to a therapeutic device which provides for the application of concentrated alternating electromagnetic energy, mechanical vibrational energy, and thermal energy to a localized area of the body such as bone joints of a hand, arm and the like. ... The use of electromagnetic energy and magnetic energy alone as a therapeutic aid for various types of diseases occuring to various mammals is well known in the prior art. A vast spectrum of various diseases has been purported to be reduced or totally eliminated by several of these devices. In U.S. Pat. No. 3,658,051, issued to MacLean, a method of treating living things using high intensity pulsating magnetic fields is shown. The method is alleged to be effective for curing a plethora of varying diseases by applying a unidirectional pulsed magnetic field to the particular part of the body that is ailing. In the instant invention, Applicant has discovered that the application simultaneously of concentrated, magnetic field energy which is alternating in direction at a low frequency in combination with mechanical vibration which vibrates the joint area and heat application to the body will reduce the symptomatic effects of arthritis, rheumatism, rheumatoid-arthritis, osteoarthritis, radiohumeral bursitis, and other similar disorders related to the musculoskeletal and connective tissues. ... The device includes an electromagnet having a core which is designed to intensify the flux lines by concentrating them into a central supporting area which has connected thereacross an elasticized band having a pair of ceramic permanent magnets, one on each side of the band supporting therein. An alternating current applied to the coil of the electromagnet generates an alternating magnetic field that vibrates the permanent magnets, producing mechanical vibration across the elastic band which can be utilized to engage the skin area surrounding the particular joint or tissue being subjected to the intensified field. Furthermore, heat is generated by the electromagnetic field in combination with the core due to hysterisis caused by the alternating magnetic field. Web site: http://www.delphion.com/details?pn=US04177796__ ·
Method and composition for treating arthritis Inventor(s): Petrus; Edward J. (Austin, TX) Assignee(s): Advanced Medical Instruments (Austin, TX) Patent Number: 6,346,519 Date filed: July 8, 1999 Abstract: This invention relates to the composition and method of treating arthritis, repairing of articular joint surfaces and the relief of symptoms associated with arthritis. The composition comprises a nitric oxide synthase inhibitor and amino sugars. The nitric oxide synthase inhibitor reduces the level of nitric oxide, the free radical believed responsible for the degradation of articular cartilage. Amino sugars are the building blocks of articular cartilage and have anti-inflammatory actions. Excerpt(s): The present invention concerns compositions and methods of treating arthritis, repairing of articular joint surfaces and relief of symptoms associated with arthritis. ... Osteoarthritis usually presents as pain, which worsens with exercise or simply an X-ray that clearly shows thinning cartilage. Common joints affected are the
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knees, hips and spine, finger, base of thumb and base of the big toe. Osteoarthritis is characterized by degenerative changes in the articular cartilage and subsequent new bone formation at the articular margins. The primary defect in hyaline cartilage, at the articular surface of the joint, is an alteration in the ratio of total glycosaminoglycans to that of the collagen fiber content in the matrix. Yasuda K. Hokkaido Igaku Zasshi 1997 Jul;72(4):369-76. Paleontologists have found osteoarthritis to exist in almost every vertebrate. Joint cartilage consists of only 5 percent cells, and joint cartilage lesions do heal Tindall W N. Business & Health Dec 1997;47-48. Bones directly underneath the cartilage in joints is called subchondral bone. This bone nourishes the cartilage with oxygen, water, and nutrients conveyed through microscopic channels. This supply route carries "chondroprotective agents" from the bloodstream to the cartilage. ... Cartilage is the supporting structure of the body, but has no blood vessels, nerves or lymphatics, and consists of thick bundles of fibrous protein (collagen) which are woven to form the articular surface. Proteoglycans fill the extracellular spaces not occupied by collagen, and are a combination of protein and sugar. Each proteoglycan subunit contains a protein core attached to hundreds of long chains of specially modified sugars called glycosaminoglycans (GAGS). Glucosamine is the single most important component and precursor for GAGs. Glucosamine is almost completely absorbed by the GI tract into the bloodstream. Cartilage rebuilding is only as good as its GAG synthesis. Chondrocytes in the cartilage obtain glucosamine from the subchondral blood vessels and manufacture N-acetylglucosamine (NAG) and glucuronic acid, which make hyaluronan, which is half glucosamine, and provides the lubricating ability of joints. Web site: http://www.delphion.com/details?pn=US06346519__ ·
Method and compositions for treating arthritis Inventor(s): Root-Bernstein; Robert S. (East Lansing, MI) Assignee(s): Board of Trustees Operating Michigan State University (E. Lansing, MI) Patent Number: 5,942,491 Date filed: October 22, 1996 Abstract: The present invention provides a process for the treatment of arthritis including the step of administering to an animal or human patient in need of such treatment a plurality of peptides each of which peptides contains a sequence of amino acid residues that is identical to or homologous to residues 110-121 or 152-161 of myelin basic protein. Novel peptides for use in that process are also provided. Excerpt(s): The field of this invention is the treatment of arthritis. More particularly, the present invention provides a process of treating arthritis using peptides that are identical to or homologous to anti-arthritic portions of myelin basic protein. ... Arthritis is a very common human bane. Although many animals models of arthritis exist and have been extensively studied, no adequate treatment exists for most forms of arthritis or for related autoimmune diseases with rheumatoid sequelae such as lupus erythematosis. Rheumatoid arthritis presents a particular problem, since it often results in the crippling of affected individuals. While working with one animal model of arthritis (Lewis rats inoculated in the footpad with Mycobacteria, which normally develop adjuvant arthritis), the unexpected observation was made that rats inoculated with a combination of mycobacteria and measles or mycobacteria and measles-mumpsrubella vaccines did not develop arthritis. It was also observed that rats pretreated with porcine myelin basic protein prior to footpad inoculation with mycobacteria were also protected against arthritis. Further experiments showed that the vaccines or MBP were
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capable of suppressing arthritis once induced. ... A literature search has revealed two additional striking observations. First, measles proteins and MBP share extensive regions of homology, suggesting that their common action may share a common mechanism mediated by peptides. This prediction was verified by synthesis of homologous peptides, which also protected and suppressed arthritis. A second observation suggests how important these results may be. Several clinicians have noted that measles infections occasionally mitigate or cure Still's disease, the juvenile form of rheumatoid arthritis. Thus, the treatment regimens described here may represent a significant step towards a treatment or cure for rheumatoid and other forms of arthritis, both in human beings and animals. Web site: http://www.delphion.com/details?pn=US05942491__ ·
Method and compositions for treating psoriasis, eczema, seborrhea and arthritis Inventor(s): Smith; Steven A. (5801 E. 41st, Ste 200, Tulsa, OK 74135) Assignee(s): none reported Patent Number: 6,613,800 Date filed: December 3, 2001 Abstract: A method and composition for treating psoriasis, eczema, seborrheic dermatitis, and possibly arthritis. The present invention involves treatment of these conditions with an oral administration of a mixture comprised of three primary ingredients: fumaric acid and/or fumarate compounds, inorganic nickel compound(s) such as nickel sulfate, and inorganic bromide compound(s) such as potassium bromide. Excerpt(s): The present invention relates to a method and composition for treating psoriasis, eczema, seborrheic dermatitis, and possibly arthritis. More specifically, the present invention involves treatment of these conditions with an oral administration of a mixture of fumaric acid, inorganic nickel compound(s), and inorganic bromide(s). ... Psoriasis is a chronic skin disorder that proliferates in nature and is widespread throughout the world, afflicting millions of humans and even afflicting domesticated animals having similar proliferative integument problems. The skin disorder is characterized by recurrent, elevated red lesions, plaques and on rarely pustules on the skin. These plaques are the result of an excessively rapid growth and shedding of epidermal or skin cells. ... No one knows what causes this abnormal cell proliferation. Its severity and course vary greatly from case to case, and also vary in the individual afflicted with the disease. Recurrences are almost the rule with intervals varying from one month to many years. One person may go through life with a single patch on the elbow, knee or scalp, while another will have repeated attacks of a generalized eruption or widespread chronic lesions lasting for years without remission. As discouraging as it may be, medical science and literature are replete with indications that patients exhibiting such lesions are destined for life to be "psoriatic". With all of the advances in medical science, no one knows what causes this abnormal cell growth. With some of it, it is felt that some type of biochemical stimulus triggers this abnormal cell growth. It is still unknown whether the origin of this biochemical malfunction resides in the skin, in the immune system, in the white blood cells, or is possibly psycho-neural. It is know that certain environmental factors can "trigger" the initial appearance or worsening of psoriasis. Conversely, the symptoms can spontaneously clear for reasons scientists do not understand. Treatment of the psoriasis is aimed at clearing the lesions for as long as possible. This is what is meant by the term `remission" or "clearance". In any event,
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medical science has fairly well agreed that psoriasis is a heritable disease in which the specific defect seems to be unknown. Web site: http://www.delphion.com/details?pn=US06613800__ ·
Method and medical agent for diagnosis of arthritis Inventor(s): Aizawa; Katsuo (Yokohama, JP), Kuroiwa; Yukari (Urawa, JP) Assignee(s): Nippon Petrochemicals Company, Ltd. (Tokyo, JP) Patent Number: 5,567,409 Date filed: December 12, 1994 Abstract: A method and medical agents for the photodynamic diagnosis of rheumatoid arthritis of mammals, which agent comprises at least one member of fluorescent compounds selected from the group consisting of tetrapyrrole carboxylic acids having at least one carboxyl group, corresponding di- or tetrahydrotetrapyrrole carboxylic acids, and mono-, di- or polyamides of the tetrapyrrole carboxylic acids with amino-mono- or dicarboxylic acids and their salts. Excerpt(s): This invention relates to a method and medical agents for the photodynamic diagnosis and photodynamic therapy of the arthritis, especially the arthritis of mammals. More particularly, the medical agents used in the present invention belong to specific fluorescent compounds having a tetrapyrrole skeletal structure. When an effective quantity of the medical agent is administered to an animal patient, the agent is accumulated in the affected part of the body. ... When light rays of necessary wavelength are applied to an affected joint to be diagnosed or treated, the agent generates fluorescence in the affected portion, thereby enabling the detection of arthritis. This is called as photodynamic diagnosis. In the therapeutic treatment, when light rays of appropriate wavelength and intensity are applied to a lesion, the agent is excited to produce a cytotoxic effect and the affected cells in arthritic lesion are necrosed. This is called as photodynamic therapy. The present invention relates to the diagnosis and the therapy of this kind applied to arthritis, especially rheumatoid arthritis. ... Rheumatoid arthritis is a chronic systemic disease mainly causing to occur polyarthritis as a cardinal symptom. This disease is initiated by the pain and swelling in small joints of hands and feet, or in elbow joints and knee joints, and other joints in whole body are then affected little by little. In the initial phase of the disease, the hyperplasia of the synovia of the affected joint begins by some stimulation of the unknown antigen, and the synovial hyperplasia is maintained and prolonged by the monokine cascade system to be a tumor-like condition. The constituents of the joint such as cartilage or ligament or bone are destroyed by the enzymes produced by these synovia and followed by the destruction of the joints. Web site: http://www.delphion.com/details?pn=US05567409__
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Method and product using sturgeon notochord for alleviating the symptoms of arthritis Inventor(s): Aoyagi; Seiji (Kobe, JP), Demichele; Stephen J. (Dublin, OH), Johns; Paul W. (Columbus, OH), Mazer; Terrence B. (Reynoldsburg, OH) Assignee(s): Abbott Laboratories (Abbott Park, IL) Patent Number: 6,423,347 Date filed: October 3, 2000 Abstract: This invention provides a composition comprising notochord and extracts thereof in therapeutic amounts. The invention more specifically relates to a method of treating arthritis in mammals, more particularly rheumatoid arthritis in humans through the enteral administration of notochord, notochord extracts or mixtures thereof. In a preferred embodiment, collagen obtained from sturgeon is enterally administered to a human at from 1.0 .mu.g to 1.05 gms per day. Excerpt(s): The present invention pertains to a method for treating the symptoms of arthritis in mammals and, more particularly, relates to the enteral administration of compositions comprising notochord and/or notochord extracts. The invention preferably uses sturgeon notochord, collagen derived from sturgeon notochord, or mixtures thereof to suppress the clinical manifestations of arthritis. The invention also relates to enteral compositions that contain notochord and its structural components to suppress and/or treat arthritis in mammals. ... Arthritis, and particularly rheumatoid arthritis (RA), is a painful and often crippling disease that initially results in swollen and inflamed joints, but often progresses to deform or completely destroy joints. This is a result of the body mistakenly attacking its own cartilage. Cartilage is a specialized kind of connective tissue which is found in human adults in three forms: hyaline or glossy cartilage; elastic cartilage; and fibrocartilage. Hyaline cartilage is the type found in the ventral ends of ribs, in joints, and in the walls of the larger respiratory passages. It is the hyaline cartilage that provides a low friction surface to prevent bone from rubbing on bone during motion. As arthritis progresses, cartilage is damaged and bone may also start to erode. This results in severe pain and ultimate destruction of the joint itself. ... Arthritis is a group of diseases affecting joints and the component tissues. Several types of arthritis are recognized, and these can be divided into several groups by their clinical course or pathological manifestations. The most common form of arthritis is Osteoarthritis (OA). Osteoarthritis is mainly caused by mechanical damage to the joints, either by repetitive use of particular joints as seen in athletes and physical laborers, or by overloading structural joints as seen in the knee joints of obese individuals. Web site: http://www.delphion.com/details?pn=US06423347__
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Method for administration of azauridine and pyridoxine for the treatment of rheumatoid arthritis Inventor(s): Drell; William (San Diego, CA) Assignee(s): UR Labs, Inc. (San Diego, CA) Patent Number: 5,389,617 Date filed: November 12, 1993 Abstract: A method for treating patients with rheumatoid arthritis comprises administering azaribine to the patient at a dosage level of 10 to 50 mg/kg/day for an
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initial period of from about 1 to about 3 weeks and then administering azaribine to the patient at dosage levels of at least 50 mg/kg/day and preferably at least 100 mg/kg/day. Excerpt(s): This invention relates to the treatment of rheumatoid arthritis and more particularly to a method for administering, 6-azauridine, azaribine or other 6-azauridine compound for treating rheumatoid arthritis. ... Azaribine (2', 3', 5'-triacetyl-6-azauridine) has been found to be effective in oral dosage form for the treatment of psoriasis, psoriatic arthritis, mycosis fungoides, herpes simplex, and small pox. Typical dosage levels for the treatment of such conditions are 125 to 250 mg/kg/day. It has been found that such a dosage level may be given for many weeks without side effects, particularly when administered in combination with pyridoxine or other pyridoxine compound, such as pyridoxal phosphate. ... At high doses, azaribine demonstrates antiinflammatory properties. For this reason, azaribine has been tested for the treatment of rheumatoid arthritis. However, at dosage levels of azaribine of 100 mg/kg/day or higher given to patents with rheumatoid arthritis, severe side effects have been reported including fever, joint pain, joint swelling, edema, nausea, emesis, exanthema, painful and rigid muscles and depression. Elis and Raskova, "New Indications for 6-Azauridine Treatment in Man, A Review," Europ.J.Clin. Pharmacol. 4, 77-81 (1972); Elis, Slavik, Ruskova, "Side Effects of 6-Azauridine triacetate in Rheumatoid Arthritis," Clin. Pharmacol. & Therap., II., 404-407 (1970) It has further been reported that slight side effects were produced even at dosage levels of 50 mg/kg per day. Ruskova, Elis, Perlik, Polansky and Slavik, "Unexpected Side Effects of 6-Azauridine in Rheumatoid Arthritis and Feedback in Animal Experiments," Proc. Soc. Europ for the Study of Drug Toxicity," Upsala: June 1970, 12 191 (1971). It is believed that for this reason, no work has been done on this indication for the last 20 years. Web site: http://www.delphion.com/details?pn=US05389617__ ·
Method for alleviating arthritis in mammals Inventor(s): Nimni; Marcel E. (2800 Nelson Way, Apt. 908, Santa Monica, CA 90405) Assignee(s): none reported Patent Number: 6,372,794 Date filed: August 26, 1999 Abstract: A method for alleviating arthritis in mammals by the oral administration of a pharmaceutical composition compound of native Type II collagen in helical form and sulfated polysaccharides found in mammalian cartilage, the Type II collagen and sulfated polysaccharides being ionically bound. Excerpt(s): The major constituents of cartilage are collagen and a variety of anionic high molecular weight carbohydrates (sulfated polysaccharides) associate with proteins in the form of proteoglycans. Both cartilage collagen and the cartilage specific carbohydrate moieties, more specifically the chondroitin sulfatate components of these carbohydrate fractions, are used with various degrees of success in treating patients afflicted with arthritis. The method of the present invention generates a mixture of these native molecules in concentrations and quality which reflect their proportions found in the native tissue. Ionic interactions between the collagen, which retains a fibrillar configuration, and the negatively charged sugars stabilizes the composition in the acid environment of the stomach and facilitates its dissociation in the alkaline environment of the small intestine. This has been found to be extremely effective in ameliorating
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symptoms and reversing changes associated with joint diseases in afflicted dogs and cats and appears to be equally effective in humans. ... Arthritis, particularly rheumatoid arthritis (RA), is a chronic, inflammatory disorder of unknown etiology, affecting approximately 1% of the world's population. Women are affected three to four times more often than men. Some populations are less affected (Asians and Nigerians), and others, such as certain Native American Indians, show a much higher incidence (5-6%). ... In most patients symptoms begin as gradually increasing malaise and fatigue, likely to be accompanied by diffuse musculoskeletal pain. Joint involvement is appreciated as pain, tenderness, swelling, and redness. Symmetry is characteristic, most commonly involving the joints of the hands, wrists, elbows, and shoulders, but also involving the knees, ankles, and feet; virtually any diarthrodial joint can be affected. Web site: http://www.delphion.com/details?pn=US06372794__ ·
Method for alleviating the symptoms of arthritis in mammals Inventor(s): Moore; Eugene R. (5600 Woodview Pass, Midland, MI 48642) Assignee(s): none reported Patent Number: 5,750,144 Date filed: April 9, 1996 Abstract: This invention provides a method for alleviating the symptoms of arthritis in mammals which comprises orally administering a composition obtained by separating water-insoluble undenatured Type II collagen containing animal tissue from animal tissue not containing Type II collagen, subdividing and sterilizing said tissue under conditions which do not change the original structure of the Type II collagen, in an amount effective and for time effective to alleviate such symptoms. Excerpt(s): The present invention pertains to means for treating the symptoms of autoimmune arthritis in mammals and, more particularly, relates to means for preparing animal tissue for oral administration to mammals, compositions comprising said animal tissue and methods for alleviating the symptoms of autoimmune arthritis, particularly rheumatoid arthritis, in humans. ... Autoimmune arthritis, and particularly rheumatoid arthritis, is a painful and often crippling disease that initially results in swollen and inflamed joints, but often progresses to deformed or completely destroyed joints. This is a result of the body mistakenly attacking collagen, which is the major portion of cartilage tissue. Cartilage tissue serves the function of a lubricant in the joints, keeping bone from rubbing on bone. As the disease progresses and more of the cartilage is destroyed, bone does begin to wear on bone. ... This results in even more severe pain and ultimately destruc- tion of the joint itself. As the disease progresses, the body sometimes attacks other collagen in the soft tissues of the body which can cause a variety of arthritis-related diseases. Web site: http://www.delphion.com/details?pn=US05750144__
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Method for detecting bacteria in urine and for treating rheumatoid arthritis, essential hypertension and other diseases associated with bacteriuria Inventor(s): Hyman; Edward S. (3420 Jefferson Ave., New Orleans, LA 70125) Assignee(s): none reported Patent Number: 4,673,637 Date filed: April 23, 1984 Abstract: A novel method of urine specimen preparation comprising intense centrifugation and a lipid wash mitigates or prevents loss of bacteria-containing sediment prior to examination. Modifications of the method facilitate examination of urines with interfering constituents such as glucose, phosphates, and soluble and insoluble proteins. By this method, bacteria have been found in the urine of patients suffering from rheumatoid arthritis and essential hypertension. These bacteria were not detected in standard urine preparations. Administration of antibiotic agents effective against the bacteria detected, such as clindamycin, destroyed these bacteria and provided therapeutic relief. Excerpt(s): This invention relates to a new method of detecting abnormal levels of bacteria in urine, and to new methods for the treatment of patients suffering from rheumatoid arthritis, essential hypertension, and other diseases in which significant bacteriuria was detected by the novel specimen preparation of the present invention that would not have been easily demonstrated by known procedures. ... The direct microscopy and the culture methods each have pitfalls In the past 20-25 years the direct visualization of bacteria in urine has largely been abandoned in favor of the methods involving culturing and counting the colonies of bacteria. Indeed virtually all of the studies of the significance of bacteriuria are based upon culturing the urine, and the direct microscopic examination of urine has been relegated to the status of a quick but inadequate screening procedure which may be helpful because it can be correlated with the culture methods. ... Rheumatoid arthritis (RA) is a chronic inflammation of the joints, generally regarded as a systemic autoimmune disorder. Its etiology is unknown, but it has been postulated that it is associated with microbial infection. See, e.g., D. C. Demonde, ed., Infection and Immunity in the Rheumatic Diseases, 95-287 (Blackwell Scientific Publications, London: 1976). The evidence, however, until the present discovery, was inconclusive. See, e.g., D. J. McCarty, et al., ed., Arthritis and Allied Conditions: A Textbook of Rheumatology, ch 28 at 417 (9th ed. 1979); R. G. Petersdorf, et al., ed., Harrison's Principles of Internal Medicine, Part Six, Chapter 346, at 1977 (McGraw Hill: 1983). Bacteriuria has not been associated with RA, and indeed one authority remarks "Urinary abnormalities are relatively uncommon in RA . . . Urinary tract infection was not found to be increased in RA patients." McCarty, supra, chapter 33, page 499, citing Ann. Rheum. Dis., 27: 345 (1968). Hypertension is a chronic elevation of blood pressure resulting from the obstruction of blood flow within the kidney (secondary hypertension) or without apparent cause (essential hypertension). One kidney disorder associated with secondary hypertension is pyelonephritis, the inflammation of the renal pelvis of the kidney as a result of bacterial infection, usually responsive to antibiotics. It has not been reported, however, that there is any correlation between essential hypertension and asymptomatic bacteriuria (bacteriuria observed in patients not reporting symptoms of urinary tract disorders). According to N. M. Kaplan, Clinical Hypertension, 14 (3d. ed. 1982), bacteriuria is found in 2-5% of hypertensives. Most of these positive cultures were of gram-negative rods. The method of the present invention has demonstrated a much higher incidence of bacteriuria in hypertensives,
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perhaps as high as 90%, and that cocci or "exploded cocci" are found in considerable numbers. Web site: http://www.delphion.com/details?pn=US04673637__ ·
Method for diagnosing rheumatoid arthritis Inventor(s): Prakash; Ramesh K. (Salt Lake City, UT) Assignee(s): Theratech, Inc. (Salt Lake City, UT) Patent Number: 5,395,753 Date filed: February 19, 1993 Abstract: A method is described for diagnosing rheumatoid arthritis by providing a recombinant IgM-specific rheumatoid arthritis-associated antigen and detecting antibodies against the antigen in patient sera. Preliminary steps of making a cDNA library from polyadenylated RNA purified from human cells, selecting recombinants that express the antigen, recloning cDNA containing the antigen gene in a high level expression vector, expressing the antigen in transformed cells, and purifying the antigen are also described. Excerpt(s): This invention relates to a method for diagnosing rheumatoid arthritis. More particularly, this invention relates to a method for objectively diagnosing rheumatoid arthritis by quantitative determination of the presence or absence of rheumatoid arthritis-associated antibodies in patient sera that react with a recombinant antigen. ... Rheumatoid arthritis is a chronic systemic rheumatic disease that affects a significant percentage of the population. Traditionally, it has been diagnosed subjectively through clinical observation and dominant complaints by a patient. P. Lipsky, Rheumatoid Arthritis, in Harrison's Principles of Internal Medicine 1423 (1987). Thus, clinical diagnosis of rheumatoid arthritis is subject to the skill of the diagnostician and the severity of disease symptoms in the patient. ... For an objective diagnosis of rheumatoid arthritis, the presence of rheumatoid factor (Rf) in the serum of rheumatoid arthritis patients is routinely determined. Rf has been detected in approximately 70% of patients exhibiting clinical symptoms of rheumatoid arthritis. These patients are thus termed "seropositive." The remaining 30% are classified as having "seronegative" rheumatoid arthritis. Numerous conditions besides rheumatoid arthritis are associated with the presence of rheumatoid factor. Therefore, the presence of Rf does not establish a conclusive diagnosis of rheumatoid arthritis. An objective method of diagnosing rheumatoid arthritis that is more closely correlated with clinical diagnoses than is the presence of Rf in sera is needed. Ideally, such an objective diagnostic test would be quick and easy to perform and would not involve radioisotopes or be invasive to the patient. Web site: http://www.delphion.com/details?pn=US05395753__
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Method for diagnosis of rheumatoid arthritis Inventor(s): Yamanaka; Naoki (Nagoya, JP), Yoshida; Makoto (Kawasaki, JP) Assignee(s): Asahi Medical Co., Ltd (Tokyo, JP), Medecs Co., Ltd. (Aichi, JP) Patent Number: 4,863,850 Date filed: February 16, 1988
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Abstract: A substantially pure rheumatoid arthritis specific protein (RASP) and an antibody against the rheumatoid arthritis specific protein (anti-RASP antibody) are disclosed. The RASP is found specifically in the serum or plasma of a patient suffering from rheumatoid arthritis, and may be detected using an anti-RASP antibody easily and effectively. Therefore, the anti-RASP antibody of the present invention is useful for the diagnosis of rheumatoid arthritis by the criterion of the presence of RASP. Excerpt(s): This invention relates to a substantially pure rheumatoid arthritis specific protein. The present invention also relates to an antibody against the rheumatoid arthritis specific protein. More particularly, the present invention is concerned with a protein specifically found in the plasma of a patient suffering from rheumatoid arthritis and an antibody specific for the antigenic determinant of the rheumatoid arthritis specific protein. ... Conventionally, the diagnosis of rheumatoid arthritis has been effected according to the criteria proposed by the American Rheumatism Association. However, such criteria depend on doctor's observations and dominant complaints by a patient, and therefore, such criteria are insufficient with respect to objectivity and quantitative analysis of the degree of rheumatoid arthritis. ... For the quantitative analysis of the degree of rheumatoid arthritis, the presence and amount of rheumatoid factor (RF), immune complex (IC) or C-reactive protein (CRP) in the serum or plasma of a patient have been determined. However, such substances are not necessarily specific for the plasma or serum of a patient suffering from rheumatoid arthritis, and therefore, such substances are not useful as a conclusive factor. Web site: http://www.delphion.com/details?pn=US04863850__ ·
Method for preparing animal tissue for use in alleviating the symptoms of arthritis in mammals Inventor(s): Moore; Eugene R. (5600 Woodview Pass, Midland, MI 48642) Assignee(s): none reported Patent Number: 5,637,321 Date filed: April 9, 1996 Abstract: This invention provides a method of preparing animal tissue containing water-insoluble undenatured Type II collagen for use in treating autoimmune arthritis, particularly rheumatoid arthritis. Excerpt(s): The present invention pertains to means for treating the symptoms of autoimmune arthritis in mammals and, more particularly, relates to means for preparing animal tissue for oral administration to mammals, compositions comprising said animal tissue and methods for alleviating the symptoms of autoimmune arthritis, particularly rheumatoid arthritis, in humans. ... Autoimmune arthritis, and particularly rheumatoid arthritis, is a painful and often crippling disease that initially results in swollen and inflammed joints, but often progresses to deformed or completely destroyed joints. This is a result of the body mistakenly attacking collagen, which is the major portion of cartilage tissue. Cartilage tissue serves the function of a lubricant in the joints, keeping bone from rubbing on bone. As the disease progresses and more of the cartilage is destroyed, bone does begin to wear on bone. This results in even more severe pain and ultimately destruction of the joint itself. As the disease progresses, the body sometimes attacks other collagen in the soft tissues of the body which can cause a variety of arthritis-related diseases. ... In order to initiate the disease, it is apparent that an individual must have an inherent (perhaps genetic) susceptibility. Given this
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susceptibility, there is now strong evidence that the disease is initiated by exposure to the Epstein-Barr virus. The ability of the Epstein-Barr virus to initiate Rheumatoid Arthritis has been linked to a key amino acid sequence which is identical to a sequence found in human collagen. Thus, in generating antibodies to destroy the Epstein-Barr virus, the body generates antibodies that are also capable of attacking its own collagen. In a similar manner, arthritis has been initiated in rats by the intradermal injection of water-soluble highly purified Type II procollagen extracted from chicken cartilage or by the well known complete Freund Adjuvant. Web site: http://www.delphion.com/details?pn=US05637321__ ·
Method for preventing and treating arthritis, osteo-traumatic pain, and neuralgias with trimebutine Inventor(s): Grouhel; Agnes (Meudon, FR), Brunelle; Gilles (Antony, FR), Roman; Fran.cedilla.ois (Vitry-sur-Seine, FR), Hamon; Jacques (Orsay, FR) Assignee(s): Warner-Lambert Company (Morris Plains, NJ) Patent Number: 6,353,024 Date filed: January 24, 2000 Abstract: The invention relates to the use of trimebutine [2-dimethylamino-2phenylbutyl-3,4,5-trimethoxy-benzoate hydrogen maleate] or its corresponding stereoisomers for the preparation of a medicament to prevent and/or treat arthritis, osteo-traumatic pain, and neuralgias. Excerpt(s): The field of the invention is related to methods for preventing and/or treating inflammatory somatic pain and chronic pain. More particularly the invention concerns the use of trimebutine [2-dimethylamino-2-phenylbutyl 3,4,5trimethoxybenzoate hydrogen maleate] for preventing and/or treating inflammatory somatic pain as well as chronic pain. ... Trimebutine [2-dimethylamino-2-phenylbutyl 3,4,5- trimethoxybenzoate hydrogen maleate; TMB] has been used in many countries since 1969 for the treatment of functional bowel disorders, including irritable bowel syndrome (IBS). The efficacy of the compound to relieve abdominal pain has been demonstrated in various clinical studies using different protocols of treatment (Luttecke, 1980; Moshal and Herron, 1979, Toussaint et al., 1981; Ghidini et al. 1986). Trimebutine was found to display weak agonist activity for rat brain and guinea-pig (Roman et al., 1987) or canine (Allescher et al., 1991) intestinal opioid receptors, without selectivity for any of the .mu.-, .delta.- and .kappa.-subtypes. This weak activity was confirmed when using isolated intestinal fragments under transmural stimulation (Pascaud et al., 1987). This property could be responsible for the modulatory action of trimebutine on intestinal motility in fasted dog. Trimebutine given either intravenously or orally delays the appearance of a phase III of the migrating motor complex (MMC) in the stomach and the duodenum by inducing a premature phase III, migrating along the whole intestine (Bueno et al., 1987). In man, trimebutine stimulates intestinal motility in both fed and fasted states (Grandjouan et al., 1989). Furthermore, trimebutine reverses the effect of stress in jejunal motility (Delis et al., 1994). ... More recently, trimebutine has been shown to be able to influence the activity of visceral afferents by decreasing the intensity of the recto-colonic reflex in rats as evidenced by the inhibition of colonic motility consecutive to rectal distension (Julia et al., 1996). This result may be related to the beneficial effects found with trimebutine in patients with IBS and more specifically in the treatment of attacks of abdominal pain.
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Web site: http://www.delphion.com/details?pn=US06353024__ ·
Method for the diagnosis of rheumatoid arthritis Inventor(s): Hayakawa; Taro (Nagoya, JP), Kodama; Shuji (Takaoka, JP), Iwata; Kazushi (Takaoka, JP), Kishi; Junichi (Nagoya, JP), Yamashita; Kyoko (Nagoya, JP), Iwata; Hisashi (Nagoya, JP) Assignee(s): Fuji Yakuhin Kogyo Kabushiki Kaisha (Toyama, JP) Patent Number: 5,190,861 Date filed: April 25, 1989 Abstract: A method for diagnosing rheumatoid arthritis, which is characterized by enzyme-immunologically measuring the amount of collagenase inhibitor present in sera, plasmas or synovial fluids by way of a sandwich assay wherein two different monoclonal antibodies which specifically bind to different antigenic determinants of the collagenase inhibitor are used, and comparing the measured amount with that for normal subjects. Excerpt(s): The present invention relates to a method of the diagnosis of rheumatoid arthritis by way of quantitation of collagenase inhibitor. More particularly the invention relates to a method for carrying out the diagnosis of rheumatoid arthritis, by means of a sandwich enzyme immunoassay for human collagenase inhibitor using monoclonal antibodies to bovine collagenase inhibitor (tissue inhibitors of metallproteinases: TIMP), on the basis of the fact that the amount of collagenase inhibitor in sera, plasmas or synovial fluids from patients with rheumatoid arthritis is clearly higher than the amount of collagenase inhibitor in sera, plasmas or synovial fluids, respectively, from normal subjects. The enzyme immunoassay mentioned above is used to mean a method for determining collagenase inhibitor which is characterized in that there are used two different monoclonal antibodies which specifically bind to different antigenic determinants of collagenase inhibitor as an antibody to be bound to a solid phase support and an antibody to be labeled with an enzyme. ... Among heretofore used methods for the diagnosis of rheumatoid arthritis may be mentioned: Rose's method based on the detection of rheumatoid factor, modified Rose's method by Heller, RAHAtest and RA-test. These methods, however, have such disadvantages that they use complex experimental methods or that it takes many days to go through with the diagnosis. ... Collagenase inhibitor has been known to exist in human's and other animals' bones, skins, dental pulps, amniotic fluids, bloods and synovial fluids as well as in cultures of joint chondrocytes, synovial cells, fibroblasts derived from varied tissues and fibrosarcomatous cells. As means for determining the amount of collagenase inhibitor methods have heretofore been known which are based on measurement of its biological activity. As described by Eisen et al. in J. Lab. Clin. Med. 75, 258-263 (1973) and also by Cawston et al. in Arthritis and Rheumatism 27, 285-290 (1984), however, it is impossible, with the heretofore known methods of determination, to assay sera, plasmas or synovial fluids for collagenase inhibitor activity since there exist in such fluids proteins, such as .alpha..sub.2 -macroglobulin, which interfere disturbingly with the measurement. Hayakawa, Iwata et al. have already developed a sandwich enzyme immunoassay (EIA) using monoclonal antibodies to bovine collagenase inhibitor, a method which enables specific quantitation of collagenase inhibitor with very small volumes of samples in a precise, straightforward and rapid manner (Japanese Patent Application No. Sho 62-42781). The present inventors have discovered that the level of collagenase inhibitor present in human sera, plasmas or synovial fluids apparently
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increases in association with affliction with rheumatoid arthritis, and found that it is possible to make a diagnosis of rheumatoid arthritis by determining, by the enzyme immunoassay mentioned above, the amount of collagenase inhibitor present in sera, plasmas or synovial fluids. Web site: http://www.delphion.com/details?pn=US05190861__ ·
Method for the treatment of arthritis and inflammatory joint diseases Inventor(s): Gordon; Robert T. (4936 W. Estes, Skokie, IL 60077) Assignee(s): none reported Patent Number: 4,758,429 Date filed: November 4, 1985 Abstract: The present invention describes a method for the treatment of arthritis and joint diseases with diagnostic applications to enhance the treatment process. The process involves the utilization of magnetic or electric dipoles which are present, capable of being induced, or introduced into the cell of the joint and are capable of being activated by an external alternating electromagnetic field. The activation of these magnetic or electric dipoles (particles) allows destruction of the reactive cells and alteration of the intracellular processes with a dimunition of the destructive process. Excerpt(s): Arthritis and joint diseases while having some modes of therapy are currently only treated symptomatically. Various medications and drugs are used to decrease the inflammatory response. The mechanism of action of many of these drugs is very poorly understood. When the destructive process has advanced too far, the joint may require surgical intervention and even prosthetic replacement. These prosthesis, while of assistance, do not provide the mobility and feelings inherent in the natural joint. ... The cause of arthritis and joint disease processes is multiple. Inflammatory joint disease may be related to stimulation of the immune system to the normal joint tissues. Similarly the various collagen diseases can stimulate the inflammatory process i.e. systemic lupus, erythemtosis. Rheumatoid arthritis and osteoarthritis are also examples of disease processes which affect the joint. Infection with bacteria, viruses and fungus can initiate a degenerative process. Tumors both primary and metastatic can invade the joint space and cause destruction. In all of these processes the mechanism is quite similar. Inflammatory cells invade the synovial lining of the joint. A pannus forms and eventually destruction of the joint ensues. The present invention describes a method to stop and/or measureably alter the process before destruction of the joint occurs, thereby preserving the normal joint. ... The electromagnetic field interacts with joint tissues in several ways. There are displacement currents due to the drift of electrons, polarization of atoms or molecules to produce dipoles and the interaction with dipoles already present. The coupling of electromagnetic energy to the joint tissues depends on the electrical conductivity (.delta.) and the dielectric constant (.epsilon.). The power imparted to the joint issues depends on the square of the amplitude of the field and the coupling constant to the joint tissues. The dielectric properties of the material depend on its composition and structure (i.e. ions, polar molecules, etc.). Web site: http://www.delphion.com/details?pn=US04758429__
Patents 347
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Method for therapeutically treating psoriatic arthritis using vitamin D analogues and metabolites Inventor(s): Gilbert; Lawrence (Hingham, MA), Holick; Michael F. (Sudbury, MA) Assignee(s): Trustees of Boston University (Boston, MA) Patent Number: 5,098,899 Date filed: December 14, 1990 Abstract: A novel and effective treatment of psoriatic arthritis is provided using biologically active forms of vitamin D analogues and metabolites, and preferrably 1,25dihydroxy vitamin D.sub.3. The administration of vitamin D analogues and metabolites may be made orally, topically, or parenterally. Substitive improvements in both the arthritic condition and skin lesions result after approximately two month's treatment when effective dosages are provided and maintained. Excerpt(s): The present invention is concerned with specific disease states and pathological disorders, and is particularly directed to therapeutically treating psoriatic arthritis as a singular disease and pathological state. ... Although psoriatic arthritis is today recognized and as a distinct disease and pathological state based on its natural evolution, prognosis, and response to available modes of treatment, its consideration and present status as a distinct and separate clinical entity separate from either psoriasis and/or rheumatoid arthritis required both time and in-depth medical knowledge. In retrospect, the first detailed description of psoriatic arthritis appeared in the doctoral thesis of Charles Bourdillion [Psoriasis et Arthropathies, These de Paris, Volume 298, 1988]; and in several mid-19th century case reports of a unique relationship between psoriasis and arthritis published by 1904 [Menzen, J., Arch. Dermatol. Syph. 70:239-240 (1904)]. For about 30 years thereafter, the idea of psoriatic arthritis being an individual and discrete entity, as opposed to the coincidental occurrence of rheumatoid arthritis and psoriasis, was not generally accepted. Consequently, it was not until the demonstration of rheumatoid factor (RF) in the serum of most patients with typical rheumatoid arthritis in 1948 that the distinction became firmly established. The demonstration and meaning of rheumatoid factor (RF) divided inflammatory arthritis into seropositive and seronegative groupings. Consequently, the realization that the majority of patients with coincident psoriasis and arthritis were in fact seronegative, coupled with the introduction of specific and reliable criteria for the diagnosis of rheumatoid arthritis itself, then firmly established psoriatic arthritis as a separate and distinct disease entity [Rose et al., Proc. Soc. Exp. Biol. Med. 68:1-6 (1948); Ragan, C., Arthritis And Allied Conditions, (J.L. Hollander and D.J. McCarthy, editors) 8th Edition, Lee & Febiger, Philadelphia, 1972; Ropes et al., Bull. Rheum. Dis. 7:121-124 (1956); and Ropes et al., Bull. Rheum. Dis. 9:175-176 (1959)]. ... Today, rheumatologists have generally accepted the concept of distinctive clinical and radiological features for psoriatic arthritis; and employ them to identify subjects suffering from psoriasis alone and to distinguish those persons suffering from either seronegative or seropositive rheumatoid arthritis without psoriasis. A series of clinical characteristics suggestive of psoriatic arthritis have been developed and verified. Similarly, a detailed description and evaluation of the pathology, etiology, clinical features, patterns of disease onset and distribution, laboratory tests, and radiographic findings of psoriatic arthritic have been extensively investigated and documented. A comprehensive and well documented description of these diagnostic, clinical, and pathological developments and findings identifying psoriatic arthritis as a distinctive disease state and entity is provided by Robert N. Bennett in Arthritis And Allied Conditions, A Textbook Of Rheumatology,
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(Daniel J. McCarthy, Editor) Lee & Febiger, 11th Edition, 1989, pages 954-971, the text of which is expressly incorporated by reference herein. Web site: http://www.delphion.com/details?pn=US05098899__ ·
Method for treating arthritically inflamed body joints, particularly joints having gouty arthritis Inventor(s): Gertner; Sheldon (39 Ridge Dr., Berkeley Heights, NJ 07922) Assignee(s): none reported Patent Number: 5,061,724 Date filed: July 18, 1989 Abstract: A method of treating inflammations of body joints in humans by topical application of anti-inflammatory agents may be used to treat joints afflicted by arthritic conditions such as gouty arthritis. The steps of the method include dissolving a predetermined quantity of a known anti-inflammatory drug, applying the medium with dissolved anti-inflammatory drug directly onto the skin covering a body joint known to be inflamed and allowing the medium with dissolved anti-inflammatory drug to be absorbed into the skin. Possible non-steroidal, anti-inflammatory drugs which may be used with the method include indomethacin, phenylbutazone and colchicine. Steroidal non-inflammatory drugs may also be used. Excerpt(s): The present invention relates to a method for treating inflammations of body joints in humans, and in particular, joints afflicted by arthritic conditions such as gouty arthritis. ... The chronic treatment of gout affecting the big toe or other toes requires daily or prophylactic treatment with one or more drugs. These drugs, such as colchicine, allopurinol, probenecid or indomethacin or combinations of these, have numerous side effects that can cause with time considerable toxicity. In addition, they may adversely affect the action of other drugs given to the patient to treat completely different conditions. More importantly, when the drugs are used to affect small areas such as the toes, relatively high doses must be given which produce overall much greater effects on other body tissues than the toes due to the general distribution of the drug when given by the oral route. ... It would appear more logical, when the object of therapy is to produce a local anti-inflammatory effect, to treat each local site of inflammation with lower doses of the anti-inflammatory drugs than would be given orally. The local concentrations under these conditions, at the joint, would still be considerably higher than giving such anti-inflammatory drugs orally, where the drug is distributed to all the body tissues and thus diluted. This local application should be domethacin and phenylbutazone (non-steroidal anti-inflammatory agents) as well as colchicine, which works by a different mechanism. Web site: http://www.delphion.com/details?pn=US05061724__
Patents 349
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Method for treating arthritis Inventor(s): Gainer; John L. (Charlottesville, VA) Assignee(s): The University of Virginia Alumni Patents Foundation (Charlottesville, VA) Patent Number: 4,176,179 Date filed: April 17, 1978 Abstract: Arthritis in mammals is treated by administering to said mammal an effective dose of a water soluble carotenoid. Excerpt(s): This invention relates to a novel technique for treating arthritis in mammals. ... In Applicant's prior applications, now U.S. Pat. Nos. 3,853,993 and 3,788,468, Applicant disclosed that certain water-soluble carotenoids had been observed to possess quite unique properties. In particular, these water-soluble carotenoids have been found to increase the diffusivity of oxygen through aqueous media. Applicant theorized that this phenomenon might be applied to effect desirable biological effects. In particular, Applicant theorized that if oxygen diffusivity in aqueous media could be enhanced, that this effect could be applied to increase the diffusivity of oxygen in blood. Applicant theorized further that by increasing the diffusivity of oxygen in the blood, atherosclerosis, which has long been theorized to be a disease resulting from local hypoxia of the vascular walls, could be successfully treated. This theory was applied to certain test animals, and, to the satisfaction of the inventors, the theory was proven to be correct, and in fact, a seemingly successful treatment of atherosclerosis was obtained. ... Applicant has now continued to study the biological properties of this most unusual class of compounds, with the result that a new biological property has been discovered which is the subject matter of this application. Web site: http://www.delphion.com/details?pn=US04176179__
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Method for treating arthritis or inflammation with Il-1.alpha. or derivatives thereof Inventor(s): Nakai; Satoru (Takushima, JP), Hirai; Yoshikatsu (Takushima, JP) Assignee(s): Otsuka Pharmaceutical Co., Ltd. (Tokyo, JP) Patent Number: 5,342,615 Date filed: July 30, 1990 Abstract: Interleukin-1.alpha. (IL-1-.alpha.) and derivatives, and their pharmaceutical compositions for use in treating arthritis or inflammation. Excerpt(s): The present invention relates to novel polypeptides, and more particularly to novel derivatives of interleukin-1.alpha. (IL-1.alpha.) and to the medicinal use of IL1.alpha. and the novel derivatives thereof. ... The Second International Lymphokine Workship decided to adopt a unified name, interleukin-1 (IL-1), for the physiologically active substances which had been referred to as lymphocyte activating factor (LAF), mitogenic protein, helper peak-1, T-cell replacing factor III (TRF-III), T-cell replacing factor M.phi. (TRFM), B-cell activating factor, B-cell differentiation factor, etc. (Cellular Immunol., 48, 433-436 (1979)). This decision is based on the reason that these physiologically active substances can not be distinguished from one another as different substances but are expressed variously merely with reference to physiological activities as interpreted from different angles. ... Further it is reported that IL-1 activates T lymphocytes and B lymphocytes, has activity to promote production of interleukin-2
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and antibodies, acts on liver tissues to promote protein synthesis and possesses activity to promote production of prostaglandins (see Reviews of Infectious Disease, Vol. 6, No. 1, 51-59 (1984), New England J. of Med., 311, 1413 (1984), etc.). Web site: http://www.delphion.com/details?pn=US05342615__ ·
Method for treating arthritis with 6-aryl pyrimidine compounds Inventor(s): Fast; Patricia E. (Kalamazoo, MI), Wierenga; Wendell (Kalamazoo, MI) Assignee(s): The Upjohn Company (Kalamazoo, MI) Patent Number: 4,507,302 Date filed: September 21, 1981 Abstract: This invention relates to 6-aryl pyrimidine compounds which have now been found to be useful for treatment or prevention of arthritis. Excerpt(s): The preparation and use of 2-amino-5-halo-6-alkyl-4-pyrimidinols as antiviral agents is known (U.S. Pat. No. 3,956,302 and Nichols, Weed and Underwood, Antimicrobial Agents and Chemotherapy 9,433, 1976). Preparation of 2-amino-5-bromo6-phenyl-4-pyrimidinol (V, where X.sub.3 is Br and X.sub.1 is phenyl) has been reported (Brown and Stevens, JCS Perkin I, 1023, 1975) but no utility has been described for this material. Snell, Elias and Freeman in GB 1,223,686 (1967) disclose a variety of 5,6disubstituted 2-amino-4-pyrimidinols, such as 2-dimethylamino-5-bromo-6-methyl-4pyrimidinol. Various 5-unsubstituted 2-amino-6-arylpyrimidinols are known (e.g., Shirahawa, Yakugaku Zasshi 80, 1542-50 (1960) (CA 55, 10450e); Kulkarni et al., J. Sci. & Ind. Res. India 19C, pp. 6-8 (1960) (CA 54, 22576c) and U.S. Pat. No. 2,776,283. Diuretics and cardioregulatory properties are described for various 2-amino and 2-substituted amino-5-aminomethyl and 5-aryl-6-aryl-4-pyrimidinols, U.S. Pat. No. 2,704,285, U.S. Pat. No. 2,723,977 and U.S. Pat. No. 2,776,283. ... This invention relates to 6-aryl pyrimidine compounds which have now been found to be useful for treatment or prevention of arthritis. ... The compounds of this invention are prepared from .beta.-keto ester compounds. The starting .beta.-keto esters are prepared as follows. Web site: http://www.delphion.com/details?pn=US04507302__
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Method for treating rheumatoid arthritis Inventor(s): Schulthess; Adrian (Begnins, CH), Farine; Jean-Claude (Eysins, CH) Assignee(s): Laboratoires OM Societe Anonyme (Geneva, CH) Patent Number: 4,322,405 Date filed: April 6, 1981 Abstract: Lysates derived from strains of Escherichia coli, especially wherein said lysates are derived from at least one of the strainsNCTC 8603, 8621, 8622, 8623, 9026, 9111, 9119, 9707, 9708,I-081, I-082, I-083, I-084, I-085, I-086, I-087, I-088, I-089are useful for treating rheumatoid arthritis. Excerpt(s): is known as an immunobiotherapeutic agent, used against infectious diseases of the urinary and the gastro-intestinal tract (see German OS 30 19 448.0). This latter specification gives full details for the preparation of lysates of these strains. The above-mentioned strains NCTC are listed by the National Collection of Type Cultures,
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London (Great Britain), and are accessible to the public, whereas the above-mentioned strains I-081 to I-089 have been deposited by the assignee of the present patent application on Mar. 7, 1979, at Collection Nationale de Cultures de Microorganismes, Institut Pasteur, Paris (France). ... We have now surprisingly found that bacterial lysates of Escherichia coli, and especially bacterial lysates of the above-mentioned strains NCTC and I, produce an anti-inflammatory action in animals. They have a non-specific immunostimulatory action in humans and are useful in patients with rheumatoid arthritis (RA). RA is known as an inflammatory disease with immunological etiology. ... In the following animal model, lysates of Escherichia coli showed an action in the chronic inflammatory phase. Web site: http://www.delphion.com/details?pn=US04322405__ ·
Method for treating rheumatoid arthritis with composition containing histone Inventor(s): Bae; Insoo (Daejon, KR), Kim; Dong-soo (Seoul, KR), Yim; Heajoon (Daejon, KR), Jung; Neon-Cheol (Daejon, KR), Yi; Yong-Weon (Daejon, KR), Hong; Seung-Suh (Daejon, KR), Lee; Hyun-Soo (Seoul, KR) Assignee(s): Samyang Genex Corporation (Seoul, KR) Patent Number: 6,204,242 Date filed: January 19, 2000 Abstract: The present invention relates to a novel use of histone and provides a pharmaceutical composition containing histone as an active ingredient to improve the symptoms of progressive, inflammatory and autoimmune arthritis. The pharmaceutical composition of the present invention includes histone, especially histone H1 as an active ingredient, and could include pharmacologically approved carriers if necessary. Histone H1 lowered induction of arthritis and reduced arthritis index more effectively than steroidal dexamethasone and also had a significant preventive effect. Excerpt(s): The present invention relates to the use of histone H1 in improving inflammatory symptoms of arthritis. Histone H1 lowers an induction of arthritis and reduces arthritis index more effectively than conventional drugs and also has a significant preventive effect. ... The present invention relates to a biologically active compound and compositions containing the same to improve symptoms of progressive, inflammatory and autoimmune arthritis. Despite the development of many arthritis drugs, arthritis remains to be a world wide serious disease due to an increasing aging population. Even though the death rate due to arthritis is low, the quality of life of an individual who suffers from this disease is sacrificed with lowered activity level and productivity. ... Among many types of arthritis, the most significant one is rheumatoid arthritis. Rheumatoid arthritis is an autoimmune disease by the action of auto-reactive T lymphocytes. T lymphocyte causes rheumatoid anthritis via delated type hypersensitivity. It is not fully understood which antigen is recognized by T lymphocyte to cause this disease. Type II collagen is known to be the most probable one, but other possibilities cannot be excluded. Anti-histone autoantibody has been discovered even though it is not clear that this antibody is the cause of the disease. Web site: http://www.delphion.com/details?pn=US06204242__
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Method for treatment of non-rheumatoid arthritis Inventor(s): Macias; William Louis (Indianapolis, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 6,610,728 Date filed: February 24, 2000 Abstract: A method is disclosed for the treatment of non-rheumatoid arthritis by administering to a mammal in need thereof a therapeutically effective amount of an sPLA.sub.2 inhibitor. Excerpt(s): The present invention is directed to a method for treating non-rheumatoid arthritis. More specifically, the present invention is directed to a method for treating the causes and/or the symptoms of various forms of non-rheumatoid arthritis in mammals by administering a therapeutically effective amount of an sPLA.sub.2 inhibitor. ... The most common form of non-rheumatoid arthritis is osteoarthritis, a degenerative joint disease which primarily affects cartilage that covers and cushions the ends of the bones causing it to fray, wear, ulcerate, and in extreme cases, to disappear entirely leaving a bone on bone joint. The disease can result in severe disability particularly in the weight bearing joints such as the knees, hips, and spine. Osteoarthritis is distinguishable, for example, from rheumatoid arthritis in that osteoarthritis involves little or no inflammation and is confined to the joints and surrounding tissue where there is a breakdown or disintegration of cartilage and other tissue thereby making it difficult for the joints to operate properly. The occurrence of osteoarthritis frequently increases with advancing years. ... Non-rheumatoid arthritis is often treated with acetaminophen and ibuprofen. In addition, non-steroidal anti-inflammatory drugs (NSAIDSs) may be used to relieve pain by blocking the production of prostaglandins (e.g., choline magnesium salicylate, salicylsalicyclic acid). Corticosteroids such as methylprednisone, prednisone, and cortisone may be used to relieve pain and swelling. Each of these known drug therapies has possible long-term disadvanges such as kidney or liver damage, heartburn, stomach upset, ulcers, gastrointestinal bleeding, mood swings, weight fain, high blood pressure, muscle weakness and lowered resistance to infection. Web site: http://www.delphion.com/details?pn=US06610728__
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Method for treatment of reactive arthritis or bursitis Inventor(s): Bonner, Jr.; Ernest L. (1406 Park St., Suite 400, Alameda, CA 94501), Hines; Robert (3637 Cape Center Dr., Fayetteville, NC 28304) Assignee(s): none reported Patent Number: 6,197,776 Date filed: July 10, 2000 Abstract: An improved method for treatment of conditions in human beings associated with either or both reactive arthritis or bursitis comprising administration of a combination of acyclovir, L-lysine, minocycline hydrochloride, and metronidazole. An alternate method comprises administration of isonicotinic acid hydrazide. Excerpt(s): This invention relates to an improved treatment for symptoms associated in humans with reactive arthritis or idiopathic bursitis. ... Reactive arthritis refers to a spondyloarthritity which usually arises as a complication of an infection elsewhere in the body. Reactive arthritis can be caused by species of Shigella bacteria (most notably
Patents 353
Shigella flexneri), Yersinia enterocolitica, Campylobacter jejuni, several species of Salmonella, genitourinary pathogens, Chlamydia trachomatis, Neisseria gonorrhea, Ureaplasma urealyticum, Streptococcus pyogenes, and other yet unidentified infectious agents. ... Reactive arthritis commonly occurs in young men and women, but can occur at any age. Sufferers experience joint pain, stiffness, redness or swelling. Common symptoms may include fatigue, malaise, fever, and weight loss. The joints of the lower extremities, including the knee, ankle, and joints of the foot, are the most common sites of involvement, but symptoms can also occur in the wrists, fingers, elbows, shoulders, neck, and lower back. Other symptoms may include urethritis and prostatitis in males, and cervicitis or salpingitis in females. Ocular disease is common ranging from transient, asymptomatic conjunctivitis to aggressive anterior uveitis that occasionally results in blindness. Mucocutaneous lesions and nail changes are frequent. On less frequent or rare occasions manifestations of reactive arthritis include cardiac conduction defects, aortic insufficiency, central or peripheral nervous system lesions, and pleuropulmonary infiltrates. Web site: http://www.delphion.com/details?pn=US06197776__ ·
Method for treatment of reactive arthritis or bursitis Inventor(s): Bonner, Jr.; Ernest L. (1406 Park St., Suite 400, Alameda, CA 94501), Hines; Robert (3637 Cape Center Dr., Fayetteville, NC 28304) Assignee(s): none reported Patent Number: 6,465,473 Date filed: February 22, 2000 Abstract: An improved method for treatment of conditions in human beings associated with either or both reactive arthritis or bursitis comprising administration of a combination of L-lysine, minocycline hydrochloride, metronidazole, and valacyclovir hydrochloride. A first alternate method comprises administration of L-lysine, minocycline hydrochloride, and metronidazole. A second alternate method comprises administration of L-lysine, minocycline hydrochloride, metronidazole, and isonicotinic acid hydrazide. Excerpt(s): This invention relates to an improved treatment for symptoms associated in humans with reactive arthritis or idiopathic bursitis. ... Reactive arthritis refers to a spondyloarthritity which usually arises as a complication of an infection elsewhere in the body. Reactive arthritis can be caused by species of Shigella bacteria (most notably Shigella flexneri), Yersinia enterocolitica, Campylobacter jejuni, several species of Salmonella, genitourinary pathogens, Chlamydia trachomatis, Neisseria gonorrhea, Ureaplasma urealyticum, Streptococcus pyogenes, and other yet unidentified infectious agents. ... Reactive arthritis commonly occurs in young men and women, but can occur at any age. Sufferers experience joint pain, stiffness, redness or swelling. Common symptoms may include fatigue, malaise, fever, and weight loss. The joints of the lower extremities, including the knee, ankle, and joints of the foot, are the most common sites of involvement, but symptoms can also occur in the wrists, fingers, elbows, shoulders, neck, and lower back. Other symptoms may include urethritis and prostatitis in males, and cervicitis or salpingitis in females. Ocular disease is common ranging from transient, asymptomatic conjunctivitis to aggressive anterior uveitis that occasionally results in blindness. Mucocutaneous lesions and nail changes are frequent. On less frequent or rare occasions manifestations of reactive arthritis include cardiac conduction
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defects, aortic insufficiency, central or peripheral nervous system lesions, and pleuropulmonary infiltrates. Web site: http://www.delphion.com/details?pn=US06465473__ ·
Method for treatment of rheumatoid arthritis Inventor(s): Jones; Frank R. (Edmonds, WA), Snyder, Jr.; Harry W. (Seattle, WA), Balint, Jr.; Joseph P. (Seattle, WA) Assignee(s): Cypress Bioscience, Inc. (San Diego, CA) Patent Number: 5,782,792 Date filed: December 12, 1994 Abstract: Rheumatoid arthritis is treated by the extra corporeal removal of IgG and IgGcontaining circulating immune complexes from the patient's blood. Removal is preferably accomplished by exposing the blood or blood plasma to a protein A immunoadsorbent which binds to IgG-containing immune complexes with high affinity. Excerpt(s): The present invention relates generally to the treatment of autoimmune disorders by extracorporeal plasma perfusion to remove immunoglobulin and immune complexes. More particularly, the present invention relates to the treatment of rheumatoid arthritis (RA) by continuous or discontinuous plasma perfusion through an immunoadsorbent capable of binding immunoglobulins and immune complexes. ... Autoimmune disorders are characterized by the destruction of a patient's body tissues by the patient's own immune system. Severe harm can arise from such a misdirected immune response, causing illness and even death to the patient. Rheumatoid arthritis is an autoimmune disorder of unknown etiology which is characterized by the presence of auto-antibodies. ... Rheumatoid arthritis (RA) is a chronic disease which can exhibit a variety of systemic manifestations. This disease has an unknown etiology and characteristically exhibits a persistent inflammatory synovitis which usually involves peripheral joints in a symmetric distribution. Despite the destructive potential of RA, its course can be quite variable. In about two-thirds of patients, a chronic polyarthritis begins insidiously with fatigue, anorexia, generalized weakness and vague musculoskeletal symptoms until the appearance of synovitis becomes apparent. In about 10% of patients, the onset can be more acute with rapid development of polyarthritis. In about one-third of patients, symptoms may initially be confined to one or a few joints. Overall, most patients will experience an intermediate course of the disease. As described above, the potential of the inflammation to cause cartilage destruction, bone erosions and, ultimately, joint deformities is the most important feature of this disease. Web site: http://www.delphion.com/details?pn=US05782792__
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Method of diagnosing caprine arthritis-encephalitis virus infection Inventor(s): Douvas; Angeline (345 S. Grand Oaks Ave., Pasadena, CA 91107), Ehresmann; Glenn (1941 Meadowbrook Rd., Altadena, CA 91101) Assignee(s): none reported Patent Number: 5,770,357 Date filed: March 15, 1996
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Abstract: The present invention provides a method of diagnosing caprine arthritisencephalitis virus infection (CAEV) in a human sample suspected of being infected with CAEV. Excerpt(s): This invention relates generally to the fields of immunology and medicine and more specifically to a method of diagnosing caprine arthritis-encephalitis virus infection in an individual. ... Caprine arthritis-encephalitis virus (CAEV) is a retrovirus that is closely related to the human immunodeficiency virus (HIV-1), which causes AIDS in humans. CAEV is known to infect goats, where it causes various pathologic conditions, including arthritis and encephalitis. CAEV infection occurs world wide and can result in costly losses to the goat farming industry. ... In many parts of the world, goat milk commonly is consumed and, particularly, in less developed countries, is an important source of nutrition. However, goat milk seldom is pasteurized in such countries prior to human consumption. Also, the consumption of raw goat milk is increasing in the United States due to its availability in health food markets. It now has been recognized that CAEV can infect humans, particularly those individuals who are occupationally exposed to goats or consume raw goat milk. While it has not yet been determined whether CAEV can cause a pathologic condition in humans, the close relationship of CAEV and HIV-1 suggests that it would be best to minimize the occurrence of CAEV infection in humans. Web site: http://www.delphion.com/details?pn=US05770357__ ·
Method of stimulating an immune response to caprine arthritis-encephalitis virus (CAEV) in humans through the administration of CAEV immunogens Inventor(s): Douvas; Angeline (Pasadena, CA), Ehresmann; Glenn (Altadena, CA) Assignee(s): University of Southern California (Los Angeles, CA) Patent Number: 6,033,672 Date filed: March 15, 1996 Abstract: The present invention provides a vaccine comprising a caprine arthritisencephalitis virus (CAEV) immunogen and a pharmaceutically acceptable carrier. The invention also provides a method of stimulating an immune response in an individual against human immunodeficiency virus-1 infection or against CAEV infection by administering a therapeutically effective amount of a CAEV immunogen to the individual. The invention further provides a method of stimulating an immune response in vitro by contacting a lymphocyte with a therapeutically effective amount of a CAEV immunogen. Excerpt(s): This invention relates generally to the fields of immunology and medicine and more specifically to methods for providing immunoprotection against HIV-1 infection. ... The incidence of acquired immunodeficiency syndrome (AIDS) has reached an epidemic level, particularly in third world countries in Africa, Asia and the Caribbean. Despite the expenditure of billions of dollars for research to discover drugs to treat or cure the disease, however, only modest progress has been made in identifying drugs that can delay the progress of the disease. ... The causative agent of AIDS is the human immunodeficiency virus (HIV-1). HIV-1 infects a particular cell type of the immune system, the T cell. Upon entering a T cell, the HIV-1 genomic DNA is incorporated into the T cell genome, where it directs synthesis of viral proteins. New copies of the HIV-1 virus then are released from the infected T cell and further infect additional T cells. Ultimately, the infected T cells die and the HIV-1 infected individual's
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immune system becomes depleted and cannot ward off subsequent infections. As a result, victims of AIDS typically die from infections that normally would cause, at worst, a mild illness in a healthy individual. Web site: http://www.delphion.com/details?pn=US06033672__ ·
Method of treating arthritis using gallium compounds Inventor(s): Matkovic; Velimir (Columbus, OH), Gerber; Nicholas (Worthington, OH) Assignee(s): The Ohio State University (Columbus, OH) Patent Number: 5,175,006 Date filed: September 21, 1990 Abstract: Gallium compounds are utilized to treat or inhibit arthritis. Excerpt(s): This invention relates generally to a method of treating or inhibiting arthritis. In particular, it relates to a method of treating arthritis by the administration of gallium compounds. ... Gallium has been known for many years to be useful in the treatment of calcium bone disorders. Gallium is a metal which belongs to the Group III A Elements of the Periodic Table. The metallic compounds used, have, of course, a low order of toxicity and are pharmaceutically acceptable. ... Prior U.S. Pat. Nos. 4,529,593 issued Jul. 16, 1985 to Warrell et al; 4,686,104 issued Aug. 11, 1987 to Bockman et al.; and 4,704,277 issued Nov. 3, 1987 to Bockman et al. describe methods of preventing excessive loss of calcium from human bone by the administration of pharmaceutically acceptable gallium-containing compounds. The '593 patent teaches the use of pharmaceutically acceptable gallium salts to reduce the excessive loss of bone calcium. The patent specifically teaches the use of gallium to prevent or treat disorders associated with extensive loss of calcium from bone in humans by administering to the individual a pharmaceutically acceptable gallium compound. Of special importance among the disorders which, may be thus treated are hypercalcemia, osteopenia, osteoporosis, bone destruction due to metastasis from malignant tumors and hyperparathyroidism. Gallium salts which are disclosed to be of use include nitrate, citrate, and halide, preferably the chloride, carbon, acetate, titrate, oxylate, oxide or hydrated oxide. Web site: http://www.delphion.com/details?pn=US05175006__
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Method of treating arthritis with etodolac Inventor(s): Martel; Rene (Candiac, CA) Assignee(s): American Home Products Corporation (New York, NY) Patent Number: 4,533,551 Date filed: February 17, 1984 Abstract: The effect of prolonged treatment with etodolac on the articular pathology associated with adjuvant arthritis in the rat has been compared to the effects produced by similar treatment with naproxen and ibuprofen. Drug effects were assessed by radiologic and histopathologic examinations. The effects on hindpaw edema, hindleg function, and body weight gain were also evaluated. Treatment was initiated on day 16 after adjuvant injection and continued for 28, 56 or 84 days. The degree of relapse which occurred during 28 days of non-treatment after dosage was stopped after 28 or 56 days of treatment was also assessed. Etodolac prevented the progression of the disease.
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Further, it appeared to diminish the severity of the articular lesions already present on day 16 before drug treatment began. All the parameters measured were improved and there was good agreement between the radiologic and histopathologic assessments of articular damage. The onset of drug activity was more rapid with etodolac than with the other drugs. By comparison naproxen and ibuprofen decreased edema, increased hindleg function and body weight gain and inhibited the progression of joint damage, but neither drug consistently decreased the magnitude of the articular damage present on day 16. With all three drugs there was less resurgence of disease symptoms when treatment was stopped after 56 days rather than 28 days of drug administration. Excerpt(s): Following treatment of adjuvant arthritic rats with the novel antiinflammatory drug etodolac (1,8-diethyl-1,3,4,9-tetrahydropyrano[3,4-b]indole-1acetic acid, Ultradol.RTM.) there was less bone and articular damage than before the start of treatment. Thus after 28 days dosage etodolac appeared to produce some reversal of the articular pathology already present 16 days after the initiation of the disease. In the same experiment naproxen stopped the further progression of the joint pathology but did not reduce it, while aspirin merely prevented the damage from progressing to maximum intensity. For the present study the period of treatment has been extended (from day 16 up to day 100 after adjuvant) to ascertain whether a longer treatment period could reduce further the joint pathology. In addition the possibility of recurrence of the disease was explored by stopping treatment after different time intervals. The effects produced by etodolac have been compared to the results achieved by naproxen and ibuprofen under the same experimental conditions. The effects of the different treatment on joint damage were assessed by radiologic and histopathologic methods at the end of each experimental period. The evolution of the disease were also monitored by measuring hindleg volume, hindleg function and body weight periodically. ... Male inbred Wistar Lewis rats (180-220 g, initial weight) obtained from Charles River Breeding Laboratories, Boston, Mass., were injected intradermally in the distal third of the tail with 0.1 ml of Freund's Complete Adjuvant (FCA) composed of a fine suspension of killed and dried Mycobacterium butyricum (Difco) in liquid paraffin at a concentration of 5 mg/ml. The day of FCA injection was designated as day 0 of the experiments. ... On day 16 after administration of FCA, the volume of both hindpaws was measured by mercury displacement according to the method of Hall, J. M. and Hallett, C.: A simple precise method for measuring rodent paw volume, J. Pharm. Pharmacol. 27:623 (1975). Web site: http://www.delphion.com/details?pn=US04533551__ ·
Method of treating arthritis, including rheumatoid arthritis, with 166 Holmium radionuclide Inventor(s): Lieberman; Ephraim (Suffern, NY), Bordoni; Maurice E. (Westtown, NY), Thornton; Alfred K. (New Hampton, NY) Assignee(s): Cadema Medical Products, Inc. (Middletown, NY) Patent Number: 5,026,538 Date filed: June 16, 1989 Abstract: .sup.166 Holmium in a carrier metallic hydroxide aggregate is disclosed for the treatment of arthritis and, in particular, rheumatoid arthritis. The compound disclosed preferably has a particle size of 1 to 40 microns, Beta energy emissions in the range of 1.76-1.84 MeV, low levels of gamma ray emissions and a radioactive half-life of 26.8 hours. The preferred metallic hydroxide is selected from the group consisting of Ferric
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Hydroxide, Aluminum Hydroxide, Bismuth Hydroxide, Chromium Hydroxide, Cupric Hydroxide, Manganese Hydroxide and Stannous Hydroxide. Methods are also disclosed for the preparation of the compound, as well as for the methods of its administration to a patient in need thereof. Excerpt(s): The present invention relates to radioactive compounds, methods for the preparation thereof and a method for the treatment of arthritis, including rheumatoid arthritis. ... Arthritic disorders are the second leading cause of losses in time and earnings in the United States. Approximately six million of all arthritis sufferers are afflicted rheumatoid arthritis. Of these, over fifty percent (50%) ultimately will have involvement of the knee joint, over eighty percent (80%) will involve the hand joint and somewhat smaller percentages will have involvement of other joints such as the ankle, elbow and shoulder. ... Rheumatoid arthritis is believed to be an autoimmune disease wherein parts of the body are attacked by antibodies manufactured in the body. These antibodies may be produced in response to viruses present in the body. While the mechanism for rheumatoid arthritis is not defined, it is a systemic disease. When the disease is active, the erythrocyte sedimentation rate (ESR) is elevated and the blood tests positive for rheumatoid factor. Web site: http://www.delphion.com/details?pn=US05026538__ ·
Method of treating pain cause by bursitis tendinitis arthritis Inventor(s): Pak; Kyoungsik (371 Sweetbriar Rd., King of Prussia, PA 19406) Assignee(s): none reported Patent Number: 5,952,367 Date filed: April 25, 1997 Abstract: Disclosed herein is a method of treating pain caused by bursitis, tendinitis, arthritis, and the like, comprises ingesting an effective amount of a non-steroidal antiinflammatory drug, and ingesting an effective amount of L-or DL-Methionine and a sugar which provides relief from stomach discomfort caused by the non-steroidal antiinflammatory drug and which in combination with the non-steroidal anti-inflammatory drug results in relieving the pain more effectively than the non-steroidal antiinflammatory drug alone. Excerpt(s): This invention relates to the field of treating pain caused by bursitis, tendinitis, arthritis, and the like, and is specifically concerned with a composition for treating such pain, a dosage unit for treating such pain, and a method of treating such pain. ... To ease the pain suffered by bursitis, tendinitis, arthritis, and the like, millions of people ingest daily high doses of non-steroidal anti-inflammatory drugs (hereinafter called "NSAIDs") such as ibuprofen. Unfortunately, NSAIDs irritate the stomach and the intestines in many people causing ulcers and bleeding. It has been reported in the Archives of Internal Medicine that ulcers and gastrointestinal bleeding caused by NSAIDs lead to as many as 20,000 deaths each year. ... It is an object of the invention to provide a composition, a dosage unit thereof, and a method for treating pain caused by bursitis, tendinitis, arthritis, and the like. Web site: http://www.delphion.com/details?pn=US05952367__
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Method of treating psoriasis, arthritis and reducing the toxicity of cancer chemotherapy Inventor(s): Batts; Donald Herman (Kalamazoo, MI), Ulrich; Roger G. (Gurnee, IL) Assignee(s): Pharmacia & Upjohn Company () Patent Number: 6,040,306 Date filed: November 10, 1998 Abstract: The present invention is a method of treating a person who has psoriasis or arthritis or reducing the toxicity of cancer chemotherapy which comprises administering to the patient an anti-psoriasis effective amount of an oxazolidinone, preferably (S)-N[[3-[3-fluoro-4-(4-morpholinyl)phenyl]-2-oxo-5-oxazolidinyl]methyl]a cetamide. Excerpt(s): The present invention is the use of known oxazolidinones to treat psoriasis, arthritis and to reduce the toxicity of cancer chemotherapy. ... U.S. Pat. Nos. 5,164,510, 5,231,188, 5,565,571, 5,652,238 and 5,688,792 all disclose various oxazolidinone antibiotics which are well known to those skilled in the art. ... Psoriasis is a well known condition, a proliferative disease of the skin of unknown etiology. It is not known, or believed, to have a microbiologic cause. Web site: http://www.delphion.com/details?pn=US06040306__
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Method of treating rheumatoid arthritis Inventor(s): Wechter; William J. (Kalamazoo, MI), Brooks; Carter D. (Texas Township, Kalamazoo County, MI) Assignee(s): The Upjohn Company (Kalamazoo, MI) Patent Number: 4,118,484 Date filed: March 29, 1976 Abstract: A process of treatment for the management of the condition known as rheumatoid arthritis. The process manages rheumatoid arthritis by controlling the inflammatory process in a rheumatoid joint by the intra-articular administration to said joint of an effective amount for controlling the inflammatory process of certain N.sup.4 acyl-ara-cytidines, 5'-O-acyl-ara-cytidines and pharmaceutically acceptable acid addition salts thereof, and pharmaceutically acceptable acid addition salts of 5'-O-acyl2,2'-anhydro-ara-cytidines. Excerpt(s): The invention concerns a method of treating rheumatoid arthritis in mammals including humans. More specifically, the invention concerns a method of controlling the inflammatory process in a rheumatoid joint of a mammal. ... Belgium Pat. No. 773,027 of Mar. 24, 1972, and U.S. Pat. No. 3,920,630 issued Nov. 18, 1975, disclose 2,2'-anhydro-ara-cytidine compounds as useful in the treatment of autoimmune diseases, such as multiple sclerosis and rheumatoid arthritis. ... Belgium Pat. No. 773,027 and U.S. Pat. No. 3,920,630 do not disclose which, if any, of the compounds are effective as an intra-articularly administered agent in controlling the inflammatory process in a rheumatoid joint. Web site: http://www.delphion.com/details?pn=US04118484__
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Method of treating rheumatoid arthritis Inventor(s): Wechter; William J. (Kalamazoo, MI), Brooks; Carter D. (Texas Township, Kalamazoo County, MI) Assignee(s): The Upjohn Company (Kalamazoo, MI) Patent Number: 4,172,889 Date filed: April 12, 1978 Abstract: A process of treatment for the management of the condition known as rheumatoid arthritis. The process manages rheumatoid arthritis by controlling the inflammatory process in a rheumatoid joint by the intra-articular administration to said joint of an effective amount for controlling the inflammatory process of certain N.sup.4 acyl-ara-cytidines, 5'-O-acyl-ara-cytidines and pharmaceutically acceptable acid addition salts thereof, and pharmaceutically acceptable acid addition salts of 5'-O-acyl2,2'-anhydro-ara-cytidines. Excerpt(s): The invention concerns a method of treating rheumatoid arthritis in mammals including humans. More specifically, the invention concerns a method of controlling the inflammatory process in a rheumatoid joint of a mammal. ... Belgium Pat. No. 773,027 of Mar. 24, 1972, and U.S. Pat. No. 3,920,630 issued Nov. 18, 1975, disclose 2,2'-anhydro-ara-cytidine compounds as useful in the treatment of autoimmune diseases, such as multiple sclerosis and rheumatoid arthritis. ... Belgium Pat. No. 773,027 and U.S. Pat. No. 3,920,630 do not disclose which, if any, of the compounds are effective as an intra-articularly administered agent in controlling the inflammatory process in a rheumatoid joint. Web site: http://www.delphion.com/details?pn=US04172889__
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Method of treating rheumatoid arthritis Inventor(s): Cincotta; Anthony H. (Andover, MA), Meier; Albert H. (Andover, MA) Assignee(s): Ergo Science Incorporated (Charlestown, MA) Patent Number: 5,905,083 Date filed: June 2, 1995 Abstract: Disclosed are methods for rectifying or ameliorating abnormal responses of mammalian immune systems, such as rheumatoid arthritis. Also disclosed are methods for modifying normal responses of the mammalian immune system. Further disclosed are methods for accomplishing the foregoing by administering to a mammal a prolactin reducer and/or enhancer at a pre-determined time or times during a 24-hour period that results in modification of the mammal's abnormal prolactin profile so that it approaches or conforms to the prolactin profile of a young, healthy mammal of the same species (or to a standard profile generated from such individuals). Additionally, methods of upregulating or augmenting an immune response in a mammal are disclosed. Excerpt(s): This invention relates to methods for rectifying or ameliorating abnormal responses of the mammalian immune system, and modifying normal responses of the mammalian immune system. More particularly, this invention relates to methods employing the alteration of prolactin rhythms as a method of adjusting mammalian immune response. ... The importance of neuroendocrine regulation of immunity has become increasingly evident during the past decade (Besedovsky, H. O. et al., J.
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Immunol. 135:750s-754s, 1985; Blalock, J. E., Physiol. Rev. 69: 1-54, 1989; Berozi, I., Dev. Comp. Immunol. 13:329-341, 1989). Much of this interest has focused on the anterior pituitary hormone prolactin, which has been reported to have potent, albeit inconsistent and often conflicting, effects on immune activity (Gala, R. R., Proc. Soc. Exp. Biol. Med. 198:5-13, 1991; Nicoletti, J. et al., Reprod. Immunol. 15:113-121, 1989; Vidaller, A., et al., Clin. Immunol. Immunopathol. 38:337-343, 1986; Gerli, R. et al., Clin. Immunol. 7:463470, 1987). ... The role of prolactin in immunity is exemplified by studies demonstrating exogenous prolactin-induced restoration of immune competence in hypophysectomized mammals (Gala, R. R., Proc. Soc. Exp. Biol. Med. 198:5-13, 1991; Bercal, I. et al., Acta Endocrinol. 98:506-513, 1981). In intact animals, prolactin administration has been associated with numerous immunological effects including stimulation of cellular or antibody responses, as well as stimulation of various immune system upregulating substances such as IL-2 (both IL-2 production and IL-2 receptor expression); enhancement of lymphocyte number, activity and mitogenic responses; and augmentation of macrophage cytotoxicity (Gala, R. R., Proc. Soc. Exp. Biol. Med. 198:513, 1991; Bernton, E. W. et al., Science 239:401-404, 1988; Rovensky, J. et al., Int. J. Immuno. Pharmac. 13:267, 1991). Web site: http://www.delphion.com/details?pn=US05905083__ ·
Method of treating rheumatoid arthritis and osteoarthrosis using tetrahydro WS9326A Inventor(s): Fujii; Takashi (Ikeda, JP), Tomoi; Masaaki (Higashiosaka, JP) Assignee(s): Fujisawa Pharmaceutical Co., Ltd. (Osaka, JP) Patent Number: 5,616,556 Date filed: November 18, 1993 Abstract: Rheumatoid arthritis and osteoarthrosis are treated by administering an effective amount of tetrahydro-WS9326A to a human being or animal suffering from rheumatoid arthritis or osteoarthrosis. Excerpt(s): This invention relates to an antiinflammatory or gastrointestinal motilitymodulating composition comprising a peptide derivative of the general formula (I) presented hereafter or a pharmaceutically acceptable salt thereof as an active ingredient, which composition finds application in the field of medicine. ... The peptide derivative of the invention, represented by the general formula (I) given below, is a per se known compound and is known to possess pharmacological activities such as substance P antagonism and neurokinin A antagonism (e.g. EP 0336230A2). However, there has not been the awareness that this peptide derivative has antiinflammatory or gastrointestinal motility-modulating activity. ... is a single bond or a double bond, or a pharmaceutically acceptable salt thereof as an active ingredient. Web site: http://www.delphion.com/details?pn=US05616556__
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Method of treating rheumatoid arthritis using tetracycline Inventor(s): Cabezas; Orestes (10201 Fontainebleau Blvd., Unit 205, Miami, FL 33172) Assignee(s): none reported Patent Number: 5,250,442 Date filed: April 8, 1993 Abstract: A method of treating rheumatoid arthritis which includes first, taking a blood test to determine a rate of erythrocyte sedimentation and a rheumatoid factor, and then fasting for a 12-hour period prior to orally administering a 500 milligram dosage of tetracycline achromycin, and observing any change in the symptoms of the rheumatoid arthritis including reduction of swelling and pain in the affected sites. This process is repeated over 24-hour cycles until the rheumatoid factor has decreased by at least 50% from the first determined level prior to treatment and erythrocyte sedimentation decreased, at which point the 24-hour cycles are continued, reducing the dosage of tetracycline achromycin to 250 milligrams until the symptoms of the rheumatoid arthritis condition disappear. Excerpt(s): The present invention relates to a method for treating rheumatoid arthritis to alleviate the symptoms thereof. ... Presently, an estimated 7,000,000 Americans suffer from rheumatoid arthritis. The symptoms of rheumatoid arthritis including pain and swelling of the smaller joints in the hands and feet. The affected joints become swollen, painful and warm to the touch during the initial attack and ensuing flare-ups. Often, the joints in the hands and the feet will ache or become stiff after extended periods of motionless such as after sleeping. ... Rheumatoid arthritis is believed to be an autoimmune disease in which the body's immune system literally attacks itself. It is believed that rheumatoid arthritis initially develops from a virus which upsets the immune system. In response, the body's disease fighting cells attack the joints causing inflammation. Web site: http://www.delphion.com/details?pn=US05250442__
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Method of treating rheumatoid arthritis with soluble collagen Inventor(s): Weiner; Howard L. (Brookline, MA), Trentham; David E. (North Quincy, MA), Hafler; David A. (West Newton, MA) Assignee(s): AutoImmune, Inc. (Lexington, MA) Patent Number: 5,720,955 Date filed: June 7, 1995 Abstract: The present invention is directed to a method and pharmaceutical formulations for the treatment of autoimmune arthritis and animal models therefore in mammals, including humans, by the oral, enteral or by-inhalation administration of whole collagen protein or biologically active peptide fragments of collagen. Excerpt(s): The foregoing applications are incorporated by reference herein in their entireties. ... The present invention pertains to treatment of autoimmune arthritis in humans. Specifically, the invention is directed to oral, enteral or by-inhalation administration of collagen or fragments or analogs to humans to induce specific suppression of the autoimmune response involved in rheumatoid and more generally in autoimmune arthritis. The invention is also directed to pharmaceutical formulations useful in the treatment of arthritis in humans comprising whole collagen, arthritis-
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suppressive peptide fragments thereof, and combinations of two or more of the foregoing. ... Collagen is the most common protein in the structural support of the human or mammalian body. Collagen's basic elemental unit is the tropocollagen protein. Tropocollagen is composed of three polypeptide chains of the same size. These chains are wound about each other forming a superhelical cable or a triple-stranded helical rod. Each of the three chains in tropocollagen consists of about a thousand amino acid residues. Web site: http://www.delphion.com/details?pn=US05720955__ ·
Method of treating rheumatoid arthritis with type collagen peptide fragments containing repeating sequences Inventor(s): Weiner; Howard L. (Brookline, MA), Trentham; David E. (North Quincy, MA), Hafler; David A. (West Newton, MA) Assignee(s): AutoImmune, Inc. (Lexington, MA) Patent Number: 5,783,188 Date filed: June 7, 1995 Abstract: The present invention is directed to a method and pharmaceutical formulations for the treatment of autoimmune arthritis and animal models therefore in mammals, including humans, by the oral, enteral or by-inhalation administration of whole collagen protein or biologically active peptide fragments of collagen. Excerpt(s): The present invention pertains to treatment of autoimmune arthritis in humans. Specifically, the invention is directed to oral, enteral or by-inhalation administration of collagen or fragments or analogs to humans to induce specific suppression of the autoimmune response involved in rheumatoid and more generally in autoimmune arthritis. The invention is also directed to pharmaceutical formulations useful in the treatment of arthritis in humans comprising whole collagen, arthritissuppressive peptide fragments thereof, and combinations of two or more of the foregoing. ... Collagen is the most common protein in the structural support of the human or mammalian body. Collagen's basic elemental unit is the tropocollagen protein. Tropocollagen is composed of three polypeptide chains of the same size. These chains are wound about each other forming a superhelical cable or a triple-stranded helical rod. Each of the three chains in tropocollagen consists of about a thousand amino acid residues. ... Rheumatoid arthritis is a cell-mediated autoimmune disease, i.e. a condition where the immune system mistakenly perceives the body's own tissue as foreign and mounts an abnormal immune response against it. Rheumatoid arthritis is characterized by persistent inflammatory synovitis that causes destruction of cartilage and bone erosion, leading to structural deformities in the peripheral joints. Joints containing articular cartilage of which Type II collagen is a major component are particularly affected. Web site: http://www.delphion.com/details?pn=US05783188__
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Method of treating rheumatoid arthritis with type II collagen Inventor(s): Weiner; Howard L. (Brookline, MA), Trentham; David E. (North Quincy, MA) Assignee(s): AutoImmune, Inc. (Lexington, MA) Patent Number: 5,843,445 Date filed: September 21, 1993 Abstract: The present invention is directed to a method and pharmaceutical formulations for the treatment of autoimmune arthritis and animal models therefore in mammals, including humans, by the oral, enteral or by-inhalation administration of whole collagen protein or biologically active peptide fragments of collagen. Excerpt(s): The present invention pertains to treatment of autoimmune arthritis in humans. Specifically, the invention is directed to oral, enteral or by-inhalation administration of collagen or fragments or analogs to humans to induce specific suppression of the autoimmune response involved in rheumatoid and more generally in autoimmune arthritis. The invention is also directed to pharmaceutical formulations useful in the treatment of arthritis in humans comprising whole collagen, arthritissuppressive peptide fragments thereof, and combinations of two or more of the foregoing. ... Collagen is the most common protein in the structural support of the human or mammalian body. Collagen's basic elemental unit is the tropocollagen protein. Tropocollagen is composed of three polypeptide chains of the same size. These chains are wound about each other forming a superhelical cable or a triple-stranded helical rod. Each of the three chains in tropocollagen consists of about a thousand amino acid residues. ... Rheumatoid arthritis is a cell-mediated autoimmune disease, i.e. a condition where the immune system mistakenly perceives the body's own tissue as foreign and mounts an abnormal immune response against it. Rheumatoid arthritis is characterized by persistent inflammatory synovitis that causes destruction of cartilage and bone erosion, leading to structural deformities in the peripheral joints. Joints containing articular cartilage of which Type II collagen is a major component are particularly affected. Web site: http://www.delphion.com/details?pn=US05843445__
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Method of treatment of rheumatoid arthritis Inventor(s): Scheinberg; Israel H. (5447 Palisades Ave., Bronx, NY 10471) Assignee(s): none reported Patent Number: 4,487,780 Date filed: February 5, 1982 Abstract: Rheumatoid arthritis is treated with substituted cysteine compounds having a lower toxicity-to-effectiveness ratio than penicillamine. Such compounds are specific alpha-substituted cysteines, beta-monosubstituted cysteines, beta-di-substituted cysteines other than penicillamine, N-acetyl penicillamine and the N-acetyl derivatives of the alpha and beta-substituted compounds mentioned above.Any of the compounds may be used synergistically in combination with suitable copper compounds or with suitable gold compounds in the treatment of arthritis.The same compounds are effective in the treatment of cystinuria and heavy metal poisoning. The same compounds as well
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as penicillamine are effective in combination with copper in the treatment of heavy metal poisoning. Excerpt(s): Rheumatoid arthritis, commonly referred to as RA, is the second most crippling disease in man, ranking immediately behind cardiovascular defects. Until recently no effective treatment for RA has been known. A number of drugs which are moderately effective in the treatment of this disease have been found, examples being D-penicillamine which is .beta.,.beta.-dimethylcysteine and certain compounds of gold, such as gold sodium thiomalate, aurothioglucose and sources of auric or aurous ion. ... Of these compounds, the most promising is the recently discovered penicillamine, a natural metabolite of penicillin. Unfortunately, not all patients respond to this medication; also, it carries with it considerable toxicity so that it can, in fact, be lethal. Another difficulty is that penicillamine is slow-acting so that generally it requires 8 to 12 weeks before it can be determined whether the patient is responding and whether the dosage needs adjusting. D-penicillamine usually produces a decrease in the titer of rheumatoid factor, an index of its specific therapeutic efficacy for this human disease. There are no genuine animal models of rheumatoid arthritis. ... At the present time, most rheumatologists treat moderately severe RA that has not responded to salicylates with either a gold compound or D-penicillamine. Penicillamine is also used initially in some patients with severe RA, and those in whom rheumatoid lung disease, vasculitis, amyloidosis, Felty's syndrome or rheumatoid nodulosis complicate the clinical picture. Web site: http://www.delphion.com/details?pn=US04487780__ ·
Method using sturgeon notochord for alleviating the symptoms of arthritis Inventor(s): Aoyagi; Seiji (Westerville, OH), DeMichele; Stephen J. (Dublin, OH), Johns; Paul W. (Columbus, OH), Mazer; Terrence B. (Reynoldsburg, OH) Assignee(s): Abbott Laboratories (Abbott Park, IL) Patent Number: 5,849,336 Date filed: July 2, 1997 Abstract: This invention provides a composition comprising notochord and extracts thereof in therapeutic amounts. The invention more specifically relates to a method of treating arthritis in mammals, more particularly rheumatoid arthritis in humans through the enteral administration of notochord, notochord extracts or mixtures thereof. In a preferred embodiment, collagen obtained from sturgeon is enterally administered to a human at from 1.0 .mu.g to 1.05 gms per day. Excerpt(s): The present invention pertains to a method for treating the symptoms of arthritis in mammals and, more particularly, relates to the enteral administration of compositions comprising notochord and/or notochord extracts. The invention preferably uses sturgeon notochord, collagen derived from sturgeon notochord, or mixtures thereof to suppress the clinical manifestations of arthritis. The invention also relates to enteral compositions that contain notochord and its structural components to suppress and/or treat arthritis in mammals. ... Arthritis, and particularly rheumatoid arthritis (RA), is a painful and often crippling disease that initially results in swollen and inflamed joints, but often progresses to deform or completely destroy joints. This is a result of the body mistakenly attacking its own cartilage. Cartilage is a specialized kind of connective tissue which is found in human adults in three forms: hyaline or glossy cartilage; elastic cartilage; and fibrocartilage. Hyaline cartilage is the type found in the ventral ends of ribs, in joints, and in the walls of the larger respiratory passages. It is the
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hyaline cartilage that provides a low friction surface to prevent bone from rubbing on bone during motion. As arthritis progresses, cartilage is damaged and bone may also start to erode. This results in severe pain and ultimate destruction of the joint itself. ... Arthritis is a group of diseases affecting joints and the component tissues. Several types of arthritis are recognized, and these can be divided into several groups by their clinical course or pathological manifestations. The most common form of arthritis is Osteoarthritis (OA). Osteoarthritis is mainly caused by mechanical damage to the joints, either by repetitive use of particular joints as seen in athletes and physical laborers, or by overloading structural joints as seen in the knee joints of obese individuals. Web site: http://www.delphion.com/details?pn=US05849336__ ·
Methods and compositions for treating inflammation or arthritis Inventor(s): Maurer; Gerald L. (Fairfield, OH) Assignee(s): National Research Laboratories (Cincinnati, OH) Patent Number: 4,680,309 Date filed: February 3, 1986 Abstract: A method of treating inflammation or arthritis with metal complexes that can traverse skin and animal cell membranes intact and effectively deliver and release metal ions in a controlled manner upon demand at the targeted inflammatory or arthritic areas containing endogenous reacting moieties which demand the metal ions. The metal complexes have an aqueous proton induced dissociation property represented by a sigmoidally-shaped curve on a cartesian coordinate plot of the negative log of the metal ion concentration versus the negative log of hydrogen ion concentration. This dissociation property enables the metal complexes to release metal ions in a controlled manner upon demand at the targeted inflammatory or arthritic areas containing endogenous reacting moieties which demand the metal ions. The metal complexes can be effectively administered either topically or subcutaneously. Upon topical application, the metal complexes are dispersed in a vehicle to provide a buffered composition to neutralize the initial acidic layer of the skin. These unique and advantageous properties permit the metal complexes to be incorporated into vehicles with an adjusted pH minimizing premature release of the metal ions prior to reaching the targeted inflammatory or arthritic areas. Further, the metal complexes can be dispersed in a greaseless cold cream vehicle formulated to avoid or minimize undesirable chemical incompatibilities. An example of a topical composition employed is disodiummonocopper(II) citrate in an amount of about 10% w/w in a water-dispersible cream base vehicle comprising an oil-in-water emulsion having a pH of about 7.0. Excerpt(s): Inflammation is a local and protective response to tissure injury and destruction of cells. The precise elements constituting the inflammatory response vary according to the site of injury, the state of the body, and the injurious agent, such as bacteria or trauma. Should the inflammatory response become impaired or compromised, however, the corresponding tissue will undergo a degenerative process stimulating further injury and cell destruction. Obviously, then, the inflammatory response embodies a multifaceted process that is required to promote and rehabilitate normal tissue function. Therefore, since the inflammatory response is generally similar with various stimuli, it can be viewed and treated as a relatively nonspecific response. ... Inflammation may be manifested in numerous ways and one of the more well-known forms is arthritis. By definition, arthritis constitutes inflammation of a joint. Unfortunately, approximately 14% of the present United States population suffers from
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some type of arthritic manifestations. Further, if arthritis is ineffectively treated, it can develop into an extremely painful, degenerative and crippling disease. The present antiarthritic therapy constitutes painful, toxic, inconvenient and ineffective protocols designed primarily to alleviate the symptoms rather than the causes. Thus, in light of current knowledge and the notorious effects of arthritis, there obviously is a critical need to develop an effective, safe, painless and convenient form of treatment that can be employed to alleviate successfully the causes of arthritic inflammation. ... Today, methods of treating inflammation or arthritis with metals such as copper are well established. For instance, it has been known since ancient Egypt that copper has been indicated for therapeutically treating granulomatous inflammation. In a another instance, it has been established that the dissolution of copper from copper jewelry, for example, bracelets, worn in contact with skin appears to have therapeutic antiinflammatory effects. Whitehouse, M. W. and Walter, W. R.: The Copper Bracelet for Arthritis. Med. J. Australia. (1):938 June 18, 1977. In still another instance, subdermal copper implants in rats have been demonstrated to exhibit anti-inflammatory activity. In a further instance, a neutral copper (II) bis(glycine) complex perfused through cat skin demonstrating that skin is permeable to soluble copper. In still a further instance several oral and parenteral copper complexes have been somewhat successfully used in the treatment of inflammation or arthritis. Such examples include penicillamine, Cu(II)salicylate, Cu(II).sub.2 (aspirinate).sub.4 and Cu(II).sub.2 (acetate).sub.4. Sorenson, J. R. J.: Development of Copper Complexes for Potential Therapeutic Use. Agents and Actions. Vol. 8 Supplement, pp. 305 at 307-310, 1981. Finally, dermally applied copper complexes have been confirmed as pharmacoactive anti-inflammatory agents. Walker et al: Dermal Copper Drugs: A Copper Bracelet and Cu(II) Salicylate Complexes. Agents and Actions. Vol. 8 Supplement pp. 359-367, 1981. Unfortunately, the current copper-containing dosage forms have been somewhat ineffective as a means to maximize delivery of copper to the strategic inflammatory or arthritic sites. Web site: http://www.delphion.com/details?pn=US04680309__ ·
Methods and compositions for treating rheumatoid arthritis Inventor(s): Barlozzari; Teresa (Wellesley, MA), Banerjee; Subhashis (Shrewsbury, MA), Haupt; Andreas (Northborough, MA) Assignee(s): BASF Aktiengesellschaft (Ludwigshafen, DE) Patent Number: 6,015,790 Date filed: October 6, 1997 Abstract: The present invention provides compositions and methods for the treatment of rheumatoid arthritis in a subject wherein one or more compounds of Formula I as defined herein alone or in combination with one or more other antiarthritic drugs provide suppression of rheumatoid arthritis. Excerpt(s): Rheumatoid arthritis is generally considered an autoimmune disease that is thought to be associated with activity of autoreactive T cells (See, e.g., Harris, E. D., Jr., The New England Journal of Medicine, 322: 1277-1289 (1990)). Despite advances in treatment, rheumatoid arthritis remains a serious health problem. Although rarely fatal, arthritis is a major cause of morbidity, loss of time from work, lost productivity and decrease in quality of life. Rheumatoid arthritis causes severe pain and loss of joint mobility and can make accomplishing even simple tasks difficult. ... Current treatment methods and regimes for rheumatoid arthritis include administration of non-steroidal anti-inflammatory drugs such as acetylsalicylic acid (aspirin), ibuprofen, naproxen and
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other such agents, gold compounds, penicillamine, methotrexate, cytotoxic agents (e.g., azothrioprine), 4-aminoquinoline agents, and immunomodulators. However, improved treatments of rheumatoid arthritis, which can suppress or ameliorate symptoms such as inflammation, swelling, abnormal neovascularization, bone erosion, or cartilage erosion are needed. Preferably, such an improved method of treatment should be able to be combined with other treatment methods, should work rapidly to cause regression or stabilization of symptoms, and should be well tolerated. Preferably, such a treatment regime should also be useful in prophylaxis in susceptible individuals. ... -CH(CH.sub.3) CH(CH.sub.3).sub.2, also referred to as 1,2-dimethylpropyl. Web site: http://www.delphion.com/details?pn=US06015790__ ·
Methods and materials for evaluating rheumatoid arthritis Inventor(s): Goronzy; Jorg J. (Rochester, MN), Weyand; Cornelia M. (Rochester, MN) Assignee(s): Mayo Foundation for Medical Education and Research (Rochester, MN) Patent Number: 6,555,320 Date filed: September 1, 1999 Abstract: The invention provides methods and materials for diagnosing a rheumatoid arthritis condition in a patient. Specifically, the invention provides methods and materials for classifying a rheumatoid arthritis condition as diffuse, follicular, or granulomatous. In addition, the invention provides methods and materials for determining if an individual suffering from a rheumatoid arthritis condition will develop severe disease. Excerpt(s): The invention relates to methods and materials for evaluating rheumatoid arthritis as well as for determining an individual's predisposition to have severe rheumatoid arthritis disease. ... Rheumatoid arthritis (RA) affects individuals in the prime of their life and is feared because of its potential to cause chronic pain and irreversible damage of tendons, ligaments, joints, and bones. The symmetrical involvement of small peripheral joints has an enormous impact on hand and foot functions and poses therapeutic challenges that cannot be easily overcome by joint replacement. Also, systemic manifestations of RA are not rare and can range from relatively minor problems, such as rheumatoid nodules, to life-threatening organ disease. ... In addition, RA is a systemic inflammatory disease that primarily manifests itself as synovial inflammation of diarthrodial joints. The typical histopathological changes include dense infiltration of the synovial membrane by mononuclear cells, neoangiogenesis, and hypertrophy and hyperplasia of the synovial lining (Harris E D (ed); Rheumatoid Arthritis, Philadelphia, WB Saunders Co., pp.3-212 (1997); and Hale L P, Haynes B F: Pathology of rheumatoid arthritis and associated disorders. Arthritis and Allied Conditions. A textbook of Rheumatology. Edited by Koopman W J. Baltimore, Williams & Wilkins, pp.993-1016 (1997)). The etiopathogenesis of the syndrome is not understood. Several lines of evidence support a central role of T lymphocytes in the disease-specific pathogenic events (Todd, et al. Science, 240:1003-1009 (1988); Panayi, et al., Arthritis Rheum, 35:729-735 (1992); and Goronzy J J, Weyand C M: Rheum Dis Clin North Am, 21:655-674 (1995)). An alternative hypothesis, namely, that macrophages are the pivotal cell type in rheumatoid synovitis, has also been proposed (Firestein G S, Zvaifler N J: Arthritis Rheum 33:768-773 (1990); and Burmester, et al., Arthritis Rheum, 40:5-18 (1997)). Whether only T cells or only macrophages or both are the causative elements in RA remains a matter of controversy (Feldmann, et al., Cell, 85:307-310 (1996); and Fox, Arthritis Rheum 40:598-609 (1997)).
Patents 369
Web site: http://www.delphion.com/details?pn=US06555320__ ·
Methods and materials for treatment of rheumatoid arthritis Inventor(s): McMichael; John (P.O. Box 81, Cambridge Springs, PA 16403) Assignee(s): none reported Patent Number: 4,704,273 Date filed: February 27, 1986 Abstract: Disclosed are methods and compositions useful for alleviating the symptoms of rheumatoid arthritis. In preferred embodiments, the compositions are administered in essentially minute "neutralizing" doses. The compositions comprise mixtures of histamine, immunoglobulin G provocative of RF formation or an immunologically active fraction thereof, collagen and either attenuated measles virus or immunologically active fraction thereof. Illustratively significant relief of symptoms of arthritis disease symptoms is achieved through parenteral (e.g., subcutaneous or sublingual) administration of such compositions. Excerpt(s): This application is a continuation-in-part of my copending U.S. application Ser. No. 708,274 filed March 5, 1985 which is a division of my U.S. application Ser. No. 378,752 filed May 17, 1982, now U.S. Pat. No. 4,521,405. ... The present invention relates generally to the treatment of disease states involving immunological factors and more particularly to methods and materials for alleviation of symptoms of nonanaphylactic disorders wherein disease pathology results in whole or part from the victim's own humoral and/or cell-medicated immune response to one or more immunogenic substances. ... Disease states involving immunological factors may be seen to broadly comprise (1) immunodeficiency diseases, and (2) disorders wherein tissue injury occurs as a result of a humoral or cell-mediated response to immunogens (e.g., antigens) of endogenous or exogenous origin. This latter group of immunological disorders is frequently referred to as involving immune "hypersensitivity", with the numerous disease states comprehended by the term classified according to four hypersensitivity "reaction" types. Web site: http://www.delphion.com/details?pn=US04704273__
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Methods for the treatment of arthritis using phosphonates and NSAIDS Inventor(s): Hovancik; Kristine (Binghamton, NY), Francis; Marion David (Cincinnati, OH), Underwood; Richard Allen (Hamilton, OH) Assignee(s): The Proctor & Gamble Company (Cincinnati, OH) Patent Number: 5,869,471 Date filed: June 7, 1995 Abstract: The present invention provides methods of treating a human or other animal subject afflicted with arthritis, including rheumatoid, arthritis and osteoarthritis, comprising a sixty (60)-day treatment period, comprised of an optional NSAID administration regimen and a phosphonate administration regimen, wherein(a) said optional NSAID administration regimen which comprises the administration to said subject of NSAIDs at a level of from 20% to 80%, preferably 20% to 70%, most preferably 20% to 50% of the conventionally prescribed daily dose on each day that said NSAID is
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administered; provided that said NSAID is administered in sufficient quantities and on a sufficient number of days to alleviate symptoms of inflammation, and wherein(b) said phosphonate administration regimen comprises the administration to said subject of a phosphonate at a dose equivalent to a systemic level of from about 0.0005 mgP/kg to about 1.0 mgP/kg per day that said phosphonate is administered; provided that said phosphonate is administered at least 1 day of every said sixty (60)-day treatment period. Excerpt(s): This invention relates to methods for the treatment of arthritis, including both rheumatoid arthritis and osteoarthritis. In particular, this invention relates to such methods of treatment by the administration of bone-active phosphonate compounds and non-steroidal anti-inflammatory drugs (NSAIDs). The bone-active phosphonates and NSAIDS act in synergy with one another and their administration results in a reduction of inflammation, but also inhibits the destruction of bone and hard tissue in the intraarticular area of the joint, which permits repair of the sub-chondral bone and hard tissue. ... Bone loss, or alteration in bone turnover, can result from, or be associated with, many types of arthritis, including rheumatoid arthritis and osteoarthritis. Rheumatoid arthritis is a chronic, systemic and articular inflammatory disorder characterized by weakening of the joint capsules and ligaments, followed by destruction of cartilage, ligaments, tendon and bone, and a decrease in viscosity and other alterations in the synovial membrane and fluid. Rheumatoid arthritis symptoms include systemic weakness, fatigue, localized pain, and stiffness, weakness, swelling, and deformation of the joints of the body. Rheumatoid arthritis is most common in women in the fourth to sixth decade of life. ... The pathogenesis of rheumatoid arthritis, leading to the destruction of the joints, is characterized by two phases: 1) an exudative phase involving the microcirculation of the synovial cells that allow an influx of plasma proteins and cellular elements into the joint and 2) a chronic inflammatory phase occurring in the sub-synovium and sub-chondral bone, characterized by pannus (granulation tissue) formation in the joint space, bone erosion, and cartilage destruction. The pannus may form adhesions and scar tissue which causes the joint deformities characteristic of rheumatoid arthritis. Web site: http://www.delphion.com/details?pn=US05869471__ ·
Methods for treating arthritis by administering an apoptosis regulator Inventor(s): Firestein; Gary S. (Del Mar, CA), Zvaifler; Nathan J. (La Jolla, CA), Green; Douglas R. (San Diego, CA) Assignee(s): The Regents of the University of California (Oakland, CA) Patent Number: 6,004,942 Date filed: August 30, 1996 Abstract: The present invention provides a novel method for the treatment of cellular accumulation in chronic inflammatory diseases such as rheumatoid arthritis. The method includes gene delivery and gene expression that is capable of enhancing apoptosis of accumulating cells and those cells which recruit accumulating cells. Also provided are diagnostic methods for detecting cellular accumulation diseases. Excerpt(s): The present invention relates generally to programmed cell death (apoptosis) and more specifically to the diagnosis and treatment of diseases of excess cellular accumulation due to defective apoptosis and more specifically to diagnosis and treatment of rheumatoid arthritis. ... Rheumatoid arthritis is a chronic inflammatory arthritis that afflicts approximately 1% of adults (Mitchell, D. 1985. Rheumatoid
Patents 371
Arthritis. P D Utsinger, N J Zvaifler, G E Ehrlich, eds. J.B. Lippincott Co., Philadelphia, pp. 133-150). The distribution of affected joints is symmetric and typically involves the small articulations of the hands and feet, although the larger appendicular joints like the shoulders and hips are often affected in established disease. Joint deformities, including ulnar deviation of the metacarpal phalangeal joints of the hand or destruction of the weight bearing joints, can occur late in the disease. ... The symptoms of the disease result from a massive increase in the number of cells lining the synovium of the joint. The various cell types which are present include type A synoviocytes, which have the characteristics of monocytes or terminally differentiated macrophages, and type B synoviocytes which are fibroblast-like. As these cells increase in number, the continuous inflammation causes initial symptoms. Eventually, local release of enzymes by the synovial internal lining degrade the extracellular matrix and cause deformity. Web site: http://www.delphion.com/details?pn=US06004942__ ·
Methods for treating arthritis using collagen type II, glucosamine chondroitin sulfate, and compositions Inventor(s): Sorgente; Nino (San Clemente, CA), Nakamura; Robert M. (La Jolla, CA) Assignee(s): Immudyne, Inc. (Houston, TX) Patent Number: 6,162,787 Date filed: April 2, 1999 Abstract: The invention describes compositions and methods for treatment of rheumatoid arthritis and osteoarthritis. The compositions comprise insoluble, native collagen Type II in a particular form in combinations with other active agents, including glucosamine, chondroitin, ascorbate, boron and magnesium. Also described are methods for producing particulated insoluble native collagen Type II. Excerpt(s): The present invention provides a method for the isolation and purification of insoluble, native collagen and chondroitin sulfate from cartilages, a therapeutic method and nutriceutical formulation containing therapeutic amounts of collagen Type II, glucosamine and/or chondroitin sulfate and/or magnesium ascorbic phosphate, and/or boron for the treatment of rheumatoid arthritis and osteoarthritis in humans and animals. ... The cartilage of the joints is called hyaline cartilage (from the Greek "hyalos" which means glass); hyaline cartilage is found not only on all surface of bones that move (articular cartilage) but also in the nose, larynx, ribs and trachea. This cartilage consists of 70% water, about 10% collagen Type II, and the rest is various protein and specialized complex sugars, called proteoglycans. The collagen and the proteoglycans form a meshwork that confers upon this cartilage stiffness, viscoelasticity, and durability. The articular cartilage provides load bearing, resilience, a low friction surface and distributes the load over the entire synovial joint. Even though the articular cartilage is very thin (about one eighth of an inch thick) it performs its function for the life of the individual (80-90 years or more) without any significant deterioration, unless it becomes injured or diseased. ... There are two major diseases that affect cartilage, namely osteoarthritis and rheumatoid arthritis; both osteoarthritis and rheumatoid arthritis result in degradation and degeneration of the articular cartilage. Osteoarthritis is a disease of cartilage only and does not have an immunological component. The major symptoms of osteoarthritis are pain, stiffness, crackling, and enlargement and deformities of the affected joints; at the early stage of osteoarthritis there is little inflammation and swelling of the joints, however in advanced stages swelling and inflammation is usually present. Rheumatoid arthritis is an autoimmune systemic disease accompanied by severe inflammation of the
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joints. In most patients rheumatoid arthritis begins with a general feeling of malaise, fatigue, often accompanied by diffuse musculoskeletal pain. Eventually the disease progresses resulting in pain on motion, tenderness, swelling and deformation of multiple joints; because rheumatoid arthritis is a systemic disease, it may be accompanied by extra-articular complications, such as anemia, vasculitis, scleritis, pleurisy, pericarditis, and peripheral neuritis. Web site: http://www.delphion.com/details?pn=US06162787__ ·
Methods for treating inflammation, inflammatory diseases, arthritis and stroke using pADPRT inhibitors Inventor(s): Kun; Ernestt (Mill Valley, CA) Assignee(s): Octamer, Inc. (Mill Valley, CA) Patent Number: 6,303,629 Date filed: April 6, 1998 Abstract: The present invention is directed to a method for treating inflammation or inflammatory disease, bacterial infection, arthritis and stroke in an animal or mammal, which comprises the steps of administering an effective amount of a pADPRT inhibitory compound to said animal or mammal. Excerpt(s): The present invention relates to methods for treating inflammation and inflammatory diseases, arthritis, and stroke in animals. The invention also relates to methods for treating animals having toxicity resulting from infestation by lipopolysaccharides. These methods involve the use of therapeutically effective amounts of pADPRT inhibitory compounds. ... The use of pADPRT inhibitory compounds have been reported for treating cancer and viral infections. Examples of these methods are described in U.S. Pat. Nos. 5,464,871, 5,473,074; 5,482,975, 5,484,951; 5,516,941, and 5,583,155, the disclosures of which are incorporated herein by reference. ... In the published literature, 5-iodo-6-amino-1,2-benzopyrone (INH.sub.2 BP), a novel inhibitor of the nuclear enzyme poly-ADP ribose polymerase (PADPRT) has recently been shown to inhibit in vivo tumorigenicity in a Ha-ras transfected endothelial cell line (Bauer et al., Int. J. Oncol. 8:239-252 (1995) and Bauer et al., Biochimie 77:347-377 (1995)). Treatment with INH.sub.2 BP has also resulted in changes in topoisomerase I and II and MAP kinase activity Based on the effects observed, a hypothesis regarding the potential use of INH.sub.2 BP in the therapy of cancer has been put forward. Web site: http://www.delphion.com/details?pn=US06303629__
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Methods of treating rheumatoid arthritis using chimeric anti-TNF antibodies Inventor(s): Le; Junming (Jackson Heights, NY), Vilcek; Jan (New York, NY), Daddona; Peter (Menlo Park, CA), Ghrayeb; John (Thorndale, PA), Knight; David (Berwyn, PA), Siegel; Scott (Westborough, MA) Assignee(s): New York University Medical Center (New York, NY), Centocor, Inc. (Malvern, PA) Patent Number: 5,698,195 Date filed: October 18, 1994
Patents 373
Abstract: Anti-TNF antibodies, fragments and regions thereof which are specific for human tumor necrosis factor-.alpha. (TNF.alpha.) and are useful in vivo for diagnosis and therapy of a number of TNF.alpha.-mediated pathologies and conditions, including rheumatoid arthritis as well as polynucleotides coding for murine and chimeric antibodies, methods of producing the antibody, methods of use of the anti-TNF antibody, or fragment, region or derivative thereof, in immunoassays and immunotherapeutic approaches are provided. Excerpt(s): The present invention in the field of immunology and medicine relates to anti-tumor necrosis factor (TNF) antibodies, anti-TNF peptides and nucleic acids encoding therefor, and to pharmaceutical and diagnostic compositions and production, diagnostic and therapeutic methods thereof, and to methods for treating human TNFmediated pathologies. ... Cells other than monocytes or macrophages also make TNF.alpha.. For example, human non-monocytic tumor cell lines produce TNF (Rubin, et al., J. Exp. Med. 164:1350 (1986); Spriggs, et al., Proc. Natl. Acad. Sci. USA 84:6563 (1987)). CD4.sup.+ and CD8.sup.+ peripheral blood T lymphocytes and some cultured T and B cell lines (Cuturi, et al., J. Exp. Med. 165:1581 (1987); Sung, et al., J. Exp. Med. 168:1539 (1988)) also produce TNF.alpha.. ... Recent evidence associates TNF with infections (Cerami, et al., Immunol. Today 9:28 (1988)), immune disorders, neoplastic pathologies (Oliff, et al., Cell 50:555 (1987)), autoimmune pathologies and graft-versus host pathologies (Piguet, et al., J. Exp. Med. 166:1280 (1987)). The association of TNF with cancer and infectious pathologies is often related to the host's catabolic state. Cancer patients suffer from weight loss, usually associated with anorexia. Web site: http://www.delphion.com/details?pn=US05698195__ ·
Mouse model for rheumatoid arthritis Inventor(s): Faustman; Denise L. (Weston, MA), Hayashi; Takuma (Malden, MA) Assignee(s): The General Hospital Corporation (Boston, MA) Patent Number: 6,414,218 Date filed: January 18, 2000 Abstract: Nonobese Diabetic Mice (NOD mice) that do not develop diabetes may be bred to produce F.sub.1 offspring that develop a condition that closely mimics rheumatoid arthritis (RA) in humans. The RA-like disease in the F.sub.1 mice, designated NOD-RA mice, is similar to human RA in clinical, radiological, histological and serological characteristics. The parents (F.sub.0) and their progeny (F.sub.1) are not diabetic and never develop hyperglycemia, and the parental mice (F.sub.0) do not themselves exhibit any symptoms of the RA-like condition that afflicts some of their progeny. The incidence, penetrance, gender domination, progression, and lifelong exacerbation of symptoms after pregnancy shown in the RA-like condition afflicting NOD-RA mice are all comparable to phenomena observed in the human disease. The NOD-RA mice provide a new spontaneous model of human RA that will be useful for studying rheumatoid arthritis and testing new drugs and reagents for treating or diagnosing the disease. Excerpt(s): The present invention pertains to the field of medical research, particularly to the development of mammalian models of human rheumatoid arthritis. ... Rheumatoid arthritis (RA) is a common autoimmune disease characterized by joint swelling, deformation and, ultimately, destruction, culminating in severe physical disability. De Graaf et al., in The Epidemiology of Chronic Rheumatism, Dellgren and Ball, eds.
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(Blackwell, Oxford, 1963), pp. 446-56; Meenam et al., Arthritis Rheum., 24:544-50 (1981); Gabriel et al., J. Rheumatol., 26:1269-74 (1999); James, Clin. Exp. Rheumatol., 17:392-93 (1999). RA is a progressive condition with well-recognized symptoms including symmetrical peripheral joint swelling and synovial inflammation while sparing the axial skeleton; the presence of rheumatoid factor (RF) autoantibodies; increased concentrations of interleukin-6 (IL-6) in serum and synovial fluid; and pregnancyinduced disease remission followed by severe postpartum flares, that is, while women with RA commonly undergo remission during pregnancy, the disease returns and may be even more severe and show a new onset or more accelerated course after delivery. See, Turgen, in Immunology and Serology in Laboratory Medicine, 2.sup.nd edition, Shanahan, ed. (Mosby Year Book, St. Louis, 1996), pp. 387-98; Hirano et al., Eur. J. Immunol., 18:1797-1801 (1988); Wilder et al., Ann. N.Y. Acad. Sci., 876:14-31 (1999); Iijima et al., J. Rheumatol., 26:755-56 (1999); Ostensen, Ann. N.Y. Acad. Sci., 876:131-43 (1999). ... In medical research directed to understanding, diagnosing and treating RA, several animal models of the disease have been described, but no spontaneous animal model that closely mimics all the features of the human disease has been discovered. Thus, it would greatly advance discovery research in the field of RA research if a mammalian model faithfully exhibiting the same characteristic physical symptoms of RA could be obtained. Web site: http://www.delphion.com/details?pn=US06414218__ ·
Nucleic acid fragments and corresponding peptide fragments from the caprine arthritis-encephalitis virus (CAEV) genome, and uses thereof Inventor(s): Bertoni; Giuseppe (Uberstorf, CH), Pancino; Gianfranco (Paris, FR), Peterhans; Ernst (Berne, CH), Sonigo; Pierre (Paris, FR) Assignee(s): Centre National de la Recherche Scientifique (Paris Cedex, FR) Patent Number: 5,858,672 Date filed: April 8, 1997 Abstract: Nucleotide fragments from caprine arthritis-encephalitis virus (CAEV) env gene, corresponding peptide fragments, and uses thereof in screening for viral caprine arthritis-encephalitis, are disclosed. Antibodies to peptide fragments and uses thereof for diagnosing viral arthritis-encephalitis are also enclosed. Said nucleic acid fragments code for a peptide fragment including at least one CAEV Env protein segment comprising at least one immunodominant epitope selected from the transmembrane region of said protein, and include 15-255 nucleotides. Excerpt(s): This application is the National Stage of International Application No. PCT/FR95/00848 filed on Jun. 26, 1995. ... The present invention relates to nucleotide fragments derived from the env gene of the caprine arthritis-encephalitis virus (CAEV) and to the corresponding peptide fragments and to their applications in the screening for caprine viral encephalitis and arthritis; the present invention also relates to antipeptide fragment antibodies as well as to their applications in the diagnosis of viral encephalitis and arthritis. ... The caprine arthritis-encephalitis virus is a lentivirus which causes a leukoencephalitis in young goats and a chronic clinical arthritis in 20 to 30% of adult goats infected naturally. Arthritis is usually progressive and is particularly severe at the level of the synovial spaces of the carpal joints. Web site: http://www.delphion.com/details?pn=US05858672__
Patents 375
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Ointment for treatment of arthritis Inventor(s): Richards; Levie (R.D. 2, Box 126, Whitehouse Station, NJ 08889) Assignee(s): none reported Patent Number: 4,271,154 Date filed: September 11, 1978 Abstract: The present application relates to the treatment of arthritis and related disorders and to a particular composition suitable thereto. The composition comprises a mixture of white petroleum jelly and the reaction products of lead-free gasoline in combination with dried and ground pods or seeds of the capsicum plants mixed to form an ointment to application to the affected part of the body. Excerpt(s): This application is a substitute for my previous U.S. application, Ser. No. 44,873 filed Mar. 6, 1974, now abandoned. ... The present invention relates to a composition of matter and to a method of making an ointment for the treatment of arthritis. The composition comprises an admixture of white petroleum jelly and the reaction product of lead-free gasoline with vegetable products derived from the seed and pods of the capsicum plant commonly known as red pepper. In particular this invention concerns on ointment particularly useful in the treatment of arthritis and related diseases as they occur in humans, lower primates and other animals. The ointment may be utilized for the temporary relief of aches and pains resulting from arthritis. The ointment is devised for external application to the affected area of the body by applying to the area adjacent to the joint and rubbing it into the skin to alleviate the aches and pains of the disease. ... Arthritis is medically termed as an inflamation of a joint or joints and is one of a number of diseases and disorders of the skeleton and body system commonly called rheumatism. It arises from many causes, some well-defined, some still unknown, and it is treated in many different ways. There are two common types know as rheumatoid arthritis and degenerative arthritis. The former is a disease not of the joints alone but of the whole bodily system, in particular, the connective body tissue. The latter is a chronic joint disease of age, rarely occurring before the age of 40 in humans. In both cases the manifestations are the same. The joints in the hands, feet and legs are affected. For example, they become swollen and gnarled, so that the digits tend to slant away to the outside. In severe cases unused muscles surrouding the affected area become painful and swollen and joints may become atrophied through non-use. Web site: http://www.delphion.com/details?pn=US04271154__
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Oral remedy for rheumatoid arthritis and functional food Inventor(s): Matsumoto; Takashi (Tsukuba, JP), Taguchi; Yasuki (Tsukuba, JP), Fujita; Kotaro (Tsukuba, JP), Ametani; Akio (Tokyo, JP), Kaminogawa; Syuichi (Kasukabe, JP), Nakagami; Masayo (Nishinomiya, JP) Assignee(s): Nippon Meat Packers, Inc. (Osaka, JP) Patent Number: 6,010,722 Date filed: May 18, 1998 Abstract: Oral drugs and functional foods of the present invention contain type-II collagen denatured (fragmented) under specific conditions. Rheumatoid arthritis (RA) has been considered to be an autoimmune disease against type-II collagen as an antigen. Since denatured type-II collagen of the invention induces high oral immune tolerance
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and inhibits immune responses against type-II collagen, it can prevent and treat RA. Particularly, RA can effectively be prevented and treated by simple oral administration of type-II collagen. Excerpt(s): This invention provides oral drugs and functional foods for treating and preventing rheumatoid arthritis. More particularly, the invention provides drugs and functional foods containing denatured type-II collagen to effectively treat and prevent rheumatoid arthritis. ... Rheumatoid arthritis (referred to as RA in the following description) is one of chronic diseases with many patients, systemically causing inflammation in connective tissues. This disease induces nonspecific inflammation mainly in synovial membranes of joints, resulting in systemic multiple arthritis and injuries of cartilage and bone. ... Although details of the mechanism have not been well clarified, RA has been considered to be an autoimmune disease related to lymphocyte antigen (HLA) DR4 and activated T cells (Lancet, 341, 283,1993). Since experimental animals given type-II collagen, a main structural protein of cartilage, exhibit symptoms morphologically similar to those of RA, type-II collagen is believed to be an autoantigen of this disease (J. Exp. Med., 146, 857, 1977; Lab. Invest., 54, 26, 1986). Web site: http://www.delphion.com/details?pn=US06010722__ ·
Pharmaceutical composition for the treatment of the anemia of rheumatoid arthritis Inventor(s): Cynshi; Osamu (Tokyo, JP), Mizuno; Koji (Saitama, JP) Assignee(s): Chugai Seiyaku Kabushiki Kaisha (Tokyo, JP) Patent Number: 4,732,889 Date filed: February 3, 1986 Abstract: A pharmaceutical composition for the treatment of the anemia of rheumatoid arthritis comprising a therapeutically effective amount of human erythropoietin (EPO) in a parenterally acceptable vehicle is disclosed. Human EPO may be extracted from human urine or also be prepared by expressing in a host cell the gene coding for the amino acid sequence of human EPO. Excerpt(s): The present invention relates to a pharmaceutical composition for the treatment of the anemia of rheumatoid arthritis that comprises a therapeutically effective amount of human erythropoietin (hereinafter referred to as "human EPO") in a parenterally acceptable vehicle. ... The term "human EPO" as used hereinafter means a polypeptide having the amino acid sequence inherent in human beings, with or without sugar chains. Examples of the human EPO include one that is derived from human urine (hereinafter referred to as "human urinary EPO"), one obtained by expressing in a host cell the gene coding for the amino acid sequence of human EPO (this type of human EPO is hereinafter referred to as "human rEPO"), one obtained from a tissue culture of human kidney cancer cells, and one obtained by cultivating a hybridoma resulting from cell fusion of a human cell line having the ability to produce human EPO. The term "erythropoietin"(hereinafter referred to as "EPO") will mean a trace physiologically active substance that acts on erythroblastic stem cells present not only in humans but also in other animals so as to accelerate the differentiation of such stems cells into mature erythrocytic cells, and proliferation of the latter. While numerous studies on human urinary EPO have been reported, the pharmaceutical utility of human EPO still remains unknown in many respects. ... High incidence of anemia as one of the complications in patients with rheumatoid arthritis has been known for many years (see, for example, Nilsson, F., Acta. Med. Scand. Suppl., 210, 193 (1948), and Roberts, F. D. et
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al.; Blood, 21, 470 (1983)), and severe anemia associated with rheumatoid arthritis is of particular clinical concern in the treatment of the disease. Web site: http://www.delphion.com/details?pn=US04732889__ ·
Pharmaceutical compositions containing dehydroepiandrosterone and anesthetic steroids in the treatment of arthritis and other joint disabilities
other
Inventor(s): Peat; Raymond F. (P.O. Box 3427, Eugene, OR 97403) Assignee(s): none reported Patent Number: 4,628,052 Date filed: May 28, 1985 Abstract: The present invention is concerned with compositions and methods of treating rheumatoid arthritis, osteoarthritis, and arthritis associated with psoriasis and with lupus and other auto-immune diseases, and also for treating non-specific joint pain associated with stress or incidental to another ailment, using dehydroepiandrosterone and/or other anesthetic steroids dissolved in an oily vehicle, and preferably administered topically or orally. Excerpt(s): This invention is concerned with compositions and methods of treating rheumatoid arthritis, osteo-arthritis, and arthritis associated with psoriasis and with lupus and other auto-immune diseases, and also for treating non-specific joint pain associated with stress or incidental to another ailment, using dehydroepiandrosterone (DHEA) and/or other anesthetic steroids dissolved in an oily vehicle, and preferably administered topically or orally. ... The extensive use of cortisone and related antiinflammatory steroids in treating arthritis has been limited by the knowledge of several side effects, including calcium loss and osteoporosis, immune suppression, and atrophy of various tissues, including the adrenal glands. Nonsteroidal anti-inflammatory agents have been used with some success to avoid the glucocorticoids' side effects, but generally are ineffective in preventing the advance of the disease process. Other agents have been used or proposed which retard the advance of the disease, possibly by inhibiting mitosis, but they generally have toxic side effects. ... It would be desirable to use in treatment substances which are normally present in the body at high levels, since these normal substances, especially when used in physiological quantities, rarely have harmful side effects. Web site: http://www.delphion.com/details?pn=US04628052__ ·
Photodynamic therapy for the destruction of the synovium in the treatment of rheumatoid arthritis and the inflammatory arthritides Inventor(s): Trauner; Kenneth (Sacramento, CA), Hasan; Tayyaba (Arlington, MA) Assignee(s): The General Hospital Corporation (Boston, MA) Patent Number: 5,368,841 Date filed: February 11, 1993 Abstract: A method of treating proliferative diseases of the synovial joint using photodynamic therapy. In particular the method of the invention may be used to destroy synovial tissue in inflammatory joint conditions associated with diseases such as
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rheumatoid arthritis, lupus erythematosus and other rheumatoid variants. A number of methods of delivery are provided, some of which are non invasive. Excerpt(s): The invention relates to the use of photodynamic therapy for the destruction of diseased synovium. ... Photodynamic therapy generally refers to an experimental cancer treatment modality that selectively kills cancer cells by an interaction between absorbed light an a retained photoactivatable agent (Kessel, Photochem. Photobiol. 44:489-493; Bottiroli et al., Photochem. Photobiol. 47:209-214, 1988; Salet et al., Photochem. Photobiol. 53:391-3, 1991; Gross, Photobiological Techniques (chapter 9), Valenzeno et al. eds., Plenum Press, New York, 1991; Star et al., Photochem and Photobiol, B: Biology 1:149-167, 1987; and Jori et al., Photodynamic Therapy of Neoplastic Disease, Kessel ed., CRC Press, Boca Raton, Fla., 1989). Chemical sensitization of live tissues by light was first reported in 1900 by Raab. Uptake of hematoporphyrin derivative (HPD) in neoplastic tissue was first described by Auler and Banzer (Z. Krebforsch 53:65-68, 1942). Uptake was later confirmed by fluorescence by Figge et al (Proc. Soc. Exp. Biol. Med. 68:640-641, 1948). Lipson et al. demonstrated tumor localization of HPD in 1960 (JNCI 26:1-12, 1961). ... The HPD semipurified mixture of porphyrins was later further purified to a combination of esters and ethers of dihematoporphyrin (DHE). The formulation predominantly in use is marketed as Photofrin.RTM. and HPD/Photofrin.RTM. was the first FDA approved photosensitizing agent available for PDT trials. Photofrin.RTM. has subsequently been tested extensively for the destruction of multiple tumors in numerous medical disciplines (Dougherty et al., In Photodynamic Therapy of Neoplastic Disease, Kessel ed., CRC Press, Boca Raton, Fla., 1989). Web site: http://www.delphion.com/details?pn=US05368841__ ·
Polynucleotides encoding MIP-1.alpha., MCP-1, MIP-1.beta., Rantes and TNF-.alpha., and methods for treating rheumatoid arthritis Inventor(s): Karin; Nathan (Haifa, IL) Assignee(s): Rappaport Family Institute for Research in the Medical Sciences (Haifa, IL) Patent Number: 6,420,346 Date filed: February 7, 2000 Abstract: A method of treating rheumatoid arthritis of an individual is disclosed. The method comprises the step of expressing within the individual at least an immunologically recognizable portion of a cytokine from an exogenous polynucleotide encoding the at least a portion of the cytokine, wherein a level of expression of the at least a portion of the cytokine is sufficient to induce the formation of anti-cytokine immunoglobulins which serve for neutralizing or ameliorating the activity of a respective and/or cross reactive endogenous cytokine, to thereby treat rheumatoid arthritis. Excerpt(s): The present invention relates to pharmaceutical compositions and methods for treating rheumatoid arthritis in an individual. More particularly, the present invention relates to DNA vaccination approaches which induce the breakdown of selftolerance to cytokines and as such inhibit the progression of the disease. ... Rheumatoid arthritis (RA) is an inflammatory disorder characterized by infiltration of leukocytes into the synovial tissue (ST) and synovial fluid (SF) of joints (Harris, 1990). Depending on the type of immunization, a single administration of complete Freund's adjuvant (CFA) may result in the development of a local inflammatory process or chronic poly adjuvant
Patents 379
induced arthritis (AIA, also termed AA) which histologically and clinically resembles human RA (Holoshitz et al., 1983). In the scientific and medical communities, AIA is considered a reliable animal model for testing drugs and treatments for RA. ... In both diseases proinflammatory cytokines and chemokines are believed to play a pivotal role in the attraction of leukocytes to the site of inflammation and in the initiation and progression of the inflammatory process. The role of proinflammatory cytokines, particularly TNF-.alpha. and IL-1, in disease manifestation has been intensively studied and explored in experimental models that have been expanded to clinical trials (Arend and Dayer, 1995; Arend et al., 1994; Elliott et al., 1994; Feldmann et al., 1997; Moreland et al., 1997; Moreland et al., 1996; for a general review, see also, Feldmann et al., 1996). Other cytokines such as IL-4, TGF-.beta., IL-8, IL-17, IL-10, IL-11, IL-12 and IL-15 have also been implicated in the regulation of the disease. Such regulation can be attributed to either their direct effect on disease manifestation, their synergistic effect with other proinflammatory cytokines/chemokines, or their involvement in the regulation of chemokine transcription, and production (Badolato and Oppenheim, 1996; Badolato et al., 1997; Butler et al., 1999; Chabaud et al., 1998; Evans et al., 1998; Feldmann et al., 1996; Kasama et al., 1999; Ma et al., 1998; Parks et al., 1998; Sato et al., 1996; Schimmer et al., 1998; Schrier et al., 1998; Wahl et al., 1993). Web site: http://www.delphion.com/details?pn=US06420346__ ·
Polyvalent equine immune serum composition and method for treating rheumatoid arthritis Inventor(s): Stephan; Peter M. (London, GB2) Assignee(s): Peter Stephan Center, Ltd. (Miami, FL) Patent Number: 4,732,752 Date filed: October 23, 1986 Abstract: A composition and method for treating rheumatoid arthritis, osteoarthritis, and related diseases which comprises administering an effective amount of an equine immune serum, in dosage form, to a patient. The equine immune serum is obtained from horses which have been immunized with a solution containing tissue from prenatal or pregnant pigs. Excerpt(s): The present invention relates to a composition and method for treating rheumatoid arthritis, osteoarthritis, non-specific rheumatism and other related diseases in humans. ... Arthritis is a term generally used to describe a condition of inflammed joints which is characterized by pain and swelling. Both osteoarthritis and rheumatoid arthritis may result in stiffness, swelling and a considerable amount of pain. Treatment generally includes rest, the application of heat, and the administration of antiinflammatory drugs. Often, the treatment further includes the administration of diseasemodifying anti-rheumatic drugs such as gold, methotrexate and penicillamine. However, since these drugs are quite toxic and often result in serious side-effects, they must be used with caution. In view of the severity of rheumatoid arthritis, osteoarthritis, and other related diseases, there is a great need for a drug which is easily tolerated and free from serious side-effects. ... Thus, it is an object of the present invention to provide a novel composition for the treatment of rheumatoid arthritis, osteoarthritis, and related diseases. Web site: http://www.delphion.com/details?pn=US04732752__
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Prevention and treatment of rheumatioid arthritis Inventor(s): Stolle; Ralph J. (Lebanon, OH), Beck; Lee R. (Birmingham, AL) Assignee(s): Stolle Research and Development Corporation (Cincinnati, OH) Patent Number: RE33,565 Date filed: August 11, 1988 Abstract: There is disclosed a novel method and product for the treatment and prevention of rheumatoid arthritis. The method involves passive immunization against a mixed spectrum of infectious bacteria which reside in the human gastrointestinal tract. The passive immunization is accomplished by oral.[.injestion.]. .Iadd.ingestion .Iaddend.of IgG immunoglobulin obtained from the milk of cows that have been immunized against a specific spectrum of bacterial types. A unique combination of bacterial species is formulated into a vaccine which is used to immunize dairy cattle. The IgG antibody obtained from the milk of the immunized cows constitutes the product of the invention. Excerpt(s): This application is related to an application in the name of Lee Randolph Beck, Ser. No. 776,249 filed Mar. 10, 1977. ... A number of years ago it was commonly believed that rheumatoid arthritis had an infectious etiology. This view is not popular today, although the inflammatory features and constitutional manifestations of rheumatoid arthritis-the synovitis and granulomatous lesions, the fever, tachycardia, leukocytosis, lymphadenopathy and ocassional spelnomegaly, the accelerated erythrocyte sedimentation rate and other changes in "acute phases reactants" are all compatible with an infectious process. Competent and repeated bacteriologic studies have failed to recover consistently a single infectious agent from the blood, synovial fluid, synovial tissues or subcutaneous nodules. Attempts to transmit the disease by injecting joint fluid from patients with rheumatoid arthritis into the joints of other human subjects have been unsuccessful. Subcutaneous nodules have failed to survive following homologous transplantation (Bauer, et al, 1951) the Practitioner 166:5. ... An infectious process may appear to precipitate the onset of rheumatoid arthritis in a significant number of patients, and may exert a deleterious influence on the course of the disease when it has already been established. There is statistical evidence to support this clinical impression (Lewis-Faning, 1950) Ann Rheum. Dis., Suppl. 9. Web site: http://www.delphion.com/details?pn=US0RE33565__
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Prevention and treatment of rheumatoid arthritis Inventor(s): Stolle; Ralph J. (Lebanon, OH), Beck; Lee R. (Birmingham, AL) Assignee(s): Stolle Research and Development Corporation (Cincinnati, OH) Patent Number: 4,732,757 Date filed: December 9, 1983 Abstract: There is disclosed a novel method and product for the treatment and prevention of rheumatoid arthritis. The method involves passive immunization against a mixed spectrum of infectious bacteria which reside in the human gastrointestinal tract. The passive immunization is accomplished by oral injestion of IgG immunoglobulin obtained from the milk of cows that have been immunized against a specific spectrum of bacterial types. A unique combination of bacterial species is formulated into a vaccine
Patents 381
which is used to immunize dairy cattle. The IgG antibody obtained from the milk of the immunized cows constitutes the product of the invention. Excerpt(s): This application is related to an application in the name of Lee Randolph Beck, Ser. No. 776,249 filed March 10, 1977. ... A number of years ago it was commonly believed that rheumatoid arthritis had an infectious etiology. This view is not popular today, although the inflammatory features and constitutional manifestations of rheumatoid arthritis--the synovitis and granulomatous lesions, the fever, tachycardia, leukocytosis, lymphadenopathy and occasional spelnomegaly, the accelerated erythrocyte sedimentation rate and other changes in "acute phases reactants"--are all compatible with an infectious process. Competent and repeated bacteriologic studies have failed to recover consistently a single infectious agent from the blood, synovial fluid, synovial tissues or subcutaneous nodules. Attempts to transmit the disease by injecting joint fluid from patients with rheumatoid arthritis into the joints of other human subjects have been unsuccessful. Subcutaneous nodules have failed to survive following homologous transplantation (Bauer, et al, 1951) the Practitioner 166:5. ... An infectious process may appear to precipitate the onset of rheumatoid arthritis in a significant number of patients, and may exert a deleterious influence on the course of the disease when it has already been established. There is statistical evidence to support this clinical impression (Lewis-Faning, 1950) Ann Rheum. Dis., Suppl. 9. Web site: http://www.delphion.com/details?pn=US04732757__ ·
Process and product for treatment of rheumatoid arthritis Inventor(s): Moore; Eugene R. (5600 Woodview Pass, Midland, MI 48642) Assignee(s): none reported Patent Number: 5,529,786 Date filed: February 28, 1994 Abstract: This invention provides a therapeutic pill comprising animal tissue containing a therapeutic amount of Type II collagen and a method of preparing animal tissue containing Type II collagen for treatment of Rheumatoid Arthritis in humans. Excerpt(s): Rheumatoid Arthritis is a painful and often crippling disease that initially results in swollen and imflammed joints, but often progresses to deformed or completely destroyed joints. This is a result of the body mistakenly attacking collagen, which is the major portion of cartilage tissue. Cartilage tissue serves the function of a lubricant in the joints, keeping bone from rubbing on bone. As the disease progresses and more of the cartilage is destroyed, bone does begin to wear on bone. This results in even more severe pain and ultimately destruction of the joint itself. As the disease progresses, the body sometimes attacks other collagen in the soft tissues of the body which can cause a variety of arthritis-related diseases. ... In order to initiate the disease, it is apparent that an individual must have an inherent (perhaps genetic) susceptibility. Given this susceptibility, there is now strong evidence that the disease is initiated by exposure to the Epstein-Barr virus. The ability of the Epstein-Barr virus to initiate Rheumatoid Arthritis has been linked to a key amino acid sequence which is identical to a sequence found in human collagen. Thus, in generating antibodies to destroy the Epstein-Barr virus, the body generates antibodies that are also capable of attacking its own collagen. In a similar manner, arthritis has been initiated in rats by the intradermal injection of highly purified Type II collagen extracted from chicken cartilage or by the well known complete Freund Adjuvant. ... It was also shown that rats could be
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prevented from getting arthritis or the effects greatly reduced from this injection of highly purified collagen. This was accomplished by feeding the same highly purified collagen to the rats for several days prior to the injection. It was also shown with rats that, once arthritis had been induced, the effects of the disease could be reduced by the oral administration of the same highly purified collagen. In a later study with humans having severe arthritis it has been shown that the oral administration of the highly purified collagen is similarly beneficial to humans in reducing the effects of the disease. Web site: http://www.delphion.com/details?pn=US05529786__ ·
Product for alleviating the symptons of arthritis in mammals Inventor(s): Moore; Eugene R. (5600 Woodview Pass, Midland, MI 48642) Assignee(s): none reported Patent Number: 5,645,851 Date filed: April 9, 1996 Abstract: This invention provides a composition useful as an edible supplement for alleviating the symptoms of arthritis for oral consumption by mammals, said composition comprising animal tissue containing water-insoluble Type II collagen, which has been separated from non-Type II collagen containing tissue and has been sterilized in subdivided form without changing the original structure of the Type II collagen. Excerpt(s): The present invention pertains to means for treating the symptoms of autoimmune arthritis in mammals and, more particularly, relates to means for preparing animal tissue for oral administration to mammals, compositions comprising said animal tissue and methods for alleviating the symptoms of autoimmune arthritis, particularly rheumatoid arthritis, in humans. ... Autoimmune arthritis, and particularly rheumatoid arthritis, is a painful and often crippling disease that initially results in swollen and inflammed joints, but often progresses to deformed or completely destroyed joints. This is a result of the body mistakenly attacking collagen, which is the major portion of cartilage tissue. Cartilage tissue serves the function of a lubricant in the joints, keeping bone from rubbing on bone. As the disease progresses and more of the cartilage is destroyed, bone does begin to wear on bone. This results in even more severe pain and ultimately destruction of the joint itself. As the disease progresses, the body sometimes attacks other collagen in the soft tissues of the body which can cause a variety of arthritis-related diseases. ... In order to initiate the disease, it is apparent that an individual must have an inherent (perhaps genetic) susceptibility. Given this susceptibility, there is now strong evidence that the disease is initiated by exposure to the Epstein-Bart virus. The ability of the Epstein-Bart virus to initiate Rheumatoid Arthritis has been linked to a key amino acid sequence which is identical to a sequence found in human collagen. Thus, in generating antibodies to destroy the Epstein-Bart virus, the body generates antibodies that are also capable of attacking its own collagen. In a similar manner, arthritis has been initiated in rats by the intradermal injection of water-soluble highly purified Type II procollagen extracted from chicken cartilage or by the well known complete Freund Adjuvant. Web site: http://www.delphion.com/details?pn=US05645851__
Patents 383
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Protein which is characteristic of rheumatoid arthritis Inventor(s): Hurwitz; Charles (108 Mosher Rd., Delmar, NY 12054), Rosano; Carmen L. (23 Nancy Dr., Troy, NY 12180), Parhami; Nourollah (349 Torquay Blvd., Westmere, NY 12203), Hechemy; Karim (29 Pico Rd., Clifton Park, NY 12065) Assignee(s): none reported Patent Number: 4,645,748 Date filed: February 1, 1985 Abstract: Describes rheumatoid arthritis factor present in detectable amounts in rheumatoid arthritis patients, but not in patients with other arthritedes; preparation of antibodies to the factor; use of factor and antibodies to test for rheumatoid arthritis; and test kits for conducting the tests. Excerpt(s): Rheumatoid arthritis (RA) has been described as an unresolved systemic inflammation in which immune dysfunction and genetic susceptibility play roles. In earlier stages it is characterized by fluctuating remissions and exacerbations, and in later stages by a chronic granulatomous response (panus formation) leading to tissue destruction. The synovial membrane in RA has many of the characteristics of a hyperactive immunologically stimulated lymphoid organ and the ratio of T suppressor to T helper lymphocytes has been shown to be significantly reduced. ... Although a number of attempts have been made to implicate bacteria, viruses and mycoplasms as etiological agents, no specific causative agent has been clearly proven. It is possible that there is no specific etiological agent, and that the important agent or factor may be the result of an interplay of hereditary factors and physiological changes on non-specific inflammatory states. ... A great deal of work has been expended on the late, destructive phase of this disease in which anaphylactically induced leukotrienes and prostaglandins may play a chemotactic role in migration of neutrophils and macrophages into the rheumatoid synovium leading to destruction of bone and cartilage. Many attempts have been made to intervene between these events and the subsequent destructive phase occurring in the rheumatoid synovia. Web site: http://www.delphion.com/details?pn=US04645748__
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Radiolabeled compositions containing a calcific matrix and their use for treatment of arthritis Inventor(s): McMillan; Kenneth (Richwood, TX), Simon; Jaime (Angleton, TX) Assignee(s): The Dow Chemical Company (Midland, MI) Patent Number: 5,300,281 Date filed: July 1, 1992 Abstract: Radioactive compositions containing a calcific matrix and methods for using the compositions for therapeutic radiation treatment including rheumatoid arthritis are disclosed. Excerpt(s): This invention relates to radioactive compositions containing a calcific matrix and use of these compositions in treating arthritis and other diseases. ... Rheumatoid arthritis is a prevalent disease characterized by chronic inflammation of the synovial membrane lining the afflicted joint. Current treatment methods for severe cases of rheumatoid arthritis include the removal of the synovial membrane, e.g., synovectomy. Surgical synovectomy has many limitations including the risk of the surgical procedure
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itself, and the fact that a surgeon often cannot remove all of the membrane. The diseased tissue remaining may eventually regenerate, causing the same symptoms which the surgery was meant to alleviate. ... Radiation synovectomy is radiation-induced ablation of diseased synovial membrane tissue accomplished by injecting a radioactive compound into the diseased synovium. Early attempts to perform radiation synovectomy were hampered by an instability of the radioactive compositions utilized and by leakage of such compounds from the synovium into surrounding healthy tissues. The instability of labile radionuclide-complexes resulted in displacement of the radionuclide from the colloid complex and retention of the radionuclide in soft tissues. Significant leakage of the radioactive compound from the injection site exposed normal tissues to dangerous levels of radiation. Because of these limitations, new radiolabeled compositions were sought which would have minimal leakage. Web site: http://www.delphion.com/details?pn=US05300281__ ·
Radiolabeled metal-binding protein for the treatment of arthritis Inventor(s): Garlich; Joseph R. (Lake Jackson, TX), McMillan; Kenneth (Richwood, TX), Simon; Jaime (Angleton, TX) Assignee(s): The Dow Chemical Company (Midland, MI) Patent Number: 5,133,956 Date filed: May 30, 1991 Abstract: Radioactive high molecular weight metal-binding protein compositions and a method for therapeutic radiation treatment including the treatment of rheumatoid arthritis comprising injection of a radioactive high molecular weight metal-binding protein compositions are disclosed. Excerpt(s): This invention relates to radioactive high molecular weight metal-binding protein compositions and to a method for the treatment of rheumatoid arthritis by administering such radioactive high molecular weight metal-binding protein compositions. ... Rheumatoid arthritis is a prevalent disease characterized by chronic inflammation of the synovial membrane lining the afflicted joint. Current treatment methods for severe cases of rheumatoid arthritis include the removal of the synovial membrane, e.g., synovectomy. Surgical synovectomy has many limitations including the risk of the surgical procedure itself, and the fact that a surgeon often cannot remove all of the membrane. The diseased tissue remaining may eventually regenerate, causing the same symptoms which the surgery was meant to alleviate. ... Radiation synovectomy is radiation-induced ablation of diseased synovial membrane tissue accomplished by injecting a radioactive compound into the diseased synovium. Early attempts to perform radiation synovectomy were hampered by an instability of the radioactive compounds utilized and by leakage of such compounds from the synovium into surrounding healthy tissues. The instability of labile radionuclide-complexes resulted in displacement of the radionuclide from the colloid complex and retention of the radionuclide in soft tissues. Significant leakage of the radioactive compound from the injection site exposed normal tissues to dangerous levels of radiation. Because of these limitations, new radiolabeled compositions were sought which would have minimal leakage. Web site: http://www.delphion.com/details?pn=US05133956__
Patents 385
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Recombinant antigen for diagnosing rheumatoid arthritis Inventor(s): Prakash; Ramesh K. (Salt Lake City, UT) Assignee(s): Research Corporation Technologies, Inc. (Tucson, AZ) Patent Number: 5,723,314 Date filed: April 10, 1996 Abstract: A method is described for diagnosing rheumatoid arthritis by providing a recombinant antigen (RAMA) and detecting rheumatoid arthritis-associated IgM antibodies against the RAMA antigen in patient sera. The RAMA antigen comprises SEQ ID NO:3 and peptides substantially homologous thereto. A purified and isolated DNA encoding the RAMA antigen and a transformed host containing the DNA are also disclosed. Excerpt(s): This invention relates to a method for diagnosing rheumatoid arthritis. More particularly, this invention relates to a method for objectively diagnosing rheumatoid arthritis by quantitative determination of the presence or absence of rheumatoid arthritis-associated antibodies in patient sera that react with a recombinant antigen. The invention also relates to the recombinant antigen and a molecular clone of the gene thereof. ... Rheumatoid arthritis is a chronic systemic rheumatic disease that affects a significant percentage of the population. Traditionally, it has been diagnosed subjectively through clinical observation and dominant complaints by a patient. P. Lipsky, Rheumatoid Arthritis, in Harrison's Principles of Internal Medicine 1423 (1987). Thus, clinical diagnosis of rheumatoid arthritis is subject to the skill of the diagnostician and the severity of disease symptoms in the patient. ... For an objective diagnosis of rheumatoid arthritis, the presence of rheumatoid factor (Rf) in the serum of rheumatoid arthritis patients is routinely determined. Rf is an autoantibody that binds to the constant region of IgG immunoglobulins. The standard test for determining the presence of Rf in blood is an aggregation test wherein Rf causes aggregation of IgG. Rf has been detected in approximately 70% of patients exhibiting clinical symptoms of rheumatoid arthritis. These patients are thus termed "seropositive." The remaining 30% are classified as having "seronegative" rheumatoid arthritis. Numerous conditions besides rheumatoid arthritis are associated with the presence of rheumatoid factor. Therefore, the presence of Rf does not establish a conclusive diagnosis of rheumatoid arthritis. An objective method of diagnosing rheumatoid arthritis that is more closely correlated with clinical diagnoses than is the presence of Rf in sera is needed. Ideally, such an objective diagnostic test would be quick and easy to perform and would not involve radioisotopes or be invasive to the patient. Web site: http://www.delphion.com/details?pn=US05723314__
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Remedy for anemia and arthritis Inventor(s): Cheng; Theodore (1209 W. Wynnewood Rd., Wynnewood, PA 19096) Assignee(s): none reported Patent Number: 4,767,626 Date filed: February 27, 1986 Abstract: A method for the treatment of anemia associated with viral and bacterial infection in a patient wherein symptoms of rheumatoid arthritis are present, by administering to the patient an effective amount of a composition capable of increasing
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thyroxine in the blood stream of said patient and thereby increasing stem cells in the blood stream. The composition preferably comprises fat soluble alkaloid extracts from the root of Zanthoxylum Simulans. Excerpt(s): The present invention relates to a method and composition for the alleviation of certain symptoms associated with rheumatoid arthritis. Also, the present invention is concerned with a method for diagnosing and monitoring patients suffering from rheumatoid arthritis. More particularly, the present invention relates to the treatment of anemia associated with rheumatoid arthritis. A still further part of the invention is the treatment of anemia which results from bacterial or viral infections and indicates also the presence of arthritis. ... There have been a number of investigations which indicate that certain bacterial and viral infections contribute to a subsequent development of the syndrome of rheumatoid arthritis as well as mild anemia. Some of these reports have indicated that there is a high incidence of anemia in patients which are suffering from rheumatoid arthritis. Such anemia is characterized as being moderately hypochromic and normocytic. ... Freireich et al, in the article entitled "Radioactive Iron Metabolism & Erythrocyte Studies of the Mechanism of the Anemia Associated With Rheumatoid Arthritis", J. Clinical Investigation 36: 1055 (1957), reported the mechanism of said anemia in arthritic patients, appears to be the rate of said red cell destruction was increased while the rate of said red cell synthesis was comparable to normal. Said anemia results because erythropoiesis fails to increase in order to compensate for said increased rate of red cell destruction. Said erythropoiesis, includes the synthesis of stem cells maturing into red blood cells in the bone marrow and in said blood stream with its continuous division and differentiation, appears to be self-regulating and also under the influence of thyrotropin, a thyroid hormone. Web site: http://www.delphion.com/details?pn=US04767626__ ·
Rose-hip formulations as anti-inflammatory natural medicine alleviating/reducing symptoms associated with inflammation and arthritis
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Inventor(s): Kharazmi; Arsalan (Hellerup, DK), Winther; Kaj (Randb.o slashed.l, DK), Rein; Eydbj.o slashed.rg (Randb.o slashed.l, DK) Assignee(s): Otto Torbjorn Hansen and Marianne Hansen (Tullebolle, DK) Patent Number: 6,024,960 Date filed: April 17, 1998 Abstract: A formulation having a rose hip concentrate is used to treat and/or alleviate the symptoms associated with inflammation including arthritis or to prevent development of arthritis. The rose hip concentrate has a high vitamin content relative to conventionally dried material, and is shown, in vitro, to inhibit the chemotaxis and oxidative burst response of human peripheral blood inflammatory cells, as well as the chemotaxis of monocytes. The formulation, in vivo, was found to inhibit chemotaxis of human peripheral blood inflammatory cells and to reduce the level of C-reactive protein, to alleviate pain and reduce inflammation in patients with arthritis. Excerpt(s): The present invention relates to the use of dried rose-hip for the preparation of formulations for the treatment or prophylaxis of a number of conditions associated with inflammation including arthritis. The invention also relates to methods of preparing these formulations. ... Inflammatory diseases such as arthritis involve a broad spectrum of different clinical manifestations. The most well known and best studied form of arthritis is rheumatoid arthritis (RA). A number of general principles apply to
Patents 387
the pathogenesis of arthritis: 1) different cell types such as polymorphonuclear leukocytes, monocyte/macrophages and T-cells are involved and that these cells interact with each other in this disease; 2) inflammatory cytokines such as tumor necrosis alpha (TNF.alpha.), interleukine-I (IL-1) and interleukine-6 (IL-6) control and amplify the inflammatory cycles at many points of the evolution of the disease; 3) other biological pathways are down- or up-regulated during inflammation; and 4) spontaneous remissions are not infrequent in some forms of arthritis such as RA. This may mean that minor adjustments in regulatory factors that activate or suppress the arthritic process are sufficient to dampen the entire process, resulting in control of the immune response and suppression of inflammation and tissue damage. Based on the principles involved in the pathogenesis of arthritis one can conclude that, a truly effective remission inducing therapy for arthritis probably will not necessarily involve a cytotoxic drug or a potent immunosuppressive drug but rather a less harmful preferably natural product that, if introduced or applied in the right manner to the patient, can trigger a healing process and prevent disease progression. ... Incidence of arthritis appears to be approximately the same in most populations throughout the world, about 1% of adult females and 0.5% of adult males. Some pockets of higher incidence has been observed in certain parts of the world. However, the role of sex appears to be stronger than any geographical or racial factors as a disease determinant. It is claimed that in the Western World approximately 70% of the population over the age of 70 have symptoms of osteoarthritis. Web site: http://www.delphion.com/details?pn=US06024960__ ·
Sports glove for arthritis Inventor(s): Marando; Don (13-3315 Makama St., Pahoa, HI 96778) Assignee(s): none reported Patent Number: 6,035,442 Date filed: September 19, 1997 Abstract: The present invention is a sports glove for arthritis having a thick padding securely attached to the palm and fingers. The padding functions to increase the relative diameter of an item grasped in the hand of the user. This permits the same grip to be retained on an item with less flexing of the fingers. Primarily the present invention is used by individuals experiencing pain when flexing the fingers to grip an item. A strap is provided which functions to securely and removably attached the user's hand to a sports club. Excerpt(s): The present invention relates to sports equipment. More particularly, the present invention relates to a sports glove for use with people having a joint ailment preventing a proper grip on a sports club. Further, the present invention assists a person, lacking strength in their hands, to maintain a grip on the sports club. ... Many people afflicted with an ailment or length of proper grip strength have difficulty grasping a sports club firmly enough to assure a proper swing, contact and follow through when hitting a sports object such as a ball. This especially affects people having arthritis, rheumatism and other crippling diseases of the hands and joints. Certain diseases cause the individual pain when the joints of the hand are flexed beyond a certain point, yet prior to that point the pains is bearable. A solution is to increase the diameter of the handle of the sports club. However, typical this is done in a permanent fashion resulting in the sports club being dedicated to one individual. Custom sports clubs with an enlarged grip are very expensive and can effect the performance of the
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club. ... A second problem with people having a joint deceases is that often their grip is inadvertently relaxed in the back swing. Often this is an affliction in the elderly resulting in the embarrassing loss of the sports club. Web site: http://www.delphion.com/details?pn=US06035442__ ·
Substantially pure rheumatoid arthritis specific protein and an antibody against the same Inventor(s): Yamanaka; Naoki (Nagoya, JP), Yoshida; Makoto (Kawasaki, JP) Assignee(s): Asahi Medical Co., Ltd. (Tokyo, JP), Medecs Co., Ltd. (Aichi, JP) Patent Number: 4,742,157 Date filed: September 13, 1985 Abstract: A substantially pure rheumatoid arthritis specific protein (RASP) and an antibody against the rheumatoid arthritis specific protein (anti-RASP antibody) are disclosed. The RASP is found specifically in the serum or plasma of a patient suffering from rheumatoid arthritis, and may be detected using an anti-RASP antibody easily and effectively. Therefore, the anti-RASP antibody of the present invention is useful for the diagnosis of rheumatoid arthritis by the criterion of the presence of RASP. Excerpt(s): This invention relates to a substantially pure rheumatoid arthritis specific protein. The present invention also relates to an antibody against the rheumatoid arthritis specific protein. More particularly, the present invention is concerned with a protein specifically found in the plasma of a patient suffering from rheumatoid arthritis and an antibody specific for the antigenic determinant of the rheumatoid arthritis specific protein. ... Conventionally, the diagnosis of rheumatoid arthritis has been effected according to the criteria proposed by the American Rheumatism Association. However, such criteria depend on doctor's observations and dominant complaints by a patient, and therefore, such criteria are insufficient with respect to objectivity and quantitative analysis of the degree of rheumatoid arthritis. ... For the quantitative analysis of the degree of rheumatoid arthritis, the presence and amount of rheumatoid factor (RF), immune complex (IC) or C-reactive protein (CRP) in the serum or plasma of a patient have been determined. However, such substances are not necessarily specific for the plasma or serum of a patient suffering from rheumatoid arthritis, and therefore, such substances are not useful as a conclusive factor. Web site: http://www.delphion.com/details?pn=US04742157__
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Substituted chromans and their use in the treatment of asthma, arthritis and related diseases Inventor(s): Eggler; James F. (Stonington, CT), Marfat; Anthony (Mystic, CT), Masamune; Hiroko (Noank, CT), Melvin, Jr.; Lawrence S. (Ledyard, CT) Assignee(s): Pfizer Inc. (New York, NY) Patent Number: 5,298,512 Date filed: September 30, 1991 Abstract: Substituted chromans which by inhibiting 5-lipoxygenase enzyme are useful in the prevention or treatment of asthma, arthritis, psoriasis, ulcers, myocardial infarction, stroke and related disease states in mammals, pharmaceutical compositions
Patents 389
thereof, a method of treatment therewith, and to intermediates useful in the synthesis thereof. Excerpt(s): The chemical nomenclature employed herein generally follows that of "I.U.P.A.C Nomenclature of Organic Chemistry, 1979 Edition," Pergammon Press, New York, 1979. ... a pharmaceutically acceptable cationic salt when . the compound contains a carboxy group. ... Because of their ease of preparation and valuable biological activity, the preferred compounds of the formula (I) have R as either 3-pyridyl or 3carboxyphenyl. When R.sup.1 and R.sup.2 are in the first alternative, the most preferred value of R.sup.1 is unsubstituted naphthyl and the most preferred value of R.sup.2 is hydrogen When R.sup.1 and R.sup.2 are in the second alternative, the preferred value of R.sup.1 is 2-quinolyl and the preferred value of R.sup.2 is methyl. Web site: http://www.delphion.com/details?pn=US05298512__ ·
Substituted tetralins, chromans and related compounds in the treatment and related compounds in the treatment of asthma, arthritis and related diseases Inventor(s): Eggler; James F. (Stonington, CT), Marfat; Anthony (Mystic, CT), Melvin, Jr.; Lawrence S. (Ledyard, CT) Assignee(s): Pfizer Inc (New York, NY) Patent Number: 5,998,451 Date filed: May 6, 1991 Abstract: Substituted tetralins, chromans and related compounds which, by inhibiting 5lipoxygenase enzyme and/or blocking leukotriene receptors, are useful in the prevention or treatment of asthma, arthritis, psoriasis, ulcers, myocardial infarction and related disease states in mammals, pharmaceutical compositions thereof, a method of treatment therewith, and to intermediates useful in the synthesis thereof. Excerpt(s): The present intention is directed to substituted tetralins, chromans and related compounds of the formula (I), depicted below, which by inhibiting 5lipoxygenase enzyme and/or blocking leukotriene receptors, are useful in the prevention or treatment of asthma, arthritis, psoriasis, ulcers, myocardial infarction and related disease states in mammals. The present invention is also directed to pharmaceutical compositions, a method of treatment, and to intermediates useful in the synthesis of said compounds of the formula (I). ... The chemical nomenclature employed herein generally follows that of "I.U.P.A.C. Nomenclature of Organic Chemistry, 1979 Edition," Pergammon Press, New York, 1979. ... a pharmaceutically acceptable cationic salt when the compound contains a carboxy group. Web site: http://www.delphion.com/details?pn=US05998451__
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Substituted tetralins, chromans and related compounds in the treatment of asthma, arthritis and related diseases Inventor(s): Eggler; James F. (Stonington, CT), Marfat; Anthony (Mystic, CT), Melvin, Jr.; Lawrence S. (Ledyard, CT) Assignee(s): Pfizer Inc. (New York, NY) Patent Number: 5,059,609 Date filed: August 4, 1989
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Abstract: Substituted tetralins, chromans and related compounds which, by inhibiting 5lipoxygenase enzyme and/or blocking leukotriene receptors, are useful in the prevention or treatment of asthma, arthritis, psoriasis, ulcers, myocardial infarction and related disease states in mammals, pharmaceutical compositions thereof, a method of treatment therewith, and to intermediates useful in the synthesis thereof. Excerpt(s): The present invention is directed to substituted tetralins, chromans and related compounds of the formula (I), depicted below, which by inhibiting 5lipoxygenase enzyme and/or blocking leukotriene receptors, are useful in the prevention or treatment of asthma, arthritis, psoriasis, ulcers, myocardial infarction and related disease states in mammals. The present invention is also directed to pharmaceutical compoitions, a method of treatment, and to intermediates useful in the synthesis of said compounds of the formula (I). ... The chemical nomenclature employed herein generally follows that of "I.U.P.A.C. Nomenclature of Organic Chemistry, 1979 Edition," Pergammon Press, New York, 1979. ... a pharmaceutically acceptable cationic salt when the compound contains a carboxy group. Web site: http://www.delphion.com/details?pn=US05059609__ ·
Synergistic composition of codine and ibuprofen to treat arthritis Inventor(s): Miller; Ronald Brown (Basel, CH), Douglas; Stephen Gordon (Shropshire, GB), Miller; Allan John (Surrey, GB) Assignee(s): Euro-Celtique, S.A. (Luxembourg, LU) Patent Number: 5,908,848 Date filed: May 12, 1997 Abstract: The invention relates to the use of a non-steroidal anti-inflammatory drug together with an opioid analgesic in the manufacture of a medicament for the treatment of arthritis. Excerpt(s): This invention relates to the treatment of arthritis and to pharmaceutical compositions and usages therefor. ... In general, the treatment of arthritic conditions has been limited to symptomatic treatment, for example to relieve symptoms such as inflammation and pain. Thus, for example, it has been proposed to use so-called nonsteroidal anti-inflammatory drug (NSAID's) in the treatment of arthritic conditions. It has also been proposed to use a variety of analgesics, including opioid analgesics, in the relief of pain in arthritic conditions. ... It has now been found, in accordance with the present invention, that the treatment of arthritic conditions with both (i) an NSAID, and (ii) an opioid analgesic can serve to treat the arthritic condition itself, that is to inhibit the arthritic process. Web site: http://www.delphion.com/details?pn=US05908848__
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Synthetic peptide for treatment of autoimmune arthritis Inventor(s): Myers; Linda K. (Memphis, TN), Seyer; Jerome M. (Memphis, TN), Kang; Andrew H. (Memphis, TN) Assignee(s): The University of Tennessee Research Corp. (Knoxville, TN) Patent Number: 6,423,315 Date filed: April 20, 1995
Patents 391
Abstract: Peptides that are capable of suppressing autoimmune arthritis are disclosed. The polypeptides described by the present invention which are capable of suppressing autoimmune arthritis in mammals include analogues of CII 245-270. The peptides do not provoke a material immunogenic response from T cells, and thus are useful therapeutic agents for suppressing autoimmune arthritis, rheumatoid arthritis, juvenile arthritis, psoriatic arthritis, spondylo arthritis, relapsing polychondritis and other connective tissue diseases. A method of surpressing autoimmune arthritis in mammals is also provided by the present invention. Excerpt(s): The present invention provides peptides for suppressing autoimmune arthritis that do not provoke a material immunogenic response from T cells. ... Autoimmune arthritis afflicts a large number of people and takes many forms including, rheumatoid arthritis, juvenile arthritis, psoriatic arthritis, spondylo arthritis, relapsing polychondritis and other connective tissue diseases. These arthritic conditions occur in mammals when T cells are activated by particular antigens or complexes containing antigens. When such activation occurs, proteolytic enzymes are produced which degrade tissues of the person or mammal afflicted by arthritis. The tissue targets of autoimmune arthritis are constituents of connective tissues in joints and tendons of mammals and ordinarily include type II collagen. Indeed autoimmune arthritis can be induced in mice, humans and other mammal by immunizing them with type collagen II derived from cartilage of the same or different mammals. See, Andriopoulos N A, Mestecky J. Miller E J, Bradley E L: Antibodies to native and denatured collagen in sera of patients with rheumatoid arthritis. Arth. Rheum. 19:613-617, 1976; Wooley P H, Luthra S. Singh S. Huse A, Stuart J M, David C S: Passive transfer of arthritis in mice by human anti-type II collagen antibody. Mayo Clinic Proc. 59:737-743, 1984. ... Autoimmune arthritis in mammals develops when T cells are activated by immunogenic complexes referred to as trimolecular complexes. These complexes are formed between antigenic peptides and major histocompatibility complex molecules (MHC). Buus, S., A. Sette, and H. M. Grey, (1987) "The interaction between protein-derived immunogenic peptides and Ia". Immuno. Rev. 98:115. These complexes then are recognized by the T cell receptors of antigen-specific T cells to form the tri-molecular complexes which result in the activation and subsequent functioning of T cells and in the development of arthritis. Web site: http://www.delphion.com/details?pn=US06423315__ ·
Therapeutic composition including plantain and aloe vera for treatment of arthritis and other afflictions Inventor(s): Sobczak; Nancy Laning (c/o Nancy Laning Sobczak Consulting, 2509 N. Humboldt, Milwaukee, WI 53212) Assignee(s): none reported Patent Number: 6,514,540 Date filed: September 6, 2001 Abstract: A therapeutic composition for treating arthritis and other afflictions includes plantain and aloe vera constituents, which are approximately 0.01% to 0.1% and 0.1% to 1.0% by weight of the therapeutic composition, respectively. Other constituents, such as herbal tinctures, added for various purposes, may be approximately 5% to 10% by weight of the therapeutic composition. A joint compatible solution for injection directly into a human joint makes up approximately 99 to 99.9% by weight of the plantain constituent, and approximately 90 to 99.9% by weight of the aloe vera constituent, with
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the remaining approximately 0.1 to 1.0% by weight of the plantain constituent being extract from a plantain plant and the remaining approximately 0.1 to 10.0% by weight of the aloe vera constituent being extract from an aloe vera plant. The plantain extract acts as a medication, while the aloe vera extract acts as a vehicle to carry the plantain extract. Excerpt(s): The present invention generally relates to compositions of matter and more particularly, to a therapeutic composition including plantain and aloe vera as its main ingredients in a particular percentage by weight arrangement with respect to each other in order for the therapeutic composition to be useful in the treatment and relief of the symptoms of arthritis and other afflictions. ... Plants and herbs have long been used for medicinal purposes. Indeed, native Americans have long known of the healing powers of certain herbs as remedies for various illnesses. However, much research still needs to be done in the area of herbal remedies and it is believed that present day healers have only begun to scratch the surface of the limitless possible cures offered by plants and herb. ... One recent inroad into herbal cures came with the discovery that aloe vera may be used as a biological vehicle for the delivery of drugs. U.S. Pat. No. 5,708,038 (the '038 patent) discloses an embodiment wherein aloe vera is used as a biological vehicle to deliver the estrogen, .beta.-estradiol and the androgen, testosterone propionate. The '038 patent also discloses a method of treating symptoms and diseases mediated by hormonal deficiencies or amenable to treatment by hormones using aloe vera as the biological vehicle for allowing penetration of drugs via a topical method. Web site: http://www.delphion.com/details?pn=US06514540__ ·
Therapeutic treatment of rheumatoid arthritis and polymyalgia rheumatica Inventor(s): Bennett; Robert M. (Portland, OR) Assignee(s): Research Corporation Technologies (DE) Patent Number: 5,965,520 Date filed: July 25, 1996 Abstract: Disclosed is a therapeutic regime for treating patients with rheumatoid arthritis (RA) Supplemental growth hormone is periodically administered to raise insulin-like growth factor 1 (IGF-1) levels, and the IGF-1 levels are monitored until they reach optimal levels and RA symptoms subside. Excerpt(s): The present invention relates to an effective treatment of the symptoms of rheumatoid arthritis and other rheumatic diseases. ... Several publications are referenced herein. The disclosures of these publications are hereby incorporated herein by reference in their entirety, unless otherwise noted. ... Fibromyalgia (FM) is a common rheumatic condition with core symptoms of musculoskeletal pain and fatigue (1,2). Specifically, FM is a group of common nonarticular rheumatic disorders characterized by achy pain, tenderness, and stiff muscles, tendon insertion areas and adjacent soft-tissue structures (47). Although patients with this condition are readily recognized, there is an ongoing controversy as whether it is or should be considered a distinctive pathophysiological entity (3). As most FM patients have multiple somatic complaints such as irritable bowel syndrome, unexplained paresthesia, cold intolerance, recurrent headaches and intermittent cognitive problems (4), it seems intuitively unlikely that a single etiologic mechanism is at play (5). Web site: http://www.delphion.com/details?pn=US05965520__
Patents 393
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Treating arthritis in animals with dietary supplements Inventor(s): Myers; Andrew (Boise, ID) Assignee(s): Nutri-Vet, LLC (Phoenix, AZ) Patent Number: 6,524,609 Date filed: August 18, 2000 Abstract: The invention is a dietary supplement for animals, especially dogs, for treating arthritis and joint discomfort. A biscuit form of the supplement may be in the form of a conventional carrier composition of, for example, typical dog biscuit materials including cereal grains, vegetables or animal meat, fat and by-products. Typically, the biscuit contains about 89-97 weight percent (wt. %) of the conventional carrier composition. Optional vitamins and minerals may also be added to the carrier material, typically in about the 1-5 wt. % range. Importantly, the biscuit of the present invention contains about 3-7 wt. % of an arthritis-treating combination, namely, glucosamine sulfate, vitamin C and an array of intracellular ions namely potassium, sodium and iodine. The glucosamine component is present by weight at approximately the same level as the vitamin C, and at approximately 10 (ten) times the level of the sum of the above-named intracellular ions. The biscuit is formulated so that its composition is approximately:Glucosamine component, 5 mg to 5,000 mg;Vitamin C component, 5 mg to 3,000 mg;Potassium component, 50 mcg to 150 mg;Sodium component, 50 mcg to 150 mg; andIodine component, 25 mcg to 100 mg.The biscuit is dosed at approximately 10 mg glucosamine component per pound of body weight of the animal per day. Excerpt(s): This invention relates generally to animals and animal nutrition. More specifically, this invention relates to treating arthritis and joint discomfort in dogs by use of dietary supplements. ... Degenerative joint diseases or arthroses are conditions where degenerative changes in cartilage lead to a breakdown in the integrity of the structural matrix of cartilage or tendinous tissues. Conventionally referred to as arthritis, the complaints associated with the degenerative changes occur most frequently in aged individuals. ... Arthritis is much more common in dogs than other domesticated pets. Arthritis is a terrible disease, as it causes pain and restricts mobility. Any dog can be afflicted with arthritis, although older dogs and larger breeds can be more susceptible. Active dogs, like work or hunting dogs, may also be at greater risk because of their increased activity levels. Web site: http://www.delphion.com/details?pn=US06524609__
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Treatment of arthritis Inventor(s): Geschickter; Charles F. (Lorton, VA) Assignee(s): Unimed, Inc. (Somerville, NJ) Patent Number: 4,468,393 Date filed: December 6, 1982 Abstract: Arthritis is treated by administration of azaspirane compounds, either germanium or silicon azaspirane compounds, preferably spirogermanium, most preferably dimethyl, diethyl, dipropyl or dibutyl. The diethyl or dibutyl are the most preferred. Excerpt(s): Aside from the treatment of the pain associated with arthritis, with pain relievers such as aspirin and the like, the most beneficial results obtained in the
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management of arthritis is with the use of cortisone. Cortisone has, however, many limitations in its use, and there is considerable research for other drugs to be used in the management of arthritis. ... U.S. Pat. No. 3,825,546 discloses a series of azaspiranes containing silicon or germanium in a ring, in connection with the treatment of cancer. ... Generally speaking, in accordance with the present invention, it has been discovered that certain specific compounds of U.S. Pat. No. 3,825,546, namely those which contain germanium in the ring, that is the spirogermaniums, particularly the dimethyl, diethyl, dipropyl and dibutyl spirogermaniums, including their acid addition salts and bisquaternary salts, can be used in the treatment of arthritis. Web site: http://www.delphion.com/details?pn=US04468393__ ·
Treatment of arthritis and allied conditions with xenylsalate Inventor(s): Karler; Arthur (Berkeley, CA) Assignee(s): Diagnostic Data, Inc. (Mountain View, CA) Patent Number: 4,073,897 Date filed: November 15, 1976 Abstract: Xenylsalate hydrochloride taken systemically, either orally or subcutaneously, has been found to be an effective relief for the symptoms of arthritis and allied conditions. Substantially no side effects have been noted. Excerpt(s): At the present time, the most popular treatment for the relief of arthritis is aspirin. Aspirin is not fully effective for this purpose and has undesirable side effects such as internal bleeding when taken in large doses or for long periods. The steroid drugs are also used but have a variety of side effects and can only be used under close medical supervision. Other drugs which have been proposed such as phenylbutazone, indomethacin and chloroquines are only partially effective and also have very serious side effects. ... Surprisingly, it has been found that xenylsalate has a pronounced antiinflammatory action as well as pain killing action when taken internally for the treatment of arthritis. ... Xenylsalate, sometimes known as biphenamine, diethylaminoethyl 2-hydroxy-3-phenyl-benzoate, was first synthesized in the 1930's. Although the free base may be used it is preferred to use the hydrochloride; the hydrochloride was employed in the clinical studies detailed later and is referred to as XCl. It has been shown to have a variety of mild biological properties. These properties were antifungal, antibacterial, anesthetic, and analgesic; xenylsalate also manifested a very low acute toxicity in laboratory rats by oral administration. The only actual use of the compound was as an antiseborrheic agent and this has been discontinued. Except for the determination of acute toxicity, all studies were restricted to topical use of comparatively dilute solutions and ointments, approximately 0.01% and 1% respectively. Web site: http://www.delphion.com/details?pn=US04073897__
Patents 395
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Treatment of arthritis and arthritic conditions with sulfites and bisulfites Inventor(s): Arias-Alvarez; Antonio J. (Carpatos, MX) Assignee(s): T & R Chemicals, Inc. (Clint, TX) Patent Number: 4,657,764 Date filed: May 8, 1984 Abstract: Sodium bisulfite useful to treat symptoms of arthritis and arthritic conditions in humans. Excerpt(s): Sodium bisulfite (usually shown by formula to be NaHSO.sub.3) has heretofore been used for many commercial purposes, as a preservative for prevention of the deterioration of liquids, such as food stuffs and pharmaceutical solids and solutions, and has been used medically externally for parasitic skin diseases and internally as a gastrointesinal antiseptic. ... The sodium bisulfite of commerce consists chiefly of sodium metabisulfite, Na.sub.2 S.sub.2 O.sub.5, and for purposes of this invention such is believed to possess the same properties as (and to be equivalent to) the true sodium bisulfite when dissolved in an aqueous solution. ... The use of sodium bisulfite and metabisulfite in the treatment of hypertension is described in my U.S. Pat. No. 4,327,083 and is also described as an antithrombotic agent useful for prolonging both prothrombin time (PT) and partial thromboplastin time (PTT) of blood or blood plasma in my U.S. Pat. No. 4,401,654. Web site: http://www.delphion.com/details?pn=US04657764__
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Treatment of arthritis and inflammation using N,N-dimethylglycine Inventor(s): Kendall; Roger V. (Williston, VT), Lawson; John W. (Clemson, SC) Assignee(s): Foodscience Corporation (Essex Junction, VT) Patent Number: 5,026,728 Date filed: October 5, 1989 Abstract: This invention relates to a method for treating arthritis and other systemic inflammatory conditions by treating the patient systemically with N,N-dimethylglycine. Excerpt(s): This invention relates to the use of N,N-dimethylglycine (DMG) to treat arthritis and inflammation in man or animals. ... Dimethylglycine is an intermediary metabolite and amino acid found in low levels in many foods, and is produced in the body from choline. DMG is an endogenous compound and an enzyme system in the body effectively converts the substance into metabolites that are either used by the body or are safely excreted from the body. ... A great deal of research has been carried out in recent years on the physiological effects of N,N-dimethylglycine. Web site: http://www.delphion.com/details?pn=US05026728__
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Treatment of arthritis and other similar conditions Inventor(s): Hull; Peter Hugh (19 Lawson Street Midge Point, Queensland 4799, AU) Assignee(s): none reported Patent Number: 6,395,313 Date filed: February 5, 2001 Abstract: Methods for treatment of arthritis are provided, the methods including administering an effective amount of Ngali Nut Oil. Excerpt(s): The invention relates to a method for treatment of the manifestations of arthritis and other similar conditions. ... Whilst the following discussion concerns the treatment and relief of the manifestations of arthritis, it is to be understood that the same principles apply to the treatment of the manifestations of rheumatism, tendinitis, spondylitis and similar degenerative joint disease. ... Rheumatism is a general term which refers to any pain or ache originating from the muscles, joints, bones or other parts of the musculoskeletal system. Many people have rheumatic pains which vary from day to day and sometimes with the weather. Often sufferers report that their manifestations are worse when the weather is damp and cold, although other sufferers report the opposite. The reasons for these fluctuations, and the precise source and mechanism of the pain is not known. Web site: http://www.delphion.com/details?pn=US06395313__
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Treatment of arthritis and substances for use in such treatment Inventor(s): Friedmann; Charles A. (Florence, IT) Assignee(s): Proter S.p.A. (Milan, IT) Patent Number: 4,244,968 Date filed: March 1, 1977 Abstract: 1,8-Dihydroxy and 1,8-diacetoxy anthraquinones and derivatives thereof are used to treat the symptoms of arthritis. Excerpt(s): This invention relates to the treatment of arthritis and to substances for use in such treatment. ... Arthritis, both rheumatoid and osteo, has been treated using antiinflammatory substances of the corticosteroid type, e.g. hydrocortisone, and betamethazone, which function by virtue of their anti-inflammatory action. ... Other compounds used in the treatment of arthritis include anti-inflammatory substances of a non-steroid type such as indomethacin, and ketobrufen and aspirin. These substances function symptomatically and prevent synthesis of prostaglandins, the pain causing agents, which are released by the arthritic process. Web site: http://www.delphion.com/details?pn=US04244968__
Patents 397
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Treatment of arthritis disorders, rheumatoid arthritis and manifestations associated with rheumatoid disorders Inventor(s): Snorrason; Ernir (Stigahlid 80, 105 Reykjavik, IS), Murray; James (Dorfet, GB) Assignee(s): Snorrason; Ernir (Reykjavik, IS) Patent Number: 6,358,941 Date filed: May 3, 1999 Abstract: The present invention relates to the use of pharmaceutically acceptable cholinesterase inhibitors for the preparation of a pharmaceutical composition for the treatment or prophylaxis of arthritic disorders, including osteoarthritis, rheumatoid arthritis and other rheumatoid diseases such as Juvenile Arthritis, Systemic Lupus Erythematosis, Sjogren's Syndrome, Progressive Systemic Sclerosis, Polymyositis, Dermatomyositis, Ankylosing Spondilitis, Reiter's Syndrome, Psoriatic Arthritis, Relapsing Polychondritis, Relapsing Panniculitis, Crohn's Disease, Ulcerative Colitis, Heredity Complement Deficiencies, Collagen Vascular Diseases, Felty's Syndrome, rheumatological manifestations associated with bacterial and viral endocarditis or myocarditis and other rheumatological manifestations such as anaemia of chronic disorders. The invention also relates to a novel method of treatment or prophylaxis of such diseases and manifestations. Preferably, the cholinesterase inhibitors are selected from a group of nicotinic acetylcholinesterase inhibitors such as galantamine (the name of this drug was previously spelled galanthamine). Excerpt(s): The present invention relates to the use of pharmaceutically acceptable cholinesterase inhibitors of the preparation of a pharmaceutical composition for the treatment or prophylaxis of arthritic disorders, including osteoarthritis, rheumatoid arthritis and other rheumatoid diseases such as Juvenile Arthritis, Systemic Lupus Erythematosis, Sjogren's Syndrome, Progressive Systemic Sclerosis, Polymyositis, Dermatomyositis, Ankylosing Spondilitis, Reiter's Syndrome, Psoriatic Arthritis, Relapsing Polychondritis, Relapsing Panniculitis, Crohn's Disease, Ulcerative Colitis, Hereditary Complement Deficiencies, Collagen Vascular Diseases, Felty's Syndrome, rheumatological manifestations associated with bacterial and viral endocarditis or myocarditis and other rheumatological manifestations such as anaemia of chronic disorders. The invention also relates to a novel method of treatment or prophylaxis of such diseases and manifestations. ... Preferably, the cholinesterase inhibitors are selected from a group of nicotinic acetylcholinesterase inhibitors such as galantamine (The name of this drug was previously spelled galanthamine). ... In the present description and claims, the term "rheumatoid" covers any of a variety of disorders marked by degeneration or metabolic derangement of the connective tissue structures of the body, especially the joints and related structures, including muscles, bursae (snyovial membranes), tendons and fibrous tissue. They are attended by pain, stiffness, or limitation of motion of these parts. Rheumatoid Arthritis is a chronic, recurrent systemic inflammatory disease primarily of the joints, usually polyarticular, marked by inflammatory changes in the snyovial membranes and articular structures and by atrophy and rarefaction of the bones. In late stages deformity and ankylosis develop. Extra-articular manifestations include vasculitis, atrophy of the skin and muscle, subcutaneous nodules, lymphadenopathy, splenomegaly, leukopaenia and often chronic anaemia. Web site: http://www.delphion.com/details?pn=US06358941__
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Treatment of arthritis using derivatives of porphorins Inventor(s): Aizawa; Katsuo (Yokohama, JP), Kuroiwa; Yukari (Urawa, JP) Assignee(s): Nippon Petrochemicals Company, Limited (Tokyo, JP) Patent Number: 5,430,051 Date filed: April 19, 1994 Abstract: A method for the photodynamic therapy of rheumatoid arthritis of mammals, which agent comprises at least one member of fluorescent compounds selected from the group consisting of tetrapyrrole carboxylic acids having at least one carboxyl group, corresponding di- or tetrahydrotetrapyrrole carboxylic acids, and mono-, di- or polyamides of the tetrapyrrole carboxylic acids with amino-mono- or dicarboxylic acids and their salts. Excerpt(s): This invention relates to a method and medical agents for the photodynamic diagnosis and photodynamic therapy of the arthritis, especially the arthritis of mammals. More particularly, the medical agents used in the present invention belong to specific fluorescent compounds having a tetrapyrrole skeletal structure. When an effective quantity of the medical agent is administered to an animal patient, the agent is accumulated in the affected part of the body. ... When light rays of necessary wavelength are applied to an affected joint to be diagnosed or treated, the agent generates fluorescence in the affected portion, thereby enabling the detection of arthritis. This is called as photodynamic diagnosis. In the therapeutic treatment, when light rays of appropriate wavelength and intensity are applied to a lesion, the agent is excited to produce a cytotoxic effect and the affected cells in arthritic lesion are necrosed. This is called as photodynamic therapy. The present invention relates to the diagnosis and the therapy of this kind applied to arthritis, especially rheumatoid arthritis. ... Rheumatoid arthritis is a chronic systemic disease mainly causing to occur potyarthritis as a cardinal symptom. This disease is initiated by the pain and swelling in small joints of hands and feet, or in elbow joints and knee joints, and other joints in whole body are then affected little by little. In the initial phase of the disease, the hyperplasia of the synovia of the affected joint begins by some stimulation of the unknown antigen, and the synovial hyperplasia is maintained and prolonged by the monokine cascade system to be a tumor-like condition. The constituents of the joint such as cartilage or ligament or bone are destroyed by the enzymes produced by these synovia and followed by the destruction of the joints. Web site: http://www.delphion.com/details?pn=US05430051__
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Treatment of arthritis with bisulfite Inventor(s): Arias-Alvarez; Jose A. (Carpatos, MX) Assignee(s): T&R Chemicals, Inc. (Clint, TX) Patent Number: 4,462,988 Date filed: May 26, 1983 Abstract: The treatment of arthritis with sulfites and bisulfites. Excerpt(s): Sodium bisulfite (usually shown by formula to be NaHSO.sub.3) has heretofore been used for many commercial purposes, such as a preservative for prevention of the deterioration of liquids, such as food stuffs and pharmaceutical solids and solutions, and has been used medically externally for parasitic skin diseases and
Patents 399
internally as a gastrointestinal antiseptic. ... The sodium bisulfite of commerce consists chiefly of sodium metabisulfite, Na.sub.2 S.sub.2 O.sub.5, and for purposes of this invention such is believed to possess the same properties as (and to be equivalent to) the true sodium bisulfite when dissolved in an aqueous solution. ... The use of sodium bisulfite and metabisulfite in the treatment of hypertension is described in my U.S. Pat. No. 4,327,083 and is also described as an antithrombotic agent useful for prolonging both prothrombin time (PT) and partial thromboplastin time (PTT) of blood or blood plasma in my copending application Ser. No. 281,951 filed July 9, 1981, now U.S. Pat. No. 4,401,654. Web site: http://www.delphion.com/details?pn=US04462988__ ·
Treatment of arthritis, including rheumatoid arthritis with .sup.166 Holmium radionuclide Inventor(s): Lieberman; Ephraim (Suffern, NY), Bordoni; Maurice (Westtown, NY), Thornton; Alfred (New Hampton, NY) Assignee(s): Cadema Medical Products, Inc. (Middletown, NY) Patent Number: 4,849,209 Date filed: January 28, 1987 Abstract: .sup.1/3 Holmium in a carrier metallic hydroxide aggregate is disclosed for the treatment of arthritis and, in particular, rheumatoid arthritis. The compound disclosed preferably has a particle size of 1 to 40 microns, Beta energy emissions in the range of 1.76-1.84 MeV, low levels of gamma ray emissions and a radioactive half-life of 26.8 hours. The preferred metallic hydroxide is selected from the group consisting of Ferric Hydroxide, Aluminum Hydroxide, Bismuth Hydroxide, Chromium Hydroxide, Cupric Hydroxide, Manganese Hydroxide and Stannous Hydroxide. Methods are also disclosed for the preparation of the compound, as well as for the methods of its administration to a patient in need thereof. Excerpt(s): The present invention relates to radioactive compounds, methods for the preparation thereof and a method for the treatment of arthritis, including rheumatoid arthritis. ... Arthritic disorders are the second leading cause of losses in time and earnings in the United States. Approximately six million of all arthritis sufferers are afflicted rheumatoid arthritis. Of these, over fifty percent (50%) ultimately will have involvement of the knee joint, over eighty percent (80%) will involve the hand joint and somewhat smaller percentages will have involvement of other joints such as the ankle, elbow and shoulder. ... Rheumatoid arthritis is believed to be an autoimmune disease wherein parts of the body are attacked by antibodies manufactured in the body. These antibodies may be produced in response to viruses present in the body. While the mechanism for rheumatoid arthritis is not defined, it is a systemic disease. When the disease is active, the erythrocyte sedimentation rate (ESR) is elevated and the blood tests positive for rheumatoid factor. Web site: http://www.delphion.com/details?pn=US04849209__
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Treatment of arthritis, including rheumatoid arthritis, with radioactive isotopes Inventor(s): Lieberman; Ephraim (Suffern, NY), Bordoni; Maurice E. (Westtown, NY), Thornton; Alfred K. (New Hampton, NY) Assignee(s): Cadema Medical Products, Inc. (Middletown, NY) Patent Number: 4,752,464 Date filed: June 7, 1985 Abstract: Treatment of rheumatoid arthritis by administering a radioactive compound to the inflamed synovium of the articular joint. The compound comprises an aggregate suspension having a radionuclide entrapped therein. The aggregate suspension is a ferric or aluminum hydroxide aggregate, and the radionuclide is selected from the group consisting of .sup.166 Holmium, .sup.153 Samarium, .sup.175 Ytterbium, .sup.169 Erbium, and .sup.176m Lutetium. The radionculide may also consist of .sup.51 Chromium. Suitable leakage inhibitors or agents to reduce leakage of the radionuclide from the articular joint is included as part of the chemical composition of the final drug form. Excerpt(s): The present invention relates to a radioactive compound, the methods for the preparation thereof and a method for the treatment of arthritis and, more particularly, radioactive compounds and a method for the treatment of rheumatoid arthritis. ... Arthritic disorders are the second leading cause of losses in time and earnings in the United States. Approximately nine percent (9%) of all arthritis sufferers are afflicted with a type of arthritis known as rheumatoid arthritis. Of these, approximately fifty-six percent (56%) ultimately will have involvement of the knee joint, eighty-seven percent (87%) of the hand joint and somewhat smaller percentages will have involvement of other joints such as the ankle, elbow and shoulder. ... The source of disability for the sufferer of rheumatoid arthritis is an inflammatory response, of unknown origin, in the synovium, or lining, of the afflicted joint. This chronic inflammation, or synovitis, leads to pannus formation and, eventually, enzymatic destruction of the joint cartilage. Web site: http://www.delphion.com/details?pn=US04752464__
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Treatment of arthritis, including rheumatoid arthritis, with the radionuclide, tin SN121 Inventor(s): Lieberman; Ephraim (1 Victory Rd., Suffern, NY 10901), Bordoni; Maurice E. (R.D. 1, Box 680, Westtown, NY 10998), Thornton; Alfred K. (Box 500 Lower Rd., New Hampton, NY 10958) Assignee(s): none reported Patent Number: 4,906,450 Date filed: March 26, 1987 Abstract: The radionuclide Tin, Sn-121 in a carrier hydroxide aggregate is disclosed for the treatment of arthritis and, in particular, rheumatoid arthritis of the hands, the interphalangeal joints of the fingers and the metacarpal joints of the hand.The radioactive compound disclosed preferably has a particle size of <90 microns. The beta energy emission associated with Tin, Sn-121 has an energy of 0.38 meV. There are no gamma photons emited during the decay of Tin, Sn-121 to stable Antimony Sb-121. The half life of Tin, Sn-121 is 27.06 hours.The method of preparation of the compound is disclosed along with the method of administration to the patient in need thereof.
Patents 401
Excerpt(s): The present invention relates to the use of a compound, radioactive Tin, Sn121, for treating arthritis, in particular rheumatoid arthritis of the fingers (interphalangeal joints and the metacarpal joints of the hand). ... Methods for the preparation of the compound are described. ... Arthritic disorders are the second leading cause of losses in time and earnings in the United States. Approximately six million (6,000,000) people are afflicted with rheumatoid arthritis. Of these, over eighty percent (80%) ultimately will have involvement of the hand joint, over fifty percent (50%) will involve the knee joint, and somewhat smaller percentages will have involvement of other joints such as the ankle, elbow, and shoulder. Rheumatoid arthritis is believed to be an autoimmune disease wherein parts of the body are attacked by antibodies manufactured in the body. These antibodies may be produced in response to viruses present in the body. While the mechanism for rheumatoid arthritis is not known, it is a systemic disease. When the disease is active, the erythrocyte sedimentation rate (ESR) is usually elevated and the blood tests usually positive for rheumatoid factor. Web site: http://www.delphion.com/details?pn=US04906450__ ·
Treatment of autoimmune diseases such as rheumatoid arthritis with suppressor factor Inventor(s): Lau; Catherine Y. (Unionville, CA) Assignee(s): Ortho Pharmaceutical (Canada) Ltd. (CA) Patent Number: 4,705,687 Date filed: June 17, 1985 Abstract: Method of treating autoimmune diseases such as rheumatoid arthritis by administration of a suppressor factor obtained in the supernatant of a human cell line. A particular human cell line is CEM which has survived treatment with 6-thioguanine. Excerpt(s): The mammalian immune system includes a complex array of organs, cells and soluble products of cells. Organs involved in the immune system include the bone marrow, spleen and lymph nodes; a wide variety of cells populate the immune system and this includes macrophages, granulocytes and T and B lymphocytes. Examples of soluble products produced by immune system cells include antibodies (produced by B lymphocytes) and lymphokines (produced by T-lymphocytes). The latter play an important role in regulating the immune system. ... (a) identification of substances or cells within the body to determine whether they are "self" or "non-self". ... (b) communication between cells to facilitate a response to "non-self" entities. Web site: http://www.delphion.com/details?pn=US04705687__
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Treatment of rheumatoid arthritis and related diseases Inventor(s): Wyburn-Mason; Roger (Richmond Surrey, GB2) Assignee(s): Simoons; John R. A. (Summit, NJ) Patent Number: 4,119,723 Date filed: July 8, 1977 Abstract: It is believed that rheumatoid arthritis and related collagen and auto-immune diseases are an infection and that various species of free-living (limax) amoebae are the aetiological agent of these diseases. It has been discovered that tinidazole and related
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compounds, antimycotic drugs with anti-protozoal activity, are effective for the treatment of rheumatoid arthritis and other collagen and auto-immune (rheumatoid) diseases. Excerpt(s): Men and other animals are continually exposed to infection and re-infection by various species and strains of free-living limax amoebae which can be detected in the faeces, nasopharynx and bronchi. In all parts of the world they form part of the environment. Experimentally in animals they induce changes like those of collagen and auto-immune diseases and are characterized by vasculitis, myosotis, hepatitis, pyelitis and spelenomegaly. They can often be seen in the tissues of animals. Such animals shown lymphadenopathy with an appearance like that of human Hodgkin's disease or a state like that of advanced malignant disease. These organisms may also be recovered from all the tissues of cases of collagen and auto-immune diseases and from human and many animal tumors and may also occur in the tissues of apparently healthy individuals. They cannot be identified in ordinary histological sections, but can be demonstrated by immunofluorescent methods. ... The definite cause of rheumatoid arthritis is presently unknown. Rheumatoid arthritis is a crippling disease, characterized by the inflammation of several joints of the body, with swelling, pain and stiffness. Rheumatoid arthritis is a disorder that afflicts about fifteen million people in the Western World alone. Successful early treatment may avert the destructive, deforming phase of the disease. Therapy has been directed largely at non-specific suppression of inflammatory and immunoligic processes. Aspirin is the cornerstone of therapy for rheumatoid arthritis and can reduce synovial inflammation, improve function and reduce pain in a majority of patients in view of its analgesic action. Widespread interest in rheumatoid arthritis arose when Hench (1949) introduced the use of cortisone in treatment. Chemical compounds which have been commonly used in treating rheumatoid arthritis are corticosteroids, gold salts, antimalarial drugs, immunosuppressive agents and a whole range of so-called non-steroidal drugs, e.g. indomethacin, phenylacetic acid (Ibuprofen), propionic acid (Naproxen) and DPenicillamine. Most of these drugs bring temporary relief to the arthritic patient but present the danger of side effects and the physician has to balance the potential benefit against the risks. However, arthritis reoccurs following withdrawal of such chemical treatment. For many years rheumatoid arthritis was considered to be an infection (Hollander et al., 1960; Robinson, 1967), but with the advent of the concept of autoimmunity this idea lost favor. Such a view has recently been revived (Lancet, 1970, 2, 303) and is supported by many observations. It is highly likely that the limax amoebae, found in all the collagen and auto-immune diseases, may well be the aetiological agent of these conditions and that anti-protozoal drugs may help by their action on these organisms. ... The use of a bis-phenyl (2-halophenyl)-1-imidazolylmethane and clotrimazole for treatment of Rheumatoid Arthritis is disclosed in my U.S. patent application Ser. No. 700,914 filed June 29, 1976. It has also been suggested to use a nitroimidazole in the treatment of rheumatoid arthritis in the Journal of Tropical Medicine and Hygiene (vol. 75) pgs. 64 to 66 March 1972. It is believed that the nitro group in the imidazole ring is related to metronidiazole which is not effective in the treatment of rheumatoid arthritis. Web site: http://www.delphion.com/details?pn=US04119723__
Patents 403
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Treatment of rheumatoid arthritis and related diseases Inventor(s): Wyburn-Mason; Roger (Richmond, GB2) Assignee(s): Simoons; John R. A. (Summit, NJ) Patent Number: 4,183,941 Date filed: August 21, 1978 Abstract: It is believed that rheumatoid arthritis and related collagen and auto-immune diseases are an infection and that various species of free-living (limax) amoebae are the aetiological agent of these diseases. It has been discovered that certain nitroimidazole compounds, anti-mycotic drugs with anti-protozoal activity, are effective for the treatment of rheumatoid arthritis and other collagen and auto-immune (rheumatoid) diseases. Excerpt(s): Men and other animals are continually exposed to infections and re-infection by various species and strains of free-living limax amoebae which can be detected in the faeces, nasopharynx and bronchi. In all parts of the world they form part of the environment. Experimentally in animals they induce changes like those of collagen and auto-immune diseases and are characterized by vasculitis, myositis, hepatitis, pyelitis and splenomegaly. They can often be seen in the tissues of animals. Such animals show lymphadenopathy with the appearance like that of human Hodgkin's disease or a state like that of advanced malignant disease. These organism may also be recovered from all the tissues of cases of collagen and auto-immune diseases and from human and many animal tumors and may also occur in the tissues of apparently healthy individuals. They cannot be identified in ordinary sections, but can be demonstrated by immunofluorescent methods. ... The definite cause of rheumatoid arthritis is presently unknown. Rheumatoid arthritis is a crippling disease, characterized by the inflammation of several joints of the body, with swelling, pain and stiffness. Rheumatoid arthritis is a disorder that afflicts about fifteen million people in the Western World alone. Successful early treatment may avert the destructive, deforming phase of the disease. Therapy has been directed largely at non-specific suppression of inflammatory and immunologic processes. Aspirin is the cornerstone of therapy for rheumatoid arthritis and can reduce pain in a majority of patients in view of its analgesic action. Widespread interest in rheumatoid arthritis arose when Hench (1949) introduced cortisone in treatment. Chemical compounds which have been commonly used in treating rheumatoid arthritis are corticosteroids, gold salts, anti-malarial drugs, immunosuppressive agents and a whole range of so-called non-steroidal drugs, e.g. indomethacin, phenylacetic acid (Ibuprofen), propionic acid (Naproxen) and DPenicillamine. Most of these drugs being temporary relief to the arthritic patient but present the danger of side effects and the physician has to balance the potential benefit against the risks. However, arthritis reoccurs following withdrawal of such chemical treatment. For many years rheumatoid arthritis was considered to be an infection (Hollander et al., 1960; Robinson, 1967), but with the advent of the concept of autoimmunity this idea lost favor. Such a view has recently been revived (Lancet, 1970, 2, 303) and is supported by many observations. It is highly likely that the limax amoebae, found in all the collagen and auto-immune diseases, may well be the aetiological agent of these conditions and that anti-protozoal drugs may help by their action on these organisms. ... The use of a bis-phenyl (2-halophenyl)-1-imidazolylmethane (e.g. clotrimazole) for the treatment of rheumatoid arthritis is disclosed in my U.S. Pat. No. 4,073,922 issued on Feb. 14, 1978. The use of tinidazole and related compounds is disclosed in my U.S. patent application Ser. No. 813,922, filed July 8, 1977, now U.S. Pat. No. 4,119,723. It has also been suggested to use a nitroimidazole derivative in the
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treatment of rheumatoid arthritis in the Journal of Tropical Medicine and Hygiene v. 75, p. 64 to 66, Mar. 1972. Web site: http://www.delphion.com/details?pn=US04183941__ ·
Treatment of rheumatoid arthritis and related diseases Inventor(s): Wyburn-Mason; Roger (Richmond, GB2) Assignee(s): Simoons; John R. A. (Summit, NJ) Patent Number: 4,218,449 Date filed: March 8, 1979 Abstract: It is believed that rheumatoid arthritis and related collagen and auto-immune diseases are an infection and that various species of free-living (limax) amoebae are the aetiological agent of these diseases. It has been discovered that certain nitroimidazole compounds, anti-mycotic drugs with anti-protozoal activity, are effective for the treatment of rheumatoid arthritis and other collagen and auto-immune (rheumatoid) diseases. Excerpt(s): Men and other animals are continually exposed to infections and re-infection by various species and strains of free-living limax amoebae which can be detected in the faeces, nasopharynx and bronchi. In all parts of the world they form part of the environment. Experimentally in animals they induce changes like those of collagen and auto-immune diseases and are characterized by vasculitis, myositis, hepatitis, pyelitis and splenomegaly. They can often be seen in the tissues of animals. Such animals show lymphadenopathy with the appearance like that of human Hodgkin's disease or a state like that of advanced malignant disease. These organism may also be recovered from all the tissues of cases of collagen and auto-immune diseases and from human and many animal tumors and may also occur in the tissues of apparently healthy individuals. They cannot be identified in ordinary sections, but can be demonstrated by immunofluorescent methods. ... The definite cause of rheumatoid arthritis is presently unknown. Rheumatoid arthritis is a crippling disease, characterized by the inflammation of several joints of the body, with swelling, pain and stiffness. Rheumatoid arthritis is a disorder that afflicts about fifteen million people in the Western World alone. Successful early treatment may avert the destructive, deforming phase of the disease. Therapy has been directed largely at non-specific suppression of inflammatory and immunologic processes. Aspirin is the cornerstone of therapy for rheumatoid arthritis and can reduce pain in a majority of patients in view of its analgesic action. Widespread interest in rheumatoid arthritis arose when Hench (1949) introduced cortisone in treatment. Chemical compounds which have been commonly used in treating rheumatoid arthritis are corticosteroids, gold salts, antimalarial drugs, immunosuppressive agents and a whole range of so-called non-steroidal drugs, e.g. indomethacin, phenylacetic acid (Ibuprofen), propionic acid (Naproxen) and DPenicillamine. Most of these drugs bring temporary relief to the arthritic patient but present the danger of side effects and the physican has to balance the potential benefit against the risks. However, arthritis reoccurs following withdrawal of such chemical treatment. For many years rheumatoid arthritis was considered to be an infection (Hollander et al., 1960; Robinson, 1967), but with the advent of the concept of autoimmunity this idea lost favor. Such a view has recently been revived (Lancet, 1970, 2, 303) and is supported by many observations. It is highly likely that the limax amoebae, found in all the collagen and auto-immune diseases, may well be the aetiological agent of these conditions and that anti-protozoal drugs may help by their action on these
Patents 405
organisms. ... The use of a bis-phenyl (2-halophenyl)-1-imidazolylmethane (e.g. clotrimazole) for the treatment of rheumatoid arthritis is disclosed in my U.S. Pat. No. 4,073,922 issued on Feb. 14, 1978. The use of tinidazole and related compounds is disclosed in my U.S. patent application Ser. No. 813,922, filed July 8, 1977. It has also been suggested to use a nitroimidazole derivative in the treatment of rheumatoid arthritis in the Journal of Tropical Medicine and Hygiene v. 75, p. 64 to 66, March 1972. Web site: http://www.delphion.com/details?pn=US04218449__ ·
Treatment of rheumatoid arthritis and related diseases Inventor(s): Wyburn-Mason; Roger (Richmond, GB2) Assignee(s): Simoons; John R. A. (Durham, NC) Patent Number: 4,402,965 Date filed: August 5, 1982 Abstract: It is believed that rheumatoid arthritis and related collagen and auto-immune diseases are an infection and that various species of free-living (limax) amoebae are the aetiological agent of these diseases. It has been discovered that furazolidone is effective for the treatment of rheumatoid arthritis and other collagen and auto-immune (rheumatoid) diseases. Excerpt(s): Men and other animals are continually exposed to infection and re-infection by various species and strains of free-living limax amoebae which can be detected in the faeces, nasopharnyx and bronchi. In all parts of the world they form part of the environment. Experimentally in animals they induce changes like those of collagen and autoimmune diseases and are characterized by vasculities, myosotis hepatitis, pyelitis and splenomegaly. They can often be seen in the tissues of animals. Such animals shown lymphadenopathy with an appearance like that of human Hodgkin's disease or a state like that of advance malignant disease. These organisms may also be recovered from all the tissues of cases of collagen and auto-immune diseases and from human and many animal tumors and may also occur in the tissues of apparently healthy individuals. They cannot be identified in ordinary histological sections, but can be demonstrated by immunofluoresence methods. ... The definite cause of rheumatoid arthritis is presently unknown. Rheumatoid arthritis is a crippling disease involving any tissue including inflammation of several joints of the body, with swelling, pain and stiffness. Rheumatoid arthritis is a disorder that afflicts about fifteen million people in the United States alone. Successful early treatment may avert the destructive, deforming phase of the disease. Therapy has been directed largely at non-specific suppression of inflammatory and immunologic processes. Aspirin is the cornerstone of therapy for rheumatoid arthritis and can reduce synovial inflammation, improve function and reduce pain in a majority of patients in view of its analgesic action. Widespread interest in rheumatoid arthritis arose when Hench (1949) introduced the use of cortisone in treatment. Chemical compounds which have been commonly used in treating rheumatoid arthritis are corticosteroids, gold salts, antimalarial drugs, immunosuppressive agents and a whole range of so-called non-steroidal drugs, e.g. indomethacin, phenylacetic acid (Ibuprofen), propionic acid (Naproxen) and DPenicillamine. Most of these drugs bring temporary relief to the arthritic patient but present the danger of side effects and the physician has to balance the potential benefit against the risks. However, arthritis reoccurs following withdrawal of such chemical treatment. For many years rheumatoid arthritis was considered to be an infection (Hollander et al., 1960; Robinson, 1967), but with the advent of the concept of auto-
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immunity this idea lost favor. Such a view has recently been revived (Lancet, 1970, 2, 303) and is supported by many observations. It is highly likely that the limax amoebae, found in all the collagen and auto-immune diseases, may well be the aetiological agent of these conditions and that antiprotozoal drugs may help by their action on these organisms. The term rheumatoid arthitis and related diseases is to be understood to include diseases such as lupus erythematosis, scleroderma, psoriasis, dermatomyositis, polymyositis, periartheritis nodosa, chronic ulcerative colitis, Still's disease. ... The use of a bis-phenyl(2-halophenyl)-1-imidazolylmethane or clotrimazole for treatment of Rheumatoid Arthritis is disclosed in my U.S. patent application Ser. No. 700,914 filed June 29, 1976 now U.S. Pat. No. 4,073,922, issued Feb. 14, 1978, and the use of tinidazole is disclosed in my U.S. Pat. No. 4,119,723. It has also been suggested to use a nitroimidazole in the treatment of rheumatoid arthritis in the Journal of Tropical Medicine and Hygiene (Vol. 75) pags. 64 to 66 March 1972. It is believed that the nitro group in the imidazole ring is related to metronidiazole which is not effective in the treatment of rheumatoid arthritis in small doses. Web site: http://www.delphion.com/details?pn=US04402965__ ·
Treatment of rheumatoid arthritis and related diseases Inventor(s): Wyburn-Mason; Roger (Richmond, GB2) Assignee(s): Simoons; John R. A. (Durham, NC) Patent Number: 4,426,384 Date filed: August 5, 1982 Abstract: It is believed that rheumatoid arthritis and related collagen and auto-immune diseases are an infection and that various species of free-living (limax) amoebae are the aetiological agent of these diseases. It has been discovered that pyrimidines with antiprotozoal activity, are effective for the treatment of rheumatoid arthritis and other collagen and auto-immune (rheumatoid) diseases. Excerpt(s): Men and other animals are continually exposed to infection and re-infection by various species and strains of free-living limax amoebae which can be detected in the faeces, nasopharynx and bronchi. In all parts of the world they form part of the environment. Experimentally in animals they induce changes like those of collagen and auto-immune diseases and are characterized by vasculitis, myosotis hepatitis, pyelitis and splenomegaly. They can often be seen in the tissues of animals. Such animals shown lymphadenopathy with an appearance like that of human Hodgkin's disease or a state like that of advance malignant disease. These organisms may also be recovered from all the tissues of cases of collagen and auto-immune diseases and from human and many animal tumors and may also occur in the tissues of apparently healthy individuals. They cannot be identified in ordinary histological sections, but can be demonstrated by immunofluoresence methods. ... The definite cause of rheumatoid arthritis is presently unknown. Rheumatoid arthritis is a crippling disease involving any tissue including inflammation of several joints of the body, with swelling, pain and stiffness. Rheumatoid arthritis is a disorder that afflicts about fifteen million people in the United States alone. Successful early treatment may avert the destructive, deforming phase of the disease. Therapy has been directed largely at non-specific suppression of inflammatory and immunologic processes. Aspirin is the cornerstone of therapy for rheumatoid arthritis and can reduce synovial inflammation, improve function and reduce pain in a majority of patients in view of its analgesic action. Widespread interest in rheumatoid arthritis arose when Hench (1949) introduced the use of cortisone in
Patents 407
treatment. Chemical compounds which have been commonly used in treating rheumatoid arthritis are corticosteroids, gold salts, antimalarial drugs, immunosuppressive agents and a whole range of so-called non-steroidal drugs, e.g. indomethacin, phenylacetic acid (Ibuprofen), propionic acid (Naproxen) and DPenicillamine. Most of these drugs bring temporary relief to the arthritic patient but present the danger of side effects and the physician has to balance the potential benefit against the risks. However, arthritis reoccurs following withdrawal of such chemical treatment. For many years rheumatoid arthritis was considered to be an infection (Hollander et al., 1960; Robinson, 1967), but with the advent of the concept of autoimmunity this idea lost favor. Such a view has recently been revived (Lancet, 1970, 2, 303) and is supported by many observations. It is highly likely that the limax amoebae, found in all the collagen and auto-immune diseases, may well be the aetiological agent of these conditions and that antiprotozoal drugs may help by their action on these organisms. The term rheumatoid arthritis and related diseases is to be understood to include diseases such as lupus erythematosis scleroderma, psoriasis, dermatomyositis, polymyositis. periartheritis nodosa. chronic ulcerative colitis, Still's disease. ... The use of a bis-phenyl (2-halophenyl)-1-imidazolylmethane or clotrimazole for treatment of Rheumatoid Arthritis is disclosed in my U.S. patent application Ser. No. 700,914 filed June 29, 1976 now U.S. Pat. No. 4,073,922, issued Feb. 14, 1978, and the use of tinidazole is disclosed in my U.S. Pat. No 4,119,723. It has also been suggested to use a nitroimidazole in the treatment of rheumatoid arthritis in the Journal of Tropical Medicine and Hygiene (Vol. 75) pags. 64 to 66 March 1972. It is believed that the nitro group in the imidazole ring is related to metronidiazole which is not effective in the treatment of rheumatoid arthritis in small doses. Various other anti-protozoal drugs were tried on the cases of rheumatoid disease or of various localized manifastations of this. The substances investigated were 4-aminoquinolines (chloroquine), hydroxychloroquine (plaquenil), amodiaquine (camoquin); copper sulphate; bile salts (dehydrocholine), which are effective in killing the trophozooites of many amoebae in the concentration found in the small intestine; and clotrimazole (canesten). All of these were actually shown experimentally to kill limax amoebae. In addition, other antiprotozoal drugs were also investigated. They included suramin, pentamidine, dehydroemetine (DHE or mebadin), metronidazole (flagyl), nimorazole (naxogin (Erba)), phanquone (entobex) and diloxanide (furamide). Web site: http://www.delphion.com/details?pn=US04426384__ ·
Treatment of rheumatoid arthritis by oral administration of pooled human immunoglobulin Inventor(s): Weisbart; Richard (Los Angeles, CA) Assignee(s): Research Corporation Technologies, Inc. (Tucson, AZ) Patent Number: 6,090,380 Date filed: May 22, 1995 Abstract: Pooled human immunoglobulin may be administered orally to rheumatoid arthritis patients to treat the rheumatoid arthritic condition of those patients. Oral administration of pooled human immunoglobulin can result in significant clinical improvement in the level of disease activity in patients with rheumatoid arthritis. Excerpt(s): The present invention relates generally to the treatment of rheumatoid arthritis. More particularly, the invention relates to the treatment of rheumatoid arthritis by oral administration of pooled human immunoglobulin. ... The publications and other
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reference materials referred to herein to describe the background of the invention and to provide additional detail regarding its practice are hereby incorporated by reference. ... Rheumatoid arthritis ("rheumatoid arthritis") is a systematic inflammatory disease that commonly affects the joints, particularly those of the hands and feet. The onset of rheumatoid arthritis can occur slowly, ranging from a few weeks to a few months, or the condition can surface rapidly in an acute manner. Web site: http://www.delphion.com/details?pn=US06090380__ ·
Treatment of the articular symptoms of rheumatoid arthritis Inventor(s): Cagnoni; Mario (178, Via Bolognese, 50139 Firenze, IT) Assignee(s): none reported Patent Number: 5,609,877 Date filed: November 30, 1994 Abstract: The present invention relates to the employment of melatonin in the preparation and use of pharmaceuticals effective in the treatment of the articular symptoms of rheumatoid arthritis. Excerpt(s): The present invention concerns the field of rheumatology and more precisely relates to the use of melatonin (MLT) in the treatment of articular inflammatory symptoms. ... The most common of the diseases characterized by acute and chronic inflammation of the joints is rheumatoid arthritis. As regards its etiology, none of the hypotheses proposed over time has ever found persuasive confirmation. Recently the etiopathogenetic hypothesis according to which the disease can be ascribed to the group of forms of hypersensitivity (the immune theory) has won the greatest agreement. ... In the therapy of this disease, pharmaceuticals of various types are used with the object of controlling the inflammatory process and also to remedy the damage that the inflammatory process itself caused to the osteocartilaginous structures. Among these we have gold salts, antimalarials, penicillamine, and furthermore all the analgesic and steroid and nonsteroid anti-inflammatory pharmaceuticals. In particular, the symptomatic therapy is carried out by resorting to antiphlogistic drugs (nonsteroidal anti-inflammatory agents and cortisone compounds) and the base therapy using synthesized antimalarials, penicillamine, azathioprine, cyclophosphamide, gold salts, etc. Web site: http://www.delphion.com/details?pn=US05609877__
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Treatments for arthritis and cast dermatitis Inventor(s): Hosick; Thomas A. (Box PMB 12-8, Atlanta, GA 30315) Assignee(s): none reported Patent Number: 4,120,976 Date filed: December 13, 1977 Abstract: This invention relates to treatments for arthritis and cast dermatitis by the administration to patients of 3,4-methylenedioxyamphetamine and its non-toxic addition salts.
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Excerpt(s): Arthritis is a series of degenerative diseases of the joints. Some of the diseases are of inflammatory etiology, such as rheumatoid arthritis and juvenile rheumatoid arthritis, and others are noninflammatory in nature, such as osteoarthritis. Two types of osteoarthritis are: (1) geriatric osteoarthritis (generally occurring in older persons), and (2) post-traumatic osteoarthritis (resulting from joint fractures and other injuries). Arthritis is characterized by pain and swelling of the joints, which may lead to increasing immobility thereof. The disease may finally lead to deformity and ankylosis, the fusing of the bones of the joint together through unnatural boney growth, permanently and totally immobilizing the joint with resulting crippling of the subject. ... Millions of people throughout the world suffer daily with the pain and discomfort of arthritis and it is the world's leading crippling disease and can affect both young and old. The cause is unknown, but autoimmune mechanisms and virus infections have been postulated. Various therapeutic agents have been prescribed and administered by medical professionals in an effort to curb the effects of arthritis, such as aspirin, cortisone, adrenocorticotropic hormone (ACTH), gold salts, and indomethacin, but all have met with limited success. ... With this background in mind, the present invention is presented and one of its objectives is to provide a better treatment for the effects of arthritis. Web site: http://www.delphion.com/details?pn=US04120976__ ·
Use of 6-halo-4-quinolone compounds and pharmaceutical compositions thereof for the preparation of a medicament for the therapeutical application in rheumatoid arthritis Inventor(s): Caruso; Innocenzo (Via Wittgens, 5, 20100 Milan, IT) Assignee(s): none reported Patent Number: 4,978,661 Date filed: August 11, 1989 Abstract: The present invention relates to the use of 6-halo-4-quinolone derivatives and pharmaceutical compositions comprising them as active ingredient, for the preparation of a medicament for the therapeutical application in rheumatoid arthritis.Quinolone derivatives can be intra-articularly administered and act on different points of the pathological process of rheumathoid arthritis without local and general toxicity. Excerpt(s): The present invention relates to the use of 6-halo-4-quinolone compounds and to pharmaceutical compositions thereof for the preparation of a medicament useful in therapy of rheumatoid arthritis. ... Rheumatoid arthritis (RA) is a primary illness of the articulations (synovitis) that may cause systemic complications, very often later in its clinical course. The pathologic process is characterized by an unceasable proliferation of the synovial tissue causing the formation of the so called "pannus" which yields the gradual destruction of the articulation by invading the cartilage and subchondral bone. It is generally accepted that a genetic predisposition may exist which causes an abnormal reactivity in these patients and/or a loss of the mechanisms of tissue control. ... It has been hypothized that rheumatoid inflammatory process, started by a yet unknown etiologic agent, becomes self-perpetuating either for the unability of the patient to get rid of the exogenous antigen inducing it (retained antigen), or for an induced autoimmunization against a structure of the same organism (Ig G, Collagen proteins, etc.), such structure being degraded during an aspecific inflammation. Web site: http://www.delphion.com/details?pn=US04978661__
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Use of a cytokine regulatory agent to treat rheumatoid arthritis Inventor(s): Girten; Beverly E. (San Diego, CA), Tuttle; Ronald R. (Escondido, CA) Assignee(s): Trega Biosciences, Inc. (San Diego, CA) Patent Number: 5,741,774 Date filed: September 27, 1996 Abstract: The present invention relates to the use of a cytokine regulatory agent to reduce the severity of rheumatoid arthritis. Excerpt(s): This invention relates generally to the fields of medicine and immunopathology and, more specifically, to methods of using a cytokine regulatory agent to reduce the severity of rheumatoid arthritis in an individual. ... Cytokines are a class of proteins produced by macrophages and monocytes in response to viral or bacterial infection and in response to T cell stimulation during an immune response. Cytokines are normally present in very low concentrations in a tissue and mediate their effects through binding to high affinity receptors on specific cell types. ... The cytokines, including TNF, IL-1, IL-2, IL-6 and IL-8, mediate host defense responses, cell regulation and cell differentiation. These cytokines can induce fever in a subject, cause activation of T and B cells and affect the levels of other cytokines, which result in a cascade effect whereby other cytokines mediate the biological action of the first cytokine. Web site: http://www.delphion.com/details?pn=US05741774__
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Use of beta.sub.2 antagonists in the treatment of inflammatory diseases, in particular, rheumatoid arthritis Inventor(s): Levine; Jon D. (San Francisco, CA), Basebaum; Allan I. (San Francisco, CA) Assignee(s): The Regents of the University of California (Berkeley, CA) Patent Number: 4,908,387 Date filed: June 6, 1988 Abstract: A method of treating inflammation and joint deterioration in mammals which comprises administering a therapeutically effective amount of a selective beta.sub.2 adrenergic receptor antagonist. The method is particularly useful for the treatment of rheumatoid arthritis in humans. Excerpt(s): This invention concerns the use of selective beta.sub.2 antagonists as active agents in the treatment of inflammatory diseases, particularly rheumatoid arthritis. ... Inflammatory diseases, in particular rheumatoid arthritis, have been treated with a wide variety of compounds representing many different structural and pharmacologic classes, including, for example, aspirin and related compounds, non-steroidal anti inflammatory agents (NSAIDS) such as indomethacin, naproxen, ibuprofen and the like, corticosteroids, immunosuppressive, opiates, antimalarials such as hydroxychloroquine and chloroquine, cytotoxics such as cyclophosphamide, chlorambucil and azathioprine, penicillamine and its derivatives, and heavy metals such as the gold salts. No representative of any of these classes is regarded as ideal. Moreover, of these, only penicillamine, some gold compounds and possibly the corticosteroids in high doses have been shown to significantly suppress the progress of rheumatoid arthritis disease (disease modification). The magnitude of thee effects, however, are small, and decrease
Patents 411
with time. Further, these compounds possess such severe toxicities that they are reserved for patients whose disease progresses rapidly inspite of treatment with less toxic agents. Finally, all of the drugs available for treating inflammatory disease, whether for symptomatic relief or disease modification, possess side effects which make drug tolerance a serious problem for many patients. The available therapies are especially poorly tolerated by aged individuals, in whom inflammatory diseases are particularly prevalent and debilitating. ... None of the drugs presently available for treating inflammatory disorders are known to act via the nervous system. However, researchers have recently noted an apparent contribution of the sympathetic nervous system to the proliferation of inflammatory conditions and processes. It has been reported that dogs chronically maintained on beta adrenergic agonists develop a rheumatoid arthritis like syndrome [Vyden et al. Arthritis Rheum. 14, 420, (1971)]. The inventors of the present invention, in conjunction with colleagues, have reported on studies showing that sympathectomy markedly attenuates the signs of inflammation and severity of joint injury in rats with experimentally induced arthritis and that intracerebroventricular administration of morphine, which is known to decrease sympathetic tone, decreases arthritic severity [Levine et al., J.Neurosci. 6, 3423-3429 (1986)]. The inventors have also reported that regional sympathetic blockade with guanethidine reduces pain and increases pinch strength in patients with active rheumatoid arthritis [Levine et al., J. Rheumatol., 13, 1040-1043 (1986)]. Finally, propranolol, a beta adrenergic blocker, has been shown, in very high doses that produce significant toxicity, to decrease signs and symptoms of inflammation, in patients with active rheumatoid arthritis; suppression of joint deterioration was not shown. [Kaplan et al., Arthritis Rheum. 23, 253-255 (1980)]. Web site: http://www.delphion.com/details?pn=US04908387__ ·
Use of bis-(5-amidino-2-benzimidazolyl) methane (BABIM) to treat arthritis Inventor(s): Tidwell; Richard R. (Chapel Hill, NC), Geratz; Joachim D. (Chapel Hill, NC), Schwab; John H. (Chapel Hill, NC), Pryzwansky; Katherine B. (Chapel Hill, NC), Anderle; Sonia K. (Chapel Hill, NC) Assignee(s): University of North Carolina, Chapel Hill (Chapel Hill, NC) Patent Number: 4,940,723 Date filed: October 20, 1988 Abstract: A method of treating arthritis, and/or bone marrow hyperplasia, osteitis and synovitis, and/or granulomatosis including of the liver and spleen, which comprises administering to a patient an effective amount of BABIM and a pharmaceutically acceptable carrier. Excerpt(s): The present application relates to a method for treating arthritis and more particularly relates to treating arthritis by use of bis-(5-amidino-2-benzimidazoly) methane (BABIM). The use of BABIM represents a novel approach to the suppression of arthritis and coincidental conditions including liver and spleen granulomata. ... Arthritis is a polyarticular inflammatory process characterized by episodic remissions and exacerbations and by progressive loss of joint function. It has a prevalence rate of about 0.5% in women and 0.1% in men begins commonly in the prime of life and exacts a high toll in morbidity and personal suffering. Treatment has been with a variety of nonsteroidal antiinflammatory agents (NSAIA), usually in combination with a modifying drug. NSAIA can mitigate pain and inflammation by interference with prostaglandin synthesis, but are unable to arrest the basic destructive properties of the
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disease. Response-modifying compounds, such as gold salts or methotrexate can retard or block the pathogenic events, yet are restricted in their long-term usefulness by significant adverse side effects. ... A novel approach to the treatment of arthritis has been newly found employing the realization that proteolytic enzymes are prominently involved in many phases of inflammation and that inhibitors may succeed in interrupting the undue enzymatic activity. Many of the suspect protease, such as Factor XIIa, thrombin, plasmin and kallikrein, are trypsin-like in nature. They have in common the ability to hydrolyze arginyl and lysyl bonds and also share the susceptibility to inhibition by synthetic amidino compounds. Amidines have already proven themselves as potent drugs in a variety of pathologic states. They can serve as strong anticoagulants, block protease-dependent replication of respiratory syncytial virus and rotavirus, retard tumor invasion and metastasis, and eliminate the characteristic glomerular necrosis seen in immune complex-mediated glomerulonephritis. Web site: http://www.delphion.com/details?pn=US04940723__ ·
Use of interleukin-4 (IL-4) to treat rheumatoid arthritis Inventor(s): Lee; Frank (Palo Alto, CA), Yokota; Takashi (Palo Alto, CA), Arai; Ken-ichi (Palo Alto, CA), Mosmann; Timothy (Atherton, CA), Rennick; Donna (Los Altos, CA) Assignee(s): Schering Corporation (Kenilworth, NJ) Patent Number: 5,951,973 Date filed: June 6, 1995 Abstract: A method of treating rheumatoid arthritis comprising administering human Interleukin-4 (IL-4) to an individual afflicted with the disease. The IL-4 is administered with a pharmaceutically acceptable carrier in a dose ranging from 1 .mu.g to 100 mg. Excerpt(s): This invention relates generally to the application of recombinant DNA technology to elucidate the control mechanisms of the mammalian immune response and, more particularly, to the isolation of nucleic acid clones coding for polypeptides capable of exhibiting B-cell, T-cell, macrophage and mast cell stimulatory activity, as well as colony stimulating factor enhancing activity. ... Recombinant DNA technology refers generally to the technique of integrating genetic information from a donor source into vectors for subsequent processing, such as through introduction into a host, whereby the transferred genetic information is copied and/or expressed in the new environment. Commonly, the genetic information exists in the form of complementary DNA (cDNA) derived from messenger RNA (mRNA) coding for a desired protein product. The carrier is frequently a plasmid having the capacity to incorporate cDNA for later replication in a host and, in some cases, actually to control expression of the cDNA and thereby direct synthesis of the encoded product in the host. ... For some time, it has been documented that the mammalian immune response is based on a series of complex cellular interactions, called the "immune network." Recent research has provided new insights into the inner workings of this network. While it remains clear that much of the response does, in fact, revolve around the network-like interactions of lymphocytes, macrophages, granulocytes and other cells, immunologists now generally hold the opinion that soluble proteins (e.g., the so-called "lymphokines") play a critical role in controlling these cellular interactions. Thus, there is considerable interest in the isolation, characterization, and mechanisms of action of cell modulatory factors, an understanding of which should yield significant breakthroughs in the diagnosis and therapy of numerous disease states.
Patents 413
Web site: http://www.delphion.com/details?pn=US05951973__ ·
Use of oligosaccharides for treatment of arthritis Inventor(s): Rademacher; Thomas W. (Oxford, GB), Dwek; Raymond A. (Oxford, GB) Assignee(s): Monsanto Company (St. Louis, MO) Patent Number: 5,164,374 Date filed: December 17, 1990 Abstract: A method for the treatment of arthritis or a related autoimmune disease that exhibits immune complexes in serum or synovial fluid is provided which comprises exposure of the serum or synovial fluid to an oligosaccharide containing a structural component that inhibits or disrupts the degree of occupancy of the Fc carbohydrate binding site on IgG, e.g., sialyllactose. Excerpt(s): This invention relates to compositions and method for the treatment of arthritis and related autoimmune diseases. ... A known feature of autoimmune diseases is the presence of immune complexes. Immune complexes help eliminate foreign bodies such as microorganisms. In patients with diseases associated with immune complexes, the formation of the immune complex can be a malfunction of the normal system whereby in some cases the antibody response is directed against native material (selfantigen). In other cases the immune response is directed against the foreign substance repeatedly introduced into the system. ... In rheumatoid arthritis, for example, the chronic inflammation of the synovial membrane of affected joints, as well as many of the extra-articular manifestations of the disease, have been ascribed to immune complexes (either localized in the joint or circulating). The immune complexes in patients with rheumatoid arthritis consist of IgG homopolymer complexes [i.e. IgG-(IgG)n, selfassociated] or heteropolymers [i.e. IgM-(IgG)n], thereby suggesting that the immunoglobulins are both the antigen and the antibody. In addition, complement components are frequently bound to these complexes. The IgG molecules found in the complexes are referred to as IgG-rheumatoid factor (IgG-RF) while the IgM molecules in the complexes are called IgM-rheumatoid factors (IgM-RF). Web site: http://www.delphion.com/details?pn=US05164374__
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Use of pharmaceutical composition in the treatment of traumatic arthritis in horses Inventor(s): Ameys; Jean-Paul (Brussels, BE) Assignee(s): Continental Pharma Incorporated (Louvain-la-Neuve, BE) Patent Number: 6,218,433 Date filed: March 20, 2000 Abstract: The present invention is related to the use of a pharmaceutical composition comprising a suitable pharmaceutical carrier and an effective amount of an active compound selected from the group consisting of phenylacetydroxamic acid, phenoxyacetydroxamic acid, arylacetydroxamic acid and/or their corresponding amides, for the preparation of a medicament in the prevention and/or the treatment of equine arthritis. Excerpt(s): The present invention is related to a new use of a pharmaceutical composition comprising an effective amount of phenylacetydroxamic acid,
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phenoxyacetydroxamic acid, arylacetydroxamic acid, possibly substituted, and/or their corresponding amides. ... It is generally accepted that lameness due to traumatic joint disease in its various forms is a common clinical problem in horses, and one of the most important sources of financial loses in the equine industry (1-9). ... Traumatic arthritis can develop after single or repetitive episodes of trauma, but continued repeated trauma to the joint is held as the most important etiologic factor in traumatic arthritis. The mechanical trauma in the form of stretching, impingement and concussion of articular tissues may perturb cellular membranes, resulting in release of inflammatory mediators inciting joint inflammation. In many cases, extended periods of rest are required for the complete resolution of the joint inflammation. Simple resting of the affected horses is therefore seldom an acceptable therapeutic alternative in working horses, considering the limitations of economics, season and competition schedules (6, 10). Web site: http://www.delphion.com/details?pn=US06218433__ ·
Use of rifamycin SV and its related salts in the treatment of rheumatoid arthritis, and related formulations suited for the purpose Inventor(s): Caruso; Innocenzo (Milan, IT), Montrone; Franco (Milan, IT), Molteni; Luigi (Malnate, IT) Assignee(s): Dr. L. Zambeletti S.p.A. (Milan, IT) Patent Number: 4,312,866 Date filed: July 7, 1980 Abstract: The invention concerns new salts of rifamycin SV and a new use of rifamycin SV in the treatment of rheumatoid arthritis and analogous affections, by intra-articular injection of the sodium salt of rifamycin SV or, better, of salts of said anti-biotic with basic aminoacid, e.g. with arginine, lysine or histidine. Excerpt(s): The present invention concerns a new use of rifamycin SV in the treatment of rheumatoid arthritis, and analogous pathologic affections, by an intra-articular injection of rifamycin SV itself, preferably in a salified form. All the operations pertaining to the preparation of the salts as per re, with inclusion of their purification, their formulation into pharmaceutical dosage forms suited for its administration, and/or of their packaging into containers suited for administration shall be covered by the term "use", to be intended according to the present invention. ... Rifamycin SV has been used for over 15 years in human and veterinary medicine as a therapeutic agent in all the range of infections due to Gram-positive and Gram-negative pathogens, Mycobacterium tuberculosis and Mycobacterium leprae. ... 8. leprosy. Web site: http://www.delphion.com/details?pn=US04312866__
Patents 415
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Use of selenium-containing compounds for negating the toxic effects of gold compounds used in the treatment of rheumatoid arthritis, and a novel seleniumcontaining gold compound and use thereof as an anti-rheumatoid arthritis medicine Inventor(s): Stockel; Richard F. (457 Rolling Hills Rd., Bridgewater, NJ 08807), Dumas; Phillip E. (137 Louise Dr., Morrisville, PA 19067) Assignee(s): none reported Patent Number: 4,680,286 Date filed: April 9, 1985 Abstract: The toxic effects of gold compounds used in the treatment of rheumatoid arthritis can be negated by the use of a selenium-containing compound. A new selenium-containing gold compound has been found to be useful as a gold compound type anti-rheumatoid arthritis medicine which can self-detoxify gold toxicity. Excerpt(s): The present invention relates to a method of negating the toxic effects of gold compounds. More particularly, the present invention relates to a method of negating the toxic effects of gold compounds used in the treatment of rheumatoid arthritis, which method comprises administering to a patient a selenium-containing compound. The present invention is also concerned with a novel selenium-containing gold compound which can be effectively used as a so-called gold compound type anti-rheumatoid arthritis medicine which can self-detoxify gold toxicity. ... The most common form of chronic inflammatory arthritis is rheumatoid arthritis, which is characterized by symmetrical inflammatory polyarthritis, morning stiffness and positive rheumatoid factor. Over more than 100 diseases have been classified as arthritis, in addition to chronic inflammatory arthritis. ... Each decision to treat with a drug requires careful therapeutic weighing of the hazards and the benefits of the drug versus the disability caused by the symptoms. Various groups of drugs useful for arthritis include salicylates, indole derivatives, propionic acid derivatives, phenylbutazone and oxyphenbutazone, penicillamine, corticosteroids, cytotoxic drugs and anti-gout agents. For an excellent review on these anti-arthritic drugs, a review article written by J. A. Markenson, appearing in Drug Therapy, January, 1981, page 45 dives a comparative overview of these types of classes of drugs. As mentioned above, there are various drugs effective in the treatment of arthritis, however, gold compounds used in gold therapy are most effective as anti-rheumatoid agents, and the gold therapy should be considered in patients with active disease who fail to respond to the plethora of drugs previously mentioned to reduce inflammation. Web site: http://www.delphion.com/details?pn=US04680286__
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Use of taxol in the treatment of rheumatoid arthritis Inventor(s): Brahn; Ernest (Encino, CA) Assignee(s): Regents of the University of California (Oakland, CA) Patent Number: 5,583,153 Date filed: October 6, 1994 Abstract: An improved method of suppression of a progressive, inflammatory, autoimmune arthritis in a mammal involves the use of the drug Taxol. In general, such a method comprises administering to a mammal having or susceptible to arthritis Taxol in a pharmacologically acceptable carrier capable of solubilizing Taxol in a dose sufficient
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to suppress at least one symptom of arthritis selected from the group of inflammation, swelling, abnormal neovascularization, bone erosion, and cartilage erosion. The use of Taxol can be combined with the use of other antiarthritic drugs, such as the angiogenesis inhibitor AGM-1470, to produce a greater therapeutic effect than with either Taxol or the other antiarthritic drug alone. Excerpt(s): This invention is directed to a method of suppression of a progressive, inflammatory, autoimmune arthritis in a mammal, such as rheumatoid arthritis. Despite advances in treatment, arthritis remains an extremely serious health problem, particularly in view of the aging population in the United States and other developed countries, because arthritis is typically a disease of the elderly. Although rarely fatal, arthritis is a major cause of morbidity, loss of time from work, lost productivity and decrease in quality of life. It causes severe pair and loss of joint mobility and can make doing even simple tasks difficult. ... Among the most serious forms of arthritis is rheumatoid arthritis. Rheumatoid arthritis is generally believed to be an autoimmune disease that is believed to be associated with activity of autoreactive T cells. It is believed that these cells cause the disease via a delayed-type hypersensitivity reaction. Although it is not completely certain which antigen these T cells recognize, one significant candidate is type II collagen. The possibility exists that other antigens may also play a role in the disease. ... Substantial work has been done on genetic bases for susceptibility to the disease. This work has focused on MHC haplotypes. Thus, it may be possible to determine, from familial studies or direct genomic analysis, that some individuals are at particular risk for the development of rheumatoid arthritis. Web site: http://www.delphion.com/details?pn=US05583153__ ·
Use of zofenopril for the treatment of rheumatoid arthritis Inventor(s): Devlin; Richard G. (Sea Girt, NJ) Assignee(s): E. R. Squibb & Sons, Inc. (Princeton, NJ) Patent Number: 4,855,315 Date filed: September 2, 1988 Abstract: Zofenopril, and pharmaceutically acceptable salts thereof, can be used for the treatment of rheumatoid arthritis. Excerpt(s): Rheumatoid arthritis is a lifelong, crippling, multisystem disease whose principal manifestation is joint inflammation. The prevalence of definite rheumatoid arthritis in the United States is approximately 1 percent (2,400,000 individuals). This estimated prevalence increases to 3 percent (7,200,000 individuals) when a more liberal definition of disease as specified by the American Rheumatism Association ("probable" and "possible" rheumatoid arthritis) is applied. ... In the majority of individuals the disease is characterized by a fluctuating and variable course with lifelong periods of exacerbation and regression, but with ever worsening joint deformity and systemic disability. Approximately 10 percent of patients develop only a short-lived inflammatory process which remits spontaneously without permanent residua, while at the opposite end of the spectrum another 10 percent experience a relentlessly progressive disease leading rapidly to marked deformity and disability. The principal manifestation of rheumatoid arthritis is joint inflammation and deformity, usually accompanied by constitutional symptoms such as weakness, easy fatigability, anorexia or weight loss. Approximately 10-20 percent of individuals with definite rheumatoid arthritis experience significant extra-articular manifestation including vasculitis, skeletal
Patents 417
muscle weakness and atrophy, polyneuropathy, pleuropulmonary disease, pericarditis or hematologic abnormalities. ... Chemotherapeutic agents available for the treatment of rheumatoid arthritis are characterized by low efficacy and high toxicity. These agents fall into categories including steroids, nonsteroidal anti-inflammatory agents (NSAID's) and disease modifying anti-rheumatoid drugs (DMARD's). The NSAID's which include salicylates, as well as ibuprofen, fenoprofen, naproxen, piroxicam, tolmetin, indomethacin, sulindac, meclofenamate and others are primariy cycloxygenase inhibitors, inhibiting production of prostaglandins, prostacycline and thromboxanes. Thus, they all produce nonspecific analgesic, anti-inflammatory and antipyretic effects and are prescribed for the control of a variety of inflammatory states. Although they are perceived to be quite potent, in fact none have been demonstrated to be more effective than aspirin in the treatment of rheumatoid arthritis. NSAID's are generally prescribed as first line therapy for this condition and are administered episodically for control of acute exacerbation of disease. Patients commonly develop tachyphylaxis or therapeutic tolerance to these agents over time and it is common practice for individuals to be switched frequently from one to another agent in the group. It is unclear whether such decreased efficacy is a function of disease progression or physiologic tolerance. Despite their status as first line treatment for rheumatoid arthritis, the NSAID's are associated with a wide spectrum of toxic side effects, especially at the doses needed to control rheumatoid arthritis. All are associated with gastrointestinal irritation (and bleeding), azotemia, platelet dysfunction, liver function abnormalities, bone marrow depression and exacerbation of allergic conditions such as rhinitis or asthma. Although the incidence of each of these effects varies somewhat with the specific agent, elderly patients receiving diuretics, common in populations with rheumatoid arthritis, may be at higher than average risk for such phenomena. Web site: http://www.delphion.com/details?pn=US04855315__ ·
Vaccine compositions and methods useful in inducing immune protection against arthritogenic peptides involved in the pathogenesis of rheumatoid arthritis Inventor(s): Carson; Dennis A. (Del Mar, CA), Albani; Salvatore (Encinitas, CA) Assignee(s): The Regents of the University of California (Oakland, CA) Patent Number: 6,153,200 Date filed: June 30, 1998 Abstract: Vaccine compositions useful in inducing immune protection in a host against arthritogenic peptides involved in the pathogenesis of rheumatoid arthritis are disclosed. Each vaccine composition provides antigenic dnaJp1 peptide (by including the peptide or a polynucleotide which encodes the peptide) and, optionally, other peptide fragments of the microbial dnaJ protein and/or human homologs thereof. Methods for identifying persons who are predisposed to develop rheumatoid arthritis and methods for use of the inventive vaccines are also disclosed. Excerpt(s): The invention relates to the control and prevention of autoimmune disease, in particular rheumatoid arthritis. More specifically, the invention relates to methods and reagents which reduce or prevent the response of a host to arthritogenic peptides which include an amino acid sequence (Q(K/R)RAA) that is homologous to a sequence contained in certain HLA proteins. ... In humans, autoimmune diseases such as rheumatoid arthritis tend to be associated with particular HLA specificities. Rheumatoid arthritis (RA) in particular is presently believed to be associated on a genetic level with the Class II HLA haplotypes DW4, DW14, DW15 (all with DR4 specificity) and/or DR1.
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Each of these haplotypes include an amino acid sequence which is commonly referred to as the "susceptibility sequence" (hereafter, "RA susceptibility sequence"; see, SEQ.ID.NOs: 1 and 2). The RA susceptibility sequence is known to vary at one amino acid; to wit, QRRAA and QKRAA (hereafter, "Q(R/K)RAA"). More than 90% of adult patients with seropositive RA have also been found to have HLA DR antigens with the RA susceptibility sequence in the third hypervariable region of the molecule. The RA susceptibility sequence has not been implicated in the onset of juvenile RA (JRA), except in patients suffering from severe, seropositive JRA. ... The QRRAA variant of the susceptibility sequence has been identified on HLA haplotypes DW14, DW15 and DR1. The QKRRA variant has been identified on HLA haplotype DW4. Highly conserved homologs of the variants have also been identified in the Epstein-Barr virus glycoprotein gp110, as well as the dnaJ heat shock proteins from Escherichia coli, as well as the bacterial species Klebsiella, Proteus, Salmonella, and Lactococcus. Web site: http://www.delphion.com/details?pn=US06153200__ ·
Vinblastine in rheumatoid arthritis Inventor(s): Schinitsky; Michael R. (Indianapolis, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 4,208,414 Date filed: May 14, 1979 Abstract: Vinblastine (vincaleucoblastine, VLB) and other anti-mitotic vinca alkaloid is useful in the treatment of rheumatoid arthritis and related diseases, alone or in combination with an anti-inflammatory agent. Excerpt(s): Vinblastine (U.S. Pat. No. 3,097,137) has been employed for a number of years as an oncolytic agent particularly useful in the treatment of Hodgkin's Disease and other lymphomas. It is generally administered by the intravenous route to patients suffering from one of these diseases. There has been a sparse amount of research work reported involving vinblastine, or other oncolytic vinca alkaloids and their derivatives, directed toward their physiological action in non-neoplastic conditions. For example, vinblastine has been used to induce leucopenia in experimental animals and the effect of that leucopenia on other conditions studied. Phelps and McCarty, writing in J. Exp. Med., 124 115 (1966), induced a gouty arthritis type of inflammation in dogs by the injection into the joint of microcrystalline sodium urate. An acute inflammatory reaction was ordinarily produced, but, in dogs pretreated with vinblastine at such a dose level that there was a profound leukocyte depletion, significant phagocyte accumulation was prevented and the inflammatory response was almost completely abolished. This finding led the authors to the conclusion that, in the particular experimental model, the polymorphonuclealeukocyte was necessary to the urate-crystal induced inflammation. Chang and Gralla, writing in Arthritis and Rheumatism, 11, 145 (1968), investigated the possibility that the effects of vinblastine on joint inflammation found by Phelps and McCarty were mediated by means other than the reduction in the number of polymorphs. These authors produced a leucopenia in dogs by using rabbit-anti-dogpolymorphonuclear serum. It was their conclusion that their findings were in accord with those of Phelps and McCarthy as regards the role of a vinblastine-induced leucopenia in preventing inflammation subsequent to the injection of mycrocrystalline urate into canine joints. Floresheim, et al. writing in Agents and Actions, 3 24 (1973) induced an acute arthritis in pigeons or chickens by the injection of microcrystalline sodium urate into the intertarsal joint. They found no inhibition of the arthritic response
Patents 419
from a number of agents including both vinblastine and vincristine. Fitsgerald, et al., Pharmacology, 6, 265 (1971) used a different model--the sodium urate-induced paw swelling in mice. The authors found that various anti-mitotics including vinblastine and vincristine produced a significant depression of paw swelling at similar dose levels. The effects of the various anti-mitotic agents did not seem to bear any relation to their antimitotic potency. T. Y. Shen, in an article titled "The Expanding Vistas of Non-acidic Anti-arthritic Agents" in Drugs in Experimental Clinical Research Vol II (1) (1977) speculates that one approach, among many, for regulation of the immuno-pathology of arthritis would be to investigate the effect of selective membrane modulators upon this disease. According to Shen, "[p]hagocytosis and the function of membrane receptors and enzymes are subject to the regulation by the fluidity of the bi-layer membrane by the submembrane structures, microtubules and microfilaments . . . . " He reports that among the classical inhibitors of microtubules are included the vinca alkaloids, vinblastine and vincristine, the anti-tumor drug, maytensine, phodphyllotoxin and colchicin. Finally, in June, 1977, a question was raised as to whether it would be useful to use vinblastine in the treatment of systemic sclerosis (Abstracts of the 14th International Congress of Rheumatism--June 26, 1977, San Francisco, California-Abstract No. 661). The authors concluded that it would be. At the same meeting, a paper was presented (Abstract No. 426) concerning the effect of the intravenous administration of vinblastine on inflammation induced by the injection of pulverized calcium pyrophosphate dihydrate crystals into the pleural cavity. The authors concluded that vinblastine may have a suppressive effect on the inflammation thus induced. ... This invention provides a method of treating rheumatoid arthritis which comprises administering to a mammal suffering from rheumatoid arthiritis and in need of treatment, an amount of a vinca-derived oncolytic agent, specifically vinblastine, effective to arrest the progress of the disease. Administration can be parenteral, specifically by the intrevenous route, or, preferably, oral. The amount of vinblastine administered varies according to the route employed. For example, by the intravenous route, a dose of 0.1 to 0.5 mg./kg. can be employed (3.7 to 18.5 mg. per meter squared), whereas the oral dosage would be roughly ten times as great (1 to 5 mg./kg.). The drug is customarily administered once (as contrasted with the daily, every third day, or weekly dosage regimen when vinblastine is used to treat Hodgkin's Disease or related neoplasms). If required, the dosage can be repeated, but not more often than every two weeks or once a month in order to avoid cumulative side-effects. ... In a second aspect of this invention, vinblastine is administered in conjunction with an anti-inflammatory agent of the profen class including ibuprofen, (.+-.) .alpha.-methyl-4-(2methylpropyl)benzeneacetic acid; carprofen, .alpha.-methyl-6-chlorocarbazole-2-acetic acid; cicloprofen, .alpha.-dl-2-methylfluorene-2-acetic acid; fenoprofen, dl-.alpha.methyl-3-phenoxybenzeneacetic acid; indoprofen, .alpha.-methyl-4-(1,3-dihydro-1-oxo2H-isoindolyl-2-yl)benzenacetic acid; ketoprofen, .alpha.-methyl-3benzoylbenzeneacetic acid; naproxyn, (.+-.) .alpha.-methyl-6-methoxy-2naphthaleneacetic acid; pirprofen, dl-.alpha.-methyl-3-chloro-4-(3-pyrrolidinol-1yl)benzeneacetic acid; suprofen, dl-.alpha.-methyl-4-(thienylcarbonyl)-benzeneacetic acid and benoxoprofen, dl-.alpha.-methyl-2-(p-chlorophenyl)benzoxazoleacetic acid and the like drugs. Other non-profen type anti-inflammatory drugs such as indomethacin can also be used advantageously with VLB and like drugs to treat rheumatoid arthritis. Such combinations of drugs, a vinca alkaloid and an anti-inflammatory agent, are particularly valuable because the primary effect of vinblastine and related alkaloids is to arrest further progress of the rheumatoid process and administration of the drug afords little if any symptomatic relief whereas, by contrast, the chief effect of the antiinflammatory drug is to alleviate the arthritic symptoms but with little or no hindrance to the progress of the arthritic process.
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Web site: http://www.delphion.com/details?pn=US04208414__
Patent Applications on Arthritis As of December 2000, U.S. patent applications are open to public viewing.10 Applications are patent requests which have yet to be granted. (The process to achieve a patent can take several years.) The following patent applications have been filed since December 2000 relating to arthritis: ·
CD44 splice variant associated with rheumatoid arthritis Inventor(s): Golan, Itshak ; (Ashdod, IL), Naor, David ; (Jerusalem, IL), Nedvetzki, Shlomo ; (Jerusalem, IL) Correspondence: COOLEY GODWARD, LLP; 3000 EL CAMINO REAL; 5 PALO ALTO SQUARE; PALO ALTO; CA; 94306; US Patent Application Number: 20030108984 Date filed: December 7, 2001 Abstract: A novel variant mRNA transcript of CD44 found in synovial cells of rheumatoid arthritis (RA) patients is described. This novel transcript contains the known CD44 constant and variant exons but also comprises three additional nucleotides (CAG) that are transcribed from the end of the intron bridging Exon v4 to Exon v5 and are inserted at the 5' end of Exon v5. This extra CAG sequence results in the insertion of a new codon for the amino acid alanine. The novel CD44 transcript found to date in eighteen RA patients and not found in healthy (non-RA) individuals, is useful in the diagnosis, prognosis, prevention and treatment of RA, of other diseases in which the variant CD44 transcript is involved and possibly in disorders and diseases which involve cells expressing other forms of the CD44 protein. Excerpt(s): This application is a continuation-in-part of International Application PCT/IL00/00326, filed Jun. 7, 2000, which claims priority to Israeli application No. 130356, filed Jun. 8, 1999, and Israeli application 133647, filed Dec. 21, 1999. All of which applications are incorporated by reference herein. ... The present invention concerns a novel nucleic acid coding sequence, vectors and host cells comprising said sequence, amino acid sequences encoded by, said sequence, antibodies reactive with said amino acid sequences and pharmaceutical compositions comprising any of the above. The invention also concerns methods for the diagnosis, prognosis, prevention and treatment of various diseases, mainly infectious and other inflammatory diseases and autoimmune diseases, and cancer. ... Aune, T. M., et al., Published EP Application No. 501233 (1992). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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This has been a common practice outside the United States prior to December 2000.
Patents 421
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Chronic rheumatoid arthritis therapy containing IL-6 antagonist as effective component Inventor(s): Oshugi, Yosiyuki ; (Gotenba-shi, JP), Moriya, Yoichiro ; (Gotenba-shi, JP), Mihara, Masahiko ; (Gotenba-shi, JP), Kishimoto, Tadamitsu ; (Osaka, JP) Correspondence: Harold C. Wegner; FOLEY & LARDNER; Washington Harbour; 3000 K Street, N.W., Suite 500; Washington; DC; 20007-5109; US Patent Application Number: 20010001663 Date filed: January 9, 2001 Abstract: There is provided a synovial cell growth inhibitor, or a pharmaceutical composition for treatment of chronic rheumatoid arthritis based on the synovial cell growth inhibitor.The pharmaceutical composition for treatment of chronic rheumatoid arthritis or synovial cell growth inhibitor contains an IL-6 antagonist, such as IL-6 antibody or IL-6R antibody, as an effective component. Excerpt(s): The present invention relates to a chronic rheumatoid arthritis therapy or synovial cell growth inhibitor comprising an interleukin-6 antagonist as an effective component. ... Chronic rheumatoid arthritis is a systemic chronic inflammatory disease in which abnormal growth of connective tissue, including synovial tissue, occurs in the joints (Melnyk et al., Arthritis Rheum. 33: 493-500, 1990). The joints of chronic rheumatoid arthritis patients have been shown to have marked growth of synovial cells, formation of a multilayer structure due to abnormal growth of the synovial cells (pannus formation), invasion of the synovial cells into cartilage tissue and bone tissue, vascularization toward the synovial tissue, and infiltration of inflammatory cells such as lymphocytes and macrophages. Mechanisms of onset of chronic rheumatoid arthritis have been reported to be based on such factors as heredity, bacterial infection and the contribution of various cytokines and growth factors, but the overall mechanism of onset has remained unclear. ... In recent years, cytokines and growth factors including interleukin-1 (IL-1), interleukin-8 (IL-8), tumor necrosis factor .alpha. (TNF.alpha.), transforming growth factor .beta. (TGF.beta.), fibroblast growth factor (FGF) and platelet-derived growth factor (PDGF) have been detected in the synovial membrane and synovial fluid of chronic rheumatoid arthritis patients (Nouri et al., Clin. Exp. Immunol. 55:295-302, 1984; Thornton et al., Clin. Exp. Immunol. 86:79-86, 1991; Saxne, et al., Arthritis Rheum. 31:1041-1045, 1988; Seitz et al., J. Clin. Invest. 87:463-469, 1991; Lafyatis et al., J. Immunol. 143:1142-1148, 1989; Melnyk et al., Arthritis Rheum. 33:493500, 1990). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Composition and method of treating arthritis Inventor(s): Petrus, Edward J. ; (Austin, TX) Correspondence: EDWARD J. PETRUS; 3413 SPANISH OAK DR.; AUSTIN; TX; 78731; US Patent Application Number: 20020119952 Date filed: February 5, 2002 Abstract: This invention relates to the compositions and method of treating and preventing arthritis, repairing of articular joint surfaces and the relief of symptoms associated with arthritis. The composition comprises bio-affecting agents to reduce nitric
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oxide production and increase chondroprotective agents. The preferred composition comprises; nitric oxide synthase inhibitors, nitric oxide scavangers, and amino sugars. Nitric oxide synthase inhibitors and nitric oxide scavengers reduce the level of nitric oxide, the free radical responsible for the degradation of articular cartilage. Amino sugars are the building blocks of articular cartilage and have anti-inflammatory actions. Excerpt(s): This application is a continuation-in-part of Ser. No. 09/149,241 filed Sep. 9, 1998 abandoned; continuation-in-part of Ser. No. 09/350,380 filed Jul. 8, 1999. ... The present invention concerns compositions and methods of treating and preventing arthritis, repairing of articular joint surfaces and relief of symptoms associated with arthritis. ... Approximately 1-2% of the population suffers from rheumatoid arthritis (RA), which is characterized as an imbalance in the immune system that causes an overproduction of pro-inflammatory cytokines, e.g., tumor necrosis factor alpha (TNF.alpha.), interleukin 1 (IL-1), and a lack of anti-inflammatory cytokines, e.g. IL-10, IL-11. RA is characterized by synovial inflammation, which progresses to cartilage destruction, bone erosion and subsequent joint deformity. The primary symptoms of RA are joint inflammation, swelling, difficulty moving, and pain. During the inflammatory process, polymorphonuclear cells, macrophages, and lymphocytes are released. Activated T-lymphocytes produce cytotoxins and pro-inflammatory cytokines, while macrophages stimulate the release of prostaglandins and cytotoxins. Vasoactive substances (histamine, kinins, and prostaglandins) are released at the site of inflammation and cause edema, warmth, erythema, and pain associated with inflamed joints. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
Compositions and methods for treating an arthritic condition Inventor(s): Roubenoff, Ronenn ; (Sharon, MA), Selhub, Jacob ; (Brookline, MA) Correspondence: MINTZ, LEVIN, COHN, FERRIS,; GLOVSKY and POPEO, P.C.; One Financial Center; Boston; MA; 02111; US Patent Application Number: 20020094970 Date filed: December 14, 2001 Abstract: The present invention features compositions and methods for the treatment of an arthritic condition. The compositions contain a reduced folate compound and a cobalamin compound. Excerpt(s): This application claims priority to U.S. provisional application No. 60/255,600, filed on Dec. 14, 2000, the entire contents of which is hereby incorporated by reference. ... The present invention makes available compositions and methods for treatment of osteoarthritis. ... Arthritis is a common form of joint disease. For example, one form of arthritis, osteoarthritis ("OA"), afflicts countless millions of people worldwide, including more than 50 million Americans. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
Patents 423
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Crude drug compositions for treating or preventing arthritic diseases and the preparation process Inventor(s): Kim, Sunyoung ; (Seoul, KR), Kim, Bongcheol ; (Kyeonggi-do, KR), Eo, Hae-Kwan ; (Seoul, KR), Jeon, Hyang ; (Seoul, KR), Shin, Sung-Seup ; (Seoul, KR), Jung, Hyung-Jin ; (Seoul, KR), Jin, Mirim ; (Seoul, KR), Cho, Byung-Wook ; (Seoul, KR), Oh, Jin-Hwan ; (Suwon-si, KR) Correspondence: FOLEY AND LARDNER; SUITE 500; 3000 K STREET NW; WASHINGTON; DC; 20007; US Patent Application Number: 20030143290 Date filed: January 16, 2003 Abstract: The present invention is related to pharmaceutical composition essentially comprising herbal extract of Chaenomelis Fructus, Achyranthis Radix, Acanthopanax, Phlomidis Radix, Gentianae Radix, Clematidis Radix, and additionally comprising herbal extract selected from group consisting of Angelicae Radix, Cnidii Rhizoma, Gastrodiae Rhizoma, Safflower, Cinnamomi Cortex, Job's tear, Aurantii nobilis Pericapium, Ledebouriellae Radix, Lonicera japonica, Akebiae caulis, Caragana chamlagu, Licorice root, Notopterygium incisum, Persicae semen, Eucommia ulmoides, Atractylodes Rhizoma, Torilis japonica according to the need for the prevention and treatment of arthritic diseases and methods of using the above extracts and composition as potent anti-inflammatory and anti-arthritic agents. Excerpt(s): This application is a continuation patent application of U.S. Provisional Application No. 60/350,085 filed Jan. 18, 2002 abandoned. ... The present invention relates to pharmaceutical composition comprising a herbal extract from various herbs, e.g., Chaenomelis Fructus, Achyranthis Radix, Acanthopanax, Phlomidis Radix, Gentianae Radix, Clematidis Radix, based on the known functions of each herb described in various literatures of traditional Chinese and Korean medicine for the prevention and treatment of arthritic diseases and methods of using such extracts and compositions as potent anti-inflammatory and anti-rheumatic agents. ... Arthritis is an autoimmune disease characterized by their symptoms such as pain, swelling and stiffness in the joints. The two major forms of arthritis in mammals are inflammatory arthritis such as rheumatoid arthritis (RA), and osteoarthritis (OA), a progressive, degenerative loss of cartilage often secondary to mechanical stress, aging, dysplastic conditions and/or injury. The symptoms of arthritis generally relate to arthrosis of spine, e.g., hallux rigidus, arthrosis psoriaticum and rheumatic arthritis. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Device and method for treating arthritis of knee Inventor(s): Toda, Yoshitaka ; (Osaka, JP) Correspondence: Nancy Lord Johnson; Sierra Patent Group; P.O. Box 6149; Stateline; NV; 89449; US Patent Application Number: 20010047146 Date filed: March 28, 2001 Abstract: The present invention relates generally to a therapeutic device and related methods for treating arthritis of the knee. The therapeutic device comprises a stretchable band having a predetermined length, a flexible and resilient body installed in the
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longitudinal middle of the stretchable band with a substantially triangular cross-section whose height is greater at one side of the stretchable band than at the other, such that the higher portion of the flexible and resilient body is applied to the sole at a position nearer to the inner or outer side thereof, and the stretchable band may be used to wrap and fix the ankle. Excerpt(s): The present invention relates to a therapeutic device for treating arthritis of the knee, including osteoarthritis of the knee. ... Osteoarthritis of the knee commonly begins with cartilage degeneration secondary to varus deformity that is multifactorial and often age-related. Varus deformity, whether or not age related, disturbs the positional relationship between the femur and tibia, resulting in partial wear and gradual loss of elasticity of the cartilage between the femur and the tibia. This causes local pressure directly on the bone and consequent bony proliferation at the joint edge and deformity. Overwork may wear or partly wear the joint due to its inherent disorder and similar proliferative change at the joint edge and the induction of osteoarthritis. ... Osteoarthritis has been treated with an insole known as a sole plate. For an insole to function as a therapeutic device, the right or left side is higher than the opposite side. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
DIAGNOSIS OF RHEUMATOID ARTHRITIS IN VIVO USING A NOVEL SPECTROSCOPIC APPROACH Inventor(s): EYSEL, HANS H. ; (WINNIPEG, CA), CANVIN, JAN M. ; (WINNIPEG, CA), MANTSCH, HENRY H. ; (WINNIPEG, CA), MANSFIELD, JAMES R. ; (WINNIPEG, CA), SOWA, MICHAEL G. ; (WINNIPEG, CA), JACKSON, MICHAEL ; (WINNIPEG, CA), EL-GABALAWY, HANI ; (WINNIPEG, CA) Correspondence: ADRIAN D BATTISON; ADE & COMPANY; 1700 360 MAIN STREET; WINNIPEG; RCC3Z3; CA Patent Application Number: 20020007121 Date filed: June 17, 1999 Abstract: A novel near infrared spectroscopic technique was used to characterize the joints in arthritis with comparison against normal joints. A beam of near infrared light was passed to joints through a fiber optic cable. Scattered light was collected by the same fiber bundle and a spectrum of the joint computed. Multivariate pattern recognition techniques identified regions of the spectrum which allowed discrimination between healthy and affected joints. Linear discriminant analysis resulted in correct classification of 74% of the joints.The high degree of similarity between mean spectra representing the early, late and control groups along with the significant between-subject variability in the data make diagnosis based on visual assessment of the spectra impossible. Linear discriminant analysis was therefore applied to spectra to determine if spectra could be classified by statistical methods as arising from early or late RA. Application of LDA resulted in correct classification of 74% of the joints. Interestingly, the spectral regions in which diagnostic differences were found by the multivariate analysis contain absorption bands related to tissue oxygenation status (oxy and deoxyhaemoglobin) and oxygen utilization (cytochrome aa.sub.3), suggesting that ischaemic changes within the joint are being detected. Excerpt(s): The present invention relates generally to the fields of diagnostic devices and methods of use thereof. More specifically, the present invention relates to a device for diagnosing rheumatoid arthritis. ... There are almost 100 disorders that fall under the
Patents 425
umbrella classification of arthritis. The most prevalent are osteoarthritis and rheumatoid arthritis. Osteoarthritis (OA) is a disease of wear and tear commonly affecting the elderly. Rheumatoid arthritis (RA) is a systemic auto-immune disorder causing a symmetric inflammatory polyarthritis. Once the inflammatory process is activated, there can be rapid destruction of joints that can, in some cases, be very aggressive. It has been shown that erosive damage occurs within weeks of the onset of the clinical symptoms. Typically, RA involves the small joints of the hands and feet leading to the clinical signs of joint tenderness and swelling. ... Despite its prevalence, arthritis can often be a difficult disease to diagnose. Clinical history and physical examination by a specialised medical practitioner are of key importance in diagnosis. However, any diagnosis based upon the personal skills and experience of the examining physician must of necessity contain an element of subjectivity. Among the more objective tests are X-ray investigation and magnetic resonance imaging of the affected joints and serological and immunological analysis of synovial fluid and blood. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
Diagnostic and therapeutic agents for rheumatoid arthritis Inventor(s): Sato, Koichiro ; (Fukushima-shi, JP), Homma, Yoshimi ; (Fukushima-shi, JP) Correspondence: FITZPATRICK CELLA HARPER & SCINTO; 30 ROCKEFELLER PLAZA; NEW YORK; NY; 10112; US Patent Application Number: 20030152572 Date filed: October 4, 2002 Abstract: The present invention provides a therapeutic agent for rheumatoid arthritis which inhibits the growth of synoviocytes mediated by c-erbB-2 by clarifying the participation of c-erbB-2 in the growth of synoviocytes in rheumatoid arthritis patients and inhibiting the activation or expression of c-erbB-2. Excerpt(s): The present invention relates to diagnostic and therapeutic agents for rheumatoid arthritis which inhibit the growth of synoviocytes mediated by c-erbB-2, and a diagnostic method for rheumatoid arthritis which comprises detecting c-erbB-2. ... Rheumatoid arthritis is a systematic, chronic inflammatory disease characterized by the growth of synoviocytes at joints and the abnormality of immunoreaction, which gradually leads to the collapse of tendon, cartilage and bone tissues [Ann. Rheum. Dis., 52, S39-S47 (1993)]. ... So far, little has been elucidated about the signal transduction for excessive growth of synoviocytes in rheumatoid arthritis; however, the participation of growth factors such as EGF (epidermal growth factor), PDGF (platelet-derived growth factor) and FGF (fibroblast growth factor) which are present in synovia has been suggested [The Journal of Orthopaedic Science, 67, 859-865 (1993), Semin. Arthritis Rheum., 21, 191-199 (1991)]. There are also reports on the elevated expression levels of PDGF receptor in synoviocytes [Scand. J. Immnol., 27, 285-294 (1988)] and FGF receptor in focal T cells [Arthritis Rheum., 39, 914-922 (1996)]. However, little has been reported about EGF receptor (hereinafter referred to as EGFR) in tissues affected by rheumatoid arthritis. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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EP4 receptor inhibitors to treat rheumatoid arthritis Inventor(s): Okumura, Takako ; (Chita-gun, JP), Shimojo, Masato ; (Chita-gun, JP), Audoly, Laurent ; (Groton, CT) Correspondence: Gregg C. Benson; Pfizer Inc.; Patent Department, MS 4159; Eastern Point Road; Groton; CT; 06340; US Patent Application Number: 20020077329 Date filed: October 15, 2001 Abstract: The invention features a method of treating rheumatoid arthritis in a mammal comprising administering an agent that inhibits prostaglandin EP4 receptor (EP4) activity. Also featured is a method of identifying agents that selectively inhibit EP4 activity in vivo. Excerpt(s): This application claims priority, under 35 U.S.C. .sctn.119(e), from U.S. provisional application No. 60/241,825 filed Oct. 19, 2000. ... The present invention features methods of treating rheumatoid arthritis by administering an agent that inhibits prostaglandin EP4 receptor activity. The invention also includes methods of identifying agents that selectively inhibit prostaglandin EP4 receptor activity in vivo. ... Prostaglandin E.sub.2 (PGE.sub.2) is a potent modulator involved in the pathogenesis of arthritis. PGE.sub.2 binds to at least four subtypes of PGE receptor, designated EP1, EP2, EP3, and EP4. Molecular studies have revealed that all subtypes are 7transmembrane spanning receptors that belong to the G-protein coupled receptor superfamily (Robert et al., Am. Soc. Pharm. Exp. Ther. 46: 205-29, 1994). EP1 activation stimulates the release of intracellular calcium via a G protein-mediated mechanism; EP2 and EP4 both activate adenylate cyclase via stimulatory G proteins, but differ in their response to certain ligands; and EP3 inhibits adenylate cyclase via inhibitory G-proteins (Robert et al., supra, Negishi et al., Biochimica Biophys. Acta 1259:109-20, 1995). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Gene therapy composition for treating arthritis Inventor(s): Ho, Seong-Hyun ; (Incheon, KR), Hahn, Woong ; (Seoul, KR), Kim, JongMook ; (Seoul, KR), Kim, Sunyoung ; (Seoul, KR) Correspondence: David A. Einhorn, Esq.; Anderson Kill & Olick, P.C.; 1251 Avenue of the Americas; New York; NY; 10020; US Patent Application Number: 20030130223 Date filed: December 27, 2002 Abstract: An intramuscular injection composition for treating arthritis in a mammal, which comprises a DNA encoding interleukin-1 receptor antagonist (IL-1Ra) and pharmaceutically acceptable carriers Excerpt(s): This application is a non-provisional application of U.S. Serial No. 60/344,316, which was filed on Dec. 28, 2001. ... The present invention relates to an intramuscular injection composition for treating arthritis which comprises a DNA encoding interleukin-1 receptor antagonist; and a method for treating arthritis by injecting same into the muscles. ... Rheumatoid arthritis (RA) is a chronic disease characterized by inflammation of the joints with concomitant destruction of cartilage and bone (Kaklamanis P. M., Clin. Rheumatol, 11: 41-7(1992)). Although the causes of RA are not fully understood, various experimental and clinical studies have suggested
Patents 427
that proinflammatory cytokines, particularly interleukin-1 (IL-1) has an important role in RA pathogenesis(Arend W P and Dayer J M, Arthritis Rheum, 38: 151-60(1995); Arner E C, Arthritis Rheum, 32: 288-97(1989); Miyasaka N, et al., Arthritis Rheum., 31: 4806(1988); and van de Loo F A, et al., J Rheumatol., 19: 348-56(1992)). It is well known that IL-1 can stimulate monocytes, recruit inflammatory cells, and induce secretion of factors that degrade cartilage (Dinarello C A, Blood, 77: 1627-52(1991)). In animal studies, systemic administration of IL-1 has been found to accelerate the development of CIA (collagen-induced arthritis) (Hom J T, et al., J. Immunol., 141: 834-41(1988)). IL-1 is present in the synovial fluid of patients with RA and in RA synovium (Nouri A M, et al., Clin. Exp. Immunol., 55: 295-302(1984); and MacNaul K L, et al., J. Immunol., 145: 415466(1990)). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
HUMAN T CELL CLONE SPECIFIC FOR RHEUMATOID ARTHRITIS Inventor(s): TSURUTA, YUJI ; (OSAKA, JP), SUZUKI, RYUJI ; (NARA, JP), TOYOSAKI-MAEDA, TOMOKO ; (HYOGO, JP), TAKEMOTO, HIROSHI ; (HYOGO, JP) Correspondence: FOLEY & LARDNER; WASHINGTON HARBOUR; 3000 K STREET NW SUITE 500; PO BOX 25696; WASHINGTON; DC; 20007-8696; US Patent Application Number: 20020076725 Date filed: September 14, 1998 Abstract: A human T cell clone recognizing an antigen expressed by a synovial cell of a rheumatoid arthritis (RA) patient in HLA-DR-restricted manner is disclosed, which clone is very useful in exploring the pathogenesis of RA and developing a method for treating and preventing RA. Excerpt(s): The present invention relates to an agent useful in diagnosing, preventing and/or treating an autoimmune disease, and particularly, to a T cell clone which is specifically reactive to an antigen presented on a certain HLA-DR which is expressed by a synovial cell of a patient suffering from rheumatoid arthritis (RA). ... An immune response, which is primarily a reaction to destroy and eliminate exogenous material invading from external ambient, is usually induced specifically for a non-self molecule (antigen). However, when the recognizability between a self and a non-self molecule is disordered by some reasons (failure in self tolerance), various autoimmune diseases develop, such as systemic erythematodes, pachydermia, multiple sclerosis (MS), rheumatoid arthritis (termed as RA, hereinafter), and the like. RA frequently attacks women after middle-age. Predominant symptoms of RA include the swelling and deformation, pain, and motor function failure in joints, and its histopathological finding is an abnormal outgrowth of synovial tissues lining capsula articularis joint capsule). At the outgrowing tissues, a large number of immunocompetent cells (neutrophile, macrophage, lymphocyte), as well as a folicle formation of B cells, which are responsible for antibody production, and a population of helper T cells, are observed. Previous epidemiologic survey has shown that RA is associated with HLA-DRB1 allele as a disease-sensitive gene, and that RA frequently attacks women at pre- and postmenopausal period. Pathologically, the infiltration of memory type CD4-positive, CD45RO-positive T cells into lesions (synovial tissue) has been found, suggesting that the helper T cells having a memory for a certain antigen would be highly responsible for the onset of RA. ... Nowadays, although non-steroidal anti-inflammatory agents, immunomodulators, and steroid agents are predominately utilized in the therapy for
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RA, these medicaments may produce various side effects (gastrointestinal injury, nephropathy, and the like). Additional disadvantages in the usage of immunomodulators include the delayed exertion of effect, and besides a possible ineffectiveness due to its repetitive administration, and therefore, the usage of immunomodulators is questionable. Recently, it is begining that immunosuppressants are used in order to control more efficiently the inflammation. Unfortunately, imuunosuppressants may produce severe side effects such as myelopathy, and therefore, there is a large demand of the exploration for a treatment targeting the lesion. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
ISOLATED NUCLEOTIDE SEQUENCES ASSOCIATED WITH MULTIPLE SCLEROSIS OR RHEUMATOID ARTHRITIS AND A PROCESS OF DETECTING Inventor(s): MANDRAND, BERNARD ; (VILLEURBANNE, FR), TUKE, PHILIP WILLIAM ; (LONDON, GB), GARSON, JEREMY ALEXANDER ; (GUILDFORD, GB), KOMURIAN-PRADEL, FLORENCE ; (SAINT CYR AU MONT D'OR, FR), PARANHOS-BACCALA, GLAUCIA ; (LYON, FR), BEDIN, FREDERIC ; (LYON, FR), BESEME, FREDERIC ; (VILLEFONTAINE, FR), PERRON, HERVE ; (LYON, FR), JOLIVET-REYNAUD, COLETTE ; (BRON, FR) Correspondence: OLIFF & BERRIDGE, PLC; P.O. BOX 19928; ALEXANDRIA; VA; 22320; US Patent Application Number: 20030039664 Date filed: November 26, 1997 Abstract: The invention provides viral material and nucleotide fragments associated with multiple sclerosis and/or rheumatoid arthritis for use in methods of diagnosis, prophylaxis, and therapy. Excerpt(s): This application is a continuation-in-part of U.S. application Ser. No. 08/756,429, filed Nov. 26, 1996. ... Multiple sclerosis (MS) is a demyelinating disease of the central nervous system (CNS), the cause of which remains as yet unknown. ... "Multiple sclerosis (MS) is the most common neurological disease of young adults with a prevalence in Europe and North America of between 20 and 200 per 100,000. It is characterized clinically by a relapsing/remitting or chronic progressive course, frequently leading to severe disability. Current knowledge suggests that MS is associated with autoimmunity, that genetic background has an important influence and that "infectious" agent(s) may be involved. Indeed, many viruses have been proposed as possible candidates but as yet, none of them has been shown to play an aetiological role. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
Patents 429
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Method and apparatus for arthritis diagnosis Inventor(s): Reuss-Borst, Monika ; (Bad Kissingen, DE), Tresp, Volker ; (Muenchen, DE), Rost, Helmut ; (Uttenreuth, DE), Metzger, Georg ; (Hagenau, DE), Mayer, Peter ; (Muenchen, DE), Beuthan, Juergen ; (Berlin, DE), Scheel, Alexander ; (Gottingen, DE) Correspondence: SCHIFF HARDIN & WAITE; 6600 SEARS TOWER; 233 S WACKER DR; CHICAGO; IL; 60606-6473; US Patent Application Number: 20010037811 Date filed: February 1, 2001 Abstract: In a method and apparatus for determining the circumference of a finger or toe joint, in particular a proximal interphalangeal joint, to be evaluated in the context of an arthritis examination of an examination subject, the joint is irradiated using a light source and at least one two-dimensional projection image is recorded using a camera apparatus. From the projection image, the diameter of the joint is determined by means of an automatic edge detection method, and the circumference is calculated on the basis of the diameter. Additionally, a diaphanoscopic examination of the joint can be made with the same apparatus, and the results combined with the diameter information to identify or monitor a degree or progress of the inflamation. Excerpt(s): The present invention is directed to a method for determining the circumference of a digit joint (finger joint or toe joint,) in particular a proximal interphalangeal joint, to be evaluated in the context of an arthritis examination of an examination subject. ... In the field of medicine, the task increasingly arises of being able to detect and evaluate pathological changes in tissue caused by metabolism in a simple manner that disturbs the patient as little as possible. An example of such pathological tissue changes is represented by rheumatic joint changes or rheumatic diseases in the area of the tissue. The finger joints, and above all the proximal interphalangeal joints, are particularly affected by such changes. Chronic arthritis often occurs as a symptom of aging, but also can be observed in younger people. The rheumatoid inflammation process of synovialis, i.e., an inflammation in the region of the joint, is associated with a swelling in the joint region. The stronger the degree of inflammation and thus of the rheumatic attack, the stronger is the swelling and thus the greater the circumference at the joint. This characteristic value describing the state of the joint is recorded in the context of an arthritis examination for diagnostic purposes, but the determination of the circumference is made manually by means of a flexible measuring strip that is placed around the joint. The measurement value is read from the measuring strip by the rheumatologist or by a medical technician, and is allocated to the respective finger joint and entered into the patient's database. The measurement precision is thereby at least +/-0.5 mm, but has proven to be larger in practice, which is related to the fact that the measuring strip can be drawn around or placed on the joint with varying strength, because the tissue and the skin are compressible. Reliable measurement values, which in particular could be used in the context of a running diagnosis, thus are not obtained. ... An object of the present invention is to provide a method which allows the circumference of a digit joint, which represents an important characteristic value for the diagnosis of arthritis, to be measured with sufficient precision. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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METHOD FOR TRATMENT OF NON-RHEUMATOID ARTHRITIS Inventor(s): MACIAS, WILLIAM LOUIS ; (INDIANAPOLIS, IN) Correspondence: ELI LILLY AND COMPANY; PATENT DIVISION; P.O. BOX 6288; INDIANAPOLIS; IN; 46206-6288; US Patent Application Number: 20030119860 Date filed: February 24, 2000 Abstract: A method is disclosed for the treatment of non-rheumatoid arthritis by administering to a mammal in need thereof a therapeutically effective amount of an sPLA 2 inhibitor. Excerpt(s): The present invention is directed to a method for treating non-rheumatoid arthritis. More specifically, the present invention is directed to a method for treating the causes and/or the symptoms of various forms of non-rheumatoid arthritis in mammals by administering a therapeutically effective amount of an sPLA.sub.2 inhibitor. ... "Arthritis" is the name given to disease states encompassing many different conditions frequently having entirely different symptoms, causes, and known treatments. Although, the word "arthritis" means joint inflammation, it has come to encompass disorders that affect not only the joints but other connective tissue of the body including supporting structures such as muscles, tendons, and ligaments as well as the protective coverings of internal organs. Some of the most commonly occurring forms of arthritis are osteoarthritis, ankylosing spondylitis, rheumatic fever, and gout. Some forms of inflammatory arthritis are characterized by lymphokine-mediated inflammation of the joints. The use of selected secretory phospholiase A2 (sPLA.sub.2) inhibitors to treat rheumatoid arthritis is described in European Patent No. 0675110 (published Oct. 4, 1995) and in U.S. Pat. No. 5,654,326. ... The most common form of non-rheumatoid arthritis is osteoarthritis, a degenerative joint disease which primarily affects cartilage that covers and cushions the ends of the bones causing it to fray, wear, ulcerate, and in extreme cases, to disappear entirely leaving a bone on bone joint. The disease can result in severe disability particularly in the weight bearing joints such as the knees, hips, and spine. Osteoarthritis is distinguishable, for example, from rheumatoid arthritis in that osteoarthritis involves little or no inflammation and is confined to the joints and surrounding tissue where there is a breakdown or disintegration of cartilage and other tissue thereby making it difficult for the joints to operate properly. The occurrence of osteoarthritis frequently increases with advancing years. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Method for treating rheumatoid arthritis with composition containing histone Inventor(s): Hong, Seung-Suh ; (Daejon, KR), Bae, Insoo ; (Daejon, KR), Kim, Dong-soo ; (Seoul, KR), Yim, Heajoon ; (Daejon, KR), Jung, Neon-Cheol ; (Daejon, KR), Lee, Hyun-Soo ; (Seoul, KR), Yi, Yong-Weon ; (Daejon, KR) Correspondence: DARBY & DARBY P.C.; Post office Box 5257; New York; NY; 101505257; US Patent Application Number: 20030007964 Date filed: June 12, 2002 Abstract: The present invention relates to a novel use of histone and an active fragment thereof and provides a pharmaceutical composition containing histone as an active
Patents 431
ingredient to improve the symptoms of progressive, inflammatory and autoimmune arthritis. The pharmaceutical composition of the present invention includes histone, especially histone H1, histone H2A, histone H2B, histone H3, histone H4, an active fragment thereof, and a mixture thereof as an active ingredient, and could include pharmacologically approved carriers if necessary. Histone or its active fragment lowered induction of arthritis and reduced arthritis index more effectively than steroidal dexamethasone and also had a significant preventive effect. Excerpt(s): The present invention relates to the use of histone or an active fragment thereof in improving inflammatory symptoms of arthritis by many possible mechanisms. Histone or an active fragment thereof lowers induction of arthritis and reduces the arthritis index more effectively than steroidal dexamethasone and also has a significant preventive effect. ... The present invention relates to biologically active compositions to improve symptoms of progressive, inflammatory and autoimmune arthritis. Despite the development of many arthritis drugs, arthritis remains a world wide serious disease due to an increasing aging population. Even though the death rate due to arthritis is low, the quality of life of an individual who suffers from this disease is sacrificed with lowered activity level and productivity. ... Among many types of arthritis, the most significant one is rheumatoid arthritis. Rheumatoid arthritis is an autoimmune disease caused by the action of auto-reactive T lymphocytes. T lymphocytes cause rheumatoid arthritis via secondary hypersensitivity. It is not fully understood which antigen is recognized by T lymphocytes to cause this disease. Type II collagen is known to be the most probable one, but other possibilities cannot be excluded. Anti-histone autoantibody has been discovered even though it is not clear that this antibody is the cause of the disease. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
Methods for treating arthritic disorders Inventor(s): Hu, Baihua ; (Audubon, PA), Clark, James D. ; (Acton, MA), Sum, FukWah ; (Pomona, NY), Thakker, Paresh ; (Boston, MA), Chen, Lihren ; (Cambridge, MA), Lee, Katherine L. ; (West Newton, MA), Tam, Steve Y. ; (Wellesley, MA), McKew, John C. ; (Arlington, MA), Behnke, Mark ; (Sommerville, MA) Correspondence: WYETH; PATENT LAW GROUP; FIVE GIRALDA FARMS; MADISON; NJ; 07940; US Patent Application Number: 20030166649 Date filed: November 22, 2002 Abstract: This invention provides methods for treating in mammals arthritic or rheumatic disorders using substituted indole compounds of the general formula: 1and pharmaceutically acceptable salt forms thereof, and methods for using the compounds as inhibitors of the activity of various phospholipase enzymes, particularly phospholipase A.sub.2 enzymes, and for the medical treatment, prevention and inhibition of pain and inflammation. Excerpt(s): The present invention relates to methods of treating or alleviating the symptoms of arthritic and rheumatic disorders in mammals, including humans, the methods utilizing chemical inhibitors of the activity of various phospholipase enzymes, particularly cytosolic phospholipase A.sub.2 enzymes (cPLA.sub.2), more particularly including inhibitors of cytosolic phospholipase A.sub.2 alpha enzymes (CPLA.sub.2.alpha.). ... Leukotrienes and prostaglandins are important mediators of
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inflammation, each of which contributes to the development of an inflammatory response in a different way. Leukotrienes recruit inflammatory cells such as neutrophils to an inflamed site, promote the extravasation of these cells and stimulate release of superoxide and proteases which damage the tissue. Leukotrienes also play a pathophysiological role in the hypersensitivity experienced by asthmatics [See, e.g. B. Samuelson et al., Science, 237:1171-76 (1987)]. Prostaglandins enhance inflammation by increasing blood flow and therefore infiltration of leukocytes to inflamed sites. Prostaglandins also potentiate the pain response induced by stimuli. ... Prostaglandins and leukotrienes are unstable and are not stored in cells, but are instead synthesized [W. L. Smith, Biochem. J., 259:315-324 (1989)] from arachidonic acid in response to stimuli. Prostaglandins are produced from arachidonic acid by the action of COX-1 and COX-2 enzymes. Arachidonic acid is also the substrate for the distinct enzyme pathway leading to the production of leukotrienes. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
Methods for treating rheumatoid arthritis using IL-17 antagonists Inventor(s): Mohler, Kendall M. ; (Poulsbo, WA) Correspondence: IMMUNEX CORPORATION; LAW DEPARTMENT; 51 UNIVERSITY STREET; SEATTLE; WA; 98101 Patent Application Number: 20020136724 Date filed: October 18, 2001 Abstract: A method of treating a mammal afflicted with rheumatoid arthritis comprising administering a soluble form of IL-17 receptor is disclosed. Excerpt(s): This application claims the benefit under U.S.C. 119(e) of U.S. provisional application serial number 60/241,230, filed Oct. 18, 2000. All of which is incorporated by reference herein. ... The invention pertains to methods for treating certain diseases and disorders associated with inflammatory and immunoregulatory responses. More particularly, the present invention involves treating rheumatoid arthritis by administering an IL-17 inhibitor or IL-17 antagonist, in particular IL-17 receptor, to an individual afflicted with such rheumatoid arthritis. ... Cytokines are hormone-like molecules that regulate various aspects of an immune or inflammatory response. Cytokines exert their effects by specifically binding receptors present on cells, and transducing a signal to the cells. Rouvier et al. (J. Immunol. 150:5445; 1993) reported a novel cDNA which they termed CTLA-8; cloning of the human homolog led to the identification of this family of molecules as Interleukin-17 (IL-17; Yao et al., Immunity 3:811; 1995). IL-17 is a cytokine produced by activated T cells that stimulates the secretion of various proinflammatory molecules, including tumor necrosis factor .alpha. (TNF-.alpha.), Interleukin-1 .beta. (IL-1.beta.) and prostaglandin E.sub.2 (PGE.sub.2) from macrophages (Jovanovic et al., J. Immunol. 160:3513; 1998). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
Patents 433
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Methods of ameliorating arthritis by modulating JNK signalsome activity Inventor(s): Firestein, Gary S. ; (Del Mar, CA) Correspondence: GARY CARY WARE & FRIENDENRICH LLP; 4365 EXECUTIVE DRIVE; SUITE 1600; SAN DIEGO; CA; 92121-2189; US Patent Application Number: 20030068660 Date filed: September 10, 2002 Abstract: Methods for identifying an agent that modulates JNK signalsome mediated signal transduction are provided. As provided are methods of ameliorating an arthritis in a subject by inhibiting JNK signalsome activity in cells of the subject. Excerpt(s): This application claims the benefit under 35 U.S.C. 119(e) of U.S. Serial No. 60/323,195, filed Sep. 12, 2001, which is incorporated herein by reference in its entirety. ... This invention relates generally to the identification of protein complex that regulate a signal transduction pathway in synoviocytes of subjects with arthritis, and, more specifically, to complexes formed by the specific association of a c-Jun N-terminal kinase (JNK) and at least one MAP kinase kinase (MKK), including, for example, a JNK signalsome comprising a complex of JNK, MKK4 and MKK7; to complexes formed by the specific association of MKK4 or MKK7 with a MAP kinase kinase kinase (MAP3K); to methods of identifying agents that modulate JNK mediated signal transduction in synoviocytes; and to methods of ameliorating a disorder associated with abnormal JNK signalsome mediated signal transduction, including, for example, an arthritis such as rheumatoid arthritis or osteoarthritis. ... Rheumatoid arthritis (RA) is the most common inflammatory arthritis and is characterized by synovial inflammation and hyperplasia. RA is a systemic, chronic, inflammatory disease that generally affects joints of the fingers, toes, elbows, knees, ankles and spine (see Pathology, 3d edition (ed. Rubin and Farber; Lippincott-Raven 1998); pages 1396-1400). RA is more common in women than men, and onset can occur at any age, though it generally begins in the third or fourth decade, with the incidence increasing with age. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Mouse model for rheumatoid arthritis Inventor(s): Hayashi, Takuma ; (Malden, MA), Faustman, Denise L. ; (Weston, MA) Correspondence: Leon R Yankwich; Yankwich & Associates; 201 Broadway; Cambridge; MA; 02139; US Patent Application Number: 20030005469 Date filed: July 16, 2002 Abstract: Nonobese Diabetic Mice (NOD mice) that do not develop diabetes may be bred to produce F.sub.1 offspring that develop a condition that closely mimics rheumatoid arthritis (RA) in humans. The RA-like disease in the F.sub.1 mice, designated NOD-RA mice, is similar to human RA in clinical, radiological, histological and serological characteristics. The parents (F.sub.0) and their progeny (F.sub.1) are not diabetic and never develop hyperglycemia, and the parental mice (F.sub.0) do not themselves exhibit any symptoms of the RA-like condition that afflicts some of their progeny. The incidence, penetrance, gender domination, progression, and lifelong exacerbation of symptoms after pregnancy shown in the RA-like condition afflicting NOD-RA mice are all comparable to phenomena observed in the human disease. The
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NOD-RA mice provide a new spontaneous model of human RA that will be useful for studying rheumatoid arthristis and testing new drugs and reagents for treating or diagnosing the disease. Excerpt(s): The present invention pertains to the field of medical research, particularly to the development of mammalian models of human rheumatoid arthritis. ... Rheumatoid arthritis (RA) is a common autoimmune disease characterized by joint swelling, deformation and, ultimately, destruction, culminating in severe physical disability. De Graaf et al., in The Epidemiolog of Chronic Rheumatism, Dellgren and Ball, eds. (Blackwell, Oxford, 1963), pp. 446-56; Meenam et al., Arthritis Rheum., 24:544-50 (1981); Gabriel et al., J. Rheumatol, 26:1269-74 (1999); James, Clin Exp. Rheumatol, 17:392-93 (1999). RA is a progressive condition with well-recognized symptoms including symmetrical peripheral joint swelling and synovial inflammation while sparing the axial skeleton; the presence of rheumatoid factor (RF) autoantibodies; increased concentrations of interleukin-6 (IL-6), interleukin-1.beta. (IL-1.beta.), and granulocyte/macrophage colony-stimulating factor (GM-CSF) in serum and synovial fluid; low concentrations of interleukin-ra (IL-ra); and pregnancy-induced disease remission followed by severe postpartum flares, that is, while women with RA commonly undergo remission during pregnancy, the disease returns and may be even more severe and show a new onset or more accelerated course after delivery. See, Turgen, in Immunology and Serology in Laboratory Medicine. 2.sup.nd edition, Shanahan ed. (Mosby Year Book, St. Louis, 1996), pp. 387-98; Hirano et al., Eur. J. Immunol, 18:1797-1801 (1988); Wilder et al., Ann. N. Y. Acad. Sci., 876:14-31 (1999); Iijima et al., J. Rheumatol, 26:755-56 (1999); Ostensen, Ann. N.Y Acad. Sci., 876:13143 (1999). In medical research directed to understanding, diagnosing and treating RA, several animal models of the disease have been described, but no spontaneous animal model that closely mimics all the features of the human disease has been discovered (See, for example, Hang et al., 1982. J. Exp. Med., 155:1690-1701; and Kouskoff et al., 1996. Cell, 87:811-822). ... Kouskoffet al. report a RA mouse model that exhibits aggressive arthritis, produced by mating a T cell receptor (TCR) transgenic mouse strain with a NOD strain. This RA mouse model is strictly dependent on the presence of the KRN transgene and is characterized by several inherent symptomological features of RA that distinguish it from human RA (hRA), however, including: 100% penetrance, early (i.e., 25-35 days) onset of disease, attack of the distal interphalangeal joints, inflammation of the spine, large excess of myeloid cells over T lymphocytes and plasma cells in the synovial membrane, a total absence of rheumatoid factor (RF) autoantibodies, and a coating of IgG deposits on internal organs. These features result in a more aggressive RA than the RA typically found in humans. Human RA has preferential disease expression in middle-aged females, peripheral disease sparing of the DIP joints, rheumatoid factor autoantibodies, similar peripheral and joint cytokine derangements, etc. The mechanism of development of arhritis-like disease in NOD/TCR mice differs dramatically from that of natural RA expression in humans, limiting the utility of this RA mouse as a model for hRA. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Novel drug targets for arthritis Inventor(s): Li, Jinan ; (Umea, SE), Holmdahl, Rikard ; (Lund, SE), Ny, Tor ; (Umea, SE) Correspondence: DARBY & DARBY P.C.; Post Office Box 5257; New York; NY; 101505257; US Patent Application Number: 20030096733 Date filed: July 10, 2002 Abstract: Novel drug targets for the treatment or prevention of arthritis are provided. Screening methods for inhibitors of the plasminogen-activation pathway, such as, for example, antagonists or inhibitors of the urokinase-type plasminogen activator (uPA), plasminogen-activator type 1 (PAI-1), the urokinase activator receptor (uPAR), and plasmin, are used to identify novel drugs for treating or preventing the progression of arthritis. Such screening methods, or methods for evaluating whether a drug is useful for treating or preventing arthritis, can also be conducted in animal models described herein. Methods of treating or preventing such diseases are also provided. Excerpt(s): This application claims the priority of U.S. provisional application serial Nos. 60/304,461, filed Jul. 10, 2001; 60/304,490, filed Jul. 10, 2001; and 60/305,182, filed Jul. 13, 2001. The disclosures of these applications are incorporated herein by reference in their entireties. ... This invention relates to arthritic diseases and conditions. In particular, the invention relates to novel treatment or prevention strategies for arthritis such as rheumatoid arthritis. In addition, the invention relates to animal models and screening methods for identifying and evaluating drugs against such drug targets. ... Arthritis compromises the quality of life for large numbers of people. For example, more than 5 million people suffer from rheumatoid arthritis (RA) worldwide, of which 2.5 million are in the United States. About 50,000-70,000 children in the United States have been diagnosed with juvenile RA, and psoriatic arthritis affects in the range of 2.5 to 5 million people in the United States alone. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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PEPTIDE DERIVED FROM AN ANTIGEN RECOGNIZED BY AUTOANTIBODIES FROM PATIENTS WITH RHEUMATOID ARTHRITIS, ANTIBODY DIRECTED AGAINST SAID PEPTIDE, A COMBINATORIAL ANTIGEN, AND A METHOD OF DETECTING AUTO- IMMUNE ANTIBODIES Inventor(s): RAATS, JOZEF MARIA HENDRIK ; (NIJMEGEN, NL), HOET, RENE MICHAEL A ; (NIJMEGEN, NL), VAN VENROOIJ, WALTHERUS JACOBUS W ; (NIJMEGEN, NL) Correspondence: PEACOCK MYERS AND ADAMS P C; P O BOX 26927; ALBUQUERQUE; NM; 871256927 Patent Application Number: 20020137092 Date filed: September 30, 1999 Abstract: The invention relates to a peptide derived from an antigen recognized by autoantibodies, which peptide is reactive with autoimmune antibodies from a patient suffering from rheumatoid arthritis. The peptide according to the invention possesses a modified arginine residue. The invention also relates to antibodies against the peptide and a method of detecting autoimmune antibodies.
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Excerpt(s): The present invention relates to a peptide derived from an antigen recognized by autoantibodies from patients with rheumatoid arthritis, which peptide is reactive with autoimmune antibodies from a patient suffering from rheumatoid arthritis. ... Such a peptide is known from the European patent application 0 511 116 (Clonatec S. A.). This application describes an antigen comprising a filaggrin or profilaggrin fragment. The peptide is recognized by rheumatoid arthritis-specific autoimmune antibodies. Rheumatoid arthritis (RA) is a systemic autoimmune disease. It is the most commonly occurring inflammatory disease of the joints, it is chronic and may lead to severe physical disablement. ... The object of the present is to provide a peptide which is reactive with autoimmune antibodies from a patient suffering from rheumatoid arthritis, which peptide is suitable for diagnostic research with increased specificity while also being useful for other purposes such as obtaining (raising, selecting and isolating) poly- and monoclonal antibodies. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
Peptides designed for the diagnosis and treatment of rheumatoid arthritis Inventor(s): Meheus, Lydie ; (Merelbeke, BE), Moereels, Henri ; (Ekeren, BE), Union, Ann ; (Aalter, BE) Correspondence: Patricia A. Kammerer; Howrey Simon Arnold & White, LLP; 750 Bering Drive; Houston; TX; 77057-2198; US Patent Application Number: 20020143143 Date filed: December 21, 2000 Abstract: The present invention relates to peptides that mimic the immunogenic determinants of self-proteins recognized by autoimmune antibodies in a biological sample from patients suffering from rheumatoid arthritis (RA). More particularly, the present invention relates to citrulline-containing peptides, which react with the majority of the latter antibodies. Furthermore, the present invention relates to diagnostic tools for a more convenient and sensitive diagnosis of RA and to therapeutic methods to treat RA. Excerpt(s): The present invention relates to peptides that mimic the immunogenic determinants of self-proteins recognised by autoimmune antibodies in a biological sample from patients suffering from rheumatoid arthritis (RA). More particularly, the present invention relates to citrulline-containing peptides, which react with the majority of the latter antibodies. Furthermore, the present invention relates to diagnostic tools for a more convenient and sensitive diagnosis of RA and to therapeutic methods to treat RA. ... Rheumatoid arthritis is a major crippling joint disease, which is systemic in nature and of unknown etiology. It affects 1% of the population, with a male to female ratio of 2:3. In terms of morbidity, the most important feature of RA is joint erosion which leads to pain, deformity and in some cases, severe disability. Life expectations in patients with a severe form of the disease are reduced by up to 10 years. RA has all the features of an autoimmune disease, including the presence of a variety of autoantibodies in patients' sera and the capacity to induce illness by transfer of pathogenic T cells in animal models. The classification of the disease can be challenged on the grounds that borderline forms are very common; furthermore inflammation of the joints is not only restricted to RA, but occurs also in other non-autoimmune diseases such as osteoarthritis, reactive arthritis and gout. ... The diagnosis of rheumatoid arthritis is initially based on clinical manifestations. As an early diagnosis allows an adjusted treatment, which can highly improve life quality of the patients, it is of major
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importance for rheumatologists to have reliable diagnostic criteria at their disposal. Serological support for diagnosing RA is not very well established and is based mainly on the presence of rheumatoid factors (RF). However, a substantial number of RA patients are RF-negative, while on the other hand, RF is also present in other rheumatic diseases including Sjogren's syndrome and systemic lupus erythematosus, in some chronic bacterial and acute viral infections, in certain parasitic diseases and chronic inflammatory diseases, and has furthermore been demonstrated in sera from healthy persons. The rather low specificity of RF thus necessitates additional testing for a second RA-specific antibody. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
Pet food for maintenance of joint health and alleviation of arthritic symptoms in companion animals Inventor(s): Bektash, Roger ; (Barnawartha, AU), Hodge, Jason ; (Port Lonsdale, AU), Bui, Linh M. ; (Sylmar, CA), Blackwood, Graeme ; (La Harba, CA), Bierer, Tiffany L. ; (Fullerton, CA) Correspondence: FULBRIGHT & JAWORSKI, LLP; 1301 MCKINNEY; SUITE 5100; HOUSTON; TX; 77010-3095; US Patent Application Number: 20030124219 Date filed: February 4, 2003 Abstract: A pet food product and process for producing the pet food product for use in maintenance of healthy joints and alleviation of arthritic symptoms in companion animals, the pet food comprising an effective amount of an active extract of Perna canaliculus. The extract can be either a powder or lipid extract. Preferably in an amount that provides for a dosage range of generally 0.18 to 114 mg of a powder extract/kg of body weight/day in a companion animal or an amount of generally 1.5 to 1000 mg of a powder extract of Perna canaliculus per 400 kcal of pet food product. Excerpt(s): This application is a continuation of U.S. application Ser. No. 09/273,933 filed on Mar. 22, 1999. ... The present invention relates to pet food for companion animals, and more particularly to pet food that includes an active quantity of an extract of Perna canaliculus in an amount that will provide a daily pet diet for the maintenance of joint health and for the alleviation of arthritic symptoms in companion animals such as dogs, cats and horses. ... The connective tissues of humans and non-human animals are constantly subject to stresses and strains from mechanical forces that can result in afflictions, such as arthritis (both rheumatoid and osteoarthritis), joint inflammation and stiffness. This is true for both humans and non-human animals, and particularly as they age. The underlying causes of rheumatoid arthritis and/or osteoarthritis are different such that rheumatoid arthritis is characterized as an autoimmune disease affecting both the joints and systemic immune functions, whereas osteoarthritis results from deterioration of the articular cartilage which may result in local inflammation of the joints. While a greater portion of humans with arthritis have rheumatoid arthritis, most of the arthritis occurring in companion animals is osteoarthritis. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Pipecolic acid derivatives of proline threonine amides useful for the treatment of rheumatoid arthritis Inventor(s): Hanson, Gunnar J. ; (Skokie, IL) Correspondence: J. Timothy Keane; PHARMACIA CORPORATION; Corporate Patent Department; P.O. Box 5110; Chicago; IL; 60680; US Patent Application Number: 20010027247 Date filed: February 26, 2001 Abstract: Non-peptidic compounds characterized by containing a segment condensed from pipecolic acid, aspartic acid, proline and threonine, or derivatives thereof, are useful to treat autoimmune diseases and inflammatory conditions. Compounds of particular interest are those of the formula: 1wherein R.sup.1 is phenyl or cyclohexyl; wherein R.sup.2 is hydrido or methyl; wherein R.sup.3 is selected from hydrido, hydroxy, acetylamino, acetyl(Lys/Tyr/Thr)NH--, propionylamino and benzyloxycarbonylamino; wherein R.sup.5 is selected from isopropyl, isobutyl, npropyl, n-butyl, aminopropyl, aminobutyl, phenyl, benzyl, hydroxyphenyl, hydroxybenzyl, morpholinocarbonylethyl, morpholinocarbonylpropyl, piperazinocarbonylethyl, piperazinocarbonylpropyl, pyridinylcarbonylethyl, pyridinylcarbonylpropyl, oxazolylcarbonylethyl, oxazolylcarbonylpropyl, azepinylcarbonylethyl and azepinylcarbonylethyl; wherein R.sup.6 is selected from hydrido, methyl, hydroxy, methoxy, phenyl and aminocarbonyl; wherein R.sup.7 is carboxyl or methylthiomethyl; wherein R.sup.9 is selected from hydrido, hydroxy, methoxy and phenyl; wherein R.sup.12 is selected from methyl, ethyl, propyl, butyl, isobutyl, --CH(iBu)CH.sub.2OH and --CH(iBu)CONH.sub.2; or a pharmaceuticallyacceptable amide, ester or salt thereof. A disease state of particular interest for use of the compounds would be rheumatoid arthritis. Excerpt(s): Non-peptidic compounds are described for treatment of autoimmune diseases. Of particular interest are pipecolic acid derivatives compounds incorporating a characterizing segment condensed from pipecolic acid, aspartic acid, proline and threonine, or derivatives thereof, which compounds are useful to treat rheumatoid arthritis. ... Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic inflammation of the synovium. This disease is triggered by an immune response generated via the molecular recognition of the T-cell receptor on CD4-positive T cells with a complex of disease-inducing peptides bound to Human Leukocyte Antigen (HLA) class II molecules. ... Rheumatoid arthritis (RA) is associated with the expression of certain HLA class II molecules, particularly the DR4-dw4, as well as DR1 and DR4dw14. It is known that blockade of the interaction between a given class II molecule, peptide ligand, and T cell receptor inhibits specific T cell responses both in vitro and in vivo. It is further known that blockade of the above interaction in animal models of autoimmunity prevents or ameliorates autoimmune disease. Inhibitor compounds which block the binding of disease-inducing peptides to an RA-associated HLA molecule, but which will not interfere with a patient's ability to generate other class IIrestricted immune responses, constitutes a selective immunosuppressive anti-RA therapy. Compounds which compete with disease-inducing endogenous peptides for binding to RA-associated HLA molecules and may thereby inhibit disease. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Polyacrylamide hydrogel for arthritis Inventor(s): Petersen, Jens ; (Birkerod, DK) Correspondence: Stanislaus Aksman; Hunton & Williams; Suite 1200; 1900 K Street, N.W.; Washington; DC; 20006; US Patent Application Number: 20030065389 Date filed: August 27, 2001 Abstract: A hydrogel for use as a prosthetic device for supplementing, augmenting or replacing cartilage in the intra-articular cavity of a joint and for treatment or prevention of arthritis. The hydrogel may be a polyacrylamide hydrogel obtained by combining acrylamide and methylene bis-acrylamide. A prosthetic device comprising the polyacrylamide hydrogel is also disclosed. Excerpt(s): The use of a hydrogel comprising 0.5 to 25% polyacrylamide by weight as a prosthetic device for the alleviation or prevention of pain in joints, such as weight bearing joints, is provides an advantageous treatment of arthritis. The hydrogel provides lubrication and support to existing cartilage in the intra-articular cavity of the joint. ... Arthritis is a degenerative condition which, when affecting the weight bearing joints such as the hip and knee joints, results in pain and hampered mobility. Arthritis may affect all joints. Degradation of articular and meniscal cartilage may result in damage to the surfaces separated by the cartilage and correspondingly to pain. Ageing is a primary cause of the degradation of the cartilage. The degradation may also result from, for example, congenital predisposition or trauma, such as repeated articulation of the joint. ... Arthritis has been treated traditionally with physiotherapy and more invasive treatments such as orthopaedic surgery and the introduction of artificial joint components. Non-steroidal anti-inflammatory agents have been used with some success but these agents may counterproductively hamper proteoglycan synthesis in collagen and cartilage as well as have undesirable side effects. Cortisone injections also weaken articular cartilage with time. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Polynucleotides and polypeptides associated with the development of rheumatoid arthritis Inventor(s): Lu, Pin ; (Princeton Jct., NJ), Neubauer, Michael G. ; (Skillman, NJ), Bowen, Michael ; (Rockville, MD), Nadler, Steven G. ; (Princeton, NJ), Carman, Julie ; (Lawrenceville, NJ) Correspondence: STEPHEN B. DAVIS; BRISTOL-MYERS SQUIBB COMPANY; PATENT DEPARTMENT; P O BOX 4000; PRINCETON; NJ; 08543-4000; US Patent Application Number: 20030170742 Date filed: December 3, 2002 Abstract: The present invention is directed to polynucleotides encoding polypeptides associated with the development of rheumatoid arthritis and homologs thereof. The invention further relates to diagnostic and therapeutic methods for utilizing these polynucleotides and polypeptides in the diagnosis, treatment, and/or prevention of rheumatoid arthritis and related disease states. The invention further relates to screening methods for identifying agonists and antagonists of the polynucleotides and polypeptides of the present invention, and compounds identified thereby.
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Excerpt(s): This application claims priority to U.S. Provisional Patent Application No. 60/337,429, filed Dec. 3, 2001, and hereby expressly incorporated by reference in its entirety. ... The present invention provides polynucleotides encoding polypeptides associated with the development and progression of rheumatoid arthritis and homologs thereof. Also provided are vectors, host cells, antibodies, and recombinant and synthetic methods for producing said polypeptides. The invention further relates to diagnostic and therapeutic methods for utilizing these polypeptides in the diagnosis, treatment, and/or prevention of rheumatoid arthritis and related disease states. The invention further relates to screening methods for identifying agonists and antagonists of the polynucleotides and polypeptides of the present invention. ... Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by progressive joint destruction. Initial destruction of cartilage and bone is associated with the formation of a pannus, consisting of a hypertrophic synovial membrane containing hyperplastic synoviocytes and an infiltrate of inflammatory cells including T cells, B cells, CD68+macrophages, mast cells, and endothelial cells. The causes of RA are not well understood. Genetic studies have linked expression of specific major histocompatibility complex class II antigens to the development of RA, suggesting the involvement of antigen-specific mechanisms in disease progression (Zanelli et al., Hum. Immunol. 61:1254-1261 (2000)). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
Process for production of bee venom as pharmaceutical product which can be used effectively in the treatment of rheumatoid arthritis and viral diseases Inventor(s): Abbadi, Ali Salem El ; (Giza, EG) Correspondence: NATH & ASSOCIATES; 1030 15th STREET; 6TH FLOOR; WASHINGTON; DC; 20005; US Patent Application Number: 20030118597 Date filed: October 11, 2002 Abstract: The traditional treatment for Rheumatoid Arthritis relies on a course of synthetic drugs, which range from the use of gold salts to anti-inflammatory drugs including both steroids and non-steroids. These drugs specially the steroids can affect adrenal and pituitary glands & cause impotence, edema, poor wound healing, reduce neurological response and cardiac irregularities.VACSERA began the first clinical studies with bee venom therapy and proved its efficiency for treatment of variety of diseases such as Rheumatoid arthritis and viral infections especially (HCV). Bee Venom was separated by a scientific method and then we determine the dosage form, toxicity, bioavailability, teratogenicity, (anti-teratogenic effect), safety and treatment schedule.The use of Bee venom in treatment of arthritis has been proved to be beneficial to many patients, primarily due to the presence of a number of polypeptides, peptides, enzymes and amines. The venom is administered according to the enclosed leaflet and physician instructions in doses which vary according to the disease and its severity. Excerpt(s): The invention relates to the adaptability of the traditional medicine (Bee venom) for treatment of a lot of diseases such as rheumatoid arthritis and viral diseases specially (HCV) in a pharmaceutical form and presents a noble service for many patients. ... Ancient Egyptians and Babilians were innovators; they used the Bee stings to relief pain accompanying Rheumatism and osteoarthritis since 2000 years B.C. ... Chinese have started the bee venom therapy since 1530 In the nineteenth century (1935) French.
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Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
Rheumatoid arthritis markers Inventor(s): Weyand, Cornelia M. ; (Rochester, MN), Goronzy, Jorg J. ; (Rochester, MN) Correspondence: MARK S. ELLINGER, PH.D.; FISH & RICHARDSON P.C., P.A.; Suite 3300; 60 South Sixth Street; Minneapolis; MN; 55402; US Patent Application Number: 20030027136 Date filed: March 23, 2001 Abstract: The invention provides methods and materials for evaluating arthritis conditions. Specifically, the invention provides methods and materials for determining the severity of an arthritis condition in a mammal that involve determining whether or not a sample from that mammal contains an elevated level of a CD21L polypeptide, a lymphotoxin-.beta. polypeptide, or a chemoattractant polypeptide. The invention also provides methods and materials for assisting medical or research professionals in determining the severity of an arthritis condition in a mammal. In addition, the invention provides methods and materials related to kits that can be used to determine the severity of an arthritis condition. Excerpt(s): The invention relates to methods and materials involved in determining the severity of a rheumatoid arthritis condition. ... Rheumatoid arthritis (RA) affects individuals in the prime of their life and is feared because of its potential to cause chronic pain and irreversible damage of tendons, ligaments, joints, and bones. The symmetrical involvement of small peripheral joints has an enormous impact on hand and foot functions and poses therapeutic challenges that cannot be easily overcome by joint replacement. Also, systemic manifestations of RA are not rare and can range from relatively minor problems, such as rheumatoid nodules, to life-threatening organ disease. ... In addition, RA is a systemic inflammatory disease that primarily manifests itself as synovial inflammation of diarthrodial joints. The typical histopathological changes include dense infiltration of the synovial membrane by mononuclear cells, neoangiogenesis, and hypertrophy and hyperplasia of the synovial lining (Harris (ed); Rheumatoid Arthritis, Philadelphia, WB Saunders Co., pp.3-212 (1997); and Hale and Haynes: Pathology of rheumatoid arthritis and associated disorders. Arthritis and Allied Conditions. A textbook of Rheumatology. Edited by Koopman. Baltimore, Williams & Wilkins, pp.9.sup.93-101.sup.6 (1997)). The etiopathogenesis of the syndrome is not well understood. Several lines of evidence support a central role of T lymphocytes in the disease-specific pathogenic events (Todd et al., Science, 240:1003-1009 (1988); Panayi et al., Arthritis Rheum., 35:729-735 (1992); and Goronzy and Weyand, Rheum. Dis. Clin. North Am., 21:655-674 (1995)). An alternative hypothesis, namely, that macrophages are the pivotal cell type in rheumatoid synovitis, has also been proposed (Firestein and Zvaifler, Arthritis Rheum. 33:768-773 (1990); and Burmester et al., Arthritis Rheum., 40:5-18 (1997)). Whether only T cells or only macrophages or both are the causative elements in RA remains a matter of controversy (Feldmann et al., Cell, 85:307-310 (1996); and Fox, Arthritis Rheum., 40:598-609 (1997)). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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RHEUMATOID ARTHRITIS REMEDY CONTAINING ANTI-IL-8 ANTIBODY AS ACTIVE INGREDIENT Inventor(s): MATSUSHIMA, KOUJI ; (CHIBA, JP), AKAHOSHI, TOHRU ; (TOKYO, JP) Correspondence: KATE H MURASHIGE; MORRISON & FOERSTER; 2000 PENNSYLVANIA AVENUE NW; SUITE 5500; WASHINGTON; DC; 200061888 Patent Application Number: 20010006637 Date filed: October 19, 1998 Abstract: A therapeutic agent for rheumatoid arthritis comprising anti-IL-8 antibody as an active ingredient. Excerpt(s): The present invention relates to a therapeutic agent for treating rheumatoid arthritis comprising anti-interleukin-8 (IL-8) antibody as an active ingredient. ... IL-8 is a protein that belongs to the C--X--C chemokine subfamily and was formerly designated as the monocyte-derived neutrophil chemotactic factor, the neutrophil attractant/activation protein-1, the neutrophil activating factor and the like. IL-8 is a factor that activates neutrophils and provides them with migratory ability, and is produced by a variety of cells in the presence of inflammatory cytokines such as IL1.beta., TNF.alpha., etc. (Koch, A. E. et al., J. Investig. Med. (1995) 43, 28-38; Larsen, C. G. et al., Immunology (1989) 68, 31-36), mitogens such as PMA, LPS etc. (Yoshimura, T. et al, Proc. Natl. Acad. Sci. U.S.A. (1987) 84, 9233-9237), and heavy metals such as cadmium etc. (Horiguchi, H. et al., Lymphokine Cytokine Res. (1993) 12, 421-428). ... It was reported that monocytes isolated from the synovial fluid of patients with rheumatoid arthritis had the elevated levels of expression of chemokines such as IL-8, GRO, MCAF, MIP-1.alpha., MIP-1.beta. and the like as compared to the monocytes isolated from the peripheral blood of healthy subjects or patients with rheumatoid arthritis (Hosaka, S. et al., Clin. Exp. Immunol. (1994) 97, 451-457). It is believed that overexpression of those various cytokines promotes migration of inflammatory cells to the joints, but it is not known which chemokine plays a central role in the pathogenesis. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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SYNTHETIC PEPTIDE FOR TREATMENT OF AUTOIMMUNE ARTHRITIS Inventor(s): SEYER, JEROME M. ; (MEMPHIS, TN), MYERS, LINDA K. ; (MEMPHIS, TN), KANG, ANDREW H. ; (MEMPHIS, TN) Correspondence: HOWARD M. EISENBERG,ESQ.; CHERNOFF,VILHAUER,MCCLUNG & STENCEL,LLP; 1600 ODS TOWER; 601 S.W. SECOND AVENUE; PORTLAND; OR; 972043157 Patent Application Number: 20020037844 Date filed: April 20, 1995 Abstract: Peptides for suppressing autoimmune arthritis by disrupting formation of trimolecular complexes which stimulate T cells. Excerpt(s): The present invention provides peptides for suppressing autoimmune arthritis that do not provoke a material immunogenic response from T cells. ... Autoimmune arthritis afflicts a large number of people and takes many forms including, rheumatoid arthritis, juvenile arthritis, psoriatic arthritis, spondylo arthritis, relapsing polychondritis and other connective tissue diseases. These arthritic conditions occur in
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mammals when T cells are activated by particular antigens or complexes containing antigens. When such activation occurs, proteolytic enzymes are produced which degrade tissues of the person or mammal afflicted by arthritis. The tissue targets of autoimmune arthritis are constituents of connective tissues in joints and tendons of mammals and ordinarily include type II collagen. Indeed autoimmune arthritis can be induced in mice, humans and other mammal by immunizing them with type collagen II derived from cartilage of the same or different mammals. See, Andriopoulos N A, Mestecky J. Miller E J, Bradley E L: Antibodies to native and denatured collagen in sera of patients with rheumatoid arthritis. Arth. Rheum. 19:613-617, 1976; Wooley P H, Luthra S. Singh S. Huse A, Stuart J M, David C S: Passive transfer of arthritis in mice by human anti-type II collagen antibody. Mayo Clinic Proc. 59:737-743, 1984. ... Autoimmune arthritis in mammals develops when T cells are activated by immunogenic complexes referred to as trimolecular complexes. These complexes are formed between antigenic peptides and major histocompatibility complex molecules (MHC). Buus, S., A. Sette, and H. M. Grey, (1987) "The interaction between protein-derived immunogenic peptides and Ia". Immuno. Rev. 98:115. These complexes then are recognized by the T cell receptors of antigen-specific T cells to form the tri-molecular complexes which result in the activation and subsequent functioning of T cells and in the development of arthritis. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
Treating arthritis in animals with dietary supplements Inventor(s): Myers, Andrew ; (Boise, ID) Correspondence: PEDERSEN & COMPANY, PLLC; P.O. BOX 2666; BOISE; ID; 83701; US Patent Application Number: 20030147971 Date filed: November 18, 2002 Abstract: The invention is a dietary supplement for animals, especially dogs, for treating arthritis and joint discomfort. A biscuit form of the supplement may be in the form of a conventional carrier composition of, for example, typical dog biscuit materials including cereal grains, vegetables or animal meat, fat and by-products. Typically, the biscuit contains about 89-97 weight percent (wt. %) of the conventional carrier composition. Optional vitamins and minerals may also be added to the carrier material, typically in about the 1-5 wt. % range. Importantly, the biscuit of the present invention contains about 3-7 wt. % of an arthritis-treating combination, namely, glucosamine sulfate, vitamin C and an array of intracellular ions namely potassium, sodium and iodine. The glucosamine component is present by weight at approximately the same level as the vitamin C, and at approximately 10 (ten) times the level of the sum of the above-named intracellular ions. The biscuit is formulated so that its composition is approximately:Glucosamine component, 5 mg to 5,000 mg;Vitamin C component, 5 mg to 3,000 mg;Potassium component, 50 mcg to 150 mg;Sodium component, 50 mcg to 150 mg; andIodine component, 25 mcg to 100 mg.The biscuit is dosed at approximately 10 mg glucosamine component per pound of body weight of the animal per day. Excerpt(s): This application is a continuation application of, and claims priority from, U.S. patent application Ser. No. 09/642,112, filed on Aug. 18, 2000, entitled "Treating Arthritis in Animals with Dietary Supplements", which application claims priority from Provisional Patent Application No. 60/149,779, filed Aug. 18, 1999, and which applications are hereby, incorporated by reference. ... This invention relates generally to
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animals and animal nutrition. More specifically, this invention relates to treating arthritis and joint discomfort in dogs by use of dietary supplements. ... Degenerative joint diseases or arthroses are conditions where degenerative changes in cartilage lead to a breakdown in the integrity of the structural matrix of cartilage or tendinous tissues. Conventionally referred to as arthritis, the complaints associated with the degenerative changes occur most frequently in aged individuals. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
Treatment for reactive arthritis or bursitis Inventor(s): Bonner, Ernest L. JR. ; (Alameda, CA), Hines, Robert ; (Fayetteville, NC) Correspondence: BEESON SKINNER BEVERLY LLP; ONE KAISER PLAZA, SUITE 2360; OAKLAND; CA; 94612; US Patent Application Number: 20030055022 Date filed: October 15, 2002 Abstract: A treatment for conditions in human beings associated with either or both reactive arthritis or bursitis comprising a combination of acyclovir, minocycline hydrochloride, and metronidazole. An alternate treatment comprises the combination of valacyclovir hydrochloride, minocycline hydrochloride, and metronidazole. Excerpt(s): This is a continuation of application Ser. No. 09/510,704, filed Feb. 22, 2000, which is still pending, which was a continuation-in-part of application Ser. No. 09/270,962, filed Mar. 17, 1999, now U.S. Pat. No. 6,087,382. ... This invention relates to an improved pharmaceutical formulation treatment of symptoms associated in humans with reactive arthritis or idiopathic bursitis. ... Reactive arthritis refers to a spondyloarthritity which usually arises as a complication of an infection elsewhere in the body. Reactive arthritis can be caused by species of Shigella bacteria (most notably Shigella flexneri), Yersinia enterocolitica, Campylobacter jejuni, several species of Salmonella, genitourinary pathogens, Chlamydia trachomatis, Neisseria gonorrhea, Ureaplasma urealyticum, Streptococcus pyogenes, and other yet unidentified infectious agents. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Treatment of arthritis and compositions therefore Inventor(s): Anastassiades, Tassos P. ; (Kingston, CA) Correspondence: MANELLI DENISON & SELTER; 2000 M STREET NW SUITE 700; WASHINGTON; DC; 20036-3307; US Patent Application Number: 20020045597 Date filed: August 24, 2001 Abstract: A 2-glucosamine derivative of the general formula (I): 1wherein R is an alkyl radical of the general formula C.sub.nH.sub.2n+1 and n is selected from 2-12; and pharmaceutically acceptable salts, esters and glucosides thereof, used for a treatment in a mammal selected from the group consisting of (a) arthritis, particularly osteoarthritis and inflammatory arthritis; (b) enhancing cartilage formation in a mammal; (c) enhancing chondrocytes cell proliferation; (d) production of glycosaminoglycan in a mammal; and (e) alleviating the symptoms of joint stiffness and restricted mobility.
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Excerpt(s): This invention relates to N-acylated glucosamine derivatives; methods of treating arthritis, particularly osteoarthritis and inflammatory arthritis, enhancing cartilage formulation, enhancing chondrocyte cell proliferation and glycosaminoglycan production in a mammal with said derivatives; and pharmaceutical compositions comprising said N-acylated glucosamine derivatives. ... It is known that glycoconjugates play an important role in many biological processes. The carbohydrate groups confer important physical properties such as conformational stability, protease resistance, charge and water-binding capacity; and biological recognition, where sequence diversity provides signals for protein targeting and cell-cell interactions (Paulson 1989). The glycoconjugates of connective tissue matrices consist of hexosamines that are Nacetylated. However, the function of the N-acetyl moiety is not known. ... The two major forms of arthritis in mammals are inflammatory arthritis, such as rheumatoid arthritis (RA), and osteoarthritis (OA), a progressive, degenerative loss of cartilage often secondary to mechanical stress, aging, dysplastic conditions and/or injury. Pain in OA is usually treated with NSAIDS (non-steroidal anti-inflammatory drugs). Inflammation and pain in RA is treated with NSAIDS, with new COX-2 inhibitors (also NSAIDS) and also with anti-metabolites such as methotrexate. Other immunomodulators in clinical use or trials include interleukins and TNF receptor antagonists. Glucosamine is a popular non-prescription, neutraceutical treatment for pain in OA. Since RA and OA have different pathologies, it is not obvious that a treatment for one should result in a treatment for the other. A recent review, J. Rheumatol. (1999) 26:11-Anastassiades T., notes that many reports of glucosamine/OA clinical trials indicate positive findings but the mechanism of action is unknown. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
Use of CD25 binding molecules in the treatment of rheumatoid arthritis or skin diseases Inventor(s): Schreier, Max H. ; (Basel, CH), Amlot, Peter Lloyd ; (London, GB), Schreier, Karin ; (Basel, CH) Correspondence: THOMAS HOXIE; NOVARTIS CORPORATION; PATENT AND TRADEMARK DEPT; 564 MORRIS AVENUE; SUMMIT; NJ; 079011027 Patent Application Number: 20020110558 Date filed: January 25, 2001 Abstract: Use of a CD25 binding molecule which comprises at least one antigen binding site comprising at least one domain which comprises in sequence, the hypervariable regions CDR1, CDR2 and CDR3; said CDR1 having the amino acid sequence Arg-TyrTrp-Met-His, said CDR2 having the amino acid sequence Ala-Ile-Tyr-Pro-Gly-Asn-SerAsp-Thr-Ser-Tyr-Asn-Gln-Lys-Phe-Glu-- Gly, and said CDR3 having the amino acid sequence Asp-Tyr-Gly-Tyr-Tyr-Phe-- Asp-Phe, in the treatment of rheumatoid arthritis or inflammatory or hyperproliferative skin diseases. Excerpt(s): The invention is directed to the use of a CD25 binding molecule in the treatment of rheumatoid arthritis or inflammatory and hyperproliferative skin diseases. ... More specifically the present invention provides in a first aspect the use of a CD25 binding molecule which comprises at least one antigen binding site comprising at least one domain which comprises in sequence, the hypervariable regions CDR1, CDR2 and CDR3; said CDR1 having the amino acid sequence Arg-Tyr-Trp-Met-His, said CDR2 having the amino acid sequence Ala-lle-Tyr-Pro-Gly-Asn-Ser-Asp-Thr-Ser-Tyr-Asn-GlnLys-Phe-Glu-- Gly, and said CDR3 having the amino acid sequence Asp-Tyr-Gly-Tyr-
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Tyr-Phe-- Asp-Phe; or direct equivalents thereof in the treatment of rheumatoid arthritis or inflammatory or hyperproliferative skin diseases. ... Treatment of rheumatoid arthritis includes control or amelioration of the disease and/or its sequellae, e.g. symptoms, such as number of tender and swollen joints, degree of tenderness and swelling, or pain, as well as control or amelioration of aetiological components. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
Use of harpagid-related compounds for prevention and treatment of osteoporosis, arthritis and ruptured disc and pharmaceutical composition containing the same Inventor(s): Kim, Sang Tae ; (Seoul, KR), Shin, Joon Shik ; (Seoul, KR), Han, Yong Nam ; (Seoul, KR) Correspondence: BIRCH STEWART KOLASCH & BIRCH; PO BOX 747; FALLS CHURCH; VA; 22040-0747; US Patent Application Number: 20020183264 Date filed: November 29, 2001 Abstract: In the present invention, it is discovered that a compound of formula (I) has a potent effect for treatment of osteoporosis, arthritis and ruptured disc: 1in which R.sub.1 represents hydrogen atom or alkyl group and R.sub.2 represents hydrogen atom r cinnamoyl group. Therefore, the compound of formula (I) can be used for prevention and treatment of osteoporosis, arthritis and ruptured disc. Thus, the present invention provides a pharmaceutical preparation containing as an effective component a compound of formula (I) in combination with a pharmaceutically acceptable auxiliary, diluent, isotonic agent, preservative, lubricant and solubilizing aid, which is formulated in the form of a pharmaceutically acceptable preparation and has a potent effect for osteoporosis, arthritis and ruptured disc. Excerpt(s): The present invention relates to a use of a harpagid-related compound as an agent for treating arthritis, osteoporosis and ruptured disc, and to a pharmaceutical composition containing said harpagid-related compound as an effective component. ... At present, it has been known that in Korea patients suffering from various bone diseases are on an increasing tendency annually. However, chemotherapy, operative therapy, etc. which have been currently used for the purpose of treating bone diseases have fail to realize the complete success as yet. Such bone diseases are advanced to chronic and degenerative state due to ageing, and further impose a great medical burden on a patient. Therefore, the development of novel materials which can be generally utilized in the clinical field is still urgently required. ... The constituent drugs contained in the galenic composition developed by the present inventors have been described in "Dongeubogam" and "Sinnongbonchokyung" as having various pharmacological activities including hematopoiesis, tonic, diuresis, bone marrow formation, recruitment of vitality and virility, effects on pre- and post-partum joint, lumbago, stomachic, anti-inflammatory, promotion of blood circulation and removal of blood stasis, elimination of nervous disorders, detoxication, hemostasis, effect of alleviating climacteric disorders, emmenagogic effect, nutritive effect, hematic activity, etc. Further, other activities have also been disclosed in prior reference. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Use of inhibitors of the activation of CXCR4 receptor by SDF-1 in treating rheumatoid arthritis Inventor(s): Seki, Tetsunori ; (Roosevelt Island, NY), Winchester, Robert J. ; (New York, NY), Gulko, Percio Saltz ; (Riverdale, NY) Correspondence: Cooper & Dunham LLP; 1185 Avenue of the Americas; New York; NY; 10036; US Patent Application Number: 20020039993 Date filed: January 31, 2001 Abstract: This invention provides a method for treating rheumatoid arthritis or other forms of inflammatory arthritis which comprises administering to a subject an amount of an agent effective to inhibit the activation of the CXCR4 receptor by SDF-1. This invention further provides a composition for treating rheumatoid arthritis comprising an effective amount of an agent capable of inhibiting the activation of the CXCR4 receptor by SDF-1 and a pharmaceutically acceptable carrier. This invention also provides a method for determining whether an agent is capable of inhibiting the activation of the CXCR4 receptor by SDF-1 comprising: (a) contacting cells expressing the CXCR4 receptor in the presence of SDF-1 with the agent under condition permitting activation of the CXCR4 receptor by SDF-1 if the agent is absent; and (b) determining whether the amount of activation of the CXCR4 receptor by SDF-1 is decreased in the presence of the agent relative to the amount of activation in its absence, such a decrease indicating that the agent is capable of inhibiting the activation of the CXCR4 receptor by SDF-1. Finally, this invention provides agents identified by such a method. Excerpt(s): This application claims priority of U.S. Ser. No. 09/127,651, filed Jul. 31, 1998, the content of which is hereby incorporated by reference. Throughout this application various references are referred to by arabic numbers within parenthesis. Disclosures of these publications in their entireties are hereby incorporated by reference into this application to more fully describe the state of the art to which this invention pertains. ... The architecture, cellular composition and state of cellular activation of the synovial membrane in rheumatoid arthritis have been well described(1,2), but fundamental questions still remain unanswered regarding the precise molecular nature and biologic significance of these inflammatory changes. The intimal synovial lining layer that is extensively altered in synovitis synovium through hyperplasia and infiltration is formed by the interaction of two distinct cell types: intimal synoviocytes derived from the fibroblastoid lineage and intercalated, hemopoietically-derived, monocytoid lineage cells(3-5). During histogenesis of the normal joint the lining cell apparently provides both guidance clues and receptor interactions to the specialized synovial monocytoid cells that result in its incorporation into the lining layer(1) . Together, the cells comprising the intimal layer carry out a number of functions responsible for the integrity and sustenance of the joint. ... The form and function of the intimal synoviocyte apparently distinguishes them from fibroblastoid cells found deeper in the synovium, although relatively little is known about the differences between these members of the fibroblastoid lineage(6). Several genes have been identified that are selectively expressed in the normal intimal, but not subintimal synoviocytes including vascular cell adhesion molecule 1 (VCAM-1)(7), uridine diphosphoglucose dehydrogenase (UDPGD) and decay accelerating factor (DAF)(6). In chronic synovitis immunopathologic studies have shown that the fibroblastoid intimal synoviocytes respond to the events by proliferating and altering their pattern of gene expression to include expression of a variety of molecules that range from MHC class II structures, through cytokines to enzymes that directly participate in the destructive remodelling of joint tissues (1,8-13). In parallel,
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some of the fibroblasts in subintimal locations similarly express MHC class II and VCAM-1(6,13). However, the performance of more analytic studies of synoviocyte cell biology has been constrained because there is no basement membrane that delimits intimal synoviocytes from the subintimal fibroblastoid cells in either normal or inflamed joint tissues, and the purification and separate culture of these two potentially distinct lineages has been difficult, if not impossible. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
Vaccine compositions and methods useful in inducing immune protection against arthritogenic peptides involved in the pathogenesis of rheumatoid arthritis Inventor(s): Carson, Dennis A. ; (Del Mar, CA), Albani, Salvatore ; (Encinitas, CA), Carson, Dennis A. ; (Del Mar, CA), Albani, Salvatore ; (Encinitas, CA) Correspondence: GARY CARY WARE & FRIENDENRICH LLP; 4365 EXECUTIVE DRIVE; SUITE 1100; SAN DIEGO; CA; 92121-2133; US, GARY CARY WARE & FRIENDENRICH LLP; 4365 EXECUTIVE DRIVE; SUITE 1100; SAN DIEGO; CA; 921212133; US Patent Application Number: 20030147910 Date filed: November 18, 2002 Abstract: Vaccine compositions useful in inducing immune protection in a host against arthritogenic peptides involved in the pathogenesis of rheumatoid arthritis are disclosed. Each vaccine composition provides antigenic dnaJp1 peptide (by including the peptide or a polynucleotide which encodes the peptide) and, optionally, other peptide fragments of the microbial dnaJ protein and/or human homologs thereof. Methods for identifying persons who are predisposed to develop rheumatoid arthritis and methods for use of the inventive vaccines are also disclosed. Excerpt(s): This is a continuation-in-part of U.S. patent application Ser. No. 08/246,988, now pending. ... This is a continuation-in-part of U.S. patent application Ser. No. 08/246,988, now pending. ... The invention relates to the control and prevention of autoimmune disease, in particular rheumatoid arthritis. More specifically, the invention relates to methods and reagents which reduce or prevent the response of a host to arthritogenic peptides which include an amino acid sequence (Q(K/R)RAA) that is homologous to a sequence contained in certain HLA proteins. ... The invention relates to the control and prevention of autoimmune disease, in particular rheumatoid arthritis. More specifically, the invention relates to methods and reagents which reduce or prevent the response of a host to arthritogenic peptides which include an amino acid sequence (Q(K/R)RAA) that is homologous to a sequence contained in certain HLA proteins. ... In humans, autoimmune diseases such as rheumatoid arthritis tend to be associated with particular HLA specificities. Rheumatoid arthritis (RA) in particular is presently believed to be associated on a genetic level with the Class II HLA haplotypes DW4, DW14, DW15 (all with DR4 specificity) and/or DR1. Each of these haplotypes include an amino acid sequence which is commonly referred to as the "susceptibility sequence" (hereafter, "RA susceptibility sequence"; see, SEQ. ID. NOs: 1 and 2). The RA susceptibility sequence is known to vary at one amino acid; to wit, QRRAA and QKAA (hereafter, "Q(R/K)RAA"). More than 90% of adult patients with seropositive RA have also been found to have HLA DR antigens with the RA susceptibility sequence in the third hypervariable region of the molecule. The RA susceptibility sequence has not been implicated in the onset of juvenile RA (JRA), except in patients suffering from severe, seropositive JRA. ... In humans, autoimmune diseases such as rheumatoid arthritis tend
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to be associated with particular HLA specificities. Rheumatoid arthritis (RA) in particular is presently believed to be associated on a genetic level with the Class II HLA haplotypes DW4, DW14, DW15 (all with DR4 specificity) and/or DR1. Each of these haplotypes include an amino acid sequence which is commonly referred to as the "susceptibility sequence" (hereafter, "RA susceptibility sequence"; see, SEQ. ID. NOs: 1 and 2). The RA susceptibility sequence is known to vary at one amino acid; to wit, QRRAA and QKAA (hereafter, "Q(R/K)RAA"). More than 90% of adult patients with seropositive RA have also been found to have HLA DR antigens with the RA susceptibility sequence in the third hypervariable region of the molecule. The RA susceptibility sequence has not been implicated in the onset of juvenile RA (JRA), except in patients suffering from severe, seropositive JRA. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
Vaccine compositions and methods useful in inducing immune protection against arthritogenic peptides involved in the pathogenesis of rheumatoid arthritis Inventor(s): Carson, Dennis A. ; (Del Mar, CA), Albani, Salvatore ; (Encinitas, CA), Carson, Dennis A. ; (Del Mar, CA), Albani, Salvatore ; (Encinitas, CA) Correspondence: GARY CARY WARE & FRIENDENRICH LLP; 4365 EXECUTIVE DRIVE; SUITE 1100; SAN DIEGO; CA; 92121-2133; US, GARY CARY WARE & FRIENDENRICH LLP; 4365 EXECUTIVE DRIVE; SUITE 1100; SAN DIEGO; CA; 921212133; US Patent Application Number: 20030147910 Date filed: November 18, 2002 Abstract: Vaccine compositions useful in inducing immune protection in a host against arthritogenic peptides involved in the pathogenesis of rheumatoid arthritis are disclosed. Each vaccine composition provides antigenic dnaJp1 peptide (by including the peptide or a polynucleotide which encodes the peptide) and, optionally, other peptide fragments of the microbial dnaJ protein and/or human homologs thereof. Methods for identifying persons who are predisposed to develop rheumatoid arthritis and methods for use of the inventive vaccines are also disclosed. Excerpt(s): This is a continuation-in-part of U.S. patent application Ser. No. 08/246,988, now pending. ... This is a continuation-in-part of U.S. patent application Ser. No. 08/246,988, now pending. ... The invention relates to the control and prevention of autoimmune disease, in particular rheumatoid arthritis. More specifically, the invention relates to methods and reagents which reduce or prevent the response of a host to arthritogenic peptides which include an amino acid sequence (Q(K/R)RAA) that is homologous to a sequence contained in certain HLA proteins. ... The invention relates to the control and prevention of autoimmune disease, in particular rheumatoid arthritis. More specifically, the invention relates to methods and reagents which reduce or prevent the response of a host to arthritogenic peptides which include an amino acid sequence (Q(K/R)RAA) that is homologous to a sequence contained in certain HLA proteins. ... In humans, autoimmune diseases such as rheumatoid arthritis tend to be associated with particular HLA specificities. Rheumatoid arthritis (RA) in particular is presently believed to be associated on a genetic level with the Class II HLA haplotypes DW4, DW14, DW15 (all with DR4 specificity) and/or DR1. Each of these haplotypes include an amino acid sequence which is commonly referred to as the "susceptibility sequence" (hereafter, "RA susceptibility sequence"; see, SEQ. ID. NOs: 1 and 2). The RA susceptibility sequence is known to vary at one amino acid; to wit, QRRAA and QKAA
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(hereafter, "Q(R/K)RAA"). More than 90% of adult patients with seropositive RA have also been found to have HLA DR antigens with the RA susceptibility sequence in the third hypervariable region of the molecule. The RA susceptibility sequence has not been implicated in the onset of juvenile RA (JRA), except in patients suffering from severe, seropositive JRA. ... In humans, autoimmune diseases such as rheumatoid arthritis tend to be associated with particular HLA specificities. Rheumatoid arthritis (RA) in particular is presently believed to be associated on a genetic level with the Class II HLA haplotypes DW4, DW14, DW15 (all with DR4 specificity) and/or DR1. Each of these haplotypes include an amino acid sequence which is commonly referred to as the "susceptibility sequence" (hereafter, "RA susceptibility sequence"; see, SEQ. ID. NOs: 1 and 2). The RA susceptibility sequence is known to vary at one amino acid; to wit, QRRAA and QKAA (hereafter, "Q(R/K)RAA"). More than 90% of adult patients with seropositive RA have also been found to have HLA DR antigens with the RA susceptibility sequence in the third hypervariable region of the molecule. The RA susceptibility sequence has not been implicated in the onset of juvenile RA (JRA), except in patients suffering from severe, seropositive JRA. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
Keeping Current In order to stay informed about patents and patent applications dealing with arthritis, you can access the U.S. Patent Office archive via the Internet at the following Web address: http://www.uspto.gov/main/patents.htm. Under “Services,” click on “Search Patents.” You will see two broad options: (1) Patent Grants, and (2) Patent Applications. To see a list of granted patents, perform the following steps: Under “Patent Grants,” click “Quick Search.” Then, type “arthritis” (or synonyms) into the “Term 1” box. After clicking on the search button, scroll down to see the various patents which have been granted to date on arthritis. You can also use this procedure to view pending patent applications concerning arthritis. Simply go back to the following Web address: http://www.uspto.gov/main/patents.htm. Under “Services,” click on “Search Patents.” Select “Quick Search” under “Patent Applications.” Then proceed with the steps listed above.
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CHAPTER 7. BOOKS ON ARTHRITIS Overview This chapter provides bibliographic book references relating to arthritis. In addition to online booksellers such as www.amazon.com and www.bn.com, excellent sources for book titles on arthritis include the Combined Health Information Database and the National Library of Medicine. Your local medical library also may have these titles available for loan.
Book Summaries: Federal Agencies The Combined Health Information Database collects various book abstracts from a variety of healthcare institutions and federal agencies. To access these summaries, go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. You will need to use the “Detailed Search” option. To find book summaries, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer. For the format option, select “Monograph/Book.” Now type “arthritis” (or synonyms) into the “For these words:” box. You should check back periodically with this database which is updated every three months. The following is a typical result when searching for books on arthritis: ·
Living With Rheumatoid Arthritis, Second Edition Source: Baltimore, MD: The Johns Hopkins University Press. 2003. 290 p. Contact: Johns Hopkins University Press. 2715 N. Charles St., Baltimore, MD 212184319. (410) 516-6934. Website: www.jhupbooks.com. Summary: This book seeks to educate patients with rheumatoid arthritis (RA) about their condition. The premise of this book is that the better the RA patient understands his or her condition, the better he or she can cope with the illness. The book is divided into six parts. Part one discusses RA and provides an overview of RA with chapters on joints, inflammation, disease course and prognosis, diagnostic tests, and other symptoms. Part two discusses coping with RA with chapters describing strategies for identifying problems, setting goals, and coping with fatigue, pain, and emotions. Part three discusses exercises and rehabilitation. Part four discusses traditional and current medications. Part five discusses other treatments for RA including alternative and
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complementary therapies, nutrition, and surgery. Part six discusses a range of topics including disability benefits, health insurance, financial matters, traveling, and other medical concerns. A glossary and bibliography are included. Numerous diagrams. ·
Conquering Rheumatoid Arthritis: The Latest Breakthroughs and Treatments Source: Amherst, NY: Prometheus Books. 2001. 255 p. Contact: Available from Prometheus Books. 59 John Glenn Drive, NY 14228-2197. (716) 691-0133 or (800) 421-0351. Website: www.prometheusbooks.com. PRICE: $20.00. ISBN: 1573928860. Summary: This book for patients describes the origins, disease course, and treatment of rheumatoid arthritis (RA). Rheumatoid arthritis affects over two million Americans. It is three times more common in women than men and becomes increasingly common in people as they age. RA is an inflammatory disease of the synovium, or lining of a joint, that results in pain, stiffness, swelling, joint damage, and loss of function in the joints. Chapters discuss the body's immune system; the anatomy of the synovial joints; the system by which the body's immune system attacks these joints; the genetic origins of RA and gene therapy; stem cell research and therapy; traditional treatments for RA including NSAIDS, DMARDS, and steroids; new medications including etanercept, COX-1 and COX-2 enzymes, leflunomide, and infliximab; clinical trials; and potential therapies. Appendices include related websites and a glossary. 14 figures.
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Arthritis Helpbook: A Tested Self-Management Program for Coping With Arthritis and Fibromyalgia. Fifth Edition. [Como convivir con su artritis: una guia para una vida activa y saludable] Source: Cambridge, MA: Perseus Books. 2000. 380 p. Contact: Available from Perseus Books. Group Customer Service Department, 5500 Central Avenue, Boulder, CO 80301. (800) 386-5656. Fax (303) 449-3356. Email:
[email protected]. Website: www.perseusbooks.com. ISBN 073820224X. PRICE: $18.00 plus shipping. Spanish version available from Bull Publishing. P.O. Box 208, Palo Alto, CA 94302-0208. (800) 676-2855. Fax (650) 327-3300. PRICE: $16.95 plus shipping; bulk discounts available. Summary: This book for individuals with arthritis and fibromyalgia presents a successful program for coping with these conditions. Chapters define arthritis; describe rheumatoid arthritis, osteoarthritis, and fibromyalgia and explain how to treat them; outline ways of preventing and dealing with osteoporosis; discuss various types of painful localized conditions; and explain how to become an arthritis self manager. Chapters also identify popular techniques for minimizing arthritis pain, present guidelines for developing a physical fitness program, describe flexibility and strengthening exercises and aerobic activities, offer suggestions for dealing with everyday problems, and provide help for dealing with depression and fatigue. Other topics include coping with emotional and interpersonal issues, establishing good nutrition habits, and using available medical resources. An appendix lists the international locations of the Arthritis Foundation and the Arthritis Society. 47 references, 11 tables, and numerous illustrations.
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Mayo Clinic on Arthritis Source: Rochester, MN: Mayo Clinic. 1999. 202 p.
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Contact: Available from Mayo Clinic, Health Information Division, 200 First Street SW, 5th Floor Centerplace Building, Rochester, MN 55905. (800) 291-1128 ext. 250. PRICE: $14.95 plus shipping and handling. ISBN 1893005003. Summary: This book provides people who have arthritis with practical, easy to understand information on osteoarthritis and rheumatoid arthritis. The contents are based on the self-help approach that Mayo Clinic practitioners take with those seeking health care at this facility. The book begins with a chapter describing common forms of arthritis, other arthritic disorders, and related musculoskeletal conditions. This is followed by a chapter that explains the fundamental principles of joint protection and offers tips on using various assistive devices. Other chapters provide guidelines on exercising properly, controlling pain, eating for better health, and gaining control over arthritis and enhancing quality of life. The book continues with a chapter on the effectiveness and side effects of nonsteroidal anti-inflammatory drugs, corticosteroids, disease-modifying antirheumatic drugs, immunosuppressants, pain reducers, antidepressants, muscle relaxants, tranquilizers, and hyaluronate injections. The next chapter explains how surgery can help hand and wrist joints, shoulders, hips, knees, and ankles and feet. This is followed by a chapter on alternative treatments. Topics include types of treatment available and the evaluation of alternative methods. Another chapter reports on promising trends in arthritis research and new diagnostic tools, medications, lifestyle approaches, operations, and other treatments under study. The remaining chapters offer suggestions on traveling with arthritis, discuss job-related issues, and identify sources of help. 59 figures. ·
Exercise Beats Arthritis Source: Palo Alto, CA: Bull Publishing Company. 1998. 142 p. Contact: Available from Bull Publishing Company. P.O. Box 208, Palo Alto, CA 943020208. (650) 322-2855. Fax (650) 327-3300. Website: www.bullpub.com. PRICE: $12.95 plus shipping and handling. ISBN 0923521453. Summary: This book provides people who have arthritis with an easy to follow program of exercises. The first chapter explains what arthritis is and identifies its signs and symptoms. This chapter also discusses rheumatoid arthritis, osteoarthritis, ankylosing spondylitis, neck and low back pain, fibromyalgia syndrome, and osteoporosis and examines the role of exercise in managing these conditions. Chapter two explores the impact of various factors, such as diet, mental attitude, and stress on arthritis. Other topics include visiting a doctor if arthritis symptoms are present, using various medications to treat the disease, receiving treatment from health professionals other than a primary care physician, considering surgery, using various techniques to relieve pain, and protecting joints. Chapter three provides general information about exercising and maintaining motivation. Other chapters present morning wake up exercises; a warm up sequence; exercises for the neck, arms, hands, back, hips, knees, and feet; a cool down exercise; water and aerobic exercises; and relaxation techniques. The final chapter provides guidelines on improving body movements. Numerous figures.
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Your Child With Arthritis: A Family Guide for Caregiving Source: Baltimore, MD: The Johns Hopkins University Press. 1996. 339 p. Contact: Johns Hopkins University Press, 2715 North Charles Street, Baltimore, MD 21218-4319.
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Summary: This book for health professionals, families of children with rheumatic illnesses, and older patients provides them with information on dealing with a rheumatic illness. Rheumatic diseases of childhood are described, including juvenile rheumatoid arthritis, juvenile spondyloarthropathy syndromes, systemic lupus erythematosus, dermatomyositis, scleroderma, and vasculitis. The description of each of these diseases includes an explanation of how it is diagnosed and treated, the possible course of the disease, and possible outcomes. Diagnostic laboratory tests and procedures are explained, and medications, physical and occupational therapy, and other treatments are discussed. In addition, the book covers the topics of selecting a physician, developing a positive physician-patient relationship, monitoring a child's progress, creating a positive school environment, financing health care, and coping with the impact of illness on the family. Sample forms are provided to help parents track their child's progress, maintain detailed medical records, and organize pertinent information. A glossary is also included. Appendices present a sample clinic guide and identify other sources of help. 68 references, 1 figure, and 3 tables. ·
Arthritis: A Take Care of Yourself Health Guide for Understanding Your Arthritis. Fourth Edition Source: Reading, MA: Addison-Wesley Publishing Company. 1995. 338 p. Contact: Available from Addison-Wesley Publishing Company, 1 Jacob Way, Reading, MA 01867. (800) 238-9682. PRICE: $14.00 in the U.S., $17.95 in Canada. Summary: This book for individuals with arthritis and related conditions provides information to help them understand their condition and the medical treatments available for arthritis and related conditions. Part one offers guidelines for managing arthritis and presents charts for identifying various categories of arthritis. These categories are also described in detail, and they include synovitis, attachment arthritis, crystal arthritis, infections, cartilage degeneration, muscle inflammation, and local and general conditions. Connective tissue diseases are also highlighted. Part two presents information on managing arthritis, focusing on treatments, medications, and surgery. Information is also provided on understanding tests, avoiding phony treatments, saving money, and preventing arthritis. Part three offers guidelines for solving problems with arthritis, including general and sexual problems and problems with pain, medications, mobility, and employment. Appendices provide additional resources. 8 figures, 3 tables, and 31 charts.
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Rheumatoid Arthritis: Caring for Your Hands Source: Bethesda, MD: American Occupational Therapy Association, Inc. 1995. 40 p. Contact: American Occupational Therapy Association, 4720 Montgomery Lane, P.O. Box 31220, Bethesda, MD 20824-1220. (301) 652-2682. (800) 377-8555 ( TDD ). (301) 652-7711 (fax). Summary: This book for individuals with rheumatoid arthritis (RA) provides information for minimizing joint inflammation and protecting joints from damage. Causes of pain in RA are identified, including inflammation and swelling, deterioration of cartilage, pressure on the bone, and tenosynovitis. Common causes of deformities in RA are discussed, including joint contracture , joint instability, and tenosynovitis. Specific hand deformities are described, their causes are explained, and steps that individuals can take to minimize these deformities are presented. Signs of inflammation are identified, including pain and morning stiffness. Techniques for managing pain and stiffness in hands are suggested. Guidelines are provided for protecting joints, relieving
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muscle tension, using splints, maintaining mobility, and fighting fatigue. A list of additional resources is also included. 4 references, 17 figures, and 1 table. ·
Essential Arthritis Cookbook: Kitchen Basics for People with Arthritis, Fibromyalgia and Other Chronic Pain and Fatigue Source: Mankato, MN: Appletree Press, Inc. 1995. 286 p. Contact: Available from Appletree Press, Inc. 151 Good Counsel Drive, Suite 125, Mankato, MN 56001. (800) 322-5679 or (507) 345-4848. Fax (507) 345-3002. PRICE: $24.95 plus shipping and handling. ISBN 0962047163. Summary: This cookbook for people with arthritis, fibromyalgia, and other chronic pain and fatigue explains how nutrition affects arthritis and other musculoskeletal diseases and uses this information to provide guidelines and recipes for good health. Chapters cover topics such as the relationship between diet and arthritis; the impact of diet on the reduction of pain, swelling, and stiffness; and the effect of various arthritis medications on vitamin and mineral levels in the body. Other chapters offer suggestions for developing an energy-saving plan, making cooking more relaxing, protecting joints from damaging forces, selecting appropriate tools, and planning meals. In addition, the book provides more than 120 recipes in the categories of appetizers, soups, salads, main dishes, vegetables, side dishes, breads, and desserts. The recipes are easy to prepare and require few ingredients and minimal cleanup. Appendixes offer suggestions for making eating easier for people whose illness or condition has made eating difficult, and provide advice for using convenience foods. 14 figures. 25 tables. 7 references.
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Living a Healthy Life With Chronic Conditions: Self-Management of Heart Disease, Arthritis, Stroke, Diabetes, Asthma, Bronchitis, Emphysema and Others Source: Palo Alto, CA: Bull Publishing Company. 1994. 296 p. Contact: Available from Bull Publishing Company. P.O. Box 208, Palo Alto, CA 943020208. (800) 676-2855 or (415) 322-2855. Fax (415) 327-3300. E-mail:
[email protected]. PRICE: $14.95. ISBN: 0923521283. Summary: This book is a complete self-management guide for people with chronic diseases. The authors focus on day-to-day living skills, in the context of the specific chronic diseases, including heart disease, arthritis, stroke, diabetes, asthma, bronchitis, and emphysema. General topics include the psychological aspects to self-management; finding resources; smoking and quitting; understanding common symptoms; using one's mind to manage symptoms; exercising for fun and fitness; exercising for flexibility and strength; exercising for endurance; exercising tips for people with specific chronic diseases; the importance of communication; durable powers of attorney for health care; eating well; and managing medications. The chapter on diabetes covers diabetes and its causes; maintaining an appropriate blood glucose level; symptoms of hyperglycemia and hypoglycemia; dietary management; exercise; insulin injections; oral medications; emotions; self-monitoring of blood glucose and urine; the complications of diabetes; and diabetes resources. Each chapter includes limited references and a subject index concludes the volume.
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Book Summaries: Online Booksellers Commercial Internet-based booksellers, such as Amazon.com and Barnes&Noble.com, offer summaries which have been supplied by each title’s publisher. Some summaries also include customer reviews. Your local bookseller may have access to in-house and commercial databases that index all published books (e.g. Books in PrintÒ). IMPORTANT NOTE: Online booksellers typically produce search results for medical and non-medical books. When searching for “arthritis” at online booksellers’ Web sites, you may discover non-medical books that use the generic term “arthritis” (or a synonym) in their titles. The following is indicative of the results you might find when searching for “arthritis” (sorted alphabetically by title; follow the hyperlink to view more details at Amazon.com): ·
18 Natural Ways to Stop Arthritis Now (18 Natural Ways Series) by Norman D. Ford; ISBN: 0879837268; http://www.amazon.com/exec/obidos/ASIN/0879837268/icongroupinterna
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250 Tips for Making Life With Arthritis Easier by Shelley Peterman Schwarz, Arthritis Foundation; ISBN: 1563523817; http://www.amazon.com/exec/obidos/ASIN/1563523817/icongroupinterna
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50 Ways to Cope With Arthritis by Consumer Guide (1996); ISBN: 0785311726; http://www.amazon.com/exec/obidos/ASIN/0785311726/icongroupinterna
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7 Steps to Overcoming Arthritis by Gary Null (Author); ISBN: 0743458915; http://www.amazon.com/exec/obidos/ASIN/0743458915/icongroupinterna
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A Diet to stop arthritis : the nightshades and ill health by Norman Franklin Childers; ISBN: 0938378007; http://www.amazon.com/exec/obidos/ASIN/0938378007/icongroupinterna
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A Doctor's Proven New Home Cure for Arthritis by Giraud W. Campbell, Robert B. Stone; ISBN: 0132170345; http://www.amazon.com/exec/obidos/ASIN/0132170345/icongroupinterna
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Action Plan for Arthritis by A. Lynn Millar (2003); ISBN: 0736046518; http://www.amazon.com/exec/obidos/ASIN/0736046518/icongroupinterna
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All about Bone, Joint, Muscle, and Arthritis Pain in Childhood: A Guide to Juvenile Rheumatoid Arthritis, Injuries, and Rheumatic Diseases for Parents and Professionals by Thomas J. A. Lehman (2004); ISBN: 0195157281; http://www.amazon.com/exec/obidos/ASIN/0195157281/icongroupinterna
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All About Osteoarthritis: The Definitive Resource for Arthritis Patients and Their Families by Nancy E. Lane, Daniel J. Wallace; ISBN: 0195138732; http://www.amazon.com/exec/obidos/ASIN/0195138732/icongroupinterna
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Alternative Answers to Arthritis & Rheumatism: The Complete Conventional and Laternative Guide to Treating Chronic Arthritis by Anne Charlish; ISBN: 0762102470; http://www.amazon.com/exec/obidos/ASIN/0762102470/icongroupinterna
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Alternative Therapies for Cancer & Arthritis by E. Weisenburger, Irv Boichuk (1996); ISBN: 0889821542; http://www.amazon.com/exec/obidos/ASIN/0889821542/icongroupinterna
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An Atlas of Osteoarthritis by K.D. Brandt (Editor), Kenneth D. Brandt; ISBN: 1850704945; http://www.amazon.com/exec/obidos/ASIN/1850704945/icongroupinterna
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Are You Sure It's Arthritis by Paul Davidson; ISBN: 0452258979; http://www.amazon.com/exec/obidos/ASIN/0452258979/icongroupinterna
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Are You Sure It's Arthritis?: A Guide to Soft-Tissue Rheumatism by Paul Davidson (1985); ISBN: 0025297708; http://www.amazon.com/exec/obidos/ASIN/0025297708/icongroupinterna
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Arthritis by Leon Chaitow (1998); ISBN: 0722535627; http://www.amazon.com/exec/obidos/ASIN/0722535627/icongroupinterna
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Arthritis (Diseases and Disorders) by Barbara Sheen (2002); ISBN: 156006904X; http://www.amazon.com/exec/obidos/ASIN/156006904X/icongroupinterna
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Arthritis (Health Watch) by Susan Dudley Gold; ISBN: 0766016595; http://www.amazon.com/exec/obidos/ASIN/0766016595/icongroupinterna
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Arthritis (Macrobiotic Food&Cooking Series) by Aveline Kushi, et al; ISBN: 0870406779; http://www.amazon.com/exec/obidos/ASIN/0870406779/icongroupinterna
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Arthritis (Sound Techniques for Healing) by Robert Friedman, et al (1993); ISBN: 1881451232; http://www.amazon.com/exec/obidos/ASIN/1881451232/icongroupinterna
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Arthritis (Your Personal Health Series) by John Thompson, Robert F. Meenan (Introduction) (1996); ISBN: 1550137824; http://www.amazon.com/exec/obidos/ASIN/1550137824/icongroupinterna
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Arthritis : An Alternative Medicine Definitive Guide by Eugene R. Zampieron, et al; ISBN: 1887299157; http://www.amazon.com/exec/obidos/ASIN/1887299157/icongroupinterna
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Arthritis : Struggle with Immobility by Hasnain, Ph.D. Walji, Hasnain Walji; ISBN: 1891294016; http://www.amazon.com/exec/obidos/ASIN/1891294016/icongroupinterna
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Arthritis 101: Questions You Have, Answers You Need by Arthritis Foundation, Afs (1997); ISBN: 1563523809; http://www.amazon.com/exec/obidos/ASIN/1563523809/icongroupinterna
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Arthritis A Comprehensive Guide to Understanding Your Arthritis (Revised Edition) by James F. Fries; ISBN: 0201054086; http://www.amazon.com/exec/obidos/ASIN/0201054086/icongroupinterna
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Arthritis Alternatives by Irna Gadd, Laurence Gadd; ISBN: 0871967693; http://www.amazon.com/exec/obidos/ASIN/0871967693/icongroupinterna
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Arthritis and Allied Conditions (1993); ISBN: 0812111230; http://www.amazon.com/exec/obidos/ASIN/0812111230/icongroupinterna
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Arthritis and Allied Conditions: A Textbook of Rheumatology (2 Volume Set) by William J. Koopman (Editor); ISBN: 0781722403; http://www.amazon.com/exec/obidos/ASIN/0781722403/icongroupinterna
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Arthritis and Chinese Herbal Medicine by Pi-Kwang Tsung, et al (1993); ISBN: 0941942252; http://www.amazon.com/exec/obidos/ASIN/0941942252/icongroupinterna
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Arthritis and Common Sense by Dale Alexander, H. E. Kirschner (Designer) (1981); ISBN: 0671427911; http://www.amazon.com/exec/obidos/ASIN/0671427911/icongroupinterna
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Arthritis and Common Sense by Dale Alexander, H. E. Kirschner (Designer) (1981); ISBN: 0671427911; http://www.amazon.com/exec/obidos/ASIN/0671427911/icongroupinterna
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Arthritis and Common Sense No 2 by Dale Alexander; ISBN: 0911638172; http://www.amazon.com/exec/obidos/ASIN/0911638172/icongroupinterna
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Arthritis and common sense; illustrated with menus by Dale Alexander (Author); ISBN: B00005VG5Y; http://www.amazon.com/exec/obidos/ASIN/B00005VG5Y/icongroupinterna
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Arthritis and Folk Medicine by D. C. Jarvis (1991); ISBN: 0449209229; http://www.amazon.com/exec/obidos/ASIN/0449209229/icongroupinterna
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Arthritis and Radioactivity : A Story of Montana's Free Enterprise Mine by Wade V. Lewis (1997); ISBN: 0897165500; http://www.amazon.com/exec/obidos/ASIN/0897165500/icongroupinterna
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Arthritis and Related Affections: Clinic, Pathology, and Treatment by Arnold Soren (1993); ISBN: 0387557792; http://www.amazon.com/exec/obidos/ASIN/0387557792/icongroupinterna
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Arthritis and Rheumatism (Natural Way) by Young Pat; ISBN: 1843334240; http://www.amazon.com/exec/obidos/ASIN/1843334240/icongroupinterna
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Arthritis and Rheumatism: The Facts by James Thomas Scott; ISBN: 0192611682; http://www.amazon.com/exec/obidos/ASIN/0192611682/icongroupinterna
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Arthritis and Rheumatism: The Sufferers' Guide by John Cosh (1997); ISBN: 1899308172; http://www.amazon.com/exec/obidos/ASIN/1899308172/icongroupinterna
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Arthritis and you by James William Brooke (Author); ISBN: B00005X7FH; http://www.amazon.com/exec/obidos/ASIN/B00005X7FH/icongroupinterna
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Arthritis Beaten Today by L. Sands; ISBN: 1901292045; http://www.amazon.com/exec/obidos/ASIN/1901292045/icongroupinterna
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Arthritis Begone!: A Doctor's Rx for Easy, Safe Inexpensive--And Effective-Treatments for Your Arthritis Pain by John B. Irwin (1997); ISBN: 0879838043; http://www.amazon.com/exec/obidos/ASIN/0879838043/icongroupinterna
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Arthritis Breakthrough by Henry Scammell, et al; ISBN: 0871316900; http://www.amazon.com/exec/obidos/ASIN/0871316900/icongroupinterna
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Arthritis Exercises (1996); ISBN: 0752518569; http://www.amazon.com/exec/obidos/ASIN/0752518569/icongroupinterna
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Arthritis For Dummies® by Barry Fox (Author), Nadine Taylor (Author) (2000); ISBN: 0764552589; http://www.amazon.com/exec/obidos/ASIN/0764552589/icongroupinterna
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Arthritis Handbook by Theodore, Dr. Rooney, Patty Rooney; ISBN: 0345335619; http://www.amazon.com/exec/obidos/ASIN/0345335619/icongroupinterna
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Arthritis Holistic Therapy (Dr. Donsbach Tells You) by Kurt Donsbach, Rudolf Alsleben (1993); ISBN: 1569595496; http://www.amazon.com/exec/obidos/ASIN/1569595496/icongroupinterna
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Arthritis Medicines A-Z: A Doctor's Guide to Today's Most Commonly Prescribed Arthritis Drugs by C. Michael, Md. Stein (2001); ISBN: 060980507X; http://www.amazon.com/exec/obidos/ASIN/060980507X/icongroupinterna
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Arthritis Miracle: How Extract Can Reduce Inflammatory Joint Pain by Earl Mindell, Virginia Hopkins; ISBN: 1583330593; http://www.amazon.com/exec/obidos/ASIN/1583330593/icongroupinterna
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Arthritis of the Hip and Knee: The Active Person's Guide to Taking Charge by Ronald J. Allen, et al (1998); ISBN: 1561451495; http://www.amazon.com/exec/obidos/ASIN/1561451495/icongroupinterna
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Arthritis Pain Relief: A Subliminal Persuasion/Self-Hypnosis by Barrie Konicov; ISBN: 0870823140; http://www.amazon.com/exec/obidos/ASIN/0870823140/icongroupinterna
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Arthritis Relief at Your Fingertips: The Complete Self-Care Guide for Easing Aches and Pains Without Drugs by Michael Reed Gach; ISBN: 0446514748; http://www.amazon.com/exec/obidos/ASIN/0446514748/icongroupinterna
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Arthritis Relief at Your Fingertips: Your Guide to Easing Aches and Pain Without Drugs by Michael Reed Gach, et al (1990); ISBN: 0446391565; http://www.amazon.com/exec/obidos/ASIN/0446391565/icongroupinterna
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Arthritis Relief: Breakthroughs in Natural Healing by Deborah L. Wilcox-Jamieson, Deborah L. Wilcox; ISBN: 1890394041; http://www.amazon.com/exec/obidos/ASIN/1890394041/icongroupinterna
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Arthritis Solution: The Newest Treatments to Help You Live Pain-Free by Robert G. Lahita, Rhobert G., Ph.D. Lahita; ISBN: 0380807785; http://www.amazon.com/exec/obidos/ASIN/0380807785/icongroupinterna
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Arthritis Sourcebook: Basic Consumer Health Information About Specific Forms of Arthrits and Related Disorders, Including Rheumatoid Arthritis, Osteoarthrits, Gout, polymya (Health Reference Series, Vol 46) by Allan R. Cook (Editor) (1998); ISBN: 0780802012; http://www.amazon.com/exec/obidos/ASIN/0780802012/icongroupinterna
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Arthritis Survival: The Holistic Medical Treatment Program for Osteoarthritis by Robert S., D.O. Ivker, et al (2001); ISBN: 1585420972; http://www.amazon.com/exec/obidos/ASIN/1585420972/icongroupinterna
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Arthritis Therapy: A Clinician's Manual by Thomas Kantor (1992); ISBN: 0929240405; http://www.amazon.com/exec/obidos/ASIN/0929240405/icongroupinterna
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Arthritis, Rheumatism and Osteoporosis by Bernard Jensen (1986); ISBN: 0932615031; http://www.amazon.com/exec/obidos/ASIN/0932615031/icongroupinterna
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Arthritis, Rheumatism and Psoriasis (By Appointment Only) by Jan De Vries (1988); ISBN: 185158028X; http://www.amazon.com/exec/obidos/ASIN/185158028X/icongroupinterna
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Arthritis, Rheumatism and Psoriasis (By Appointment Only) by Jan de Vries (2002); ISBN: 1840185589; http://www.amazon.com/exec/obidos/ASIN/1840185589/icongroupinterna
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Arthritis: A Take Care of Yourself Health Guide for Understanding Your Arthritis by James F. Fries, James, MD Fries; ISBN: 0738202258; http://www.amazon.com/exec/obidos/ASIN/0738202258/icongroupinterna
460 Arthritis
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Arthritis: A Take Care of Yourself Health Guide for Understanding Your Arthritis by James F. Fries, James, MD Fries; ISBN: 0738202258; http://www.amazon.com/exec/obidos/ASIN/0738202258/icongroupinterna
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Arthritis: About Osteoarthritis and Rheumatoid Disease, Including Rheumatoid Arthritis by Anthony Di Fabio, Gus J. Prosch (1997); ISBN: 0961543736; http://www.amazon.com/exec/obidos/ASIN/0961543736/icongroupinterna
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Arthritis: An American Yoga Association Wellness Guide: The Powerful Program for Greater Strength, Flexibility, and Freedom by Alice Christensen (2001); ISBN: 1575666480; http://www.amazon.com/exec/obidos/ASIN/1575666480/icongroupinterna
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Arthritis: An American Yoga Association Wellness Guide: The Powerful Program for Greater Strength, Flexibility, and Freedom by Alice Christensen (2001); ISBN: 1575666480; http://www.amazon.com/exec/obidos/ASIN/1575666480/icongroupinterna
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Arthritis: Don't Learn to Live With It by Carlton Fredericks, Carlton Fredricks (1985); ISBN: 0399511334; http://www.amazon.com/exec/obidos/ASIN/0399511334/icongroupinterna
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Arthritis: in Black and White by Anne C. Brower, et al; ISBN: 0721651526; http://www.amazon.com/exec/obidos/ASIN/0721651526/icongroupinterna
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Arthritis: Little Known Treatments by Anthony Di Fabio; ISBN: 0961543728; http://www.amazon.com/exec/obidos/ASIN/0961543728/icongroupinterna
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Arthritis: Stop Suffering, Start Moving by Darlene Cohen (1995); ISBN: 0802774660; http://www.amazon.com/exec/obidos/ASIN/0802774660/icongroupinterna
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Arthritis: The Chinese Way of Healing and Prevention (Qigong-Health and Healing) by Jwing-Ming Yang, Alan Dougall (Editor) (1996); ISBN: 1886969426; http://www.amazon.com/exec/obidos/ASIN/1886969426/icongroupinterna
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Arthritis: The Complete Guide to Relief by Dava Sobel, Arthur C. Klein; ISBN: 1854879952; http://www.amazon.com/exec/obidos/ASIN/1854879952/icongroupinterna
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Arthritis: The Doctor's Cure by Michael Loes (Editor), et al; ISBN: 0879839295; http://www.amazon.com/exec/obidos/ASIN/0879839295/icongroupinterna
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Arthritis: What Exercises Work by Dava Sobel, et al (1995); ISBN: 0312130252; http://www.amazon.com/exec/obidos/ASIN/0312130252/icongroupinterna
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Arthritis: What Exercises Work by Dava Sobel, et al (1995); ISBN: 0312130252; http://www.amazon.com/exec/obidos/ASIN/0312130252/icongroupinterna
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Arthritis: What Works (An Arthritis Survey Publication) by Dava Sobel, et al (1989); ISBN: 0312032897; http://www.amazon.com/exec/obidos/ASIN/0312032897/icongroupinterna
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Arthritis: What You Need to Know (Johns Hopkins Health , Vol 2, No 4) by Sara J. Henry, et al (1999); ISBN: 0737016000; http://www.amazon.com/exec/obidos/ASIN/0737016000/icongroupinterna
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Arthritis: Your Complete Exercise Guide (Cooper Clinic and Research Institute Fitness Series) by Neil F. Gordon, Kenneth H. Cooper (1992); ISBN: 0873223926; http://www.amazon.com/exec/obidos/ASIN/0873223926/icongroupinterna
Books 461
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Arthritis: Your Natural Guide to Healing with Diet, Vitamins, Minerals, Herbs, Exercise, and Other Natural Methods by Michael T. Murray; ISBN: 1559584912; http://www.amazon.com/exec/obidos/ASIN/1559584912/icongroupinterna
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Auranofin in Rheumatoid Arthritis by Norman L. Gottlieb (Editor) (1987); ISBN: 0941741001; http://www.amazon.com/exec/obidos/ASIN/0941741001/icongroupinterna
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Autoimmunity, Rheumatoid Arthritis and Cyclosporin A by Y. Mizushima (Editor), Amor (1991); ISBN: 1850703051; http://www.amazon.com/exec/obidos/ASIN/1850703051/icongroupinterna
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Beat Arthritis by Michael Colgan (2000); ISBN: 1896817238; http://www.amazon.com/exec/obidos/ASIN/1896817238/icongroupinterna
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Bees Don't Get Arthritis by Fred Malone (1992); ISBN: 0914960601; http://www.amazon.com/exec/obidos/ASIN/0914960601/icongroupinterna
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Beyond Aspirin : Nature's Challenge to Arthritis, Cancer & Alzheimer's Disease by Thomas M. Newmark, et al; ISBN: 0934252823; http://www.amazon.com/exec/obidos/ASIN/0934252823/icongroupinterna
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Breakthroughs in Arthritis by William L. Fischer; ISBN: 0915421151; http://www.amazon.com/exec/obidos/ASIN/0915421151/icongroupinterna
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Care of Arthritis in the Older Adult (Springer Series on Geriatric Nursing) by Ann Schmidt Luggen (Editor), et al (2002); ISBN: 0826123627; http://www.amazon.com/exec/obidos/ASIN/0826123627/icongroupinterna
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Carlson Wade's Fact/Book on Arthritis, Nutrition, and Natural Therapy. by Carlson Wade (1976); ISBN: 0879831324; http://www.amazon.com/exec/obidos/ASIN/0879831324/icongroupinterna
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Christiaan Barnard's Program for Living With Arthritis by Christiaan Barnard, Peter Evans; ISBN: 055324888X; http://www.amazon.com/exec/obidos/ASIN/055324888X/icongroupinterna
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Clinician's Manual on Osteoarthritis by Scott, et al (2001); ISBN: 1858739233; http://www.amazon.com/exec/obidos/ASIN/1858739233/icongroupinterna
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Cmo Cetyl Myristoleate: A Natural Treatment for Arthritis & Other Joint-Related Diseases (Woodland Health Ser) by Rita Elkins (1997); ISBN: 1580540104; http://www.amazon.com/exec/obidos/ASIN/1580540104/icongroupinterna
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Color Atlas and Text of Osteoarthritis by Michael Doherty (Editor), Michael Doherty M. D. (1994); ISBN: 0815127529; http://www.amazon.com/exec/obidos/ASIN/0815127529/icongroupinterna
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Columbia Presbyterian Osteoarthritis Handbook by Ronald P. Grelsamer (Editor), et al; ISBN: 0020344619; http://www.amazon.com/exec/obidos/ASIN/0020344619/icongroupinterna
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Conquering Arthritis: What Doctors Don't Tell You Because They Don't Know: 9 Secrets I Learned the Hard Way; ISBN: 0971889708; http://www.amazon.com/exec/obidos/ASIN/0971889708/icongroupinterna
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Conquering Rheumatoid Arthritis (French by William Bensen, Wynn Bensen (1997); ISBN: 0969778198; http://www.amazon.com/exec/obidos/ASIN/0969778198/icongroupinterna
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Conquering Rheumatoid Arthritis: The Latest Breakthroughs and Treatments by Thomas F. Lee (2001); ISBN: 1573928860; http://www.amazon.com/exec/obidos/ASIN/1573928860/icongroupinterna
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Contemporary Diagnosis and Management of Arthritis® by Sergio Schwartzman; ISBN: 1884065295; http://www.amazon.com/exec/obidos/ASIN/1884065295/icongroupinterna
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Cooking for Arthritis: Over 50 Delicious and Nutritious Recipes to Help Sufferers of Arthritis by Michelle Berriedale-Johnson (2002); ISBN: 075480965X; http://www.amazon.com/exec/obidos/ASIN/075480965X/icongroupinterna
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Coping With Osteoarthritis: Sound, Compassionate Advice for People Dealing With the Challenge of Osteoarthritis (Coping With...) by Robert H., Ph.D. Phillips (2001); ISBN: 1583330909; http://www.amazon.com/exec/obidos/ASIN/1583330909/icongroupinterna
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Coping With Osteoarthritis: Sound, Compassionate Advice for People Dealing With the Challenge of Osteoarthritis (Coping With...) by Robert H., Ph.D. Phillips (2001); ISBN: 1583330909; http://www.amazon.com/exec/obidos/ASIN/1583330909/icongroupinterna
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Coping With Rheumatoid Arthritis by Robert H. Phillips (1988); ISBN: 0895293714; http://www.amazon.com/exec/obidos/ASIN/0895293714/icongroupinterna
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Curing Arthritis Diet Book by Margaret Hills (1986); ISBN: 0859696049; http://www.amazon.com/exec/obidos/ASIN/0859696049/icongroupinterna
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Curing Arthritis Exercise Book by Margaret Hills, Janet Horwood (1994); ISBN: 0859697045; http://www.amazon.com/exec/obidos/ASIN/0859697045/icongroupinterna
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Curing Arthritis Naturally with Chinese Medicine by Douglas Frank, et al; ISBN: 0936185872; http://www.amazon.com/exec/obidos/ASIN/0936185872/icongroupinterna
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Curing Arthritis: More Ways to a Drug-Free Life (Transaction Large Print Books) [LARGE PRINT] by Margaret Hills, Janet Horwood (2000); ISBN: 1560004592; http://www.amazon.com/exec/obidos/ASIN/1560004592/icongroupinterna
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Curing Arthritis: The Drug Free Way by Margaret Hills, Maragret Hills (1994); ISBN: 0859696898; http://www.amazon.com/exec/obidos/ASIN/0859696898/icongroupinterna
·
Cust Arthritis Solution by J. Kandel, D. B. Sudderth (1997); ISBN: 0761512349; http://www.amazon.com/exec/obidos/ASIN/0761512349/icongroupinterna
·
Devils Claw Root and Other Natural Remedies for Arthritis by Rachel Carstons, et al (1998); ISBN: 092047036X; http://www.amazon.com/exec/obidos/ASIN/092047036X/icongroupinterna
·
Diagnosis and Nonsurgical Management of Osteoarthritis, 2nd edition by Kenneth D. Brandt; ISBN: 1884735576; http://www.amazon.com/exec/obidos/ASIN/1884735576/icongroupinterna
·
Doctor Discusses Learning to Cope with Arthritis Rheumatism and Gout by Robert E. Dunbar (1990); ISBN: 0318375044; http://www.amazon.com/exec/obidos/ASIN/0318375044/icongroupinterna
Books 463
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Dr. Mandell's Lifetime Arthritis Relief System (1986); ISBN: 9993817376; http://www.amazon.com/exec/obidos/ASIN/9993817376/icongroupinterna
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Dr. Scott's Knee Book: Symptoms, Diagnosis, and Treatment of Knee Problems, Including: Torn Cartilage, Ligament Damage, Arthritis, Tendinitis, Arthroscopic Surgery, and by W. Norman Scott, et al (1996); ISBN: 0684811049; http://www.amazon.com/exec/obidos/ASIN/0684811049/icongroupinterna
·
Dr. Scott's Knee Book: Symptoms, Diagnosis, and Treatment of Knee Problems, Including: Torn Cartilage, Ligament Damage, Arthritis, Tendinitis, Arthroscopic Surgery, and by W. Norman Scott, et al (1996); ISBN: 0684811049; http://www.amazon.com/exec/obidos/ASIN/0684811049/icongroupinterna
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Eat to Beat Arthritis: Over 60 Recipes and a Self-Treatment Plan to Transform Your Life by Marguerite Patten, et al (2001); ISBN: 0007116195; http://www.amazon.com/exec/obidos/ASIN/0007116195/icongroupinterna
·
Evening Primrose Oil: How Its Amazing Nutrients Promote Health Relief from Problems Including Acne, Arthritis and Heart Disease by Richard A. Passwater (1982); ISBN: 0879832630; http://www.amazon.com/exec/obidos/ASIN/0879832630/icongroupinterna
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Exercise Beats Arthritis: An Easy-to-Follow Program of Exercises by Valerie Sayce, Ian Fraser; ISBN: 0923521453; http://www.amazon.com/exec/obidos/ASIN/0923521453/icongroupinterna
·
Exercise Can Beat Your Arthritis by Valerie Sayce, Ian Fraser (Contributor); ISBN: 0895293927; http://www.amazon.com/exec/obidos/ASIN/0895293927/icongroupinterna
·
Exercises for Arthritis: 100 Exercises for Healthy Living by Healthy Living Institute, et al (2004); ISBN: 157826166X; http://www.amazon.com/exec/obidos/ASIN/157826166X/icongroupinterna
·
Family Guide to Natural Therapies: Easy to Prepare Remedies for More Than 120 Everyday Health Problems, from Arthritis to Warts by Nancy Beckham, D. R. Bensen (Editor); ISBN: 087983725X; http://www.amazon.com/exec/obidos/ASIN/087983725X/icongroupinterna
·
Finding Ways: Recovering from Rheumatoid Arthritis Through Alternative Medicine by Barbara Jay Nies (1997); ISBN: 0965364860; http://www.amazon.com/exec/obidos/ASIN/0965364860/icongroupinterna
·
Flax Oil As a True Aid Against Arthritis Heart Infarction Cancer and Other Diseases by Johanna Dr. Budwig (1996); ISBN: 0969527217; http://www.amazon.com/exec/obidos/ASIN/0969527217/icongroupinterna
·
Foot and Ankle in Rheumatoid Arthritis by M. Bouysset (2003); ISBN: 2287597573; http://www.amazon.com/exec/obidos/ASIN/2287597573/icongroupinterna
·
Free from Pain of Rheumotoid Arthritis by Laura Nelsen (1989); ISBN: 0925288004; http://www.amazon.com/exec/obidos/ASIN/0925288004/icongroupinterna
·
Freedom from Arthritis through Nutrition by Philip J. Welsh, et al; ISBN: 093085215X; http://www.amazon.com/exec/obidos/ASIN/093085215X/icongroupinterna
·
Gentle Yoga: For People With Arthritis, Stroke Damage, M.S., or People in Wheelchairs by Lorna Bell, Eudora Seyfer (Contributor) (1987); ISBN: 0890874883; http://www.amazon.com/exec/obidos/ASIN/0890874883/icongroupinterna
464 Arthritis
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Get a Grip! : A Take-Charge Approach to Living With Arthritis by Amye Leong, Joe Layden (2002); ISBN: 1585421480; http://www.amazon.com/exec/obidos/ASIN/1585421480/icongroupinterna
·
Getting Up is Hard to Do : Life with Rheumatoid Arthritis by Wanda James; ISBN: 0968703607; http://www.amazon.com/exec/obidos/ASIN/0968703607/icongroupinterna
·
Glucosamine: Nature's Arthritis Remedy by Ray Sahelian; ISBN: 0963975528; http://www.amazon.com/exec/obidos/ASIN/0963975528/icongroupinterna
·
God's Pathway to Healing: Joints and Arthritis by Reginald B., MD Cherry (2003); ISBN: 076422767X; http://www.amazon.com/exec/obidos/ASIN/076422767X/icongroupinterna
·
Guia Practica Para Superar LA Arthritis/Christiaan Bernard's Program for Living With Arthritis by Christiaan Barnard, Cristian Barnard (1995); ISBN: 8425317363; http://www.amazon.com/exec/obidos/ASIN/8425317363/icongroupinterna
·
Guide to Independent Living for People With Arthritis; ISBN: 091242303X; http://www.amazon.com/exec/obidos/ASIN/091242303X/icongroupinterna
·
Heal Arthritis: Physically-Mentally-Spiritually : The Edgar Cayce Approach by William A. McGarey; ISBN: 0876043996; http://www.amazon.com/exec/obidos/ASIN/0876043996/icongroupinterna
·
Healing Arthritis by Penny Kendall-Reed, Stephen Reed (2002); ISBN: 1550823124; http://www.amazon.com/exec/obidos/ASIN/1550823124/icongroupinterna
·
Healing Arthritis the Natural Way: The Breakthrough Program for Reversing Arthritis Using Nutrition and Supplements by Luke Pain Free Bucci; ISBN: 156530277X; http://www.amazon.com/exec/obidos/ASIN/156530277X/icongroupinterna
·
Healing Arthritis: Complementary Naturopathic, Orthopedic and Drug Treatments by Penny Kendall-Reed (2002); ISBN: 1553663748; http://www.amazon.com/exec/obidos/ASIN/1553663748/icongroupinterna
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Healing Arthritis: Discover Your Own Inner Healing Power by Taking an Active Role in Your Healing Process by Michio Kushi; ISBN: 0895295377; http://www.amazon.com/exec/obidos/ASIN/0895295377/icongroupinterna
·
Healing Joint Pain Naturally: Safe and Effective Ways to Treat Arthritis, Fibromyalgia, and Other Joint Diseases by Ellen Hodgson Brown (2001); ISBN: 076790561X; http://www.amazon.com/exec/obidos/ASIN/076790561X/icongroupinterna
·
Health Benefits of Cat's Claw: Its Role in Treating Cancer, Arthritis, Prostate Problems, Asthma and Many Other Chronic Conditions by Alexander Schauss; ISBN: 0879837578; http://www.amazon.com/exec/obidos/ASIN/0879837578/icongroupinterna
·
Health Journeys for People With Rheumatoid Arthritis or Lupus by Belleruth Naparstek (Reader); ISBN: 1570420114; http://www.amazon.com/exec/obidos/ASIN/1570420114/icongroupinterna
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Health Journeys: A Guided Meditation to Help You with Rheumatoid Arthritis or Lupus by Belleruth Naparstek; ISBN: 1881405699; http://www.amazon.com/exec/obidos/ASIN/1881405699/icongroupinterna
Books 465
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Healthy Bones & Joints: A Natural Approach to Treating Arthritis, Osteoporosis, Tendinitis, Myalgia & Bursitis by David Hoffmann, David Hoffman; ISBN: 1580172539; http://www.amazon.com/exec/obidos/ASIN/1580172539/icongroupinterna
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Help Yourself: Recipes and Resources from the Arthritis Foundation; ISBN: 0871974193; http://www.amazon.com/exec/obidos/ASIN/0871974193/icongroupinterna
·
Herbs to Relieve Arthritis (Keats Good Herb Guide) by C. J. Puotinen (1996); ISBN: 0879837438; http://www.amazon.com/exec/obidos/ASIN/0879837438/icongroupinterna
·
How to Beat Arthritis With Immune Power Boosters by Carlson Wade; ISBN: 0133964418; http://www.amazon.com/exec/obidos/ASIN/0133964418/icongroupinterna
·
How to Eat Away Arthritis by Lauri M. Aesoph, Norman D. Ford; ISBN: 013242892X; http://www.amazon.com/exec/obidos/ASIN/013242892X/icongroupinterna
·
How to Eat Away Arthritis and Gout by Norman D. Ford; ISBN: 0134056477; http://www.amazon.com/exec/obidos/ASIN/0134056477/icongroupinterna
·
How to Fight Arthritis & Win by William L. Fischer; ISBN: 1891434128; http://www.amazon.com/exec/obidos/ASIN/1891434128/icongroupinterna
·
I Cured My Arthritis You Can Too by Margie Garrison; ISBN: 0912835001; http://www.amazon.com/exec/obidos/ASIN/0912835001/icongroupinterna
·
Imaging of Arthritis and Related Conditions: With Clinical Perspectives by George B. Greenfield (Editor), et al; ISBN: 0781715369; http://www.amazon.com/exec/obidos/ASIN/0781715369/icongroupinterna
·
Infections and Arthritis (New Clinical Applications/Rheumatology) by John J. Calabro, W. Carson Dick (Editor) (1989); ISBN: 0746200528; http://www.amazon.com/exec/obidos/ASIN/0746200528/icongroupinterna
·
Joint Destruction in Arthritis and Osteoarthritis (Agents and Actions Supplements, Vol. 39) by W.B. Van Den Berg, et al (1993); ISBN: 0817627731; http://www.amazon.com/exec/obidos/ASIN/0817627731/icongroupinterna
·
Joints of Pain : Living my Life with Rheumatoid Arthritis by Laura Pietro; ISBN: 0970418604; http://www.amazon.com/exec/obidos/ASIN/0970418604/icongroupinterna
·
Juvenile Arthritis (Perspectives on Disease and Illness) by Judith Peacock; ISBN: 0736802797; http://www.amazon.com/exec/obidos/ASIN/0736802797/icongroupinterna
·
Kalamazoo Arthritis Book by Halpern. M.D. Alan A. (1986); ISBN: 9998064236; http://www.amazon.com/exec/obidos/ASIN/9998064236/icongroupinterna
·
Keeping A Secret: A Story About Juvenile Rheumatoid Arthritis by Elizabeth Murphy Melas, et al; ISBN: 0929173341; http://www.amazon.com/exec/obidos/ASIN/0929173341/icongroupinterna
·
Learn about Your Arthritis! Patients' Guide to Managing the Most Common Rheumatic Illnesses by Malin Prupas (2001); ISBN: 1587360284; http://www.amazon.com/exec/obidos/ASIN/1587360284/icongroupinterna
466 Arthritis
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Life Without Arthritis: The Maori Way: A Remarkable Discovery for Arthritis and Rheumatism Sufferers by Jan De Vries; ISBN: 1851584668; http://www.amazon.com/exec/obidos/ASIN/1851584668/icongroupinterna
·
Living With Arthritis: Everything You Need to Know (Your Personal Health) by John Marcus Thompson (2001); ISBN: 1552096114; http://www.amazon.com/exec/obidos/ASIN/1552096114/icongroupinterna
·
Living With Arthritis: Successful Strategies to Help Manage the Pain and Remain Active by Harry, M.D. Shen, et al (1993); ISBN: 0452269970; http://www.amazon.com/exec/obidos/ASIN/0452269970/icongroupinterna
·
Living With Juvenile Rheumatoid Arthritis (Living Well Chronic Conditions) by Susan H. Gray, Serge Bloch (2002); ISBN: 1567661041; http://www.amazon.com/exec/obidos/ASIN/1567661041/icongroupinterna
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Living with Rheumatoid Arthritis by Tammi L. Shlotzhauer, et al; ISBN: 0801871476; http://www.amazon.com/exec/obidos/ASIN/0801871476/icongroupinterna
·
Lyprinol: A Natural Solution for Arthritis and Other Inflammatory Disorders by Georges M. Halpern, Krista Edmonds (2001); ISBN: 1583331034; http://www.amazon.com/exec/obidos/ASIN/1583331034/icongroupinterna
·
Magic Herbs for Arthritis, Rheumatism, and Related Ailments by Richard Lucas; ISBN: 0135439000; http://www.amazon.com/exec/obidos/ASIN/0135439000/icongroupinterna
·
Managing and Preventing Arthritis: The Natural Alternatives by George L. Redmon (1999); ISBN: 0934252904; http://www.amazon.com/exec/obidos/ASIN/0934252904/icongroupinterna
·
Market Dynamics: Arthritis - The Ongoing Battle for Supremacy [DOWNLOAD: PDF] by Datamonitor (Author); ISBN: B00008R3X7; http://www.amazon.com/exec/obidos/ASIN/B00008R3X7/icongroupinterna
·
Maximizing the Arthritis Cure: A Step-By-Step Program to Faster, Stronger Healing During Any Stage of the Cure by Jason Theodosakis, et al; ISBN: 0312969163; http://www.amazon.com/exec/obidos/ASIN/0312969163/icongroupinterna
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Maximizing the Arthritis Cure: A Step-By-Step Program to Faster, Stronger Healing During Any Stage of the Cure by Jason Theodosakis, et al; ISBN: 0312969163; http://www.amazon.com/exec/obidos/ASIN/0312969163/icongroupinterna
·
Mayo Clinic on Arthritis by Gene G. Hunder (Editor) (2002); ISBN: 1893005259; http://www.amazon.com/exec/obidos/ASIN/1893005259/icongroupinterna
·
Mechanisms and Models in Rheumatoid Arthritis by J.C.W. Edwards, et al (1995); ISBN: 0123404401; http://www.amazon.com/exec/obidos/ASIN/0123404401/icongroupinterna
·
Monoclonal Antibodies, Cytokines and Arthritis: Mediators of Inflammation and Therapy (Inflammatory Disease and Therapy Series No 7) by Thomas F. Kresina (Editor); ISBN: 0824781163; http://www.amazon.com/exec/obidos/ASIN/0824781163/icongroupinterna
·
MSM the Definitive Guide: The Nutritional Breakthrough for Arthritis, Allergies and More by Stanley W. Jacob, Jeremy Appleton (2002); ISBN: 1893910229; http://www.amazon.com/exec/obidos/ASIN/1893910229/icongroupinterna
Books 467
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Natural Care Library Garlic: Safe and Effective Self-Care for Arthritis, High Blood Pressure and Flu by Stephanie Pedersen; ISBN: 0789451921; http://www.amazon.com/exec/obidos/ASIN/0789451921/icongroupinterna
·
Natural Medicine for Arthritis (The Dell Natural Medicine Library) by Winifred Conkling; ISBN: 0440221692; http://www.amazon.com/exec/obidos/ASIN/0440221692/icongroupinterna
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Natural Medicine for Arthritis: The Best Alternative Methods for Relieving Pain and Stiffness: From Food & Herbs to Acupuncture & Homeopathy by Glenn S. Rothfeld, et al (1996); ISBN: 0875962874; http://www.amazon.com/exec/obidos/ASIN/0875962874/icongroupinterna
·
New Treatments in Arthritis by Philip G. Conaghan, et al (2003); ISBN: 1850091889; http://www.amazon.com/exec/obidos/ASIN/1850091889/icongroupinterna
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Nicole's Story: A Book About a Girl With Juvenile Rheumatoid Arthritis by Virginia Tortorica Aldape, et al; ISBN: 082252578X; http://www.amazon.com/exec/obidos/ASIN/082252578X/icongroupinterna
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Nicole's Story: A Book About a Girl With Juvenile Rheumatoid Arthritis by Virginia Tortorica Aldape, et al; ISBN: 082252578X; http://www.amazon.com/exec/obidos/ASIN/082252578X/icongroupinterna
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Nutrients for Health: The New Zealand Green-Lipped Mussel Helping in Treatment of Osteo- & Rheu Matoid Arthritis by John Croft; ISBN: 0722531710; http://www.amazon.com/exec/obidos/ASIN/0722531710/icongroupinterna
·
Osteoarthritis by Kenneth D. Brandt (Editor), et al (2003); ISBN: 0198509677; http://www.amazon.com/exec/obidos/ASIN/0198509677/icongroupinterna
·
Osteoarthritis in Rhesus Monkeys and Gibbons: A Locomotor Model of Joint Degeneration (Contributions to Primatology, Vol 25) by C. Jean Derousseau (1988); ISBN: 3805547005; http://www.amazon.com/exec/obidos/ASIN/3805547005/icongroupinterna
·
Osteoarthritis: A Step by Step Success Story to Show Others They Can Help Themselves by Fred L. Savage (1990); ISBN: 0882680862; http://www.amazon.com/exec/obidos/ASIN/0882680862/icongroupinterna
·
Osteoarthritis: Diagnosis and Medical/Surgical Management by Roland W. Moskowitz (Editor), et al; ISBN: 0721684394; http://www.amazon.com/exec/obidos/ASIN/0721684394/icongroupinterna
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Osteoarthritis: Fundamentals and Strategies for Joint-Preserving Treatment by J. Grifka (Editor), et al; ISBN: 3540663096; http://www.amazon.com/exec/obidos/ASIN/3540663096/icongroupinterna
·
Osteoarthritis: Public Health Implications for an Aging Population by David Hamerman (Editor), M. David Hamerman (1997); ISBN: 0801855616; http://www.amazon.com/exec/obidos/ASIN/0801855616/icongroupinterna
·
Osteoarthritis: Your Questions Answered by John Dickson, Gillian Hosie (2003); ISBN: 0443073465; http://www.amazon.com/exec/obidos/ASIN/0443073465/icongroupinterna
·
Overcoming Arthritis by David Brownstein; ISBN: 0966088212; http://www.amazon.com/exec/obidos/ASIN/0966088212/icongroupinterna
468 Arthritis
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Overcoming Arthritis and Other Rheumatic Diseases by Maxi Warmbrand, Max Warmbrand; ISBN: 0517379902; http://www.amazon.com/exec/obidos/ASIN/0517379902/icongroupinterna
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Overcoming Arthritis: How to Relieve Pain and Restore Mobility Through a Unique Tai Chi Program by Paul Lam, Judith Horstman; ISBN: 0789484315; http://www.amazon.com/exec/obidos/ASIN/0789484315/icongroupinterna
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Overcoming the Pain of Inflammatory Arthritis: The Pain-Free Promise of Pantothenic Acid by Phyllis Eisenstein, et al; ISBN: 0895298104; http://www.amazon.com/exec/obidos/ASIN/0895298104/icongroupinterna
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Pain Free: The Definitive Guide to Healing Arthritis, Low-Back Pain, and Sports Injuries Through Nutrition and Supplements by Luke Bucci (1995); ISBN: 1565301617; http://www.amazon.com/exec/obidos/ASIN/1565301617/icongroupinterna
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Pain-Free Arthritis : A 7-Step Plan for Feeling Better Again by Debra Fulghum Bruce (Author), Harris H. McIlwain (Author) (2003); ISBN: 0805073256; http://www.amazon.com/exec/obidos/ASIN/0805073256/icongroupinterna
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Pain-Free with Magnet Therapy: Discover how Magnets can Help Relieve Arthritis, Sports Injuries, Fibromyalgia, and Chronic Pain by Lara Owen; ISBN: 0761520864; http://www.amazon.com/exec/obidos/ASIN/0761520864/icongroupinterna
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People with Arthritis Can Exercise (Pace): Level II (Video Cassette) by The Arthritis Foundation (1993); ISBN: 0912423366; http://www.amazon.com/exec/obidos/ASIN/0912423366/icongroupinterna
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Physical Therapy in Arthritis by Joan M. Walker (Editor), et al; ISBN: 0721649998; http://www.amazon.com/exec/obidos/ASIN/0721649998/icongroupinterna
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Pipeline Insight: Rheumatoid Arthritis and Osteoarthritis - Striving for innovation among me-toos [DOWNLOAD: PDF] by Datamonitor (Author); ISBN: B00009XGBS; http://www.amazon.com/exec/obidos/ASIN/B00009XGBS/icongroupinterna
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Playing Through Arthritis : How to Conquer Pain and Enjoy Your Favorite Sports and Activities by David, S. Silver, Jerry Buss; ISBN: 0071402241; http://www.amazon.com/exec/obidos/ASIN/0071402241/icongroupinterna
·
Pocket Reference to TNF Antagonism and Rheumatoid Arthritis by Maini, et al (2000); ISBN: 1858733758; http://www.amazon.com/exec/obidos/ASIN/1858733758/icongroupinterna
·
Preventing and Reversing Arthritis Naturally: The Untold Story by Raquel Martin, et al; ISBN: 0892818913; http://www.amazon.com/exec/obidos/ASIN/0892818913/icongroupinterna
·
Preventing Arthritis [DOWNLOAD: ADOBE READER] by Ronald M. Lawrence, Martin Zucker (2001); ISBN: B00006I4PH; http://www.amazon.com/exec/obidos/ASIN/B00006I4PH/icongroupinterna
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Preventing Arthritis: A Holistic Approach to Life Without Pain by Ronald W., Md Lawrence, et al (2002); ISBN: 0425184684; http://www.amazon.com/exec/obidos/ASIN/0425184684/icongroupinterna
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Prevention's Healing With Vitamins: The Most Effective Vitamin and Mineral Treatments for Everyday Health Problems and Serious Disease-From Allergies and Arthritis to Water Retention and by Alice Feinstein (Editor), et al (1996); ISBN: 0875962920; http://www.amazon.com/exec/obidos/ASIN/0875962920/icongroupinterna
Books 469
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Preventions Outsmart Arthritis: Expert-Endorsed Remedies for Short-Term Relief and Lifetime Control by Prevention Health Books (Editor); ISBN: 0312988117; http://www.amazon.com/exec/obidos/ASIN/0312988117/icongroupinterna
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Prolo Your Arthritis Pain Away: Curing Disabling & Disfiguring Arthritis Pain With Prolotherapy by Ross A. Hauser, et al; ISBN: 0966101057; http://www.amazon.com/exec/obidos/ASIN/0966101057/icongroupinterna
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Qigong for Arthritis: The Chinese Way of Healing and Prevention: Massage, Cavity Press, and Qigong Exercises by Jwing-Ming Yang, et al; ISBN: 0940871130; http://www.amazon.com/exec/obidos/ASIN/0940871130/icongroupinterna
·
Raising a Child With Arthritis: Parent's Guide by Arthritis Foundation (Editor) (1998); ISBN: 0912423196; http://www.amazon.com/exec/obidos/ASIN/0912423196/icongroupinterna
·
Rapid Reference to Arthritis by Frank McKenna, Lee Simon (2003); ISBN: 0723433143; http://www.amazon.com/exec/obidos/ASIN/0723433143/icongroupinterna
·
Recipes for Arthritis Health (The Johns Hopkins Cookbook Library) by John A. Flynn (Editor), Lora Brown Wilder (Editor) (2003); ISBN: 0929661761; http://www.amazon.com/exec/obidos/ASIN/0929661761/icongroupinterna
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Rehabilitation of Persons with Rheumatoid Arthritis by Rowland W. Chang (Editor), et al; ISBN: 083420679X; http://www.amazon.com/exec/obidos/ASIN/083420679X/icongroupinterna
·
Releasing Arthritis: The Seven Year Plan by Linda Frazer Fleming (1990); ISBN: 1877631027; http://www.amazon.com/exec/obidos/ASIN/1877631027/icongroupinterna
·
Relief from Arthritis: The Natural Way by John E. Croft; ISBN: 0722513771; http://www.amazon.com/exec/obidos/ASIN/0722513771/icongroupinterna
·
Relief from Chronic Arthritis Pain by Helene MacLean, et al; ISBN: 0440205964; http://www.amazon.com/exec/obidos/ASIN/0440205964/icongroupinterna
·
Revisional Surgery in Rheumatoid Arthritis (Rheumatology: The Interdisciplinary Concept, Vol 13) by M. Hamalainen, et al (1990); ISBN: 380554930X; http://www.amazon.com/exec/obidos/ASIN/380554930X/icongroupinterna
·
Rheumatoid Arthritis (Current Directions in Autoimmunity, Vol. 3) by J. J. Goronzy (Editor), C. M. Weyand (Editor) (2001); ISBN: 3805571208; http://www.amazon.com/exec/obidos/ASIN/3805571208/icongroupinterna
·
Rheumatoid Arthritis Surgery of the Complex Hand and Foot (Rheumatology, Vol 11) by F.-W. Hagena (Editor) (1987); ISBN: 3805544081; http://www.amazon.com/exec/obidos/ASIN/3805544081/icongroupinterna
·
Rheumatoid Arthritis Surgery of the Elbow (Rheumatology. the Interdisciplinary Concept, Vol 15) by M. J. Hamalainen (Editor), F. W. Hagena (Editor) (1991); ISBN: 3805553277; http://www.amazon.com/exec/obidos/ASIN/3805553277/icongroupinterna
·
Rheumatoid Arthritis Surgery of the Shoulder (Rheumatology, Vol 12) by A.W.F. Lettin, et al (1989); ISBN: 3805548044; http://www.amazon.com/exec/obidos/ASIN/3805548044/icongroupinterna
470 Arthritis
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Rheumatoid Arthritis: Current Trends in Diagnostics, Convervative Treatment and Surgical Reconstruction by Hubert Baumgartner (Editor), et al; ISBN: 3131024410; http://www.amazon.com/exec/obidos/ASIN/3131024410/icongroupinterna
·
Rheumatoid Arthritis: Epidemiology, Pathogenesis and Treatment by Sherine Gabriel, Larry Moreland (2001); ISBN: 1901346161; http://www.amazon.com/exec/obidos/ASIN/1901346161/icongroupinterna
·
Rheumatoid Arthritis: Etiology, Diagnosis, Management by Peter D. Utsinger, et al; ISBN: 0397505884; http://www.amazon.com/exec/obidos/ASIN/0397505884/icongroupinterna
·
Rheumatoid Arthritis: Everything You Need to Know by Robert G. Lahita (2001); ISBN: 1583331018; http://www.amazon.com/exec/obidos/ASIN/1583331018/icongroupinterna
·
Rheumatoid Arthritis: Frontiers in Pathogenesis and Treatment by Gary S. Firestein (Editor), et al; ISBN: 0192629727; http://www.amazon.com/exec/obidos/ASIN/0192629727/icongroupinterna
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Rheumatoid Arthritis: Plan to Win by Cheryl Koehn, et al (2002); ISBN: 0195130561; http://www.amazon.com/exec/obidos/ASIN/0195130561/icongroupinterna
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Rheumatoid Arthritis: Recent Research Advances by J.R. Kalden, et al (1992); ISBN: 038753315X; http://www.amazon.com/exec/obidos/ASIN/038753315X/icongroupinterna
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Rheumatoid Arthritis: The Infection Connection {Targeting and Treating the Cause of Chronic Illness} by Katherine M. Poehlmann; ISBN: 0961726865; http://www.amazon.com/exec/obidos/ASIN/0961726865/icongroupinterna
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Rheumatoid Arthritis: The Infection Connection {Targeting and Treating the Cause of Chronic Illness} by Katherine M. Poehlmann; ISBN: 0961726865; http://www.amazon.com/exec/obidos/ASIN/0961726865/icongroupinterna
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Rheumatoid Arthritis: Your Medication Explained (Overcoming Common Problems Series.) by Mary-Claire Mason, Elaine, Dr. Smith; ISBN: 085969836X; http://www.amazon.com/exec/obidos/ASIN/085969836X/icongroupinterna
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Rheumatology, Arthritis and Musculoskeletal Disease Two Thousand by Panush (2000); ISBN: 0815129262; http://www.amazon.com/exec/obidos/ASIN/0815129262/icongroupinterna
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Same S-Adenosylmethionine: The European Arthritis and Depression Breakthrough by Sol Grazi, Marie Costa; ISBN: 0761516271; http://www.amazon.com/exec/obidos/ASIN/0761516271/icongroupinterna
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Same: The Remarkable Substance That Promotes Detoxification, Relieves Arthritis, and Fights Depression by Rita Elkins (1999); ISBN: 1580540597; http://www.amazon.com/exec/obidos/ASIN/1580540597/icongroupinterna
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Say No to Arthritis (Optimum Nutrition Handbook) by Patrick Holford; ISBN: 0749920130; http://www.amazon.com/exec/obidos/ASIN/0749920130/icongroupinterna
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Silent Pain: Is It Arthritis?: Reflections of a Clinical Rheumatologist by William E. Byrd, Jan Sullivan (Illustrator) (1995); ISBN: 1556181558; http://www.amazon.com/exec/obidos/ASIN/1556181558/icongroupinterna
Books 471
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Simple Solutions for Arthritis: An Arthritis Patient's Practical Guide to Health and Hope by Kim Manser Hofmann (2000); ISBN: 1587213656; http://www.amazon.com/exec/obidos/ASIN/1587213656/icongroupinterna
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Sjogren's Syndrome: The Sneaky "Arthritis" by Sue Dauphin; ISBN: 0962035408; http://www.amazon.com/exec/obidos/ASIN/0962035408/icongroupinterna
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Special Report: A Doctor's Proven New Way to Conquer Rheumatism and Arthritis by James K. Van Fleet, John E. Eichenlaub (1992); ISBN: 0138326509; http://www.amazon.com/exec/obidos/ASIN/0138326509/icongroupinterna
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Staff Manual for Teaching Patients About Rheumatoid Arthritis 1982 Edition by Roberta Wallace (1982); ISBN: 0872583740; http://www.amazon.com/exec/obidos/ASIN/0872583740/icongroupinterna
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Stop Arthritis: How I Defeated It Naturally by Alan Schlines (2003); ISBN: 1589394267; http://www.amazon.com/exec/obidos/ASIN/1589394267/icongroupinterna
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Stop Osteoarthritis Now: Halting the Baby Boomers' Disease by Harris H. McIlwain (Preface), Debra Fulghum Bruce (1996); ISBN: 0684814390; http://www.amazon.com/exec/obidos/ASIN/0684814390/icongroupinterna
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Stop Suffering from Arthritis by Dac Dipl T., Dr Huang, Dac Dipl AC Ch T. Huang (2002); ISBN: 140104770X; http://www.amazon.com/exec/obidos/ASIN/140104770X/icongroupinterna
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Strong Women and Men Beat Arthritis: The Scientifically Proven Program That Allows People With Arthritis to Take Charge of Their Disease by Miriam E. Nelson, et al (2002); ISBN: 0399148523; http://www.amazon.com/exec/obidos/ASIN/0399148523/icongroupinterna
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Surgical Treatment of Rheumatoid Arthritis by Thomas P. Sculco (Editor), et al (1992); ISBN: 0801662796; http://www.amazon.com/exec/obidos/ASIN/0801662796/icongroupinterna
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T Cells In Arthritis by Pierre Miossec, et al; ISBN: 376435853X; http://www.amazon.com/exec/obidos/ASIN/376435853X/icongroupinterna
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Taking Charge of Arthritis: An Action Guide to Managing Your Health and WellBeing by Larry Katzenstein, Readers Digest Association (2002); ISBN: 0762103221; http://www.amazon.com/exec/obidos/ASIN/0762103221/icongroupinterna
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Taking Control: A New Approach to Dealing with Arthritis by Margaret Gore; ISBN: 1864486910; http://www.amazon.com/exec/obidos/ASIN/1864486910/icongroupinterna
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The 2002 Official Patient's Sourcebook on Rheumatoid Arthritis by James N. Parker, Icon Health Publications; ISBN: 0597829861; http://www.amazon.com/exec/obidos/ASIN/0597829861/icongroupinterna
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The Arthritis Action Program: An Integrated Plan of Traditional and Complementary Therapies by Michael E. Weinblatt, Harvard Medical School (2000); ISBN: 0684868024; http://www.amazon.com/exec/obidos/ASIN/0684868024/icongroupinterna
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The Arthritis Bible: A Comprehensive Guide to Alternative Therapies and Conventional Treatments for Arthritic Diseases by Leonid Gordin, Craig Weatherby; ISBN: 0892818255; http://www.amazon.com/exec/obidos/ASIN/0892818255/icongroupinterna
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The Arthritis Book of Water Exercise by Judy Jetter, Nancy Kadlec; ISBN: 0030707145; http://www.amazon.com/exec/obidos/ASIN/0030707145/icongroupinterna
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The Arthritis Cookbook: Over 50 Delicious and Healthy Recipes for People with Arthritis (The Healthy Eating Library) by Michelle Berriedale-Johnson (2000); ISBN: 0754805298; http://www.amazon.com/exec/obidos/ASIN/0754805298/icongroupinterna
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The Arthritis Cookbook: Over 50 Delicious and Healthy Recipes to Help People with Arthritis by Michelle Berriedale-Johnson; ISBN: 0754807509; http://www.amazon.com/exec/obidos/ASIN/0754807509/icongroupinterna
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The Arthritis Cure Cookbook by Brenda D. Adderly; ISBN: 0895262193; http://www.amazon.com/exec/obidos/ASIN/0895262193/icongroupinterna
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The Arthritis Cure Fitness Solution by Chanteil Miller, Brenda D. Adderly; ISBN: 0895263599; http://www.amazon.com/exec/obidos/ASIN/0895263599/icongroupinterna
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The Arthritis Cure, Revised Edition : The Medical Miracle That Can Halt, Reverse, and May Even Cure Osteoarthritis by Jason Theodosakis (Author), Sheila Buff (Author) (2004); ISBN: 0312327897; http://www.amazon.com/exec/obidos/ASIN/0312327897/icongroupinterna
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The Arthritis Diet Cookbook by Michael McIlwraith; ISBN: 0575042656; http://www.amazon.com/exec/obidos/ASIN/0575042656/icongroupinterna
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The Arthritis Foundation's Guide to Alternative Therapies by Judith Horstman, et al; ISBN: 0912423234; http://www.amazon.com/exec/obidos/ASIN/0912423234/icongroupinterna
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The Arthritis Foundation's Guide to Good Living with Osteoarthritis by Arthritis Foundation (2000); ISBN: 0912423250; http://www.amazon.com/exec/obidos/ASIN/0912423250/icongroupinterna
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The Arthritis Foundation's Guide to Good Living with Rheumatoid Arthritis by Gretchen Henkel, et al; ISBN: 0912423218; http://www.amazon.com/exec/obidos/ASIN/0912423218/icongroupinterna
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The Arthritis Foundation's Guide to Managing Your Arthritis by Mary Anne Dunkin, John H., MD Klippel (Editor); ISBN: 0912423285; http://www.amazon.com/exec/obidos/ASIN/0912423285/icongroupinterna
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The Arthritis Foundation's Guide to Pain Management by Susan Bernstein, John H. Klippel (2003); ISBN: 0912423390; http://www.amazon.com/exec/obidos/ASIN/0912423390/icongroupinterna
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The Arthritis Foundation's Tips for Good Living With Arthritis by The Arthritis Foundation (Editor), Arthritis Foundation (2001); ISBN: 0912423277; http://www.amazon.com/exec/obidos/ASIN/0912423277/icongroupinterna
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The Arthritis Handbook (1996); ISBN: 0864330820; http://www.amazon.com/exec/obidos/ASIN/0864330820/icongroupinterna
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The arthritis handbook: a patient's manual on arthritis, rheumatism and gout by Darrell C. Crain; ISBN: 0682472115; http://www.amazon.com/exec/obidos/ASIN/0682472115/icongroupinterna
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The Arthritis Healthy Exchanges Cookbook (Healthy Exchanges Cookbooks) by Joanna M. Lund (1998); ISBN: 0399523774; http://www.amazon.com/exec/obidos/ASIN/0399523774/icongroupinterna
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The Arthritis Healthy Exchanges Cookbook (Healthy Exchanges Cookbooks) by Joanna M. Lund (1998); ISBN: 0399523774; http://www.amazon.com/exec/obidos/ASIN/0399523774/icongroupinterna
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The Arthritis Helpbook by James F. Fries (Contributor), Kate Lorig; ISBN: 020105468X; http://www.amazon.com/exec/obidos/ASIN/020105468X/icongroupinterna
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The Arthritis Helpbook: A Tested Self-Management Program for Coping with Arthritis and Fibromyalgia by Kate Lorig, et al; ISBN: 073820224X; http://www.amazon.com/exec/obidos/ASIN/073820224X/icongroupinterna
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The Arthritis Helpbook: What You Can Do for Your Arthritis by Kate Lorig, James F. Fries; ISBN: 0201037963; http://www.amazon.com/exec/obidos/ASIN/0201037963/icongroupinterna
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The Arthritis Relief Diet by James Scala; ISBN: 0452262569; http://www.amazon.com/exec/obidos/ASIN/0452262569/icongroupinterna
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The Arthritis Solution by David B., Md Sudderth, et al; ISBN: 0761511725; http://www.amazon.com/exec/obidos/ASIN/0761511725/icongroupinterna
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The Arthritis Sourcebook by Earl J. Jr., Md. Brewer, et al; ISBN: 0737303816; http://www.amazon.com/exec/obidos/ASIN/0737303816/icongroupinterna
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The Bible Cure for Arthritis (Fitness and Health) by Donald, Md. Colbert, Don Colbert (1999); ISBN: 0884196496; http://www.amazon.com/exec/obidos/ASIN/0884196496/icongroupinterna
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The Duke University Medical Center Book of Arthritis by David S. Pisetsky, Susan Flamholtz Trien (Contributor) (1995); ISBN: 0449908879; http://www.amazon.com/exec/obidos/ASIN/0449908879/icongroupinterna
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The Encyclopedia of Arthritis (Library of Health and Living) by Michael, Dr Stein, et al (2003); ISBN: 081604810X; http://www.amazon.com/exec/obidos/ASIN/081604810X/icongroupinterna
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The Essential Arthritis Cookbook : Kitchen Basics for People With Arthritis, Fibromyalgia and Other Chronic Pain and Fatigue by Sarah L. Morgan (Editor), et al; ISBN: 1891011014; http://www.amazon.com/exec/obidos/ASIN/1891011014/icongroupinterna
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The Everyday Arthritis Solution: Food, Movement, and Lifestyle Secrets to Ease the Pain and Feel Your Best by Richard Laliberte, et al (2003); ISBN: 0762104767; http://www.amazon.com/exec/obidos/ASIN/0762104767/icongroupinterna
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The Hospital for Special Surgery Rheumatoid Arthritis Handbook by Stephen A. Paget (Author), et al; ISBN: 0471410454; http://www.amazon.com/exec/obidos/ASIN/0471410454/icongroupinterna
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The Johns Hopkins White Papers: Arthritis by John A. Flynn, Simeon Margolis; ISBN: 0929661133; http://www.amazon.com/exec/obidos/ASIN/0929661133/icongroupinterna
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The Many Faces of Osteoarthritis by Vincent C. Hascall (Editor), et al; ISBN: 3764365811; http://www.amazon.com/exec/obidos/ASIN/3764365811/icongroupinterna
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The Natural Pharmacist: Your Complete Guide to Arthritis by Ron Hobbs, et al; ISBN: 0761515569; http://www.amazon.com/exec/obidos/ASIN/0761515569/icongroupinterna
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The Natural Way With Arthritis & Rheumatism (Natural Way) by Pat Young; ISBN: 1852306297; http://www.amazon.com/exec/obidos/ASIN/1852306297/icongroupinterna
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The New Arthritis Breakthrough by Henry Scammell (1998); ISBN: 0871318431; http://www.amazon.com/exec/obidos/ASIN/0871318431/icongroupinterna
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The New Arthritis Relief Diet: Proven Steps to Stop Inflammation, Prevent Joint Damage, Decrease Medication, and Improve the Quality of Your Life by James Scala (1998); ISBN: 0452279518; http://www.amazon.com/exec/obidos/ASIN/0452279518/icongroupinterna
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The Official Patient's Sourcebook on Arthritis of the Knee: A Revised and Updated Directory for the Internet Age by Icon Health Publications (2002); ISBN: 0597832331; http://www.amazon.com/exec/obidos/ASIN/0597832331/icongroupinterna
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The Official Patient's Sourcebook on Arthritis of the Shoulder: A Revised and Updated Directory for the Internet Age by Icon Health Publications (2002); ISBN: 059783234X; http://www.amazon.com/exec/obidos/ASIN/059783234X/icongroupinterna
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The Official Patient's Sourcebook on Juvenile Rheumatoid Arthritis: A Revised and Updated Directory for the Internet Age by Icon Health Publications (2002); ISBN: 059783377X; http://www.amazon.com/exec/obidos/ASIN/059783377X/icongroupinterna
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The Pain Relief Breakthrough: The Power of Magnets to Relieve Backaches, Arthritis, Menstrual Cramps, Carpal Tunnel Syndrome, Sports Injuries, and More by Julian, M.D. Whitaker, Brenda D. Adderly (1998); ISBN: 0316601934; http://www.amazon.com/exec/obidos/ASIN/0316601934/icongroupinterna
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The Road Back: Rheumatoid Arthritis, Its Cause and Its Treatment by Thomas Mc Pherson Brown, et al (1988); ISBN: 0871315432; http://www.amazon.com/exec/obidos/ASIN/0871315432/icongroupinterna
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The Sam-E Handbook: The Fast, Natural Way to Relieve the Pain of Arthritis, Alleviate the Discomfort of Fibromyalgia, and Boost Your Energy by Nancy Stedman; ISBN: 0609806548; http://www.amazon.com/exec/obidos/ASIN/0609806548/icongroupinterna
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The Super Aspirin Cure for Arthritis by Harris H., MD McIlwain, H. M. D. McIlwain (1999); ISBN: 0553762826; http://www.amazon.com/exec/obidos/ASIN/0553762826/icongroupinterna
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The Super Aspirin Cure for Arthritis: What You Need to Know About the Breakthrough Drugs That Stop Pain and Reverse Arthritis Symptoms Without Side Effects by Harris H. McIlwain, et al; ISBN: 0553581074; http://www.amazon.com/exec/obidos/ASIN/0553581074/icongroupinterna
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The Surgical Management of Rheumatoid Arthritis by F. Howard Beddow (1989); ISBN: 072361007X; http://www.amazon.com/exec/obidos/ASIN/072361007X/icongroupinterna
Books 475
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The Wrist in Rheumatoid Arthritis (Rheumatology: The Interdisciplinary Concept, Vol 17) by B.R. Simmen, F.W. Hagena (Editor) (1992); ISBN: 3805555148; http://www.amazon.com/exec/obidos/ASIN/3805555148/icongroupinterna
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The Year in Rheumatic Disorders 2002: Special Issue: Rheumatoid Arthritis by D. Scott (Editor), et al (2002); ISBN: 0953733998; http://www.amazon.com/exec/obidos/ASIN/0953733998/icongroupinterna
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The Yearbook of Rheumatology, Arthritis, and Musculoskeletal Disease, 1999 by Richard S., Md. Panush (Editor), et al (1999); ISBN: 0815197381; http://www.amazon.com/exec/obidos/ASIN/0815197381/icongroupinterna
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There Is a Cure for Arthritis by Paavo O. Airola; ISBN: 0139146989; http://www.amazon.com/exec/obidos/ASIN/0139146989/icongroupinterna
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Time-Life Alternative Remedies for Common Ailments: How to Treat, Arthritis, Back Problems, Chronic Fatigue, Headaches, Insomnia, Sinusitis-- And over 40 More Common Health Conditions by Time-Life Books (Editor); ISBN: 073701105X; http://www.amazon.com/exec/obidos/ASIN/073701105X/icongroupinterna
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TNF-Inhibition in the Treatment of Rheumatoid Arthritis by Larry W. Moreland, et al; ISBN: 1841841560; http://www.amazon.com/exec/obidos/ASIN/1841841560/icongroupinterna
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Triumph Over Arthritis : A comprehensive and up-to-date guide to the help available by Anna Scott; ISBN: 0868063738; http://www.amazon.com/exec/obidos/ASIN/0868063738/icongroupinterna
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Understanding Arthritis and Rheumatism by Jennifer Worral; ISBN: 1898205973; http://www.amazon.com/exec/obidos/ASIN/1898205973/icongroupinterna
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Understanding Rheumatoid Arthritis by S. P. Newman (Editor) (1996); ISBN: 0415105412; http://www.amazon.com/exec/obidos/ASIN/0415105412/icongroupinterna
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Win the War Against Arthritis (Progressive Health Series) by Michael Colgan (1999); ISBN: 1896817203; http://www.amazon.com/exec/obidos/ASIN/1896817203/icongroupinterna
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Your Child with Arthritis: A Family guide for Caregiving by Lori B., M.D. Tucker, et al (2000); ISBN: 0801865344; http://www.amazon.com/exec/obidos/ASIN/0801865344/icongroupinterna
The National Library of Medicine Book Index The National Library of Medicine at the National Institutes of Health has a massive database of books published on healthcare and biomedicine. Go to the following Internet site, http://locatorplus.gov/, and then select “Search LOCATORplus.” Once you are in the search area, simply type “arthritis” (or synonyms) into the search box, and select “books only.” From there, results can be sorted by publication date, author, or relevance. The following was recently catalogued by the National Library of Medicine:11 11 In addition to LOCATORPlus, in collaboration with authors and publishers, the National Center for Biotechnology Information (NCBI) is currently adapting biomedical books for the Web. The books may be accessed in two ways: (1) by searching directly using any search term or phrase (in the same way as the bibliographic database PubMed), or (2) by following the links to PubMed abstracts. Each PubMed abstract has a "Books" button that displays a facsimile of the abstract in which some phrases are hypertext links. These phrases are also found in
476 Arthritis
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[Beta] 1C-globulin and trypsin inhibitors in systemic lupus erythematosus and rheumatoid arthritis. Author: Lundh, Bengt.; Year: 1964; Lund, Gleerup, 1965
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A prognostic study of juvenile rheumatoid arthritis: analysis of 544 cases. Author: Laaksonen, Anna-Liisa.; Year: 1964; Turku, Jaakkoo-Taara, 1966
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A study on a substance eluted from erythrocytes of patients with rheumatoid arthritis and patients with hemolytic anemia. Author: Blodgett, Randolph C.,; Year: 1962; [Minneapolis] 1963
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Anemia problems in rheumatoid arthritis. Author: Nilsson, Fried Alvar,; Year: 1958; Uppsala, Appelbergs boktryckeriaktiebolag, 1948
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Arthritis and allied conditions; a textbook of rheumatology. Editor: Joseph Lee Hollander. Section editors: Edward W. Boland [et al.] Contributing editors: Nathan R. Abrams [et al.]. Author: Hollander, Joseph Lee,; Year: 1963; Philadelphia, Lea; Febiger, 1966
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Arthritis source book. Author: United States. Public Health Service. Division of Chronic Diseases.; Year: 1965; Washington, U. S. Public Health Service, Division of Chronic Diseases, Diabetes and
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Ashamed of my arthritis. Author: Rostron, Lewis.; Year: 1962; Blackpool, Eng., 1965
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Balneotherapy of rheumathoid [sic] arthritis and degenerative lesions of the spine. Author: Evers, A. (Arrien); Year: 2003; Köln, Universitätsverlag [1961?]
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Cellular concepts in rheumatoid arthritis. Comp. and ed. by C. A. L. Stephens, Jr. and A. B. Stanfield with the assistance of Margaret L. Doorly. Author: Stephens, C. A. L.,; Year: 1964; Springfield, Ill., Thomas [c1966]
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Characterization of dextran eluates from erythrocytes of normal persons and patients with rheumatoid arthritis. Author: Hunder, Gene G.; Year: 1963; [Minneapolis] 1965
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Conference on criteria for, and evaluation of, orthopedic measures in the management of deformities of rheumatoid arthritis, Barbizon Plaza Hotel, New York, December 8, 1963. [Transactions. Author: American Rheumatism Association.; Year: 1963; New York, Grune; Stratton, 1964]
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First three steps towards arthritic recovery. Author: De Coti-Marsh, Charles.; Year: 1964; [London, Hursdrex] 1964
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Further in vitro studies on the cytotoxic effect of mononuclear cells from synovial fluid in arthritis, by Helge Hedberg and Bengt Källén. Author: Hedberg, Helge.; Year: 1964; Lund, Gleerup, 1964
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Home treatment for arthritis. Author: De Coti-Marsh, Charles.; Year: 1958; [London] 1966
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Practical prescribing guidelines in rheumatoid arthritis Author: Capell, Hilary A. (Hilary Allison),; Year: 1963; London; New York: Martin Dunitz; Independence, KY: Distributed in the USA by Taylor; Francis, 2003; ISBN: 1841842826 http://www.amazon.com/exec/obidos/ASIN/1841842826/icongroupinterna
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Statistical review [of] poliomyelitis, congenital defects, arthritis. Author: National Foundation.; Year: 1964; New York, 1962
the books available at NCBI. Click on hyperlinked results in the list of books in which the phrase is found. Currently, the majority of the links are between the books and PubMed. In the future, more links will be created between the books and other types of information, such as gene and protein sequences and macromolecular structures. See http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Books.
Books 477
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Symposium on rheumatoid arthritis; differential diagnosis and treatment, April 14th18th, 1957. Ed. by Nanna Svartz and Börje Olhagen. Author: Svartz, Nanna Charlotta,; Year: 1945; Stockholm, 1958
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The psychological aspects of rheumatoid arthritis. Author: Geist, Harold,; Year: 1961; Springfield, Ill. Thomas [c1966]
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The psychosomatic approach to primary chronic rheumatoid arthritis; a comparison between primary chronic rheumatoid arthritis and other psychosomatic diseases (bronchial asthma, peptic ulcer, essential hypertension) in relation to a control group of normals, by J. J. G. Prick and K. J. M. van de Loo. Tr. by T. G. Fahy. Author: Prick, J. J. G. (Joseph Jules Guillaume); Year: 1964; Philadelphia, Davis [c1964]
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The public health aspects of chronic rheumatoid arthritis and related diseases; report on a technical conference...Rome, 12-20 November 1963. Author: World Health Organization. Regional Office for Europe.; Year: 2003; Copenhagen, 1964
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The temporomandibular joint in adult rheumatoid arthritis; a clinical and roentgenologic study. Author: Uotila, Esko.; Year: 1961; Helsinki, 1964
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Treatment of epilepsy; guest editor: Russell N. DeJong. Treatment of arthritis; guest editor: Carl M. Pearson. Author: DeJong, Russell N.; Year: 1948; [New York] Harper; Row, 1964
Chapters on Arthritis In order to find chapters that specifically relate to arthritis, an excellent source of abstracts is the Combined Health Information Database. You will need to limit your search to book chapters and arthritis using the “Detailed Search” option. Go to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find book chapters, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Book Chapter.” Type “arthritis” (or synonyms) into the “For these words:” box. The following is a typical result when searching for book chapters on arthritis: ·
Chapter 10: Psoriatic Arthritis Source: in Klippel, J.H., et al., eds. Primer on the Rheumatic Diseases. 12th ed. Atlanta, GA: Arthritis Foundation. 2001. p. 233-238. Contact: Available from Arthritis Foundation. P.O. Box 1616, Alpharetta, GA 300091616. (800) 207-8633. Fax (credit card orders only) (770) 442-9742. Website: www.arthritis.org. PRICE: $69.95 plus shipping and handling. ISBN: 0912423293. Summary: This chapter provides health professionals with information on the epidemiology, pathogenesis, clinical features, treatment, and prognosis of psoriatic arthritis. This heterogeneous disease presents in various forms, including monarthritis, asymmetric oligoarthritis, or symmetric polyarthritis. Although the etiology of psoriasis and psoriatic arthritis is not known, genetic, environmental, and immunologic factors appear to influence susceptibility and disease expression. Data support a role for class I human leukocyte antigens in the pathogenesis of psoriatic arthritis. Environmental factors such as infectious agents and physical trauma are likely to be important in the pathogenesis as well. T cells have an important pathogenic role in the skin and joint manifestations of psoriatic arthritis. From a diagnostic and therapeutic standpoint, patients may be classified into the following groups: mono-or oligoarthritis with enthesitis resembling reactive arthritis, symmetric polyarthritis resembling rheumatoid
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arthritis (RA), and predominantly axial disease with or without peripheral joint disease. Nail involvement is the one clinical feature that identifies patients with psoriasis who are likely to develop arthritis. Several radiographic features are characteristic of psoriatic arthritis. The bone changes in psoriatic arthritis are a combination of erosion and bone production in a specific distribution. Although certain features distinguish psoriatic arthritis from RA, distinguishing between psoriatic arthritis and other seronegative spondyloarthropathies can be more difficult. The initial treatment for stable plaque psoriasis is topical therapy with emollients and keratolytic agents alone or in combination with anthralin, corticosteroids, vitamin D derivatives, and topical retinoids. Treatment for joint disease depends on the type and on the severity of joint and skin involvement. Physical or occupational therapy should be considered early in the course of the disease. Drugs that may be helpful include nonsteroidal antiinflammatory drugs, disease modifying antirheumatic agents, corticosteroids, and etanercept. Most people who have psoriatic arthritis have a better prognosis than people with RA. 2 figures and 23 references. ·
Chapter 12-A: Infectious Disorders: Septic Arthritis Source: in Klippel, J.H., et al., eds. Primer on the Rheumatic Diseases. 12th ed. Atlanta, GA: Arthritis Foundation. 2001. p. 259-264. Contact: Available from Arthritis Foundation. P.O. Box 1616, Alpharetta, GA 300091616. (800) 207-8633. Fax (credit card orders only) (770) 442-9742. Website: www.arthritis.org. PRICE: $69.95 plus shipping and handling. ISBN: 0912423293. Summary: This section of a chapter on infectious disorders provides health professionals with information on the risk factors, pathogenesis, microbiology, clinical features, diagnosis, treatment, prognosis, outcome, and prevention of septic arthritis. Factors that predispose to septic arthritis include age over 80 years, comorbid conditions, rheumatoid arthritis, the presence of a prosthetic joint in the knee or hip, recent joint surgery, and skin infection. Septic arthritis usually occurs as a result of bacteremic seeding of the affected joint from an extraarticular infection site. Trauma or surgical procedures may cause joint infections. The Gram-positive cocci are the major nongonococcal pathogens causing acute bacterial arthritis. Most cases of septic arthritis are monarticular, with large peripheral joints being infected more than small ones. Arthrocentesis is mandatory if septic arthritis is suspected. The synovial fluid of a septic joint usually has extremely high white blood cell counts where polymorphonuclear cells predominate. Tests that should be performed on the synovial fluid include a culture for microorganisms, a cell count and its differential, a Gram-stained smear, and a wet preparation examined under polarizing microscopy. Septic arthritis is treated with antibiotics. The choice of antibiotic agent depends on the results of the Gram-stained smear of the synovial fluid and the most likely causative microorganism. The infected joint space must be drained through needle aspiration or surgery to eradicate the infection, hasten the recovery of lost function, and reduce pain. Physical therapy is used to mobilize the inflamed joint. Antibiotic prophylaxis may be used as a preventive measure for some people. In addition, the chapter discusses septic arthritis in children, gonococcal joint infection, and septic bursitis. 2 tables and 21 references.
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Chapter 12-B: Infectious Disorders: Viral Arthritis Source: in Klippel, J.H., et al., eds. Primer on the Rheumatic Diseases. 12th ed. Atlanta, GA: Arthritis Foundation. 2001. p. 265-269.
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Contact: Available from Arthritis Foundation. P.O. Box 1616, Alpharetta, GA 300091616. (800) 207-8633. Fax (credit card orders only) (770) 442-9742. Website: www.arthritis.org. PRICE: $69.95 plus shipping and handling. ISBN: 0912423293. Summary: This section of a chapter on infectious disorders provides health professionals with information on the viruses causing arthralgia or arthritis. Infection with human parvovirus, designated B19, may be responsible for up to 12 percent of the cases of recent onset polyarthralgia or polyarthritis. Although only a small percentage of children with B19 infection may experience arthralgias or arthritis, as many as 78 percent of infected, symptomatic adults develop joint symptoms. Serologic diagnosis is possible only during a brief period because anti-B19 immunoglobulin M antibodies may be elevated for just 2 months following an acute infection. Hepatitis B virus infection may cause an immune complex mediated arthritis that occurs suddenly and is often severe. The joints of the hand and knee are most often affected. Rubella infection causes more joint complaints in adults, particularly women. Arthralgias are more common than frank arthritis. The joints of the hands, knees, wrists, ankles, and elbows are most frequently involved. Postvaccine arthralgia, myalgia, arthritis, and paresthesia have been associated with all rubella vaccine preparations. Several musculoskeletal syndromes, including Reiter's syndrome and psoriatic arthritis, have been detected in people infected with HIV. The alphavirus genus of the Togaviridae family includes various arthritogenic viruses that are mosquito borne. The known major viral pathogens of this genus include Sindbis virus, Chikungunya fever virus, O'nyong-nyong virus, Ross River virus, Barmah Forest virus, and Mayaro virus. Joint involvement is occasionally found in various commonly encountered viral syndromes, including varicella, mumps, adenovirus, and coxsackievirus A9, B2, B3, B4, and B6 infection. 1 figure and 18 references. ·
Chapter 12-D: Infectious Disorders: Mycobacterial, Fungal, and Parasitic Arthritis Source: in Klippel, J.H., et al., eds. Primer on the Rheumatic Diseases. 12th ed. Atlanta, GA: Arthritis Foundation. 2001. p. 274-279. Contact: Available from Arthritis Foundation. P.O. Box 1616, Alpharetta, GA 300091616. (800) 207-8633. Fax (credit card orders only) (770) 442-9742. Website: www.arthritis.org. PRICE: $69.95 plus shipping and handling. ISBN: 0912423293. Summary: This section of a chapter on infectious disorders provides health professionals with information on the symptoms, diagnosis, and treatment of mycobacterial, fungal, and parasitic arthritis. Mycobacteria cause mycobacterium tuberculosis. The most common form of osteoarticular infection with M. tuberculosis is tuberculosis spondylitis (Pott's disease). Symptoms include pain and tenderness. Diagnosis is based on examination of biopsy specimens obtained by open or computed tomography guided biopsy. Treatment options include combination chemotherapy or surgery. Tuberculosis arthritis, also caused by mycobacteria, presents with joint pain and swelling. Diagnosis is based on histologic and microbiologic examination of synovium. This form of arthritis usually responds to combination chemotherapy, but surgery may be needed. Musculoskeletal symptoms may also be caused by Mycobacterium bovis as a component of Bacillus Calmette-Guerin, atypical mycobacteria, and mycobacterium leprae. Fungal musculoskeletal infections include candidiasis, coccidioidomycosis, sporotrichosis, blastomycosis, cryptococcosis, and histoplasmosis. Most fungal musculoskeletal infections have an insidious onset and indolent course. Diagnosis of these infections is made by culture of synovial fluid or tissue. Antifungal agents are used to treat these infections. Parasitic organisms (protozoa, helminths, and arthropods) can induce immune responses that cause tissue
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injury and musculoskeletal manifestations. Protozoa associated with arthralgias and arthritis include Giardia lamblia, Entamoeba histolytica, Trichomona vaginalis, and Toxoplasma gondii. Helminths associated with joint symptoms include Strongyloides stercoralis, Taenia saginata, and Echinococcus granulosus. 1 figure, 1 table, and 20 references. ·
Chapter 39-B: Pediatric Rheumatic Diseases: Juvenile Rheumatoid Arthritis and Juvenile Spondyloarthropathies Source: in Klippel, J.H., et al., eds. Primer on the Rheumatic Diseases. 12th ed. Atlanta, GA: Arthritis Foundation. 2001. p. 534-542. Contact: Available from Arthritis Foundation. P.O. Box 1616, Alpharetta, GA 300091616. (800) 207-8633. Fax (credit card orders only) (770) 442-9742. Website: www.arthritis.org. PRICE: $69.95 plus shipping and handling. ISBN: 0912423293. Summary: This section of a chapter on pediatric rheumatic diseases provides health professionals with information on the epidemiology, clinical features, and treatment of juvenile rheumatoid arthritis (JRA) and juvenile spondyloarthropathies. JRA, a disease with an unknown cause, is the most common form of childhood arthritis. JRA is categorized as systemic, polyarticular, and pauciarticular. These subtypes have different clinical presentations, immunogenetic associations, and clinical courses. Diagnosis is based on data from the medical history, physical examination, and laboratory testing. Diagnostic criteria for JRA are disease onset at less than 16 years of age, persistent arthritis in one or more joints for at least 6 weeks, and exclusion of other types of childhood arthritis. JRA treatment begins during the diagnostic phase and consists of physical, social, and pharmacologic components. The physical component consists of performing range of motion exercises, wearing splints, and teaching joint protection techniques. The social program relates to psychosocial adjustments, school adaptations, and vocational issues. The pharmacologic component focuses on treatment of articular, ocular, and other manifestations of JRA with nonsteroidal antiinflammatory drugs (NSAIDs), methotrexate, etanercept, sulfasalazine, and systemic and intraarticular corticosteroids. The juvenile spondyloarthropathies encompass the discrete clinical entities of juvenile ankylosing spondylitis, reactive arthritis, psoriatic arthritis, and arthropathies associated with inflammatory bowel disease. Most of the juvenile spondyloarthropathies respond to treatment with NSAIDs. 3 tables and 27 references.
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Chapter 11-B: Seronegative Spondyloarthropathies: Reactive Arthritis and Enteropathic Arthritis Source: in Klippel, J.H., et al., eds. Primer on the Rheumatic Diseases. 12th ed. Atlanta, GA: Arthritis Foundation. 2001. p. 245-250. Contact: Available from Arthritis Foundation. P.O. Box 1616, Alpharetta, GA 300091616. (800) 207-8633. Fax (credit card orders only) (770) 442-9742. Website: www.arthritis.org. PRICE: $69.95 plus shipping and handling. ISBN: 0912423293. Summary: This chapter provides health professionals with information on the clinical features and diagnosis of reactive arthritis (ReA) and enteropathic arthritis. ReA, a seronegative spondyloarthropathy that is distinct from rheumatoid arthritis, is a form of peripheral arthritis that is often accompanied by one or more extraarticular manifestations. ReA usually begins acutely 2 to 4 weeks after venereal infections or bouts of gastroenteritis. Nongonococcal urethritis, when present, is usually the first manifestation. Chlamydia trachomatis is frequently the cause of the urethritis or cervicitis as well as the triggering agent of the ReA. Conjunctivitis, when present,
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typically accompanies urethritis or occurs within several days. Articular manifestations usually occur last. Lower leg joints are affected more commonly than joints of the upper extremities. Inflammation also usually occurs at bony sites where tendons, ligaments, or fascia have their attachments or insertions. Low back and buttock pain are common in ReA. Various mucocutaneous and visceral manifestations are associated with ReA, including keratoderma blennorrhagicum, circinate balanitis, aortitis, and amyloidosis of the serum amyloid A variety. Acute phase reactants are usually abnormal, serum globulins are frequently elevated, synovial fluid typically shows highly inflammatory changes, and tests for rheumatoid factor and antinuclear antibodies are negative. Radiographic abnormalities may be found once symptoms have been present for several months. Diagnosis is based on disease manifestations and laboratory findings. ReA has a self limited course of 3 to 12 months in most patients. Arthritis with or without other extraintestinal manifestations may be the first clinical symptom of inflammatory bowel disease (IBD). The usual pattern of joint inflammation is migratory arthralgias or arthritis. Extraarticular manifestations of IBD usually reflect active bowel disease and tend to occur at the same time as peripheral arthritis. Anemia is common in IBD. Acute phase reactants are typically elevated, serum rheumatoid factors and antinuclear antibodies are not present, and synovial fluid findings are reported infrequently. Joint disease can occur in a rare multisystem disease known as Whipple's disease. The arthritis is usually chronic but nondeforming. Diagnosis is based on finding characteristic, periodic acid Schiff staining deposits in macrophages of the small intestine and, less commonly, in biopsies of lymph nodes of joint synovia. Remission can be achieved with long term treatment with tetracyclines. 3 figures, 1 table, and 20 references. ·
Anti-Cytokine Therapy for Rheumatoid Arthritis Source: in Coggins, C.H. Hancock, E.W. Levitt, L.J., eds. Annual Review of Medicine, Volume 51, 2000. Palo Alto, CA: Annual Reviews, Inc. 2000. p. 207-229. Contact: Available from Annual Reviews. 4139 El Camino Way, P.O. Box 10139, Palo Alto, CA 94303-0139. (650) 493-4400. E-mail:
[email protected]. Website: www.AnnualReviews.org. Summary: This chapter provides health professionals with information on anticytokine therapy for rheumatoid arthritis (RA). Although the chapter focuses on studies designed to inhibit the activity of tumor necrosis factor (TNF) alpha and interleukin (IL) 1 in RA, it also considers the preliminary clinical data concerning blockade of IL-6 and strategies to augment the activity of the antiinflammatory cytokines IL-4, IL-10, and IL-11 in this disease. TNF alpha and IL-1 are important in mediating inflammation in RA. The possibility that IL-1 and TNF alpha might be implicated in the pathogenesis of inflammation and joint damage in RA arose from in vitro observations that demonstrated the proinflammatory properties of these cytokines. Both were shown to stimulate production of prostaglandin E and collagenase, and they were implicated in stimulating resorption of cartilage and inhibiting synthesis of proteoglycan. Despite evidence from in vitro experiments, there was considerable skepticism that anti-TNF agents would have significant therapeutic activity in a disease that seems to involve multiple inflammatory pathways with overlapping functions. However, two approaches in preclinical in vivo studies produced convincing data that TNF alpha was a valid therapeutic target. Randomized phase II and III clinical trials of the anti-TNF reagents infliximab and etanercept have demonstrated an acceptable safety profile and marked clinical efficacy in cases of RA that have not responded adequately to conventional therapy. Combination therapy with methotrexate (MTX) appears to be particularly
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effective in patients whose disease activity persists despite prior disease modifying antirheumatic drugs (DMARDs) and ongoing MTX monotherapy. DMARD recalcitrant disease may become the main indication for the use of anti-TNF drugs in patients with RA. Trials of IL-1 receptor antagonist show a relatively modest antiinflammatory effect and a possible retardation of joint damage. Whether anti-TNF therapy protects joints from structural damage is under investigation. One anti-TNF reagent has already been approved in the United States for the treatment of RA, and other cytokine antagonists or agonists are under development. 4 figures, 2 tables, and 78 references. (AA-M). ·
Pyogenic Arthritis in Adults Source: in Maddison, P.J. et al., Eds. Oxford Textbook of Rheumatology. Volume 2. New York, NY: Oxford University Press, Inc. 1993. p. 529-538. Contact: Available from Oxford University Press, Inc., New York, NY. Summary: This chapter for health professionals focuses on pyogenic bacterial infections in adults. The pathophysiology of bacterial infections is explained. Nongonococcal arthritis is discussed in terms of clinical manifestations and laboratory, radiographic, and bacteriological findings. The occurrence of joint infections in individuals with rheumatoid arthritis and prosthetic joints is discussed. The characteristics of gonococcal and meningococcal arthritis and septic bursitis are described. The issue of managing pyogenic joint infections is addressed. Management of these infections involves prompt diagnosis and initiation of treatment, use of appropriate antibiotics, and drainage of the infected joint. 20 references, 1 figure, and 3 tables.
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Pyogenic Arthritis in Children Source: in Maddison, P.J. et al., Eds. Oxford Textbook of Rheumatology. Volume 2. New York, NY: Oxford University Press, Inc. 1993. p. 539-543. Contact: Available from Oxford University Press, Inc., New York, NY. Summary: This chapter for health professionals focuses on pyogenic bacterial infections in children. The epidemiology and pathogenesis of joint infection are reviewed. The clinical manifestations of joint infection are described. Bacterial agents that most commonly cause suppurative arthritis are identified. Specific pathogens in septic arthritis are highlighted, including H. influenzae and Neisseria gonorrhoea. The characteristics of septic arthritis of the hip and sacroiliac joint are described. The symptoms of neonatal skeletal infection are summarized. The occurrence of septic arthritis in chronic joint disease is discussed. The principles of managing suppurative arthritis in childhood are presented. Data on the prognosis for suppurative joint infection in childhood are highlighted. 45 references and 6 tables.
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Viral Arthritis Source: in Maddison, P.J. et al., Eds. Oxford Textbook of Rheumatology. Volume 2. New York, NY: Oxford University Press, Inc. 1993. p. 552-560. Contact: Available from Oxford University Press, Inc., New York, NY. Summary: This chapter for health professionals focuses on viral causes of arthritis. Virus-host interactions are examined. The viral pathogenesis of arthritis is explained. The structure, epidemiology, clinical and rheumatic manifestations, pathogenesis, diagnosis, treatment, and outcome of various viruses or virus vaccines are discussed. These viruses or vaccines include rubella and the rubella vaccine, human parvovirus
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B19, hepatitis B and hepatitis B vaccine, mumps, and arboviruses. In addition, enteroviruses, variola and vaccinia viruses, adenovirus, varicella-zoster, Epstein-Barr virus, herpes simplex virus, and cytomegalovirus are described. 45 references. ·
Brucellar Arthritis Source: in Maddison, P.J. et al., Eds. Oxford Textbook of Rheumatology. Volume 2. New York, NY: Oxford University Press, Inc. 1993. p.581-589. Contact: Available from Oxford University Press, Inc., New York, NY. Summary: This chapter for health professionals presents an overview of brucellar arthritis. The epidemiology and general characteristics of brucellosis are discussed. The general characteristics of the brucellae organism are identified. The defense mechanisms of the host are highlighted. The clinical and radiographic characteristics of brucellararthritis are described, including arthritis of the peripheral joints, sacroiliitis, spondylitis, osteomyelitis, and reactive arthritis. General laboratory features of brucellosis are summarized. Diagnostic investigations are discussed, focusing on bacteriological and serological investigations. The treatment of brucellar arthritis is explained. 60 references, 7 figures, and 2 tables.
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Fungal Arthritis Source: in Maddison, P.J. et al., Eds. Oxford Textbook of Rheumatology. Volume 2. New York, NY: Oxford University Press, Inc. 1993. p. 599-607. Contact: Available from Oxford University Press, Inc., New York, NY. Summary: This chapter for health professionals presents an overview of fungal arthritis. The epidemiology and clinical features of fungal arthritis are discussed. Some of the drugs used to treat fungal infections are identified. The clinical features, diagnosis, and treatment of various fungal infections are highlighted. These include Candida spp. infections, blastomycosis, sporotrichosis, coccidioidomycosis, histoplasmosis, cryptococcosis, and paracoccidioidomycosis. Miscellaneous fungi that have been implicated in joint infections are also identified. 91 references, 5 figures, and 2 tables.
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Immunopathogenesis of Rheumatoid Arthritis Source: in Maddison, P.J. et al., Eds. Oxford Textbook of Rheumatology. Volume 2. New York, NY: Oxford University Press, Inc. 1993. p. 621-638. Contact: Available from Oxford University Press, Inc., New York, NY. Summary: This chapter for health professionals focuses on the immunopathogenesis of rheumatoid arthritis. A historical review of rheumatoid arthritis is presented. Factors involved in the etiology of rheumatoid arthritis are examined, including genetic factors, infectious agents, and sex hormones. Antibodies that show diagnostic specificity for rheumatoid arthritis are identified. The pathology of rheumatoid arthritis is discussed, focusing on involvement of the synovial joints, the development of pannus, and extraarticular manifestations. The pathogenesis of rheumatoid arthritis is described, focusing on cell recruitment, T-cell activation, B-cell lineage, cell interaction, cytokine expression and regulation, and immune suppression. Examples of existing and new models of rheumatoid arthritis are presented. These models include collagen-induced arthritis, adjuvant arthritis, and streptococcal cell-wall arthritis. 151 references, 9 figures, and 2 tables.
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Rheumatoid Arthritis: The Clinical Picture Source: in Maddison, P.J. et al., Eds. Oxford Textbook of Rheumatology. Volume 2. New York, NY: Oxford University Press, Inc. 1993. p. 639-661. Contact: Available from Oxford University Press, Inc., New York, NY. Summary: This chapter for health professionals focuses on the clinical features of rheumatoid arthritis. The criteria for rheumatoid arthritis are presented. Data on the epidemiology of rheumatoid arthritis are provided. The onset of rheumatoid arthritis is explained. The articular and nonarticular manifestations of rheumatoid arthritis are described. The influence of age, sex, and pregnancy on rheumatoid arthritis is examined. The complications of rheumatoid arthritis are discussed, including infections, neurological complications, cervical spine dislocation, fractures, tendon and ligament damage, amyloidosis, and Felty's syndrome. Laboratory tests and radiographic techniques useful in the diagnosis of rheumatoid arthritis are highlighted. The use of nonsteroidal anti-inflammatory drugs, antimalarials, soluble gold salts, D-penicillamine, sulphasalazine, methotrexate, auranofin, azathioprine, glucocortiocoids, and alkylating agents to treat rheumatoid arthritis is discussed. Experimental and surgical therapies are considered. Data on the prognosis for rheumatoid arthritis are also provided. 180 references, 7 figures, and 20 tables.
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Juvenile Rheumatoid Arthritis (Rheumatoid Factor Positive Polyarthritis) Source: in Maddison, P.J. et al., Eds. Oxford Textbook of Rheumatology. Volume 2. New York, NY: Oxford University Press, Inc. 1993. p. 661-666. Contact: Available from Oxford University Press, Inc., New York, NY. Summary: This chapter for health professionals presents an overview of juvenile rheumatoid arthritis. This form of arthritis is a subset of juvenile chronic arthritis. The mode of presentation and clinical manifestations of juvenile rheumatoid arthritis are described. Tests used to diagnosis this form of arthritis are identified. Studies on the course of the disease are highlighted. Research on the genetic aspects of juvenile rheumatoid arthritis is summarized. The principles involved in managing this form of arthritis are presented. Treatment involves maintenance of joint position and function and relief of pain through the use of nonsteroidal anti-inflammatory drugs. Surgical procedures may be used in certain cases. 19 references and 7 figures.
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Pauciarticular-onset Juvenile Chronic (Rheumatoid) Arthritis Source: in Maddison, P.J. et al., Eds. Oxford Textbook of Rheumatology. Volume 2. New York, NY: Oxford University Press, Inc. 1993. p. 710-722. Contact: Available from Oxford University Press, Inc., New York, NY. Summary: This chapter for health professionals presents an overview of pauciarticularonset juvenile chronic arthritis. Data on the epidemiology of this form of arthritis are presented. The clinical and laboratory features of this disease are highlighted. The course of this form of arthritis is explained. The articular and ocular complications that children with pauciarticular-onset juvenile chronic arthritis may experience are described. The differential diagnosis of this disease is discussed in terms of the conditions that may simulate it, including monarticular conditions, short-lived inflammatory conditions, spondylarthropathies, and complaints of pain in the absence of joint inflammation. The etiology of and immunogenetics involved in pauciarticularonset juvenile chronic arthritis are examined. The use of drugs to treat this disease is
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discussed, and the outcome for children with the disease is considered. In addition, illustrative cases are presented. 61 references, 3 figures, and 6 tables. ·
Systemic-onset Juvenile Chronic (Rheumatoid) Arthritis and Adult-onset Still's Disease Source: in Maddison, P.J. et al., Eds. Oxford Textbook of Rheumatology. Volume 2. New York, NY: Oxford University Press, Inc. 1993. p. 722-733. Contact: Available from Oxford University Press, Inc., New York, NY. Summary: This chapter for health professionals presents an overview of systemic-onset juvenile chronic arthritis. Data on the epidemiology and the causes of death associated with this form of arthritis are presented. The common features of systemic-onset juvenile chronic arthritis are described, including reticuloendothelial hyperplasia, serositis, and arthritis. Less common features are highlighted, including a general arrest of growth. Laboratory features of the disease are discussed. The differential diagnosis of systemic-onset juvenile chronic arthritis is explained. The course and prognosis of the disease are examined. The drug management of the disease is discussed. Amyloidosis, a common complication of the systemic-onset form of arthritis, is described. In addition, the clinical and laboratory manifestations, course, and treatment of adult-onset Still's disease are highlighted. 83 references, 5 figures, and 7 tables.
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Arthritis Associated with Inflammatory Bowel Disease Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 279-282. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: This chapter on arthritis associated with inflammatory bowel disease (IBD) is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and ulcerative colitis (UC), together known as IBD. Arthritis is a relatively common complication of UC and CD, affecting 10 to 20 percent of patients. Arthritis may predate the bowel disease and may be severe enough to warrant treatment in its own right, perhaps with nonsteroidal anti-inflammatory drugs (NSAIDs). This may, itself, exacerbate the underlying bowel disease. In this chapter, the different forms of arthritis associated with IBD are identified and their management discussed in terms of their prognosis, possible modes of treatment, and when expert help should be sought. With the exception of ankylosing spondylitis (AS, fusion of the vertebral facet joints), the IBD associated joint disease is largely non deforming and non progressive, and so can be managed symptomatically, although the use of NSAIDs should be avoided. Management involves judicious use of physical treatments (rest, range of movement exercises, and physiotherapy) in addition to pharmacological treatments. Patients with AS or persistent or erosive peripheral joint disease should be referred to a rheumatologist. 2 tables. 6 references.
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Lessons from Treatment of Rheumatoid Arthritis Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 283-288.
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Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: Rheumatoid arthritis (RA) is a disease of very complex pathophysiology, combining genetic factors, alterations of cellular and humoral immune responses, potential involvement of infectious agents, and various mechanisms of tissue destruction. When compared to inflammatory bowel diseases (IBDs), remarkable similarities both in pathophysiological mechanisms and in management of therapy exist, which may allow one to develop novel strategies for each of these disease entities derived from knowledge of the counterpart. This chapter on lessons from the treatment of RA is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and ulcerative colitis (UC), together known IBD. In this chapter, the authors offer a chart comparing the similarities of pathophysiologic features of RA and IBD covering genetic factors, involvement of microorganisms, cellular infiltrates, inflammatory mediators, cytokines, immune phenomena, tissue destruction by disease components, tissue destruction by vasculitis or fibrosis (scarring), and extrafocal manifestations. The authors then outline early and long term disease modifying drug treatments and their complications, concluding with a discussion of biologics (monoclonal antibodies and soluble cytokine receptors that can inhibit the effects of proinflammatory cytokines). 5 tables. 12 references. ·
Debilitating Diseases: Osteoporosis, Alcoholism, Arthritis, and Renal Disease Source: in Frank-Spohrer, G.C. Community Nutrition: Applying Epidemiology to Contemporary Practice. Gaithersburg, MD: Aspen Publishers, Inc. 1996. p. 535-557. Contact: Available from Aspen Publishers, Inc. 7201 McKinney Circle, Frederick, MD 21701. (800) 638-8437. PRICE: $48.00. ISBN: 0834207842. Summary: This chapter on debilitating diseases, including osteoporosis, alcoholism, arthritis, and renal disease, is from a nursing text on community nutrition. The author describes the occurrence and etiology of these four diseases, identifies secondary and tertiary prevention approaches for each one, and lists and enumerates the role of dietary components in the secondary prevention of these diseases. One chart summarizes the general dietary recommendations for renal patients. The author also relates suggestions to the Healthy People 2000 objectives. 4 figures. 7 tables. 59 references.
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Arthritis, Osteoporosis, and Chronic Back Conditions Source: in Healthy People 2010 (Conference Edition), Volume I. U.S. Department of Health and Human Services, Washington, DC, pp. 2-1-2-27, January 2000. Contact: U.S. Government Printing Office, Superintendent of Documents, P.O. Box 371954, Pittsburgh, PA 15250-7954. (202) 512-1800. Stock No. 017-001-00547-9. INTERNET/EMAIL: www.health.gov/healthypeople. Summary: Arthritis, Osteoporosis, and Chronic Back Conditions, a chapter in Healthy People 2010 (Conference Edition), notes that one goal of Healthy People 2010 is to prevent illness and disability related to arthritis and other rheumatic conditions, osteoporosis, and chronic back conditions. The current and projected growth in the number of people age 65 and older in the United States has focused attention on preserving quality of life as well as length of life. The various forms of arthritis affect
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more than 15 percent of the United States population, over 43 million persons, and more than 20 percent of the adult population. Arthritis is the leading cause of disability. Osteoporosis affects about 13 to 18 percent of women age 50 and older and 3 to 6 percent of men age 50 and older. This reduction in bone mass or density leads to deteriorated and fragile bones. Chronic low back pain is associated with various workrelated risk factors, such as heavy physical work, lifting and forceful movements, awkward postures, and whole body vibration. The national health objectives for the year 2000 included increasing the proportion of women of menopausal age who have been counseled about estrogen replacement therapy for the prevention of osteoporosis. Objectives for Healthy People 2010 include (1) increasing the mean number of days without severe pain among adults who have chronic joint symptoms; (2) reducing the proportion of adults with chronic joint symptoms who experience a limitation in activity due to arthritis; (3) reducing the proportion of all adults with chronic joint symptoms who have difficulty in performing two or more personal care activities, thereby preserving independence; (4) increasing the proportion of adults age 18 and older with arthritis who seek help in coping if they experience personal and emotional problems; (5) increasing the employment rate among adults with arthritis in the working-age population; (6) eliminating racial disparities in the rate of total knee replacements; and (7) increasing the proportion of adults who have seen a health care provider for their chronic joint symptoms. Goals for osteoporosis include reducing the overall number of cases of osteoporosis and reducing the proportion of adults who are hospitalized for vertebral fractures associated with osteoporosis. The goal for chronic back conditions is to reduce activity limitation due to chronic back conditions. ·
Socioeconomic Status and Rheumatoid Arthritis Source: in Rheumatoid Arthritis: Pathogenesis, Assessment, Outcome, and Treatment. Wolfe, F. Pincus, T. eds. New York, NY, Marcel Dekker, Inc., pp. 297-315, 1994. Contact: Marcel Dekker, Inc., 270 Madison Avenue, New York, NY 10016. Summary: Socioeconomic Status and Rheumatoid Arthritis, a book chapter in Rheumatoid Arthritis: Pathogenesis, Assessment, Outcome, and Treatment, states that socioeconomic status has been observed to be associated with the prevalence, morbidity, and mortality of most chronic diseases. Although occupational, financial, and educational status are correlated, each reflects different societal and individual forces associated with health and disease. The number of years of formal education a person has attained has been demonstrated in several studies to be a most important socioeconomic variable associated with good health. Education may enhance (1) problem-solving abilities, (2) efficiency in using medical services, (3) capacity to cope with stress, (4) social skills, (5) psychological status, and (6) economic skills, therby enabling one to insulate oneself from adversity or to cope with adverse situations more effectively. Researchers initially described the psychological and social characteristics of patients hospitalized for rheumatoid arthritis (RA), hypertension, and duodenal ulcer in 1965. When the patients with RA were compared with controls, the patients with RA had lower levels of formal education. The patients with RA were also unwilling to see changes in themselves. Increased mortality and morbidity were associated with lower formal education levels in 75 RA patients studied 9 years apart in 1973 and 1982: 9 of the 20 patients with 8 or fewer years of education had died, compared with 10 of 34 with 912 years of education and only 1 of 21 with more than 12 years of education. Overall, 79 percent of grade school-educated, 43 percent of high school-educated, and 20 percent of college-educated patients had either died or declined more than 50 percent in functional capacity over a 9-year period. Possible associations of formal education with clinical
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status were analyzed in 2,006 patients with RA from five clinical centers in Arizona (1), California (2), Canada (1), and Kansas (1); lower levels of formal education were associated with poorer Health Assessment Questionnaire disability scores in men and were weakly associated in women, even with adjustment for (1) age, (2) sex, (3) employment status, (4) occupation, (5) marital status, (6) race, (7) income, (8) erythrocyte sedimentation rate, (9) rheumatoid factor titer, (10) number of tender joints, and (11) duration of disease. Although education appears to be a powerful predictor of health status, data concerning formal education level are not collected in usual clinical practice. It would appear desirable that data concerning this variable should be collected in routine care.
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CHAPTER 8. MULTIMEDIA ON ARTHRITIS Overview In this chapter, we show you how to keep current on multimedia sources of information on arthritis. We start with sources that have been summarized by federal agencies, and then show you how to find bibliographic information catalogued by the National Library of Medicine.
Video Recordings An excellent source of multimedia information on arthritis is the Combined Health Information Database. You will need to limit your search to “Videorecording” and “arthritis” using the “Detailed Search” option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find video productions, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Videorecording (videotape, videocassette, etc.).” Type “arthritis” (or synonyms) into the “For these words:” box. The following is a typical result when searching for video recordings on arthritis: ·
Pathways to Better Living With Arthritis and Related Conditions Source: Morro Bay, CA: Mobility Limited. 1997. (videocassette). Contact: Available from Arthritis Foundation. P.O. Box 1616, Alpharetta, GA 300091616. (800) 207-8633. Fax (credit card orders only) (770) 442-9742. Website: www.arthritis.org. PRICE: $29.95 plus shipping and handling. Summary: This video presents a comprehensive exercise program for people who have arthritis and related conditions. The models in the video have arthritis, and different levels of physical fitness and ages are depicted. Most of the program can be performed while seated. This state-of-the-art program is based on yoga and includes breathing techniques, stretches, strengthening and aerobic exercises, and total body relaxation techniques. The program is broken down into a sitting section, a standing section, an aerobics section, a floor workout, and a relaxation section. These sections can be done separately, or they can be done together for one complete workout.
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Arthritis (Osteoarthritis) Source: New York, NY: Patient Education Media, Inc. 1996. Contact: Available from Patient Education Media, Inc./Time Life Medical, 1271 6th Avenue, New York, NY 10020. (212) 522-8089. (212) 522-8092 (fax). (800) 588-9959. PRICE: $19.95. Summary: This videotape for individuals with arthritis and their families provides upto-date medical information on arthritis. The information in the videotape is presented in a news magazine-style and is divided into four reports. These reports use computer animation to help viewers understand what is going on inside the body and how a diagnosis is made; explain what happens after the diagnosis is made; address practical issues concerning the types of health care professionals involved in managing arthritis and osteoarthritis and how the lifestyle changes that patients may find helpful; explore options for treating and managing arthritis and osteoarthritis, including using medications, exercising, reducing weight, and, in some cases, undergoing joint replacement surgery; and use an in-studio question-and-answer session to consider issues that frequently arise about arthritis and osteoarthritis. The videotape is accompanied by a patient workbook that includes program highlights, a glossary, a resource guide, and a personal journal.
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Arthritis and Liver Transplant Source: Alexandria, VA: PBS Video. 199x. Contact: Available from PBS Video. Public Broadcasting Service, 1320 Braddock Place, Alexandria, VA 22314-1698. (800) 344-3337. PRICE: $59.95 VHS or $79.95 U-Matic, plus $8.50 shipping and handling. Order No. LIFM-702L. ISBN: 1559519908. Summary: This videotape is one of a series of seven programs that provide an in-depth look at the internal strength and convictions of people who live active and productive lives in spite of an illness that can be crippling or fatal. The strength, persistence, and enthusiasm of patients who have chosen life over debility can provide inspiration to other patients and people who are grappling with illness. The second half of the video features Kendra Poarch of Texas, who was presented with a new liver for her 14th birthday as her only chance of living. The program explores the lives of organ transplant recipients. (AA-M).
Audio Recordings The Combined Health Information Database contains abstracts on audio productions. To search CHID, go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find audio productions, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Sound Recordings.” Type “arthritis” (or synonyms) into the “For these words:” box. The following is a typical result when searching for sound recordings on arthritis: ·
AIDS: Disease, Patient, Internist Contact: California Medical Association, Audio Digest Foundation, 1577 E Chevy Chase Dr, Glendale, CA, 91206, (213) 245-8505.
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Summary: This sound recording, along with accompanying pre-test and post-test questions, comprises part of an ongoing series of educational activities. The first speaker, Michael S. Gottlieb, of Allergy and Immunology Associates in Santa Monica, CA, discusses real and perceived risks of Human immunodeficiency virus (HIV) transmission. He points out that there are three important routes of transmission: Sexual, parenteral, and perinatal. The likelihood of transmission through insect bites or casual contact is dismissed; the risks in the health-care setting are assessed. Following his speech is a dramatization of a doctor-patient interchange presented by the Los Angeles County Medical Association. The dramatization covers awareness of the patient's sexual behavior; symptoms; asymptomatic carriers; high-risk sexual behavior, possibly risky behavior, and low-risk behavior; and other considerations. Early diagnosis and treatment is the subject of a presentation by Lowell S. Young, clinical professor of medicine at the University of California, San Francisco, School of Medicine; Chief, Division of Infectious Diseases, Pacific Presbyterian Medical Center; and Director, Kuzell Institute for arthritis and Infectious Diseases, San Francisco. He outlines the various opportunistic infections that may afflict Persons with AIDS (PWA's), including Pneumocystis carinii pneumonia (PCP), leukopenia, cryptosporidiosis, toxoplasmosis, thrush, CMV infection, mycobacterium avium infection, and Kaposi's sarcoma. He also looks at antiviral therapy and bolstering immunity as methods of treatment. ·
Serving Individuals with Diabetes who are Blind or Visually Impaired: A Resource Guide for Vocational Rehabilitation Counselors Source: Mississippi State, MS: Rehabilitation Research and Training Center on Blindness and Low Vision, Mississippi State University. 1997. 227 p. Contact: Available from Rehabilitation Research and Training Center on Blindness and Low Vision, Mississippi State University. Publications Manager, P.O. Drawer 6189, Mississippi State, MS 39762. (601) 325-2001 or (601) 325-8693. Fax (601) 325-8989. TDD (601) 325-8693. PRICE: $25.00 in any format. Summary: This resource guide is designed to help counselors better serve individuals with diabetes who are blind or visually impaired. The guide refers readers to a large collection of resources on various diabetes publications, medications, and appliances. Five sections cover an introduction to diabetes; self management; current medical issues; employment issues; and emotional aspects of diabetes. Topics include myths about diabetes; diabetic eye disease; new nutrition guidelines for diabetes management; oral diabetes medications; diabetes and medications; insulin and measurement devices and systems; maintaining the proper temperature of insulin; blood glucose control; 'talking' blood glucose monitoring systems; and noninvasive glucose monitors. The authors also discuss diabetes and the feet; kidney failure, dialysis, and transplantation; pancreas transplantation; arthritis and diabetes; diabetes and yeast infections; hypoglycemia; diabetic peripheral neuropathy; diabetes and men's sexual health; cardiovascular health; diabetic ketoacidosis; diabetic dermopathy; diabetes and the Individualized Written Rehabilitation Program (IWRP); the use of Braille; health insurance; and scleral shells. The book's appendix includes lists of diabetes-related organizations, publications, listservs, and World Wide Web sites; sources of low-sugar products and products for the blind; and diabetes equipment and supplies, including insulin syringe magnifiers. The resource guide is available in large print, Braille, audiocassette, and computer diskette.
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Bibliography: Multimedia on Arthritis The National Library of Medicine is a rich source of information on healthcare-related multimedia productions including slides, computer software, and databases. To access the multimedia database, go to the following Web site: http://locatorplus.gov/. Select “Search LOCATORplus.” Once in the search area, simply type in arthritis (or synonyms). Then, in the option box provided below the search box, select “Audiovisuals and Computer Files.” From there, you can choose to sort results by publication date, author, or relevance. The following multimedia has been indexed on arthritis (for more information, follow the hyperlink indicated): ·
Acute arthritis: diagnosis and management [slide] Source: H. Ralph Schumacher; Year: 1973; Format: Slide; [New York]: Medcom, c1973
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Arthritis: current concepts of diagnosis and treatment [slide] Source: American Academy of Orthopaedic Surgeons; Year: 1975; Format: Slide; [Chicago]: The Academy, [1975]
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Arthritis [slide] Source: [Gordon E. Madge]; Year: 1970; Format: Slide; [Richmond: G. E. Madge, 1970]
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Assessment of arthritic pain [sound recording] Source: College of Nursing, Niagara University; Year: 1977; Format: Sound recording; Buffalo: Communications in Learning, 1977
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Bed care and positioning of the patient with arthritis [motion picture] Source: The Arthritis Foundation, Southwest Chapter, University of Arizona College of Education, Rehabilitation Center and Tucson Medical Center; produced by Aztec Film Productions; Year: 1968; Format: Motion picture; [New York]:
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Gout and gouty arthritis [slide] Source: Continuing Education Committee of the New York State Podiatry Society, Western Division; Year: 1975; Format: Slide; [Buffalo, N. Y.]: Communications in Learning, 1975
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Learning to diagnose arthritis [videorecording] Source: Penn State Television, WPSXTV; Year: 1978; Format: Videorecording; University Park, Pa.: Penn State Univ.: [for loan and sale by its Audio-Visual Services], c1978
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Lubrication in healthy and arthritic joints [motion picture] Source: Eric L. Radin, Igor L. Paul; produced by Dick Turbey [sic]; Year: 1970; Format: Motion picture; Kalamazoo, Mich.: Upjohn, [1970]
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Rheumatoid arthritis: a case study [filmstrip] Source: Trainex Corporation; Year: 1975; Format: Filmstrip; Garden Grove, Calif.: Trainex, p1975
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Rheumatoid arthritis [motion picture] Source: Norman P. Schenker; with scientific collaboration of E.G.L. Bywaters... [et al]; Year: 1963; Format: Motion picture; [New York]: Pfizer, [1963?]
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Surgical treatment of arthritis [slide] Source: Western New York Medical Records Association; Year: 1976; Format: Slide; Buffalo: Communications in Learning, 1976
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Synovectomy of the proximal interphalangeal joint of the finger in rheumatoid arthritis [motion picture] Source: Alan H. Wilde; Year: 1970; Format: Motion picture; Cleveland: Wilde; [Danbury, Conn.: for loan by Davis & Geck, 1970]
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Systemic (extra-articular) manifestations of rheumatoid arthritis [slide] Source: Duncan S. Owen; Year: 1977; Format: Slide; Richmond: Medical College of Virginia: [for sale by its Learning Resource Centers, 1977]
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The Knee in rheumatoid arthritis [slide] Source: Alan H. Wilde; Year: 1972; Format: Slide; [New York]: Medcom, c1972
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The Patient with rheumatoid arthritis [slide] Source: University of Michigan Medical Center Department of Postgraduate Medicine and Health Professions Education Independent Study Unit; Year: 1975; Format: Slide; Ann Arbor: The University: [for loan or sale by its Medical Center Media Library], c1975
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The Principles of bed exercising with the arthritis patient [motion picture] Source: The Arthritis Foundation; produced by Aztec Film Productions; Year: 1968; Format: Motion picture; New York: The Foundation; [Atlanta: for loan by National Medical Audiovisual Center, 1968]
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Total hip replacement for arthritis in the adult secondary to congenital dislocation of the hip [slide] Source: American Academy of Orthopaedic Surgeons; Year: 1976; Format: Slide; [Chicago]: The Academy, [1976]
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Transferring the patient with arthritis [motion picture] Source: Southwest Chapter, The Arthritis Foundation; made by Aztec Film Productions; Year: 1968; Format: Motion picture; [New York]: The Foundation, [1968?]
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Treatment of rheumatoid arthritis including joint fluid analysis and injection [slide] Source: Department of Continuing Medical Education School of Medicine State University of New York at Buffalo, in cooperation with Lakes Area Regional Medical Program; Year: 1975; Format: Slide; Buffalo, N. Y.: Communications in Learning, 1975
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CHAPTER 9. PERIODICALS AND NEWS ON ARTHRITIS Overview In this chapter, we suggest a number of news sources and present various periodicals that cover arthritis.
News Services and Press Releases One of the simplest ways of tracking press releases on arthritis is to search the news wires. In the following sample of sources, we will briefly describe how to access each service. These services only post recent news intended for public viewing.
PR Newswire To access the PR Newswire archive, simply go to http://www.prnewswire.com/. Select your country. Type “arthritis” (or synonyms) into the search box. You will automatically receive information on relevant news releases posted within the last 30 days. The search results are shown by order of relevance.
Reuters Health The Reuters’ Medical News and Health eLine databases can be very useful in exploring news archives relating to arthritis. While some of the listed articles are free to view, others are available for purchase for a nominal fee. To access this archive, go to http://www.reutershealth.com/en/index.html and search by “arthritis” (or synonyms). The following was recently listed in this archive for arthritis: ·
Intensive exercise benefits some patients with rheumatoid arthritis Source: Reuters Medical News Date: September 12, 2003 http://www.reutershealth.com/archive/2003/09/12/professional/links/20030912clin 010.html
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Abbott gets European approval for arthritis drug Source: Reuters Industry Breifing Date: September 10, 2003
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Activity level predicts physical fitness in juvenile rheumatoid arthritis Source: Reuters Medical News Date: September 03, 2003
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Smokers have an increased risk of RF-positive rheumatoid arthritis Source: Reuters Medical News Date: August 29, 2003
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BPI and HNP are accumulated in inflamed joints of rheumatoid arthritis patients Source: Reuters Medical News Date: August 28, 2003
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Rheumatoid arthritis activity tied to atherogenic lipid profile Source: Reuters Medical News Date: August 26, 2003
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Heart risk high in arthritis patients Source: Reuters Health eLine Date: August 26, 2003
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Anti-CCP testing most useful for predicting mild disease with early arthritis Source: Reuters Medical News Date: August 25, 2003
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Combo arthritis therapy has no long-term benefit Source: Reuters Health eLine Date: August 12, 2003
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Synovial inflammation and angiogenesis are associated with osteoarthritis Source: Reuters Medical News Date: August 07, 2003
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Chemokine blockade may offer treatment of rheumatoid arthritis Source: Reuters Medical News Date: August 05, 2003
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Rheumatologists and surgeons often disagree on arthritis treatment Source: Reuters Medical News Date: August 04, 2003
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Drugs or surgery for hand arthritis? Docs disagree Source: Reuters Health eLine Date: August 04, 2003
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B lymphocytes rise before relapse of rituximab-treated rheumatoid arthritis Source: Reuters Industry Breifing Date: August 01, 2003
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Rofecoxib, celecoxib cost-effective in arthritis patients at risk for GI problems Source: Reuters Industry Breifing Date: July 28, 2003
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U.S. FDA approves new use for Amgen's Enbrel arthritis drug Source: Reuters Industry Breifing Date: July 25, 2003
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Electrical muscle stimulation good for knee arthritis Source: Reuters Health eLine Date: July 24, 2003
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Electrical stimulation improves muscle strength in older adults with arthritis Source: Reuters Medical News Date: July 23, 2003
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Osteopontin epitope tied to rheumatoid arthritis Source: Reuters Industry Breifing Date: July 21, 2003
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Fourfold increased risk of tuberculosis seen with rheumatoid arthritis Source: Reuters Medical News Date: July 21, 2003
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IL1-beta levels high in synovium of patients with end-stage rheumatoid arthritis Source: Reuters Medical News Date: July 18, 2003
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Women with rheumatoid arthritis have less favorable disease course than men Source: Reuters Medical News Date: July 11, 2003
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Arthritis outlook worse for women Source: Reuters Health eLine Date: July 11, 2003
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Aventis, Vertex start enrollment of rheumatoid arthritis trial of pralnacasan Source: Reuters Industry Breifing Date: July 10, 2003
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Anti-IL-17 therapy halts arthritis in mice with Lyme disease Source: Reuters Industry Breifing Date: July 10, 2003
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Endostatin improves rheumatoid arthritis in mouse model Source: Reuters Industry Breifing Date: July 08, 2003
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Antibiotic treatment does not alter the natural history of reactive arthritis Source: Reuters Medical News Date: July 04, 2003
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Cortisol clearance normal in women with rheumatoid arthritis Source: Reuters Medical News Date: July 02, 2003
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Beneficial effects of leflunomide for rheumatoid arthritis sustained in long term Source: Reuters Industry Breifing Date: June 27, 2003
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Use of a feedback system may reduce rheumatoid arthritis disease activity Source: Reuters Industry Breifing Date: June 25, 2003
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Rheumatoid arthritis ups overall death risk: study Source: Reuters Health eLine Date: June 24, 2003
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FDA panel backs new use for Amgen arthritis drug Source: Reuters Industry Breifing Date: June 24, 2003
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Postmenopausal rheumatoid arthritis strongly linked with osteoporosis Source: Reuters Medical News Date: June 20, 2003
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Novartis, Roche drugs show promise for arthritis Source: Reuters Industry Breifing Date: June 20, 2003
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Amgen, Wyeth study shows Enbrel plus methotrexate slows arthritis joint damage Source: Reuters Industry Breifing Date: June 20, 2003
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New IL-6 receptor blocker promising for rheumatoid arthritis Source: Reuters Industry Breifing Date: June 19, 2003
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Knee replacement helps kids with arthritis, too Source: Reuters Health eLine Date: June 19, 2003
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Infliximab plus methotrexate effective in early rheumatoid arthritis Source: Reuters Medical News Date: June 19, 2003
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DNA chip study reveals gene clues to rheumatoid arthritis Source: Reuters Medical News Date: June 19, 2003
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Adalimumab improves radiographic outcomes in arthritis Source: Reuters Medical News Date: June 19, 2003
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Abbott's Humira improves radiographic outcomes in arthritis Source: Reuters Industry Breifing Date: June 19, 2003
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New study will test Remicade for preventing rheumatoid arthritis Source: Reuters Industry Breifing Date: June 18, 2003
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Leflunomide comparable to sulfasalazine and methotrexate in rheumatoid arthritis Source: Reuters Industry Breifing Date: June 18, 2003
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FDA clears leflunomide for expanded rheumatoid arthritis indication Source: Reuters Medical News Date: June 17, 2003
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Aventis' Arava wins new rheumatoid arthritis indication Source: Reuters Industry Breifing Date: June 17, 2003
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Daily pain common in juvenile arthritis, may be undertreated Source: Reuters Medical News Date: June 13, 2003
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MIF gene polymorphism predicts poor outcome in juvenile arthritis Source: Reuters Medical News Date: June 11, 2003
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Synovial macrophage elimination could be useful in rheumatoid arthritis Source: Reuters Medical News Date: June 02, 2003
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Older adults with arthritis to double in US by 2030 Source: Reuters Health eLine Date: May 29, 2003
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Number of older adults with arthritis expected to double by 2030 Source: Reuters Industry Breifing Date: May 29, 2003
The NIH Within MEDLINEplus, the NIH has made an agreement with the New York Times Syndicate, the AP News Service, and Reuters to deliver news that can be browsed by the public. Search news releases at http://www.nlm.nih.gov/medlineplus/alphanews_a.html. MEDLINEplus allows you to browse across an alphabetical index. Or you can search by date at the following Web page: http://www.nlm.nih.gov/medlineplus/newsbydate.html. Often, news items are indexed by MEDLINEplus within its search engine.
Business Wire Business Wire is similar to PR Newswire. To access this archive, simply go to http://www.businesswire.com/. You can scan the news by industry category or company name.
Market Wire Market Wire is more focused on technology than the other wires. To browse the latest press releases by topic, such as alternative medicine, biotechnology, fitness, healthcare, legal, nutrition, and pharmaceuticals, access Market Wire’s Medical/Health channel at http://www.marketwire.com/mw/release_index?channel=MedicalHealth. Or simply go to Market Wire’s home page at http://www.marketwire.com/mw/home, type “arthritis” (or synonyms) into the search box, and click on “Search News.” As this service is technology oriented, you may wish to use it when searching for press releases covering diagnostic procedures or tests.
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Search Engines Medical news is also available in the news sections of commercial Internet search engines. See the health news page at Yahoo (http://dir.yahoo.com/Health/News_and_Media/), or you can use this Web site’s general news search page at http://news.yahoo.com/. Type in “arthritis” (or synonyms). If you know the name of a company that is relevant to arthritis, you can go to any stock trading Web site (such as http://www.etrade.com/) and search for the company name there. News items across various news sources are reported on indicated hyperlinks. Google offers a similar service at http://news.google.com/.
BBC Covering news from a more European perspective, the British Broadcasting Corporation (BBC) allows the public free access to their news archive located at http://www.bbc.co.uk/. Search by “arthritis” (or synonyms).
Newsletters on Arthritis Find newsletters on arthritis using the Combined Health Information Database (CHID). You will need to use the “Detailed Search” option. To access CHID, go to the following hyperlink: http://chid.nih.gov/detail/detail.html. Limit your search to “Newsletter” and “arthritis.” Go to the bottom of the search page where “You may refine your search by.” Select the dates and language that you prefer. For the format option, select “Newsletter.” Type “arthritis” (or synonyms) into the “For these words:” box. The following list was generated using the options described above: ·
Septic Arthritis Update Source: Bulletin on the Rheumatic Diseases. 51(1): 1-4. 2002. Contact: Available from Arthritis Foundation. 1330 West Peachtree Street, Atlanta, GA 30309. (800) 268-6942 or (404) 872-7100. Fax (404) 872-9559. Website: www.arthritis.org. Summary: This newsletter provides health professionals with information on septic arthritis, focusing on its risk factors, pathogenesis, clinical features, diagnosis, treatment, prevention, and outcome. Bacterial infections are the most serious infections affecting normal, diseased, and prosthetic joints. An impaired immune system is a predisposition to septic arthritis. Bacteremic seeding of the affected joint from an extraarticular infection site is the most common pathogenesis of septic arthritis. The Gram positive cocci are the major pathogens among nongonococcal causes of acute bacterial arthritis. Septic arthritis is usually monoarticular rather than polyarticular. Diagnosis is based on the results of arthrocentesis and synovial fluid analysis. A cell count, a Gram stained smear, and a wet preparation examined under a polarizing microscope are immediate tests to perform on the synovial fluid in addition to culturing for microorganisms. Antibiotics are used to treat septic arthritis. The type of antibiotic used is based on the identity and sensitivities of the microorganism. Factors that indicate poor outcome include young and old age, a virulent microorganism, a delay in diagnosis or treatment initiation, underlying joint disease, and occurrence in certain joints. Although opportunities to prevent septic arthritis are limited, they should be kept in mind in patients with underlying arthritis or patients who have had a total joint replacement.
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Accurate data are lacking on the cost effectiveness of antibiotic prophylaxis to prevent late infections in prosthetic joints. 18 references. ·
Sports, Exercise, and Arthritis Source: Bulletin on the Rheumatic Diseases. 50(6): 1-4. 2001. Contact: Available from Arthritis Foundation. 1330 West Peachtree Street, Atlanta, GA 30309. (800) 268-6942 or (404) 872-7100. Fax (404) 872-9559. Website: www.arthritis.org. Summary: This newsletter provides health professionals with information on the impact of exercise and sports on the musculoskeletal system. Some observations from animal studies suggest a link between the physical stress of exercise and osteoarthritis (OA). The article reviews human studies on the relationship between vigorous exercise and OA and between physical activity and OA of the knee, as well as the beneficial effects of exercise in patients with either inflammatory or degenerative arthritis. Evidence suggesting that sports participation and exercise contribute over time to degenerative arthritis is fragmentary and difficult to substantiate consistently. However, there is much evidence, even if anecdotal, to support the many benefits of exercise in health and disease. For example, one study found that a dynamic, individually tailored strength training program can be beneficial for people who have inflammatory arthritis by minimizing the effects of disease, inactivity, or both on the neuromuscular system. 22 references.
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Glucosamine and Chondroitin for Osteoarthritis? Source: Bulletin on the Rheumatic Diseases. 50(7): 1-4. 2001. Contact: Available from Arthritis Foundation. 1330 West Peachtree Street, Atlanta, GA 30309. (800) 268-6942 or (404) 872-7100. Fax (404) 872-9559. Website: www.arthritis.org. Summary: This newsletter provides health professionals and people who have osteoarthritis (OA) with information on the therapeutic effects of glucosamine and chondroitin. The article reviews laboratory studies, placebo controlled clinical trials, comparator trials, and human disease modification studies of glucosamine and chondroitin. Evidence currently supports a modest efficacy for glucosamine and chondroitin in the treatment of OA. The products are safe and could have a role in the management of this disorder. However, further independent studies are needed to confirm findings on efficacy and to determine the clinical applicability of these compounds. In addition, preliminary findings support the idea that glucosamine and chondroitin might have disease modifying effects in OA. Research is needed to confirm these findings and to evaluate the impact of glucosamine and chondroitin on all aspects of OA progression. 1 table and 16 references.
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Use of Low-Dose Prednisone in the Management of Rheumatoid Arthritis, The Source: Bulletin on the Rheumatic Diseases. 50(12): 1-4. 2001. Contact: Available from Arthritis Foundation. 1330 West Peachtree Street, Atlanta, GA 30309. (800) 268-6942 or (404) 872-7100. Fax (404) 872-9559. Website: www.arthritis.org. Summary: This newsletter provides health professionals with information on the use of low dose prednisone, a glucocorticoid, in the management of rheumatoid arthritis (RA). RA, a chronic, symmetric polyarthritis that can lead to joint deformity and destruction, is associated with a significant increase in economic loss, morbidity, and mortality. Glucocorticoids have been used in the treatment of RA since 1948. These 21 carbon
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steroid molecules activate a cytoplasmic glucocorticoid receptor that ultimately results in the prevention of gene expression of various proinflammatory proteins and the inhibition of class I and II major histocompatibility complexes, adhesion molecules, inducible nitric oxide, and cyclooxygenase 2 enzyme. The side effects of glucocorticoids are well known. However, side effects can be minimized by using low doses. Potential side effects of low dose prednisone are osteopenia, bruising, weight gain, and formation of either cataracts or glaucoma. The article reviews evidence demonstrating the effectiveness of low dose corticosteroids in managing RA and suggests appropriate dosing. The article recommends that prednisone, at a dose not to exceed 10 milligrams per day be initiated as early as possible in the treatment of RA, usually with another disease modifying antirheumatic drug. 1 table and 22 references.
Newsletter Articles Use the Combined Health Information Database, and limit your search criteria to “newsletter articles.” Again, you will need to use the “Detailed Search” option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. Go to the bottom of the search page where “You may refine your search by.” Select the dates and language that you prefer. For the format option, select “Newsletter Article.” Type “arthritis” (or synonyms) into the “For these words:” box. You should check back periodically with this database as it is updated every three months. The following is a typical result when searching for newsletter articles on arthritis: ·
Arthritis: Hip Replacement Source: Harvard Health Letter. 27(4): 4-5. February 2002. Contact: Available from Harvard Health Letter. P.O. Box 380, Department BI, Boston, MA 02117. (800) 829-9045 or (617) 432-1485. E-mail:
[email protected]. Summary: This newsletter article provides people who are considering hip replacement surgery with information on this procedure. Although hip replacement used to be performed mainly on older people, this is changing because the operation has improved, replacement parts last longer, and people have higher expectations on how active and mobile they would like to be. The operation takes 2 to 3 hours. The procedure involves cutting off the top of the femur and replacing it with a round head component that fits snugly into the part of the pelvis that forms the socket of the hip's ball and socket design. Hip replacement parts can be cemented in place, or cementless models can be used. Recovery involves staying in the hospital for 4 to 5 days, working with physical and occupational therapists several times a day while in the hospital, and walking with crutches for about 6 weeks. Early complications include having the joint dislocate or having a leg that is too long. Long term complications include inflammation of the joint. Most hip replacements last 10 to 15 years. Surgical outcomes improve with greater experience on the part of the surgeon and the specialization on the part of the hospital. 1 figure.
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Etanercept: A New Drug for the Treatment of Psoriatic Arthritis Source: Psoriasis Forum. 8(1): 1,4,5. Spring 2002. Contact: National Psoriasis Foundation. P.O. Box 9009, Portland, OR 97207-9009. (800) 723-9166 ext. 12 or (503) 244-7404. Fax: (503) 245-0626. Email:
[email protected]. Website: www.psoriasis.org.
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Summary: This newsletter article discusses etanercept, the first FDA-approved drug for treating psoriatic arthritis. This drug was approved by the FDA for treating patients with RA in 1998 and has also been used to treat juvenile rheumatoid arthritis. Both topical and systemic therapies are used to treat psoriatic arthritis. Systemic therapies which include UVB and PUVA can cause organ toxicity. Etarnercept works by inhibiting the tumor necrosis factor-alpha (TNF-alpha)that is found in elevated levels in the skin and synovium of patients with psoriatic arthritis. The drug is administered subcutaneously by the patient. The most common side effect of etanercept is injectionsite reactions. Ninety percent of these were resolved without treatment. Other side effects include infections, sepsis, and rarely, tuberculosis, neurologic events, and pancytopenia. Overall, etanercept is well tolerated with an excellent safety profile and provides patients with psoriasis a new treatment option. ·
Genetics and Rheumatic Diseases: Rheumatoid Arthritis and Ankylosing Spondylitis Source: Bulletin on the Rheumatic Diseases. 50(2): 1-4. 2001. Contact: Available from Arthritis Foundation. 1330 West Peachtree Street, Atlanta, GA 30309. (800) 268-6942 or (404) 872-7100. Fax (404) 872-9559. Website: www.arthritis.org. Summary: This newsletter article provides health professionals and patients with information on the genetics of rheumatoid arthritis (RA) and ankylosing spondylitis (AS). The article explains the approaches that researchers can take to identify the nonHLA (Human Leukocyte Antigens) genes involved in susceptibility to RA, focusing on the genome wide approach. The article also highlights genetic studies of RA and AS. Analysis of data collected by the European Consortium for RA Families suggests links to several genetic regions. Findings of research conducted by the North American Rheumatoid Arthritis Consortium have revealed the presence of at least six different genetic regions outside the major histocompatibility complex with evidence for linkage. Modeling of genetic data obtained from family studies of AS suggests that two to six independent genes, including HLA-B27, interact multiplicatively to determine the risk for AS. The article discusses the relevance of genetic research on RA and AS to clinical practice. 20 references.
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Update on Reactive Arthritis Source: Bulletin on the Rheumatic Diseases. 50(4): 1-4. 2001. Contact: Available from Arthritis Foundation. 1330 West Peachtree Street, Atlanta, GA 30309. (800) 268-6942 or (404) 872-7100. Fax (404) 872-9559. Website: www.arthritis.org. Summary: This newsletter article provides health professionals with information on the clinical features, diagnosis, etiology, and treatment of reactive arthritis (ReA). This acute or subacute inflammatory arthropathy affects people in the second to fourth decade of life and occurs 1 to 4 weeks following genitourinary or enteric infection. ReA is usually a nondestructive, asymmetric oligoarthritis of peripheral large joints that occurs more frequently in the lower extremities than in the upper ones. There is no diagnostic test for ReA, so the diagnosis is based on focused questioning of a patient with otherwise unexplained oligoarthritis. Laboratory tests may be helpful in some situations. The mechanism of active ReA must be understood in order to determine appropriate therapies. The article explains how a microorganism causes arthritis and reviews studies that have focused on identifying infectious particles within the joint. In addition, the article discusses the role of antibiotics in managing ReA and the use of nonsteroidal antiinflammatory drugs, intraarticular glucocorticoids, sulfasalazine, and methotrexate in treating ReA. 1 table and 15 references.
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Traveling With Arthritis Source: Arthritis Self-Management. 2(7): 1-2. July 2001. Contact: Available from Arthritis Self-Management. Customer Service, P.O. Box 56051, Boulder, CO 80322-6051. (800) 234-0923. Summary: This newsletter article provides people who have arthritis with information on traveling. Arthritis will likely restrict people who have arthritis from participating in some activities, so they need to think carefully about what kind of trip they will enjoy the most. Many people seek professional advice for help with planning a trip. Forms of professional help include travel agents, tour companies, and physicians. The article offers tips on packing clothing, medications, and other supplies; provides advice on travelling by train, ship, airplane, and car; and presents guidelines on seeking hotel accommodations for people with disabilities. In addition, the article identifies sources of additional information.
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Hyaluronate and Knee OA [Osteoarthritis] Source: Arthritis Self-Management. 2(7): 6. July 2001. Contact: Available from Arthritis Self-Management. Customer Service, P.O. Box 56051, Boulder, CO 80322-6051. (800) 234-0923. Summary: This newsletter article provides people who have arthritis with information on the use of hyaluronate to treat osteoarthritis (OA) of the knee. Hyaluronate is a normal constituent of the joint fluid that lubricates and cushions the joints. The osteoarthritic joint is less capable of producing and maintaining healthy levels of hyaluronate in the synovial fluid, so the joint becomes stiff and painful. Replacing hyaluronate via injection directly into the knee joint can improve joint function and reduce pain. This procedure is known as viscosupplementation. Hyalgan, Synvisc, and Supartz are the hyaluronate compounds currently approved by the Food and Drug Administration for the treatment of OA of the knee. People who do not respond adequately to nondrug treatments such as weight loss and exercise and those who respond poorly to acetaminophen or to nonsteroidal antiinflammatory drugs may be candidates for viscosupplementation. The article explains how the procedure is performed, identifies potential side effects, and reports on its efficacy. The article also lists sources of additional information.
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Arthritis: More Than Meets the Eye Source: Arthritis Frontline. Spring 2001. Contact: Available from Arthritis Foundation, Metropolitan Washington Chapter. 4455 Connecticut Avenue, NW, Suite 300, Washington, DC 20008. (202) 537-6800. E-mail:
[email protected]. Website: www.arthritis.org. Summary: This newsletter article provides people who have arthritis with information on the most commonly diagnosed forms of the disease. Osteoarthritis (OA), or degenerative joint disease, is the most common type of arthritis. OA, which occurs when cartilage begins to fray, wear, and decay, can cause severe joint pain, reduced joint motion, loss of function, and disability. Rheumatoid arthritis (RA) is an inflammatory disease of the joint lining. RA, which most often affects the hands and feet, results in pain, stiffness, swelling, deformity, and loss of function in the joints. Systemic lupus erythematosus (SLE) is an autoimmune disease in which the immune system attacks the body's own healthy cells and tissues. Gout, a very common form of arthritis, causes
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sudden, severe episodes of pain, tenderness, redness, warmth, and inflammation in some joints. Gout generally occurs in stages, and it can be controlled with medication. Fibromyalgia, a chronic condition, causes widespread pain, fatigue, and sleep disturbances. 3 figures. ·
Arthritis: Should You Be Taking a COX-2 Inhibitor? Source: Harvard Health Letter. 27(1): 1-3. November 2001. Contact: Available from Harvard Health Letter. P.O. Box 380, Department BI, Boston, MA 02117. (800) 829-9045 or (617) 432-1485. E-mail:
[email protected]. Summary: This newsletter article provides people who have arthritis with information on the use of cyclooxgenase-2 (COX-2) inhibitors in the treatment of arthritis. Celecoxib (Celebrex) and rofecoxib (Vioxx) are the most well known COX-2 inhibitors. Studies have shown that the COX-2 inhibitors cause fewer serious ulcers and gastrointestinal complications than older but far less expensive medications like ibuprofen and naproxen. These latter medications are nonprescription versions of a class of drugs known as nonsteroidal antiinflammatory drugs (NSAIDs). NSAIDs inhibit COX, which controls the production of prostaglandins, hormone like compounds critical to pain transmission. The development of COX-2 drugs was the result of the discovery that COX was not one but two enzymes. COX-1 is made continually in most cells, whereas COX-2 is made largely in response to pathological situations like tissue damage and inflammation. Most NSAIDs inhibit both COX-1 and COX-2. NSAIDs that inhibit COX-1 deprive those tissues of prostaglandins and make them vulnerable to damage. By contrast, COX-2 inhibitors focus on COX-2 activity without impeding COX-1. The American College of Rheumatology recommends that patients with arthritis begin NSAID therapy at the lowest dose possible and increase the dosage only if they continue to have pain. Candidates for COX-2 inhibitors are people who have had a prior bleeding problem with NSAIDs or anyone who is age 65 and over, has a history of ulcers, or is currently using steroids. The article includes a sidebar that discusses the possibility that COX-2 inhibitors increase the risk of heart attack. 1 figure.
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Supplements: Glucosamine for Osteoarthritis Source: Harvard Women's Health Watch. 7(9): 5. May 2000. Contact: Available from Harvard Women's Health Watch. Department SR, P.O. Box 380, Boston, MA 02117. (800) 829-5921. E-mail:
[email protected]. Summary: This newsletter article provides women who have arthritis with information on the supplement glucosamine. This popular nutritional supplement, which is derived from the shells of lobster, shrimp, and crabs, is being promoted for treating osteoarthritis (OA) naturally. Glucosamine occurs naturally in the body and encourages cartilage cells to produce glycosaminoglycans and proteoglycans. Mild and moderate OA cases have generally been treated with nonsteroidal antiinflammatory drugs, but long term use of these medications can cause serious gastrointestinal side effects. Thus, people who have OA are looking for gentler, less expensive ways to treat their pain. Numerous studies conducted in Europe and Asia suggest that glucosamine has promise as a pain reliever. The National Institutes of Health awarded the University of Utah School of Medicine a $6.6 million grant to coordinate the first multicenter, randomized, double blind clinical trial of glucosamine and chondroitin, a companion supplement, in patients with OA of the knee. The 1,000 patients participating in the study will take either glucosamine, chondroitin, a combination of both, or a placebo for 16 weeks and be
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evaluated monthly for improvement of pain. The article offers suggestions on taking glucosamine safely. ·
Sex and Arthritis Source: Bulletin on the Rheumatic Diseases. 49(7): 1-4. 2000. Contact: Available from Arthritis Foundation. 1330 West Peachtree Street, Atlanta, GA 30309. (404) 872-7100. Fax (404) 872-9559. Summary: This newsletter article provides health professionals with information on sexual dysfunction in people who have rheumatic diseases. Despite the lack of studies, in patients with rheumatic disease, there is consensus that arthritis can interfere with sexual functioning. Osteoarthritis, rheumatoid arthritis, Sjogren's syndrome, systemic lupus erythematosus, systemic sclerosis, and fibromyalgia may all have a negative impact on sexual functioning. Medications commonly used to treat rheumatic diseases, including glucocorticoids, immunosuppressants, tricyclic antidepressants, and selective serotonin reuptake inhibitors, may also affect sexual function. Although arthritis affects each person's sexuality in a different manner, there are some common concerns that affect each person and his or her partner. Physicians can help their patients who have sexual problems by inquiring about sexual issues as a part of routine care, giving patients limited information to help them understand the possible changes that may occur as a result of the disease or treatment, offering patients specific strategies, and referring patients to other health professionals skilled in marital relationships and sexual disturbances. 1 table and 24 references.
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Elbow Surgery for Arthritis: Relief When Other Therapies Don't Work Source: Mayo Clinic Health Letter. 18(10): 4-5. October 2000. Contact: Available from Mayo Clinic Health Letter, 200 First Street SW, Rochester, MN 55905. (800) 333-9037 or (303) 604-1465. Email:
[email protected]. Summary: This newsletter article provides people who have arthritis in the elbow with information on the use of a surgical technique known as debridement to relieve elbow pain and improve function and motion. The most common types of arthritis are osteoarthritis, which is a degenerative disease, and rheumatoid arthritis, which is associated with inflammation of the lining of joints. When treatments such as medications, activity modification, and physical therapy no longer help, for arthritis pain and immobility, surgery may be needed. Joint replacement is the standard of care for people who have advanced arthritis in the elbow. However, some people with an earlier stage of disease may have the option of undergoing traditional or arthroscopic debridement. Although debridement is traditionally performed with an open incision, arthroscopic surgery is proving promising. One form of arthroscopic debridement is known as osteocapsular arthroplasty. The article outlines the characteristics of people who may benefit from arthroscopic debridement and highlights the risks associated with it. 1 figure.
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Juvenile Rheumatoid Arthritis: A Medical Perspective Source: Arthritis Frontline. Winter 2001. Page 4. Contact: Available from Arthritis Foundation, Metropolitan Washington Chapter. 4455 Connecticut Avenue, NW, Suite 300, Washington, DC 20008. (202) 537-6800. E-mail:
[email protected]. Website: www.arthritis.org.
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Summary: This newsletter article provides children who have juvenile rheumatoid arthritis (JRA) and their families with information on this inflammatory condition of the joints. JRA begins before the age of 16. It is categorized into pauciarticular, polyarticular, and systemic subgroups. Approximately half of all children with JRA have pauciarticular JRA, a form in which one to four joints are involved. In most children with this form of JRA, the course of arthritis is intermittent and mild. When more than four joints are involved, the joints tend to be symmetrically affected. Approximately 40 percent of all children with JRA have this polyarticular form of the disease. Polyarticular JRA is more likely found in girls, and most have a mild course. The systemic form affects both genders equally and accounts for 10 percent of JRA cases. There is no definitive test for JRA, so diagnosis is by exclusion. Fifty percent of children with JRA continue to have disease activity into adulthood. Treatments that can stop or slow the progression of the disease include nonsteroidal antiinflammatory drugs, disease modifying antirheumatic drugs, and biologic response modifiers. In addition, children who have JRA should exercise, rest, and use splints to keep the joints functional and the muscles strong. ·
New Osteoarthritis Treatments: Will Revolutionary Drugs Bring Relief? Source: Mayo Clinic Women's HealthSource. 3(3): 1-2. March 1999. Summary: This newsletter article provides people who have osteoarthritis with information on new drugs available for treating this chronic condition. Although there is little evidence of inflammation with osteoarthritis, pain-relieving nonsteroidal antiinflammatory drugs (NSAIDs) have been the treatment of choice. In 1971, researchers found the NSAIDs worked by inhibiting the enzyme cyclooxygenase, or Cox. Cox-2 enzymes promote the inflammation and pain of arthritis. Most NSAIDs inhibit both Cox-1 and Cox-2 molecules, however, this then leaves the stomach lining vulnerable to ulcers and bleeding. The Cox-2 inhibitors appear to provide pain relief equal to other NSAIDs with much less chance of gastrointestinal upset. Two other new treatments for osteoarthritis, hyaluronan and hylan G-F20, are injectable drugs that help relieve pain. Hyaluronan is administered in a series of five injections into the knee joint, and relief may last up to 12 months. Hylan G-F20 is similar to hyaluronan, and it is administered in three injections. This drug may produce relief for up to 6 months or longer. Both of these drugs are currently available, and the Cox-2 inhibitor Celebrex is expected to be available some time in 1999. The article also comments on the use of the nutritional supplements, glucosamine and chondroitin sulfate, to treat osteoarthritis.
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COX-2 Inhibitors: New Medication for Arthritis Pain Source: Mayo Clinic Health Letter. 17(4): 7. April 1999. Summary: This newsletter article provides people who have osteoarthritis with information on Cox-2 inhibitors, a new class of drugs approved for the treatment of osteoarthritis and rheumatoid arthritis. Cox-2 inhibitors are not 'super aspirins;' they are not aspirin, nor are they necessarily more powerful. However, these drugs target pain in ways similar to aspirin or other nonsteroidal anti-inflammatory drugs (NSAIDs), but they do not produce the gastrointestinal side effects associated with long-term use of NSAIDs. Because the long-term effects of Cox-2 inhibitors are unknown, the Food and Drug Administration has required the standard NSAID warning about the risk of gastrointestinal side effects. The article outlines issues that people should consider before taking a Cox-2 inhibitor.
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Arthritis Relief: Considering the Alternatives Source: Harvard Health Letter. 24(9): 7. July 1999. Contact: Available from Harvard Health Letter, P.O. Box 380, Department BI, Boston, MA 02117. (800) 829-9045 or (617) 432-1485. E-mail:
[email protected]. Summary: This newsletter article provides people who have arthritis with information on the purported effectiveness of the dietary supplements glucosamine, chondroitin sulfate, and S-Adenosylmethionine (SAM-e) in relieving the pain of osteoarthritis (OA). This form of arthritis involves a breakdown of cartilage. Glucosamine stimulates cartilage cells to produce glycosaminoglycans and proteoglycans, the building blocks of cartilage. Chondroitin sulfate is believed to inhibit the enzymes that contribute to the breakdown of cartilage. Some studies suggest that SAM-e may promote cartilage formation and repair by stimulating the synthesis of proteoglycans. Although these three dietary supplements have been reputed to relieve the pain of OA with fewer side effects than conventional medication and to halt and even reverse its progress, they have not been required to meet the same standards for safety, efficacy, and purity as conventional medications because of their status as dietary supplements. Therefore, the Arthritis Foundation has refused to endorse the use of glucosamine and chondroitin until long-term, controlled clinical trials with larger numbers of patients are published. However, the foundation says there is sufficient information to support the pain relief claims made for SAM-e.
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Coping With Arthritis: The Problems Kids Face and How You Can Help Source: Kids Get Arthritis Too. pp. 5-6. May-June 1999. Contact: Available from Kids Get Arthritis Too (Arthritis Foundation). P.O. Box 921907, Norcross, GA 30010-1907. (800) 268-6942. Summary: This newsletter article provides the parents of children who have arthritis with information on how to help them cope with their condition. Parents must balance the urge to give their child special treatment with the need to be realistic about what their child can do. One common challenge faced by children with arthritis is not being able to play certain sports. This may set a child up for peer rejection. Thus, parents should encourage socialization through activities that do not focus on physical abilities. Educating classmates about how arthritis affects a child and about the effects of drugs used to treat arthritis may also be helpful. One of the biggest problems faced by children with arthritis is their overprotective parents. Parents should emphasize the need for a normal lifestyle so that the child feels like one of the family rather than someone special. Another problem associated with overprotecting the child with arthritis is creating resentment and rivalry among siblings. Parents should pay attention to the other children in the family and avoid overindulging the child with arthritis. As the child grows into adolescence, parents find that one of their greatest challenges is getting their child to take his or her medication. However, there are solutions to this problem as well.
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Tumor Necrosis Factor Inhibitors for Rheumatoid Arthritis Source: Bulletin on the Rheumatic Diseases. 48(3): 1-4. 1999. Contact: Available from Arthritis Foundation. 1330 West Peachtree Street, Atlanta, GA 30309. (404) 872-7100. Fax (404) 872-9559. Summary: This newsletter article provides people who have arthritis with information on the efficacy and safety of etanercept and infliximab for treating rheumatoid arthritis
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(RA). These new agents are tumor necrosis factor (TNF) antagonists that block the actions of TNF, a cytokine that mediates the clinical and pathologic sequelae of RA. The article explains the immunobiology of TNF and discusses its role in RA. The article then highlights studies on etanercept and infliximab. Studies of etanercept have demonstrated its efficacy in arthritis. A study investigating combination therapy with etanercept and methotrexate in people with RA unresponsive to moderate doses of methotrexate also showed promise. In a study evaluating etanercept in children with juvenile RA, children receiving treatment with etanercept had significant clinical improvement as defined by standard arthritis activity criteria of the pediatric population. Both open label and placebo controlled trials have demonstrated the effectiveness of using infliximab to treat RA. Etanercept has been approved by the Food and Drug Administration (FDA) for use in people with moderate to severe RA who fail to respond to treatment with a disease modifying antirheumatic drug. FDA approval for the use of infliximab in RA is pending. Adverse affects of TNF inhibitors include injection site reactions, development of antibodies to the TNF inhibitor, development of antinuclear and anti-DS DNA antibodies, infections, and lymphomas. 1 table and 16 references. ·
Should You Try Acupuncture for Arthritis? Source: Health After 50. 9(11):3; January 1998. Contact: Johns Hopkins Medical Letter, Health After 50, 550 North Broadway, Suite 1100, Baltimore, MD 21205-2011. Summary: This newsletter article for individuals with arthritis discusses the use of acupuncture to relieve the pain caused by arthritis and other musculoskeletal disorders. It explains the belief underlying the principle of acupuncture and reports on studies that provide evidence of the effectiveness of acupuncture for relieving pain. Several studies have found that osteoarthritis patients experienced pain relief following acupuncture treatments. However, another study found that arthritis symptoms improved in individuals receiving acupuncture and in those who had needles inserted in nontraditional acupuncture sites. The article stresses that more testing is needed to determine whether the positive effects of acupuncture are the result of placebo effects or some other mechanism.
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On the Trail of New Arthritis Treatments Source: Harvard Health Letter. 23(1):7; 1998. Contact: Available from Harvard Health Letter, P.O. Box 380, Boston, MA 02117. Summary: This newsletter article for health professionals and individuals with arthritis reports on the progress made the finding a better class of medications for treating rheumatoid arthritis. Researchers have developed several drugs that block the release of a cytokine known as tumor necrosis factor (TNF). One anti-TNF compound that look promising is TNFR:Fc. A multicenter trial of this compound demonstrated a reduction in tender or swollen joints in 61 percent of those taking high doses of the compound. Although there are some uncertainties about its long-term side effects, TNFR:Fc and other anti-cytokines may be approved by the Food and Drug Administration by 1999.
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Nonmedical Therapies for Osteoarthritis Source: Bulletin on the Rheumatic Diseases. 47(2): 5-7. 1998.
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Contact: Available from Arthritis Foundation. 1330 West Peachtree Street, Atlanta, GA 30309. (404) 872-7100. Fax (404) 872-9559. Summary: This newsletter article provides people who have osteoarthritis (OA) with information on the efficacy and usefulness of common nonmedicinal therapies for OA, including exercise, weight loss, physical modalities, and other treatments for painful conditions. OA, which is a degenerative joint disease, is the most common form of arthritis. Evidence suggests that muscle strengthening and aerobic conditioning may be promising treatments. Despite this evidence, patient adherence to recommended programs of exercise is often poor. Thus, various tactics are necessary to enhance adherence. In addition, the issue of which types of exercise should be recommended is unresolved. Studies have shown that weight change over time has an effect on a person's risk of developing OA. People who experience weight gain increase their risk, whereas people who experience weight loss decrease their risk. Although few clinical trials have examined the efficacy of weight loss as a treatment for OA of the knee or hip, one uncontrolled study demonstrated that weight loss was an effective nonmedicinal therapy for the pain and disability of knee OA. Research has also shown that some types of biomechanical alterations, such as elastic knee supports and canes and crutches, may be effective treatment options. Other analgesic treatments, including transcutaneous electrical nerve stimulation, electromagnetic stimulation, pulsed electrical stimulation, and educational interventions, may also be useful. 10 references. ·
Arthritis Cure: Does It Really Work? Source: University of California at Berkeley Wellness Letter. 13(8):1-2,5; May 1997. Contact: Available from Health Letter Associates, P.O. Box 412, Prince Street Station, New York, NY 10012-0007. Summary: This newsletter article for individuals with osteoarthritis critiques a book that offers advice for managing osteoarthritis (OA). Although the book provides some standard advice for managing OA, it also claims that OA suffers will experience relief from their symptoms by taking the nutritional supplements glucosamine and chondroitin sulfate. The book even proclaims that some individuals may have a complete reversal of arthritis through the rebuilding of cartilage. The article explains why this claim is inaccurate. It also offers suggestions for preventing and treating OA, including adopting a regular exercise program, maintaining a healthy weight, and using acetaminophen and nonsteroidal anti-inflammatory drugs.
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Proven Relief for Arthritis Pain Source: Health After 50. 9(4):3; June 1997. Contact: Johns Hopkins Medical Letter, Health After 50, 550 North Broadway, Suite 1100, Baltimore, MD 21205-2011. Summary: This newsletter article for individuals with arthritis discusses the use of relaxation therapy for relieving osteoarthritis (OA) pain. Relaxation therapy may be beneficial because relaxation releases muscle tension, thereby diminishing the degree and perception of pain and improving the ability to cope with pain. Promising relaxation techniques include meditation, guided imagery, deep breathing, biofeedback, and hypnosis. Although relaxation therapy may reduce the need for other treatments such as medication, rest, exercise, weight control, and joint protection, these treatments are still key components of OA care. The important role that each of these treatments has in OA treatment are discussed.
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Dangers of Low-dose Corticosteroid Therapy in Rheumatoid Arthritis Source: Bulletin on the Rheumatic Diseases. 46(4):1-4; June 1997. Contact: Arthritis Foundation. 1330 West Peachtree Street; Atlanta, GA 30309. (404) 8727100. Fax (404) 872-9559. Summary: This newsletter article for health professionals considers the adverse effects of oral low-dose corticosteroid therapy in rheumatoid arthritis, focusing on osteoporosis and posterior subcapsular cataracts. Concerns related to corticosteroid use are discussed, including continued use once they are started and use of higher doses to maintain improvements. In addition, indications for low-dose steroid use are identified and recommendations for steroid use are presented, including using prednisone or prednisolone, using one dose per day rather than split doses, and considering risk factors for the development or aggravation of comorbid conditions. 19 references and 1 table.
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Benefits of Low-dose Corticosteroids in Rheumatoid Arthritis Source: Bulletin on the Rheumatic Diseases. 46(4):4-7; June 1997. Contact: Arthritis Foundation. 1330 West Peachtree Street; Atlanta, GA 30309. (404) 8727100. Fax (404) 872-9559. Summary: This newsletter article for health professionals considers the benefits of lowdose corticosteroids in treating rheumatoid arthritis (RA). The mechanism of action of corticosteroids is explained, and studies on the disease-modifying effects of corticosteroids are reviewed. Careful analysis of some study data suggests beneficial effects of corticosteroids in RA. However, the potential toxicity of corticosteroids has been well-documented. Common side effects include interfering with glucose tolerance, increasing lipoproteins and serum lipids, elevating blood pressure, increasing the likelihood of osteoporosis, and causing muscle weakness and myopathy. In addition, the use of alternate-day and pulse steroids is discussed. The article concludes that corticosteroids are an important therapeutic option for individuals with RA. 18 references.
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Foot and Ankle Issues in Rheumatoid Arthritis Source: Bulletin on the Rheumatic Diseases. 46(5):1-3; August 1997. Contact: Arthritis Foundation, 1330 West Peachtree Street, Atlanta, GA 30309. (404) 8727100. (404) 872-9559 (fax). Summary: This newsletter article for health professionals discusses foot and ankle involvement in rheumatoid arthritis. Extra-articular manifestations that affect the foot and ankle are identified, and intra-articular involvement is examined. Guidelines for the medical management of early synovitis in the foot and ankle are provided. Such management includes using appropriate nonsteroidal anti-inflammatory drugs, diseasemodifying antirheumatic drugs, and low doses of prednisone to control inflammation. Additional measures include joint injections, modifications in footwear, accommodative orthotics, ankle/foot orthoses, and bracing. Surgery may be effective in treating advanced deformity in the foot and ankle. 8 references.
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Natural Relief From Arthritis Source: Health After 50. 9(8):1-2; October 1997.
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Contact: Johns Hopkins Medical Letter, Health After 50, 550 North Broadway, Suite 1100, Baltimore, MD 21205-2011. Summary: This newsletter article for individuals with osteoarthritis (OA) discusses the use of glucosamine and chondroitin as advised in a book on managing arthritis. It explains why the use of these nutritional supplements seems to have merit and states, however, that there is no convincing evidence that glucosamine or chondroitin reaches the cartilage or helps rebuild it. The lack of rigorous studies of these supplements has created skepticism about their effectiveness within the medical community. However, because of the commercial success of the glucosamine and chondroitin combination, several studies are planned. ·
Arthritis Research Update Source: Observer. 49(3):1-2; Winter 1997. Contact: Arthritis Foundation, Rocky Mountain Chapter. Summary: This newsletter article for individuals with arthritis reports on the outcomes of arthritis research, including increasing the understanding of the causes of many forms of arthritis and enhancing the recognition by health care providers that arthritis and its associated pain are complex issues affecting body and mind. In addition, it presents research updates concerning systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). Research on SLE has yielded the identification of a gene that may contribute to lupus. RA research has focused on the identification of cytokines that cause joint damage and cells that drive inflammation in RA.
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Acute Monarthritis Source: Bulletin of the Rheumatic Diseases. 46(7): 1-2. November 1997. Summary: This newsletter article provides health professionals with information on the diagnosis and treatment of acute monarthritis. This type of arthritis is a rheumatologic emergency that requires urgent, thorough investigation with the goal of making a precise diagnosis. Diagnostic possibilities include nongonococcal and gonococcal bacterial infections. The most common nongonococcal pathogens causing acute monarthritis include Staphylococcus aureus. Pathogenic organisms enter the joint through hematogenous spread from another primary site of infection or contiguous spread from soft tissue, penetrating trauma, surgery, or underlying bone. Symptoms of acute bacterial infection include acute onset of severe pain and swelling of a single joint. The knee is the joint most commonly affected, followed by other large, diarthrodial joints. Treatment should include joint drainage either by needle aspiration or open drainage and antibiotic therapy. Disseminated gonococcal infection is the most frequent cause of septic arthritis in immunocompetent people under 40 years old. About 50 percent of these individuals present with acute monarthritis. Definitive diagnosis requires culture confirmation. Treatment involves the use of third-generation cephalosporin or a quinolone. The second broad category of acute monarthritis is crystalline arthritis. Acute gout and pseudogout are the dominate forms of crystalline arthritis. The article presents a case history that highlights some of the issues related to acute monarthritis. 8 references. (AA-M).
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Juvenile Arthritis and Back to School Source: American Juvenile Arthritis Organization Newsletter. 4; Fall 1996. Contact: American Juvenile Arthritis Organization.
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Summary: This newsletter article for children with juvenile arthritis and their families offers suggestions for ensuring that these children are able to participate to their fullest abilities in school. Advice includes providing school personnel with clear oral and written instructions, planning for the next school year at the end of the previous year, establishing at least one good relationship with a school staff member, involving children or adolescents when planning school modifications, and using American Juvenile Arthritis Organization programs and materials. ·
Know the Symptoms of Psoriatic Arthritis Source: National Psoriasis Foundation Bulletin. 27(5):8; September/October 1996. Contact: National Psoriasis Foundation. 6600 SW 92nd Avenue, Suite 300, Portland, OR 97223-7195. (503)244-7404. Fax (503) 245-0626. Summary: This newsletter article for individuals with psoriasis presents the symptoms of psoriatic arthritis. This form of arthritis affects single or multiple joints, particularly those of the hands and feet. The simultaneous presence of psoriasis and nail malformation are an indication of psoriatic arthritis. Nonpharmacological modalities used to treat psoriatic arthritis are highlighted. Drugs that have been beneficial to individuals with both rheumatoid and psoriatic arthritis are identified, including methotrexate and antimalarials. The co-occurrence of gout in individuals with psoriatic arthritis is also discussed.
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Current Surgical Treatment for Arthritis of the Hand Source: Arthritis Observer. 48(1):1,4; Spring 1996. Contact: Rocky Mountain Chapter of the Arthritis Foundation. Summary: This newsletter article for individuals with arthritis focuses on current surgical treatment for arthritis of the hand. The team concept of care for managing arthritis is discussed. Types of surgical techniques are described, including soft tissue arthroplasty , silicone implants in the joints, artificial joint replacement, and joint fusion. Types of anesthesia used in these surgical procedures are identified. The post-surgical relationship between the patient and the hand therapist is also considered.
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Career Counseling for Teenagers With Arthritis Source: Bulletin on the Rheumatic Diseases. 45(3):4-6; May 1996. Contact: Arthritis Foundation, 1314 Spring Street, NW, Atlanta, GA 30309. (404) 8727100. (404) 872-9559 (fax). Summary: This newsletter article for health professionals discusses the importance of providing adolescents and young adults with arthritis with career counseling. Factors that effect the employment situation of adolescents and young adults with arthritis are identified. Data on employment of and vocational services for the disabled are presented. Examples of exemplary programs, booklets, newsletters, and videotapes for disabled adolescents and their families are highlighted, focusing on the Adolescent Employment Readiness Center, the Special Treatment Center for Arthritis, a career guide for adolescents with arthritis, a newsletter for adolescents seeking employment, and a videotape on the journey of three young adolescents with chronic illness toward independence in health care. 4 references.
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Tufts Nutrition Research: From the Lab to Your Plate. Vitamin E for Easing Rheumatoid Arthritis Pain Source: Tufts University Health and Nutrition Letter. 18(12). Special Supplement. February 2001. Contact: 10 High Street, Suite 706, Boston, MA 02110.
[email protected] www.healthletter.tufts.edu. Summary: This article reviews research suggesting that large doses of vitamin E may help reduce pain and inflammation in people who suffer from rheumatoid arthritis. Two German studies have found that those who take vitamin E daily experience a decrease in morning stiffness, joint tenderness, and joint pain. A Danish study suggests that high enough blood levels of vitamin E may help to prevent rheumatoid arthritis. Danish researchers have found that those who start with low blood levels of vitamin E are eight times more likely than those with higher levels to end up with the disease. This may occur because people with rheumatoid arthritis use up more antioxidants (such as vitamin E) to destroy free radicals (toxic oxygen molecules involved in causing inflammation). Jeffrey Blumberg, head of the Antioxidants Research Laboratory at Tufts University, states that although vitamin E is not the new arthritis treatment, it may be an 'adjunctive treatment.'
Academic Periodicals covering Arthritis Numerous periodicals are currently indexed within the National Library of Medicine’s PubMed database that are known to publish articles relating to arthritis. In addition to these sources, you can search for articles covering arthritis that have been published by any of the periodicals listed in previous chapters. To find the latest studies published, go to http://www.ncbi.nlm.nih.gov/pubmed, type the name of the periodical into the search box, and click “Go.” If you want complete details about the historical contents of a journal, you can also visit the following Web site: http://www.ncbi.nlm.nih.gov/entrez/jrbrowser.cgi. Here, type in the name of the journal or its abbreviation, and you will receive an index of published articles. At http://locatorplus.gov/, you can retrieve more indexing information on medical periodicals (e.g. the name of the publisher). Select the button “Search LOCATORplus.” Then type in the name of the journal and select the advanced search option “Journal Title Search.”
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APPENDICES
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APPENDIX A. PHYSICIAN RESOURCES Overview In this chapter, we focus on databases and Internet-based guidelines and information resources created or written for a professional audience.
NIH Guidelines Commonly referred to as “clinical” or “professional” guidelines, the National Institutes of Health publish physician guidelines for the most common diseases. Publications are available at the following by relevant Institute12: ·
Office of the Director (OD); guidelines consolidated across agencies available at http://www.nih.gov/health/consumer/conkey.htm
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National Institute of General Medical Sciences (NIGMS); fact sheets available at http://www.nigms.nih.gov/news/facts/
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National Library of Medicine (NLM); extensive encyclopedia (A.D.A.M., Inc.) with guidelines: http://www.nlm.nih.gov/medlineplus/healthtopics.html
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National Cancer Institute (NCI); guidelines available at http://www.cancer.gov/cancerinfo/list.aspx?viewid=5f35036e-5497-4d86-8c2c714a9f7c8d25
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National Eye Institute (NEI); guidelines available at http://www.nei.nih.gov/order/index.htm
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National Heart, Lung, and Blood Institute (NHLBI); guidelines available at http://www.nhlbi.nih.gov/guidelines/index.htm
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National Human Genome Research Institute (NHGRI); research available at http://www.genome.gov/page.cfm?pageID=10000375
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National Institute on Aging (NIA); guidelines available at http://www.nia.nih.gov/health/
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These publications are typically written by one or more of the various NIH Institutes.
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National Institute on Alcohol Abuse and Alcoholism (NIAAA); guidelines available at http://www.niaaa.nih.gov/publications/publications.htm
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National Institute of Allergy and Infectious Diseases (NIAID); guidelines available at http://www.niaid.nih.gov/publications/
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National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS); fact sheets and guidelines available at http://www.niams.nih.gov/hi/index.htm
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National Institute of Child Health and Human Development (NICHD); guidelines available at http://www.nichd.nih.gov/publications/pubskey.cfm
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National Institute on Deafness and Other Communication Disorders (NIDCD); fact sheets and guidelines at http://www.nidcd.nih.gov/health/
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National Institute of Dental and Craniofacial Research (NIDCR); guidelines available at http://www.nidr.nih.gov/health/
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National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK); guidelines available at http://www.niddk.nih.gov/health/health.htm
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National Institute on Drug Abuse (NIDA); guidelines available at http://www.nida.nih.gov/DrugAbuse.html
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National Institute of Environmental Health Sciences (NIEHS); environmental health information available at http://www.niehs.nih.gov/external/facts.htm
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National Institute of Mental Health (NIMH); guidelines available at http://www.nimh.nih.gov/practitioners/index.cfm
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National Institute of Neurological Disorders and Stroke (NINDS); neurological disorder information pages available at http://www.ninds.nih.gov/health_and_medical/disorder_index.htm
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National Institute of Nursing Research (NINR); publications on selected illnesses at http://www.nih.gov/ninr/news-info/publications.html
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National Institute of Biomedical Imaging and Bioengineering; general information at http://grants.nih.gov/grants/becon/becon_info.htm
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Center for Information Technology (CIT); referrals to other agencies based on keyword searches available at http://kb.nih.gov/www_query_main.asp
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National Center for Complementary and Alternative Medicine (NCCAM); health information available at http://nccam.nih.gov/health/
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National Center for Research Resources (NCRR); various information directories available at http://www.ncrr.nih.gov/publications.asp
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Office of Rare Diseases; various fact sheets available at http://rarediseases.info.nih.gov/html/resources/rep_pubs.html
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Centers for Disease Control and Prevention; various fact sheets on infectious diseases available at http://www.cdc.gov/publications.htm
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NIH Databases In addition to the various Institutes of Health that publish professional guidelines, the NIH has designed a number of databases for professionals.13 Physician-oriented resources provide a wide variety of information related to the biomedical and health sciences, both past and present. The format of these resources varies. Searchable databases, bibliographic citations, full-text articles (when available), archival collections, and images are all available. The following are referenced by the National Library of Medicine:14 ·
Bioethics: Access to published literature on the ethical, legal, and public policy issues surrounding healthcare and biomedical research. This information is provided in conjunction with the Kennedy Institute of Ethics located at Georgetown University, Washington, D.C.: http://www.nlm.nih.gov/databases/databases_bioethics.html
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HIV/AIDS Resources: Describes various links and databases dedicated to HIV/AIDS research: http://www.nlm.nih.gov/pubs/factsheets/aidsinfs.html
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NLM Online Exhibitions: Describes “Exhibitions in the History of Medicine”: http://www.nlm.nih.gov/exhibition/exhibition.html. Additional resources for historical scholarship in medicine: http://www.nlm.nih.gov/hmd/hmd.html
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Biotechnology Information: Access to public databases. The National Center for Biotechnology Information conducts research in computational biology, develops software tools for analyzing genome data, and disseminates biomedical information for the better understanding of molecular processes affecting human health and disease: http://www.ncbi.nlm.nih.gov/
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Population Information: The National Library of Medicine provides access to worldwide coverage of population, family planning, and related health issues, including family planning technology and programs, fertility, and population law and policy: http://www.nlm.nih.gov/databases/databases_population.html
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Cancer Information: Access to cancer-oriented databases: http://www.nlm.nih.gov/databases/databases_cancer.html
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Profiles in Science: Offering the archival collections of prominent twentieth-century biomedical scientists to the public through modern digital technology: http://www.profiles.nlm.nih.gov/
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Chemical Information: Provides links to various chemical databases and references: http://sis.nlm.nih.gov/Chem/ChemMain.html
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Clinical Alerts: Reports the release of findings from the NIH-funded clinical trials where such release could significantly affect morbidity and mortality: http://www.nlm.nih.gov/databases/alerts/clinical_alerts.html
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Space Life Sciences: Provides links and information to space-based research (including NASA): http://www.nlm.nih.gov/databases/databases_space.html
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MEDLINE: Bibliographic database covering the fields of medicine, nursing, dentistry, veterinary medicine, the healthcare system, and the pre-clinical sciences: http://www.nlm.nih.gov/databases/databases_medline.html
13 Remember, for the general public, the National Library of Medicine recommends the databases referenced in MEDLINEplus (http://medlineplus.gov/ or http://www.nlm.nih.gov/medlineplus/databases.html). 14 See http://www.nlm.nih.gov/databases/databases.html.
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Toxicology and Environmental Health Information (TOXNET): Databases covering toxicology and environmental health: http://sis.nlm.nih.gov/Tox/ToxMain.html
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Visible Human Interface: Anatomically detailed, three-dimensional representations of normal male and female human bodies: http://www.nlm.nih.gov/research/visible/visible_human.html The Combined Health Information Database
A comprehensive source of information on clinical guidelines written for professionals is the Combined Health Information Database. You will need to limit your search to one of the following: Brochure/Pamphlet, Fact Sheet, or Information Package, and “arthritis” using the “Detailed Search” option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find associations, use the drop boxes at the bottom of the search page where “You may refine your search by.” For the publication date, select “All Years.” Select your preferred language and the format option “Fact Sheet.” Type “arthritis” (or synonyms) into the “For these words:” box. The following is a sample result: ·
Special Report: Arthritis Source: Boston, MA: Harvard Medical School. 1999. 46 p. Contact: Available from Harvard Medical School. Health Publications Group, Department SR, P.O. Box 380, Boston, MA 02117-0380. PRICE: $16.00 plus shipping and handling. Summary: This report provides people who have arthritis with information on the features, diagnosis, and treatment of osteoarthritis (OA), rheumatoid arthritis (RA), and ankylosing spondylitis (AS). The report begins by explaining the difference between arthritis and rheumatism. This is followed by an overview of the joints and the immune system in rheumatic diseases. Topics include types of joints, joint design, the functioning of the immune system, the occurrence of inflammation in arthritis, and the role of genetics. The report then discusses OA, RA, and AS in terms of their evolution, symptoms, possible causes, diagnosis, and treatment. Other seronegative spondyloarthropathies, including Reiter's syndrome, psoriatic arthritis, and enteropathic arthritis, are described. A section of the report is devoted to the diagnosis of rheumatic diseases, focusing on obtaining a medical history; assessing pain and stiffness; conducting a physical examination by observing how the patient moves, examining the joints for abnormalities, and moving the joints through their range of motion to detect pain, resistance, unusual sounds, and instability; and performing studies such as blood tests, radiography, other imaging techniques, and arthrocentesis. Another section focuses on using physical therapy to treat people who have arthritis. Modalities discussed are heat and cold therapy, exercise, diathermy, and transcutaneous electrical nerve stimulation. In addition, the report provides suggestions on living with arthritis. They focus on diet; rest during periods of acute inflammation; exercise; joint protection; and ways of coping with depression, stress, and sexual needs. The report also includes a glossary and a list of resources. 1 appendix and 8 figures.
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North Carolina Arthritis Report 2002 Source: Thurston Arthritis Research Center, University of North Carolina at Chapel Hill. Behavioral Risk Factor Surveillance System, State Center for Health Statistics, 20 p., March 2002.
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Contact: State Center for Health Statistics, Department of Health and Human Services, 1908 Mail Service Center, Raleigh, NC 27699-1908. INTERNET/EMAIL: http://www.schs.state.nc.us/SCHS/about/programs/brfss/; http://www.schs.state.nc.us/SCHS/pdf/arthritis.pdf. Summary: The North Carolina Arthritis Report 2002 describes the prevalence of arthritis in North Carolina, the factors that are associated with increased risk of arthritis, and the impact that arthritis has on quality of life. The report discusses (1) background information, including terminology, used in describing arthritis; (2) the sources of data used in preparing this report; (3) the prevalence of arthritis in North Carolina and comparisons of prevalence with that of the United States; (4) the sociodemographic aspects of arthritis; (5) modifiable risk factors of arthritis; (6) quality-of-life issues of people with arthritis; (7) health care accessibility issues for people with arthritis; (8) cost issues associated with arthritis; and (9) prevention and control of arthritis. Key findings of the report are that 24.8 percent of adult North Carolina residents who responded to the Behavioral Risk Factor Surveillance System survey (BRFSS) in 2000 reported being diagnosed with arthritis by a physician and more than one-third of the respondents reported physician-diagnosed arthritis, chronic joint symptoms, or both, the latter proportion representing more than 2 million adults. When compared to the rest of the United States (37 states participated in the 2000 BRFSS), the prevalence of arthritis in North Carolina was one of the highest in the nation. The two most significant modifiable risk factors for arthritis are excess body weight and physical inactivity. The North Carolina Arthritis Program plans to address the burden of arthritis among state residents through an arthritis marketing and communication campaign to reach health and aging professionals and people with arthritis, their caregivers, and families at all levels of prevention. Other intervention activities include (1) the North Carolina Arthritis Coalition, which is made up of a range of health and aging professionals, people with arthritis and their caregivers, and advocates statewide for improved arthritis care and support; and (2) the Arthritis Self-help Course (ASHC), sponsored by the Arthritis Foundation, that trains people with arthritis to manage their condition and minimize its effects. ASHC is a 6-week course that is usually conducted in a community group setting of about 15 people. It has been shown to be effective in reducing pain by 20 percent and doctor's visits by 40 percent, thus reducing overall health care costs. ·
Reducing the Burden of Arthritis and Other Rheumatic Conditions: Final Report Source: Tallahassee, FL, University of South Florida, 29 p., July 31, 2001. Contact: University of South Florida, College of Public Health, Department of Community and Family Health, 4052 Bald Cypress Way, Bin no. A13, Tallahassee, FL 32399-1721. (850) 245-4100. INTERNET/EMAIL: http://www.doh.state.fl.us/family/arthritis/report.pdf. Summary: Reducing the Burden of Arthritis and Other Rheumatic Conditions: Final Report describes a study that identified determinants of physical activity among Hispanic Americans with arthritis. The intention of the study was to provide a basis for building a social marketing plan to promote physical activity in this group. Seven focus groups in Dade County, Florida, identified determinants of physical activity among Hispanic Americans with arthritis and pretested audio and visual educational materials. Results found that people with arthritis faced significant challenge in staying motivated to combat disability and pain. Some participants cried while talking about such challenges. All believed that people must maintain an optimistic attitude about their condition and not surrender to the disease. Many respondents understood that physical activity and exercise were recommended for people with arthritis, and many considered
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physical activity an important part of daily life. However, they tended to see exercise as burdensome and requiring more time and effort than physical activity. Participants felt motivated to stay physically active by their desire to manage joint pain, minimize stiffness, and avoid becoming disabled. Some believed exercise helped fight depression and improved overall health. They feared causing increased pain during or immediately following exercise. They also feared injuring themselves and worried about lack of time. Some respondents said they were physically unable to exercise and some doubted their ability to exercise safely. Many believed they were more likely to exercise with others than alone. ·
2001-2005 Virginia Arthritis Action Plan (VAAP) Source: Richmond, VA, Virginia Department of Health, 28 p., 2001. Contact: Virginia Department of Health, 1500 East Main Street, Suite 106, Richmond, VA 23219. (804) 225-2255. FAX: (804) 371-6152. INTERNET/EMAIL: http://www.vahealth.org/arthritis/VAAP.pdf;
[email protected]. Summary: Arthritis is one of the most common diseases in the United States. In 2000, it was estimated that 31 percent of Virginia's population reported having arthritis. Arthritis is not just a normal part of aging; the majority of those afflicted are under the age of 65. Some forms of arthritis can be prevented with weight control, physical activity, and precautions to avoid certain occupational and sports injuries. The annual medical and social costs related to arthritis total almost $65 billion nationwide. In 1999, in Virginia, there were 15,833 hospitalizations with arthritis and related diseases as the primary cause. The average charge per hospitalization was nearly $17,000. To combat the burden of arthritis in Virginia, volunteers who make up the Virginia Arthritis Task Force developed the Virginia Arthritis Action Plan to serve as a guiding document of effective steps Virginians can take to prevent, manage, and decrease the burden of arthritis on citizens and their families. Priority areas of the plan include (1) raising awareness about arthritis risk factors, prevention, myths, the importance of early diagnosis, and appropriate treatment and self-management; (2) identifying and implementing programs to support arthritis prevention and control; (3) identifying and implementing policies and health systems infrastructure to support arthritis prevention and control; and (4) collecting, analyzing, interpreting, and reporting on arthritis-related health data and the physical, social, and economic burden of arthritis.
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National Arthritis Action Plan: A Public Health Strategy Source: Atlanta, GA, Arthritis Foundation, 58 p., 1999. Contact: Arthritis Foundation National Office, 1330 West Peachtree Street, Atlanta, GA 30309. (404) 872-7100. www.arthritis.org. Centers for Disease Control an d Prevention, National Center for Chronic Disease Prevention and Health Promotion , Mail Stop K-40, 4770 Buford Highway NE, Atlanta, GA, 30341-3717. (770) 488-5131. EMAIL/INTERNET:
[email protected]. www.cdc.gov/nccdphp. Summary: National Arthritis Action Plan: A Public Health Strategy describes a plan designed to stimulate and strengthen a national, coordinated effort for reducing the occurrence of arthritis and its accompanying disability. The ultimate aims of the plan are to (1) increase public awareness of arthritis as the leading cause of disability and an important public health problem; (2) prevent arthritis whenever possible; (3) promote early diagnosis and appropriate management for people with arthritis to ensure them the maximum number of years of healthy life; (4) minimize preventable pain and disability due to arthritis; (5) support people with arthritis in developing and accessing
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the resources they need to cope with their disease; and (6) ensure that people with arthritis receive the family, peer, and community support they need. The plan focuses on three major areas: (1) Surveillance, epidemiology, and prevention research; (2) communication and education; and (3) programs, policies, and systems. The report is divided into six chapters: (1) Background; (2) strategic framework; (3) surveillance, epidemiology, and prevention research; (4) communication and education; (5) programs, policies, and systems; and (6) implementation. Appendices contain listings of the working group members, state health department reviewers, the partnership network members, and arthritis-related recommendations in the proposed Healthy People 2010 objectives. 37 references.
The NLM Gateway15 The NLM (National Library of Medicine) Gateway is a Web-based system that lets users search simultaneously in multiple retrieval systems at the U.S. National Library of Medicine (NLM). It allows users of NLM services to initiate searches from one Web interface, providing one-stop searching for many of NLM’s information resources or databases.16 To use the NLM Gateway, simply go to the search site at http://gateway.nlm.nih.gov/gw/Cmd. Type “arthritis” (or synonyms) into the search box and click “Search.” The results will be presented in a tabular form, indicating the number of references in each database category. Results Summary Category Journal Articles Books / Periodicals / Audio Visual Consumer Health Meeting Abstracts Other Collections Total
Items Found 137748 2829 737 202 47 141563
HSTAT17 HSTAT is a free, Web-based resource that provides access to full-text documents used in healthcare decision-making.18 These documents include clinical practice guidelines, quickreference guides for clinicians, consumer health brochures, evidence reports and technology assessments from the Agency for Healthcare Research and Quality (AHRQ), as well as AHRQ’s Put Prevention Into Practice.19 Simply search by “arthritis” (or synonyms) at the following Web site: http://text.nlm.nih.gov. Adapted from NLM: http://gateway.nlm.nih.gov/gw/Cmd?Overview.x. The NLM Gateway is currently being developed by the Lister Hill National Center for Biomedical Communications (LHNCBC) at the National Library of Medicine (NLM) of the National Institutes of Health (NIH). 17 Adapted from HSTAT: http://www.nlm.nih.gov/pubs/factsheets/hstat.html. 18 The HSTAT URL is http://hstat.nlm.nih.gov/. 19 Other important documents in HSTAT include: the National Institutes of Health (NIH) Consensus Conference Reports and Technology Assessment Reports; the HIV/AIDS Treatment Information Service (ATIS) resource documents; the Substance Abuse and Mental Health Services Administration's Center for Substance Abuse Treatment (SAMHSA/CSAT) Treatment Improvement Protocols (TIP) and Center for Substance Abuse Prevention (SAMHSA/CSAP) Prevention Enhancement Protocols System (PEPS); the Public Health Service (PHS) Preventive Services Task Force's Guide to Clinical Preventive Services; the independent, nonfederal Task Force on Community 15 16
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Coffee Break: Tutorials for Biologists20 Coffee Break is a general healthcare site that takes a scientific view of the news and covers recent breakthroughs in biology that may one day assist physicians in developing treatments. Here you will find a collection of short reports on recent biological discoveries. Each report incorporates interactive tutorials that demonstrate how bioinformatics tools are used as a part of the research process. Currently, all Coffee Breaks are written by NCBI staff.21 Each report is about 400 words and is usually based on a discovery reported in one or more articles from recently published, peer-reviewed literature.22 This site has new articles every few weeks, so it can be considered an online magazine of sorts. It is intended for general background information. You can access the Coffee Break Web site at the following hyperlink: http://www.ncbi.nlm.nih.gov/Coffeebreak/.
Other Commercial Databases In addition to resources maintained by official agencies, other databases exist that are commercial ventures addressing medical professionals. Here are some examples that may interest you: ·
CliniWeb International: Index and table of contents to selected clinical information on the Internet; see http://www.ohsu.edu/cliniweb/.
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Medical World Search: Searches full text from thousands of selected medical sites on the Internet; see http://www.mwsearch.com/.
The Genome Project and Arthritis In the following section, we will discuss databases and references which relate to the Genome Project and arthritis.
Online Mendelian Inheritance in Man (OMIM) The Online Mendelian Inheritance in Man (OMIM) database is a catalog of human genes and genetic disorders authored and edited by Dr. Victor A. McKusick and his colleagues at Johns Hopkins and elsewhere. OMIM was developed for the World Wide Web by the National Center for Biotechnology Information (NCBI).23 The database contains textual information, pictures, and reference information. It also contains copious links to NCBI’s Entrez database of MEDLINE articles and sequence information. Services’ Guide to Community Preventive Services; and the Health Technology Advisory Committee (HTAC) of the Minnesota Health Care Commission (MHCC) health technology evaluations. 20 Adapted from http://www.ncbi.nlm.nih.gov/Coffeebreak/Archive/FAQ.html. 21 The figure that accompanies each article is frequently supplied by an expert external to NCBI, in which case the source of the figure is cited. The result is an interactive tutorial that tells a biological story. 22 After a brief introduction that sets the work described into a broader context, the report focuses on how a molecular understanding can provide explanations of observed biology and lead to therapies for diseases. Each vignette is accompanied by a figure and hypertext links that lead to a series of pages that interactively show how NCBI tools and resources are used in the research process. 23 Adapted from http://www.ncbi.nlm.nih.gov/. Established in 1988 as a national resource for molecular biology information, NCBI creates public databases, conducts research in computational biology, develops software tools for analyzing genome data, and disseminates biomedical information--all for the better understanding of molecular processes affecting human health and disease.
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To search the database, go to http://www.ncbi.nlm.nih.gov/Omim/searchomim.html. Type “arthritis” (or synonyms) into the search box, and click “Submit Search.” If too many results appear, you can narrow the search by adding the word “clinical.” Each report will have additional links to related research and databases. In particular, the option “Database Links” will search across technical databases that offer an abundance of information. The following is an example of the results you can obtain from the OMIM for arthritis: ·
Arteritis, Familial Granulomatous, with Juvenile Polyarthritis Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?108050
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Arthritis, Sacroiliac Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?108100
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Histiocytic Dermatoarthritis Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?142730
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Osteoarthritis Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?165720
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Osteoarthritis of Distal Interphalangeal Joints Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?140600
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Psoriatic Arthritis, Susceptibility To, 1 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?607507
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Pyogenic Sterile Arthritis, Pyoderma Gangrenosum, and Acne Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?604416
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Rheumatoid Arthritis Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?180300
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Rheumatoid Arthritis, Systemic Juvenile Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?604302
Genes and Disease (NCBI - Map) The Genes and Disease database is produced by the National Center for Biotechnology Information of the National Library of Medicine at the National Institutes of Health. This Web site categorizes each disorder by system of the body. Go to http://www.ncbi.nlm.nih.gov/disease/, and browse the system pages to have a full view of important conditions linked to human genes. Since this site is regularly updated, you may wish to revisit it from time to time. The following systems and associated disorders are addressed: ·
Cancer: Uncontrolled cell division. Examples: Breast and ovarian cancer, Burkitt lymphoma, chronic myeloid leukemia, colon cancer, lung cancer, malignant melanoma, multiple endocrine neoplasia, neurofibromatosis, p53 tumor suppressor, pancreatic cancer, prostate cancer, Ras oncogene, RB: retinoblastoma, von Hippel-Lindau syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Cancer.html
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Immune System: Fights invaders. Examples: Asthma, autoimmune polyglandular syndrome, Crohn’s disease, DiGeorge syndrome, familial Mediterranean fever, immunodeficiency with Hyper-IgM, severe combined immunodeficiency. Web site: http://www.ncbi.nlm.nih.gov/disease/Immune.html
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·
Metabolism: Food and energy. Examples: Adreno-leukodystrophy, atherosclerosis, Best disease, Gaucher disease, glucose galactose malabsorption, gyrate atrophy, juvenile-onset diabetes, obesity, paroxysmal nocturnal hemoglobinuria, phenylketonuria, Refsum disease, Tangier disease, Tay-Sachs disease. Web site: http://www.ncbi.nlm.nih.gov/disease/Metabolism.html
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Muscle and Bone: Movement and growth. Examples: Duchenne muscular dystrophy, Ellis-van Creveld syndrome, Marfan syndrome, myotonic dystrophy, spinal muscular atrophy. Web site: http://www.ncbi.nlm.nih.gov/disease/Muscle.html
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Nervous System: Mind and body. Examples: Alzheimer disease, amyotrophic lateral sclerosis, Angelman syndrome, Charcot-Marie-Tooth disease, epilepsy, essential tremor, fragile X syndrome, Friedreich’s ataxia, Huntington disease, Niemann-Pick disease, Parkinson disease, Prader-Willi syndrome, Rett syndrome, spinocerebellar atrophy, Williams syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Brain.html
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Signals: Cellular messages. Examples: Ataxia telangiectasia, Cockayne syndrome, glaucoma, male-patterned baldness, SRY: sex determination, tuberous sclerosis, Waardenburg syndrome, Werner syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Signals.html
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Transporters: Pumps and channels. Examples: Cystic fibrosis, deafness, diastrophic dysplasia, Hemophilia A, long-QT syndrome, Menkes syndrome, Pendred syndrome, polycystic kidney disease, sickle cell anemia, Wilson’s disease, Zellweger syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Transporters.html
Entrez Entrez is a search and retrieval system that integrates several linked databases at the National Center for Biotechnology Information (NCBI). These databases include nucleotide sequences, protein sequences, macromolecular structures, whole genomes, and MEDLINE through PubMed. Entrez provides access to the following databases: ·
3D Domains: Domains from Entrez Structure, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=geo
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Books: Online books, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=books
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Genome: Complete genome assemblies, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Genome
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NCBI’s Protein Sequence Information Survey Results: Web site: http://www.ncbi.nlm.nih.gov/About/proteinsurvey/
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Nucleotide Sequence Database (Genbank): Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Nucleotide
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OMIM: Online Mendelian Inheritance in Man, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=OMIM
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PopSet: Population study data sets, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Popset
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ProbeSet: Gene Expression Omnibus (GEO), Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=geo
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Protein Sequence Database: Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Protein
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PubMed: Biomedical literature (PubMed), Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed
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Structure: Three-dimensional macromolecular structures, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Structure
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Taxonomy: Organisms in GenBank, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Taxonomy
To access the Entrez system at the National Center for Biotechnology Information, go to http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=search&DB=genome, and then select the database that you would like to search. The databases available are listed in the drop box next to “Search.” Enter “arthritis” (or synonyms) into the search box and click “Go.”
Jablonski’s Multiple Congenital Anomaly/Mental Retardation (MCA/MR) Syndromes Database24 This online resource has been developed to facilitate the identification and differentiation of syndromic entities. Special attention is given to the type of information that is usually limited or completely omitted in existing reference sources due to space limitations of the printed form. At http://www.nlm.nih.gov/mesh/jablonski/syndrome_toc/toc_a.html, you can search across syndromes using an alphabetical index. Search by keywords at http://www.nlm.nih.gov/mesh/jablonski/syndrome_db.html. The Genome Database25 Established at Johns Hopkins University in Baltimore, Maryland in 1990, the Genome Database (GDB) is the official central repository for genomic mapping data resulting from the Human Genome Initiative. In the spring of 1999, the Bioinformatics Supercomputing Centre (BiSC) at the Hospital for Sick Children in Toronto, Ontario assumed the management of GDB. The Human Genome Initiative is a worldwide research effort focusing on structural analysis of human DNA to determine the location and sequence of the estimated 100,000 human genes. In support of this project, GDB stores and curates data generated by researchers worldwide who are engaged in the mapping effort of the Human Genome Project (HGP). GDB’s mission is to provide scientists with an encyclopedia of the human genome which is continually revised and updated to reflect the current state of scientific knowledge. Although GDB has historically focused on gene mapping, its focus will 24 Adapted from the National Library of Medicine: http://www.nlm.nih.gov/mesh/jablonski/about_syndrome.html. 25 Adapted from the Genome Database: http://gdbwww.gdb.org/gdb/aboutGDB.html - mission.
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broaden as the Genome Project moves from mapping to sequence, and finally, to functional analysis. To access the GDB, simply go to the following hyperlink: http://www.gdb.org/. Search “All Biological Data” by “Keyword.” Type “arthritis” (or synonyms) into the search box, and review the results. If more than one word is used in the search box, then separate each one with the word “and” or “or” (using “or” might be useful when using synonyms).
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APPENDIX B. PATIENT RESOURCES Overview Official agencies, as well as federally funded institutions supported by national grants, frequently publish a variety of guidelines written with the patient in mind. These are typically called “Fact Sheets” or “Guidelines.” They can take the form of a brochure, information kit, pamphlet, or flyer. Often they are only a few pages in length. Since new guidelines on arthritis can appear at any moment and be published by a number of sources, the best approach to finding guidelines is to systematically scan the Internet-based services that post them.
Patient Guideline Sources The remainder of this chapter directs you to sources which either publish or can help you find additional guidelines on topics related to arthritis. Due to space limitations, these sources are listed in a concise manner. Do not hesitate to consult the following sources by either using the Internet hyperlink provided, or, in cases where the contact information is provided, contacting the publisher or author directly.
The National Institutes of Health The NIH gateway to patients is located at http://health.nih.gov/. From this site, you can search across various sources and institutes, a number of which are summarized below.
Topic Pages: MEDLINEplus The National Library of Medicine has created a vast and patient-oriented healthcare information portal called MEDLINEplus. Within this Internet-based system are “health topic pages” which list links to available materials relevant to arthritis. To access this system, log on to http://www.nlm.nih.gov/medlineplus/healthtopics.html. From there you can either search using the alphabetical index or browse by broad topic areas. Recently, MEDLINEplus listed the following when searched for “arthritis”:
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Guides on arthritis Arthritis http://www.nlm.nih.gov/medlineplus/arthritis.html
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Other Guides Ankle Injuries and Disorders http://www.nlm.nih.gov/medlineplus/ankleinjuriesanddisorders.html Arthritis http://www.nlm.nih.gov/medlineplus/arthritis.html Foot Injuries and Disorders http://www.nlm.nih.gov/medlineplus/footinjuriesanddisorders.html Gout and Pseudogout http://www.nlm.nih.gov/medlineplus/goutandpseudogout.html Juvenile Rheumatoid Arthritis http://www.nlm.nih.gov/medlineplus/juvenilerheumatoidarthritis.html Osteoarthritis http://www.nlm.nih.gov/medlineplus/osteoarthritis.html Rheumatoid Arthritis http://www.nlm.nih.gov/medlineplus/rheumatoidarthritis.html
Within the health topic page dedicated to arthritis, the following was listed: ·
General/Overviews Juvenile Rheumatoid Arthritis Source: Nemours Foundation http://kidshealth.org/kid/health_problems/bone/juv_rheum_arthritis.html Juvenile Rheumatoid Arthritis (JRA) Source: Arthritis Foundation http://www.arthritis.org/conditions/DiseaseCenter/jra.asp
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Diagnosis/Symptoms Antinuclear Antibody Test Source: American Association for Clinical Chemistry http://www.labtestsonline.org/understanding/analytes/ana/test.html Rheumatoid Factor Source: American Association for Clinical Chemistry http://www.labtestsonline.org/understanding/analytes/rheumatoid/test.html
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Treatment 2003 Drug Guide Source: Arthritis Foundation http://www.arthritis.org/conditions/DrugGuide/default.asp
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Arthritis: Timely Treatments for an Ageless Disease Source: Food and Drug Administration http://www.fda.gov/fdac/features/2000/300_arth.html Help Your Arthritis Treatment Work http://www.fda.gov/opacom/lowlit/arthrtis.html Kids Need Medications, Too Source: Arthritis Foundation http://www.arthritis.org/conditions/DrugGuide/kids.asp Methotrexate Source: American Academy of Family Physicians http://familydoctor.org/handouts/628.html ·
Coping Coping with Juvenile Rheumatoid Arthritis Source: American Academy of Orthopaedic Surgeons http://orthoinfo.aaos.org/fact/thr_report.cfm?Thread_ID=301&topcategory=Pedia trics&all=all Dealing with Emotional Issues Source: Arthritis Foundation http://www.arthritis.org/communities/juvenile_arthritis/emotions.asp School Success Source: Arthritis Foundation http://www.arthritis.org/resources/school_success.asp
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Specific Conditions/Aspects Dental Care Source: Arthritis Foundation http://www.arthritis.org/conditions/dentalcare.asp Eye Care Source: Arthritis Foundation http://www.arthritis.org/conditions/DiseaseCenter/JRA/treated_eye_dental_diet .asp Financial Assistance Source: Arthritis Foundation http://www.arthritis.org/communities/juvenile_arthritis/financial.asp Juvenile Arthritis - Other Types and Related Conditions Source: Arthritis Foundation http://www.arthritis.org/conditions/DiseaseCenter/ja_other.asp Juvenile Enteropathic Arthritis Source: Arthritis Foundation http://www.arthritis.org/conditions/diseasecenter/juvenileenteropathicarthritis.a sp Juvenile Reactive Arthritis Source: Arthritis Foundation http://www.arthritis.org/conditions/diseasecenter/juvenilereactivearthritis.asp
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Pauciarticular JRA Source: Arthritis Foundation http://www.arthritis.org/conditions/diseasecenter/pauciarticularJRA.asp Polyarticular JRA Source: Arthritis Foundation http://www.arthritis.org/conditions/diseasecenter/polyarticularJRA.asp Systemic Onset JRA Source: Arthritis Foundation http://www.arthritis.org/conditions/diseasecenter/systemiconsetJRA.asp ·
From the National Institutes of Health Questions and Answers About Juvenile Rheumatoid Arthritis Source: National Institute of Arthritis and Musculoskeletal and Skin Diseases http://www.niams.nih.gov/hi/topics/juvenile_arthritis/juvarthr.htm
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Law and Policy Federal Laws That Can Help Source: Arthritis Foundation http://www.arthritis.org/communities/juvenile_arthritis/federallaws.asp
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Organizations American College of Rheumatology http://www.rheumatology.org/ Arthritis Foundation http://www.arthritis.org/ National Institute of Arthritis and Musculoskeletal and Skin Diseases http://www.niams.nih.gov/
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Research Pain of Juvenile Arthritis May Reduce School and Social Activity Source: National Institute of Arthritis and Musculoskeletal and Skin Diseases http://www.niams.nih.gov/ne/highlights/spotlight/2003/pain-juvenile.htm Progress and Opportunities in Juvenile Arthritis Source: Arthritis Foundation http://www.arthritis.org/research/research_program/Juvenile_Arthritis/default.a sp
You may also choose to use the search utility provided by MEDLINEplus at the following Web address: http://www.nlm.nih.gov/medlineplus/. Simply type a keyword into the search box and click “Search.” This utility is similar to the NIH search utility, with the exception that it only includes materials that are linked within the MEDLINEplus system (mostly patient-oriented information). It also has the disadvantage of generating unstructured results. We recommend, therefore, that you use this method only if you have a very targeted search.
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The Combined Health Information Database (CHID) CHID Online is a reference tool that maintains a database directory of thousands of journal articles and patient education guidelines on arthritis. CHID offers summaries that describe the guidelines available, including contact information and pricing. CHID’s general Web site is http://chid.nih.gov/. To search this database, go to http://chid.nih.gov/detail/detail.html. In particular, you can use the advanced search options to look up pamphlets, reports, brochures, and information kits. The following was recently posted in this archive: ·
Handout on Health: Osteoarthritis Source: Bethesda, MD: National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Information Clearinghouse. 2002. 40 p. Contact: Available from National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Information Clearinghouse. 1 AMS Circle, Bethesda, MD 20892-3675. (877) 226-4267 toll-free or (301) 495-4484. Fax (301) 718-6366. TTY (301) 565-2966. E-mail:
[email protected]. Website: www.niams.nih.gov. PRICE: 1 to 25 copies free. Order Number: AR-250 HH (booklet), or AR-250L HH (large print fact sheet). Summary: This booklet uses a question and answer format to provide people who have osteoarthritis (OA) with information on the symptoms, diagnosis, and treatment of this degenerative joint disease. OA, which mostly affects the cartilage, causes pain, stiffness, swelling, and loss of motion of the joint. OA occurs most often in the hands, knees, hips, or spine. The disease affects more than 20 million people in the United States, and by 2030, about 70 million Americans will be at risk for OA. It is one of the most frequent causes of physical disability among adults, particularly those age 65 or older. Although the exact cause of OA is unknown, scientists suspect a combination of factors, including excess weight, the aging process, joint injury, and stresses on the joints from certain jobs and sports activities. In addition to physical problems, OA can affect finances and lifestyles. Diagnosis is based on clinical history, a physical examination, and tests. The goals of treatment are to improve joint care, maintain an acceptable body weight, control pain, and achieve a healthy lifestyle. OA treatment plans can involve exercise; rest and joint care; pain relief; weight control; medications such as acetaminophen, nonsteroidal antiinflammatory drugs, topical pain relievers, mild narcotic painkillers, corticosteroids, and hyaluronic acid; surgery; and nontraditional treatment approaches such as acupuncture, folk remedies, and nutritional supplements. Self care is the foundation of successful management of the pain and disability of OA. Programs that help people learn about OA, learn self care, and maintain a positive attitude include patient education programs, arthritis self management programs, and arthritis support groups. Regular exercise is also important in self care and wellness. The booklet describes the keys areas of OA research being supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases and other components of the National Institutes of Health, including animal models, diagnostic tools, genetic studies, tissue engineering, comprehensive treatment strategies, new drug therapies, and nutritional supplements. The booklet includes a list of additional resources as well. 4 figures.
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Questions and Answers About Reactive Arthritis Source: Bethesda, MD: National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Information Clearinghouse. 2002. 24 p. Contact: Available from National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Information Clearinghouse. 1 AMS Circle, Bethesda, MD 20892-3675.
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(877) 226-4267 toll-free or (301) 495-4484. Fax (301) 718-6366. TTY (301) 565-2966. E-mail:
[email protected]. Website: www.niams.nih.gov. PRICE: 1 to 25 copies free. Order Number: AR-253 QA (booklet), or AR-253L QA (large print fact sheet). Summary: This booklet uses a question and answer format to provide people who have reactive arthritis with information about the causes, symptoms, diagnosis, and treatment of this form of arthritis, which occurs as a reaction to an infection elsewhere in the body. Reactive arthritis, or Reiter's syndrome, usually begins 1 to 3 weeks after infection. Chlamydia trachomatis, the bacterium most often associated with reactive arthritis, is usually acquired through sexual contact. Infections in the digestive tract caused by Salmonella, Shigella, Yersinia, and Campylobacter may also trigger reactive arthritis. A genetic factor, human leukocyte antigen, increases the risk of developing reactive arthritis. Although reactive arthritis itself is not contagious, the bacteria that trigger it can be passed from person to person. Men aged 20 to 40 are most likely to develop reactive arthritis. Symptoms include inflammation of the urogenital tract, the joints, and the eyes. Mouth ulcers and skin rashes are less common symptoms. Diagnosis is based on clinical presentation, laboratory tests, and imaging studies. There is no cure for reactive arthritis, but some treatments relieve symptoms. Treatment options include nonsteroidal antiinflammatory drugs, corticosteroid injections, topical corticosteroids, antibiotics, immunosuppressive medicines, tumor necrosis factor inhibitors, and exercise. Most people with reactive arthritis recover fully within 2 to 6 months after the first symptoms appear. Researchers are investigating the causes and treatments for reactive arthritis. The booklet identifies sources of additional information and provides a glossary of medical terms. ·
Questions and Answers About Arthritis and Rheumatic Diseases Source: Bethesda, MD: National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Information Clearinghouse. 2002. 40 p. Contact: Available from National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Information Clearinghouse. 1 AMS Circle, Bethesda, MD 20892-3675. (877) 226-4267 or (301) 495-4484. Fax (301) 718-6366. TTY (301) 565-2966. E-mail:
[email protected]. Website: www.niams.nih.gov. PRICE: 1 to 25 copies free. Order Number: AR-27 QA (booklet), or AR-27L QA (large print). Summary: This booklet uses a question and answer format to provide people who have arthritis and other rheumatic diseases with information on their causes, symptoms, diagnosis, and treatment. Rheumatic diseases cause pain, stiffness, and swelling in joints and other supporting structures of the body. Although many people use arthritis to refer to all rheumatic diseases, the many types of arthritis comprise only a portion of the rheumatic diseases. Examples of rheumatic diseases include osteoarthritis (OA), rheumatic arthritis (RA), fibromyalgia, systemic lupus erythematosus, scleroderma, juvenile rheumatoid arthritis, ankylosing spondylitis, gout, infectious arthritis, reactive arthritis, psoriatic arthritis, bursitis, and tendinitis. The causes of rheumatic disease depend on the type of disease, and the causes of most rheumatic diseases are still being investigated. Common symptoms of arthritis include joint swelling, pain, and stiffness. Diagnosis of rheumatic diseases involves obtaining a medical history, performing a physical examination, and obtaining laboratory tests and X rays or other imaging tests. Common laboratory tests include various blood tests, arthrocentesis, and urinalysis. Treatment options for arthritis include rest and relaxation; exercise; proper diet; medications such as analgesics, nonsteroidal anti-inflammatory drugs, acetaminophen, and corticosteroids; heat and cold therapies; hydrotherapy; mobilization therapy; relaxation therapy; orthotic devices; and surgery. The National Institute of Arthritis and
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Musculoskeletal and Skin Diseases currently supports research efforts in RA, OA, lupus, and scleroderma. The fact sheet includes a list of additional sources of information and a list of key words to help readers understand the terms used in the fact sheet. ·
Questions and Answers About Arthritis Pain Source: Bethesda, MD: National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Information Clearinghouse. 2001. 24 p. Contact: Available from National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Information Clearinghouse. 1 AMS Circle, Bethesda, MD 20892-3675. (877) 226-4267 or (301) 495-4484. Fax (301) 718-6366. TTY (301) 565-2966. E-mail:
[email protected]. Website: www.niams.nih.gov. PRICE: 1 to 25 copies free. Order Number: AR-188QA (booklet), or AR-188L QA (large print). Summary: This fact sheet for people with arthritis uses a question and answer format to provide information about arthritis pain. It explains that arthritis refers to a group of more than 100 rheumatic diseases that can cause joint pain, stiffness, and swelling, and that they may affect parts of the body other than joints. The fact sheet discusses the various causes of pain, how pain varies from individual to individual, how doctors work with patients to help guide treatment, and the drug and nondrug treatment options for both short-and long-term relief. Also described are alternative therapies that may help patients cope with the stress of living with arthritis, including being an active participant in pain management and substituting distraction for pain. The fact sheet also discusses current research supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases on arthritis pain. It then refers the reader to four voluntary health organizations for additional information about arthritis. A large print version of this fact sheet is also available.
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Questions and Answers About Arthritis and Exercise Source: Bethesda, MD: National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Information Clearinghouse. 2001. 24 p. Contact: Available from National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Information Clearinghouse. 1 AMS Circle, Bethesda, MD 20892-3675. (877) 226-4267 or (301) 495-4484. Fax (301) 718-6366. TTY (301) 565-2966. E-mail:
[email protected]. Website: www.niams.nih.gov. PRICE: 1 to 25 copies free. Order Number: AR-103QA (booklet), or AR-103L QA (large print). Summary: This fact sheet for people with arthritis uses a question and answer format to provide information about the inclusion of exercise in an arthritis treatment plan. Individuals with arthritis should exercise because it reduces joint pain and stiffness and increases flexibility, muscle strength, and endurance. The best types of exercise for people with arthritis include range-of-motion, strengthening, and aerobic exercises. The fact sheet offers guidelines for starting an exercise program and outlines how often various types of exercises should be performed. It explains what type of strengthening program is best, the signs of too much exercise, and the amount of rest needed during general or local flares. The fact sheet also describes various methods of pain relief including moist heat, cold, hydrotherapy, mobilization therapies, transcutaneous electrical nerve stimulation, biofeedback, relaxation therapy, and acupuncture. It also discusses current research on arthritis and exercise. The fact sheet lists four sources for additional information. A large print version of this fact sheet is also available.
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Questions and Answers About Juvenile Rheumatoid Arthritis Source: Bethesda, MD: National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Information Clearinghouse. 2001. 24 p. Contact: Available from National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Information Clearinghouse. 1 AMS Circle, Bethesda, MD 20892-3675. (877) 226-4267 or (301) 495-4484. Fax (301) 718-6366. TTY (301) 565-2966. E-mail:
[email protected]. Website: www.niams.nih.gov. PRICE: 1 to 25 copies free. Order Number: AR-112QA (booklet), or AR-112L QA (large print). Summary: This fact sheet for children with juvenile rheumatoid arthritis (JRA) and their families uses a question and answer format to provide information. JRA is described as an autoimmune disorder, the most common type of arthritis to affect children, and different from adult rheumatoid arthritis in that, unlike adults, many children outgrow the illness. The fact sheet discusses the most common symptoms of JRA, when they occur, and that children with JRA may look different because of growth problems and the effects of medication. Also explained are diagnostic procedures and treatments including medications such as nonsteroidal anti-inflammatory drugs, disease-modifying antirheumatic drugs, methotrexate, and corticosteroids. Family support is emphasized, as is the importance of exercise to reduce the symptoms of JRA and maintain joint function and range of motion. Current research on the causes and treatments for JRA is also described, including information about a research registry for families in which two or more siblings have JRA. Readers can get additional information about JRA from the voluntary health organizations listed. A large print version of this fact sheet is also available.
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Inside Look at Osteoarthritis, An Source: South Deerfield, MA: Channing L. Bete Co., Inc. 2000. 16 p. Contact: Available from Channing L. Bete Co., Inc. 200 State Road, South Deerfield, MA 01373-0200. (800) 628-7733. Fax (800) 499-6464. E-mail:
[email protected]. PRICE: Contact company for pricing information; available in bulk. Order Number 75324A-02-00. Summary: This illustrated booklet provides people who have osteoarthritis (OA) with an overview of this common degenerative form of arthritis. OA causes morning joint stiffness; joint pain during or after use; a crackling sound or grating sensation during use; and joint tenderness, redness, or swelling. Risk factors for OA include age, heredity, overuse, excess weight, and a previous injury to a bone or joint. Joints commonly affected by OA include the hand, spine, hip, knee, and foot. The booklet describes the anatomy of a normal joint and explains how OA slowly damages joints. Other topics include taking various prescription and nonprescription medications to relieve pain; using heat or cold, massage, relaxation techniques, and complementary therapies to ease pain and stiffness; and undergoing surgery to repair joints. In addition, the booklet discusses the importance of exercise in managing OA, provides examples of good body mechanics to help protect joints, and identifies supportive devices and tools.
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Basal Joint Arthritis Source: San Bruno, CA: StayWell Company. 2000. 6 p. Contact: Available from StayWell Company. 1100 Grundy Lane, San Bruno, CA 940663030. (800) 333-3032. Website: www.staywell.com. PRICE: Call or write for current pricing on single and bulk orders.
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Summary: This illustrated brochure provides people who have arthritis with information on the causes, symptoms, and treatment of basal joint arthritis. This type of arthritis, which affects the joint at the base of the thumb, occurs as a result of wear and tear on the joint. The most common symptom is pain in the lower part of the thumb. Diagnosis is based on a physical examination. X rays can provide information on the amount of joint destruction. Treatments can be nonsurgical or surgical. Nonsurgical treatments are splints and medications. If nonsurgical treatments do not relieve pain and stiffness, or if the joint has been destroyed, a tendon graft can be used to rebuild it. Following surgery, the patient undergoes physical therapy to strengthen the muscles and make the joint more flexible. 2 figures. ·
Help Your Arthritis Treatment Work Source: US Food and Drug Administration. May 2000. 12 p. Contact: Available from US Food and Drug Administration. 5600 Fishers Lane (HFI-40) Rockville, MD 20857. Website: www.fda.gov. Summary: This brochure provides an overview of treatment methods for managing joint pain and stiffness in patients with arthritis. Doctors may prescribe medicine or suggest a nonprescription medication to help control joint pain. The patient should inform the doctor about any previous adverse reactions to medications. The doctor should advise the patient on the dosage, special instructions, and side effects of the medication. It is important for patients to read labels of nonprescription medications as they may contain pain killers that are already being taken for arthritis. The patient should discuss health foods and supplements as arthritis cures with their doctor. It is important to rest when arthritis is worse. Exercise can alleviate pain and help the patient sleep better. If all other treatments fail it may be necessary to have surgery.
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Understanding Psoriatic Arthritis Source: National Psoriasis Foundation. 200x. 10 p. Contact: Available from National Psoriasis Foundation. 6600 SW 92nd Avenue, Suite 300, Portland, OR 97223-7195. (800) 723-9166. Website: www.psoriasis.org. Summary: This brochure provides patients with an overview of psoriatic arthritis (PA), a chronic condition that causes pain, swelling, and stiffness in the joints. PA can be mild, involving few joints and minor pain, or severe, involving more joints and severe pain. Most patients that develop PA already have psoriasis. Although PA cannot be cured, it can be effectively managed using medications, exercise, splinting, surgery, other forms of therapy, or a combination of these methods. NSAIDs and DMARDs are used to control pain and swelling. Biologic drugs are used generally when other forms of treatment have not been effective and work by blocking the response of the immune system to prevent the effects of arthritis.
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Managing Your Arthritis [Information Package] Source: Shawnee Mission, KS: Searle, The Movement for Motion Program. 1999. [packet of 8 booklets]. Contact: Available from Searle, The Movement for Motion Program. P.O. Box 29278, Shawnee Mission, KS 66201-9686. (877) 732-7531 ext. 108. Website: www.arthritisconnection.com. PRICE: Single copy free.
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Summary: This information packet, which consists of numerous booklets, provides people who have arthritis with information on comfortably performing daily activities, developing a strong working relationship with their doctor and other health care professionals, being active in their own treatment, and maintaining good interpersonal relationships. Booklets that focus on living more comfortably with arthritis help people learn about various tools and techniques they can use to help make living with arthritis easier, including good body mechanics to conserve energy and use joints wisely. It is also important to be efficient, use assistive devices, and get adequate sleep and exercise. The booklet on developing a good doctor patient relationship offers tips on how to make each office visit valuable and presents a reproducible form that can be taken to each office visit so the patient remembers topics he or she would like to discuss. The booklets on self care provide guidelines on healthy eating, exercising, and making the most of arthritis care resources. The booklet dealing with interpersonal relations explains how to educate loved ones and others about arthritis and to interact with others. A final booklet describes the differences between osteoarthritis and rheumatoid arthritis and discusses the use of medications, diet, and exercise to manage arthritis. ·
Foot Care: Arthritis Source: San Bruno, CA: StayWell Company. 1999. 6 p. Contact: Available from StayWell Company. 1100 Grundy Lane, San Bruno, CA 940663030. (800) 333-3032. Website: www.staywell.com. PRICE: Call or write for current pricing on single and bulk orders. Summary: This illustrated brochure provides people who have arthritis with information on its effect on the feet. Many people develop arthritis in their feet. It can affect the big toe, midfoot, or rear foot joints; the joint where the ankle and foot meet; and other nearby joints. Diagnosis is based on information obtained through a medical history, a physical examination, and imaging tests. Treatment options include various medications and surgery to trim or fuse joints. After surgery, the foot will most likely be bandaged and immobilized for a while.
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Managing Your Arthritis for Life Source: Midland, MI: Health Enhancement Systems. 1999. 8 p. Contact: Available from Health Enhancement Systems. P.O. Box 1035, Midland, MI 48641-1035. (800) 326-2317. Fax (517) 839-0025. PRICE: Bulk prices starting at $0.98 each for 10-50, plus shipping and handling. Item No. HESAR-5. Summary: This brochure provides people who have arthritis with information on making arthritis management a permanent part of their life. The brochure begins by explaining how readers can determine whether lapses in arthritis management are just a momentary slip or a more serious cause for concern. This is followed by information on staying focused on arthritis management, renewing one's commitment to arthritis management, balancing one's life, and finding new ways to build even more healthy changes into one's life. Readers answer questions or complete written statements to determine how well they are managing their arthritis. The brochure includes a list of helpful organizations.
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Thinking About Managing Your Arthritis Source: Midland, MI: Health Enhancement Systems. 1999. 4 p.
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Contact: Available from Health Enhancement Systems. P.O. Box 1035, Midland, MI 48641-1035. (800) 326-2317. Fax (517) 839-0025. PRICE: Bulk prices starting at $0.68 each for 10-50, plus shipping and handling. Item No. HESAR-1. Summary: This brochure guides people through the process of thinking about managing their arthritis. The brochure begins by describing the features of osteoarthritis and rheumatoid arthritis and explaining what arthritis management means. This is followed by a series of questions that help readers think about arthritis management. The brochure also includes a list of helpful organizations. ·
Benefits of Managing Arthritis, The Source: Midland, MI: Health Enhancement Systems. 1999. 8 p. Contact: Available from Health Enhancement Systems. P.O. Box 1035, Midland, MI 48641-1035. (800) 326-2317. Fax (517) 839-0025. PRICE: Bulk prices starting at $0.98 each for 10-50, plus shipping and handling. Item No. HESAR-2. Summary: This brochure provides people who have arthritis with information on the benefits of arthritis management. The brochure begins by identifying the risk factors that people can and cannot control and describing the features of osteoarthritis and rheumatoid arthritis. This is followed by information on the advantages of managing arthritis and the benefits of keeping a record of arthritis symptoms. In addition, the brochure presents several scenes that readers can reflect upon to help them manage their arthritis, provides sample questions that readers can answer to learn about their arthritis and how to control it, and explains the importance of finding supportive people. The brochure also includes a list of helpful organizations.
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Preparing To Manage Your Arthritis Source: Midland, MI: Health Enhancement Systems. 1999. 16 p. Contact: Available from Health Enhancement Systems. P.O. Box 1035, Midland, MI 48641-1035. (800) 326-2317. Fax (517) 839-0025. PRICE: Bulk prices starting at $1.96 each for 10-50 plus, shipping and handling. Item No. HESAR-3. Summary: This brochure provides people with information on preparing to manage their arthritis. The brochure includes activities that readers complete to learn and practice the skills they need for arthritis management. The brochure begins by outlining the advantages of managing arthritis, identifying the risk factors that people can and cannot control, and presenting questions readers can ask themselves to help learn about their arthritis and its management. This is followed by steps people who have arthritis can take to achieve a healthier life. In addition, the brochure presents ideas to relieve symptoms through lifestyle changes, among them eating wisely, staying active, taking a stress break, resting, performing an enjoyable activity, keeping a journal, and checking out special aids. Other topics include managing pain; taking medication; putting an arthritis management plan into motion; and identifying specific, measurable, achievable, relevant, and trackable goals. The brochure also includes an arthritis log and a list of helpful organizations.
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Feeling Good About Managing Your Arthritis Source: Midland, MI: Health Enhancement Systems. 1999. 8 p.
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Contact: Available from Health Enhancement Systems. P.O. Box 1035, Midland, MI 48641-1035. (800) 326-2317. Fax (517) 839-0025. PRICE: Bulk prices starting at $0.98 each for 10-50, plus shipping and handling. Item No. HESAR-4. Summary: This brochure provides people who have arthritis with information on feeling good about managing their arthritis. The brochure begins by presenting ideas to help readers make exercise a part of each day, find time for 20 minute stress breaks twice a day, make eating wisely a part of life, deal with medication problems, and cope with increasing pain. This is followed by information on establishing goals that are specific, measurable, achievable, relevant, and trackable. Other topics include ways to reward oneself for working to control one's arthritis. The brochure includes a personal wellness contract and a list of helpful organizations. ·
Handout on Health: Rheumatoid Arthritis Source: Bethesda, MD: National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Information Clearinghouse. 1998. 36 p. Contact: Available from National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Information Clearinghouse. 1 AMS Circle, Bethesda, MD 20892-3675. (877) 226-4267 or (301) 495-4484. Fax (301) 718-6366. TTY (301) 565-2966. E-mail:
[email protected]. Website: www.niams.nih.gov. PRICE: 1 to 25 copies free. Order Number: AR-13HH (booklet), or AR-13L HH (large print). Summary: This booklet is for people with rheumatoid arthritis (RA), family members, friends, and others and focuses on the features, progression, causes, diagnosis, and treatment of RA. It discusses the prevalence of the disease, the factors that may have a role in its development, how it differs from other kinds of arthritis, and its progression in the cartilage and bone within the joint. The booklet also explains how a doctor makes a diagnosis, the treatment goals and options, the importance of routine medical care, and some alternative therapies that may help patients cope with the stress of living with a chronic illness. The booklet also describes current research on the causes and treatments for RA by the National Institute of Arthritis and Musculoskeletal and Skin Diseases and other components of the National Institutes of Health. It then refers the reader to the network of voluntary health organizations for additional information about RA. A large print version of this booklet is also available. 1 figure.
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Psoriatic Arthritis Source: Portland, OR: National Psoriasis Foundation. 1999. 12 p. Contact: National Psoriasis Foundation. 6600 SW 92nd Avenue, Suite 300, Portland, OR 97223-7195. (800) 723-9166 or (503) 244-7404. Fax (503) 245-0626. E-mail:
[email protected]. Website: www.psoriasis.org. Summary: This booklet for individuals with psoriasis presents an overview of psoriatic arthritis (PA). It lists the symptoms of PA; explains how a diagnosis of PA is made; and describes localized mild PA, generalized disabling PA, symmetric arthritis, asymmetric arthritis, distal interphalangeal predominant arthritis, spondylitis, and arthritis mutilans. The booklet discusses various treatments for PA, including aspirin, nonsteroidal anti-inflammatory drugs, sulfasalazine, gold, methotrexate, azathioprine, steroids, photochemotherapy, antimalarials, cyclosporine, retinoids, diet or climate changes, surgery, exercise, physical therapy, and splints. In addition, it lists educational literature available from the National Psoriasis Foundation.
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Decision Making for Teenagers with Arthritis Source: Atlanta, GA: Arthritis Foundation. 1998. 28 p. Contact: Available from Arthritis Foundation. P.O. Box 1616, Alpharetta, GA 300091616. (800) 207-8633. Fax (credit card orders only) (770) 442-9742. http://www.arthritis.org. PRICE: Single copy free from local Arthritis Foundation chapter (call 800-283-7800 for closest local chapter); bulk orders may be purchased from address above. Summary: This brochure for adolescents with arthritis offers guidelines for choosing a career. It explains that the career decision making process begins with an assessment of personal goals and values, interests, skills, and personal characteristics. Although arthritis may place some limitations on a person, it should not become a restriction. The brochure describes various opportunities that exist for high school students to learn about and prepare for the work world, including transition planning, guidance counseling, and hospital-based job counseling, and lists the many ways students can gain skills and experience. For students wishing to attend college, the brochure discusses preparing for college admission tests, deciding which colleges or universities to apply to, and making a final decision. It also outlines the many strategies students with arthritis can use to make the most of their college experience. Also detailed are the sources of financial assistance available, and how financial aid could affect Social Security benefits. The brochure also includes a list of helpful resources.
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Arthritis Answers Source: Atlanta, GA: Arthritis Foundation. 1998. 24 p. Contact: Available from Arthritis Foundation. P.O. Box 1616, Alpharetta, GA 300091616. (800) 207-8633. Fax (credit card orders only) (770) 442-9742. http://www.arthritis.org. PRICE: Single copy free from local Arthritis Foundation chapter (call 800-283-7800 for closest local chapter); bulk orders may be purchased from address above. Summary: This brochure for people with arthritis uses a question and answer format to provide information about the condition. It describes the symptoms of arthritis and related conditions, and states that the cause of most types of arthritis is unknown and that certain factors, such as genetic make-up, lifestyle, and the environment, may have a role in some types of arthritis. The brochure lists several of the more than 100 different types of arthritis and related conditions and explains how a diagnosis is made. It discusses the many drug and nondrug treatments available, which may involve working with different types of health care specialists. The brochure explains how people can reduce their risk for developing arthritis, and how those who already have arthritis can maintain their independence. It describes the four broad research areas under investigation, including causes, treatment, education, and lifestyle influences on arthritis. The brochure includes sources of additional information. It is also available in Spanish. 6 figures.
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Walking and Arthritis Source: Atlanta, GA: Arthritis Foundation. 1998. 6 p. Contact: Available from Arthritis Foundation. P.O. Box 1616, Alpharetta, GA 300091616. (800) 207-8633. Fax (credit card orders only) (770) 442-9742. http://www.arthritis.org. PRICE: Single copy free from local Arthritis Foundation
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chapter (call 800-283-7800 for closest local chapter); bulk orders may be purchased from address above. Summary: This brochure for people with arthritis offers guidelines for a walking regimen to keep fit and flexible. It details the physical and psychological benefits of walking, and the importance of first talking with the doctor about the best level of intensity and length of time for regular walks. Also discussed are the types of clothes to wear, checking out a proposed route, and informing family members of the walking route. Walks can be made more enjoyable if people take time to warm up and cool down, use an assistive device if necessary, walk at their own pace, begin slowly, select firm and level surfaces for walks, and walk during times of day when light and shadows do not cause problems. In addition, walking can be made more interesting by changing the location, finding a walking partner, setting different daily goals, and signing up for a fundraising walk. The fact sheet also provides information on the Arthritis Foundation. ·
Water Exercise: Pools, Spas and Arthritis Source: Atlanta, GA: Arthritis Foundation. 1998. 20 p. Contact: Available from Arthritis Foundation. P.O. Box 1616, Alpharetta, GA 300091616. (800) 207-8633. Fax (credit card orders only) (770) 442-9742. http://www.arthritis.org. PRICE: Single copy free from local Arthritis Foundation chapter (call 800-283-7800 for closest local chapter); bulk orders may be purchased from address above. Summary: This brochure for people with arthritis offers guidelines for using water exercise as a means of relieving arthritis pain and stiffness. It explains the benefits of water exercise and that it can be done in a pool or hot tub. The brochure provides guidelines for purchasing a hot tub or pool and using it safely, and describes various exercises that people can try. It also provides sources of additional information, including the Arthritis Foundation. 20 figures.
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Rheumatoid Arthritis Source: Atlanta, GA: Arthritis Foundation. 1998. 24 p. Contact: Available from Arthritis Foundation. P.O. Box 1616, Alpharetta, GA 300091616. (800) 207-8633. Fax (credit card orders only) (770) 442-9742. http://www.arthritis.org. PRICE: Single copy free from local Arthritis Foundation chapter (call 800-283-7800 for closest local chapter); bulk orders may be purchased from address above. Summary: This brochure for people with rheumatoid arthritis (RA) uses a question and answer format to provide an overview of this common form of arthritis. It explains the differences between RA and other forms of arthritis; discusses the role of heredity, infection, and immune system dysfunction; and describes the disease progression, diagnosis, and treatment. Diagnosis is based on the medical history, a physical examination, and tests. Treatment includes medications, exercise, physical therapy, surgery, and diet. Medications that may relieve symptoms are nonsteroidal antiinflammatory drugs, such as aspirin, other analgesics, glucocorticoids, and diseasemodifying medications. In addition, the brochure highlights research on RA, offers advice on managing it, and provides information on the Arthritis Foundation. 2 figures.
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Surgery and Arthritis: What You Need to Know Source: Atlanta, GA: Arthritis Foundation. 1998. 20 p. Contact: Available from Arthritis Foundation. P.O. Box 1616, Alpharetta, GA 300091616. (800) 207-8633. Fax (credit card orders only) (770) 442-9742. http://www.arthritis.org. PRICE: Single copy free from local Arthritis Foundation chapter (call 800-283-7800 for closest local chapter); bulk orders may be purchased from address above. Summary: This brochure for people with arthritis addresses issues surrounding the use of surgery to lessen the pain, disability, and deformity caused by this disease. First, it describes the structure of joints so patients can understand what surgery can do for them. Then it identifies the benefits and risks of surgery, lists questions that patients should ask before proceeding with surgical treatment, and highlights the factors that will influence its cost. The brochure describes various types of surgical procedures and explains in detail how surgery can benefit the hip and other joints. In addition, it offers guidelines on preparing for and recuperating from joint surgery. Information on the Arthritis Foundation is also provided. 7 figures.
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Osteoarthritis Source: San Bruno, CA: StayWell Company. 1998. 8 p. Contact: Available from StayWell Company. 1100 Grundy Lane, San Bruno, CA 940663030. (800) 333-3032. Website: www.staywell.com. PRICE: Call or write for current pricing on single and bulk orders. Summary: This booklet provides people who have osteoarthritis (OA) with information on this degenerative form of arthritis. Although its cause is not completely known, OA is associated with the breakdown of the articular cartilage. Symptoms of OA vary greatly among people. The booklet explains the basic anatomy of the normal, movable joint, focusing on the articular cartilage, the synovial membrane, and the joint capsule. OA occurs when the articular cartilage begins to break down and the smooth sliding surfaces of the bones become pitted and irregular. Sites include the neck, fingers, lower back, hip, and knee. Diagnosis requires a medical history, a physical examination, and laboratory and diagnostic imaging studies. Medical treatment may include taking aspirin, nonsteroidal anti-inflammatory drugs, and corticosteroids, as well as losing excess weight. Physical therapy, including exercise and heat treatments, may also be used to treat OA. Exercises can be performed to increase joint flexibility and strengthen muscles. In addition, surgical treatment, such as hip and knee replacement, may be used for pain that does not respond to conventional treatment and physical therapy.
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What People With Arthritis Need to Know About Osteoporosis Source: Washington, DC: National Osteoporosis Foundation. 1997. 12 p. Contact: National Osteoporosis Foundation. 1232 22nd Street N.W., Washington, DC 20037-1292. (202) 223-2226. Website: www.nof.org. PRICE: Single copy $0.40; 500 or more copies $0.35. Summary: This booklet for individuals with arthritis explains what they need to know about osteoporosis. It clarifies the difference between osteoporosis and osteoarthritis and defines rheumatoid arthritis. The differences among these three conditions are outlined. The booklet also offers strategies that arthritis patients can use to prevent and treat osteoporosis, including being sure of their diagnosis, knowing the side effects of
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any medications being taken, using exercise to help relieve joint stiffness and pain, eating a healthy and balanced diet, getting adequate amounts of calcium, eliminating other risk factors for osteoporosis, and undergoing a bone density test to predict the chance of a future fracture. 1 chart. ·
Exercise and Your Arthritis Source: Atlanta, GA: Arthritis Foundation. 1997. 28 p. Contact: Arthritis Foundation, P.O. Box 7669, Atlanta, GA 30357-0669. (800) 283-7800. (800) 207-8633. Summary: This booklet for individuals with arthritis focuses on the importance of exercise. It explains what could happen to these individuals if they do not exercise, who can help them start an exercise program, and whether there are any risks to exercising. The booklet describes main types of exercise, including range-of-motion, strengthening, and endurance exercises, and presents sample range-of-motion exercises. It offers guidelines for beginning an exercise program and provides suggestions for actions individuals should take prior to, during, and following exercise. In addition, the booklet presents common reasons for not exercising and suggests ways to overcome them, and it identifies sources of additional information.
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Arthritis in the Workplace Source: Atlanta, GA: Arthritis Foundation. 1997. 24 p. Contact: Available from Arthritis Foundation. P.O. Box 1616, Alpharetta, GA 300091616. (800) 207-8633. Fax (credit card orders only) (770) 442-9742. http://www.arthritis.org. PRICE: Single copy free from local Arthritis Foundation chapter (call 800-283-7800 for closest local chapter); bulk orders may be purchased from address above. Summary: This brochure for people with arthritis or an arthritis-related condition offers guidelines for choosing a career. It encourages them to use their limitations as a guide to finding appropriate careers instead of as restrictions. They should begin their job search by assessing their physical capabilities, making a detailed list of the activities that may be involved in an occupation they are considering, and assessing the impact of their condition on their ability to perform the task. The brochure outlines the many steps in a successful job search including listing job goals, compiling a well-organized resume, attending professional organization or club meetings, practicing interviewing skills, and deciding ahead of time how and when to discuss arthritis-related limitations. It also explains the various ways to find job opportunities, and the laws that can help disabled people find and keep employment. Also discussed are the many strategies that people with arthritis can use to succeed in their work environment, as well as the need to be aware of vocational education services and work disability benefits. The brochure also includes sources of additional information.
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Gardening and Arthritis Source: Atlanta, GA: Arthritis Foundation. 1997. 6 p. Contact: Available from Arthritis Foundation. P.O. Box 1616, Alpharetta, GA 300091616. (800) 207-8633. Fax (credit card orders only) (770) 442-9742. http://www.arthritis.org. PRICE: Single copy free from local Arthritis Foundation chapter (call 800-283-7800 for closest local chapter); bulk orders may be purchased from address above.
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Summary: This brochure for people with arthritis offers advice for maintaining a garden. It shows how gardening can help people with arthritis maintain joint flexibility, range of motion, and quality of life. The brochure give people advice on what to do prior to starting a garden, how to plan a gardening schedule, warming up before working, and pacing their work. It describes how gardening tasks can be made easier, more energy-conserving and more enjoyable by carefully arranging the garden, and using low maintenance plants, helpful tools, and easy watering methods. The brochure also discusses ways to protect joints by moving correctly when undertaking gardening tasks. The brochure also provides information on the Arthritis Foundation. ·
Golf and Arthritis Source: Atlanta, GA: Arthritis Foundation. 1997. 6 p. Contact: Available from Arthritis Foundation. P.O. Box 1616, Alpharetta, GA 300091616. (800) 207-8633. Fax (credit card orders only) (770) 442-9742. http://www.arthritis.org. PRICE: Single copy free from local Arthritis Foundation chapter (call 800-283-7800 for closest local chapter); bulk orders may be purchased from address above. Summary: This brochure for people with arthritis offers them guidelines for playing golf. It explains the health-enhancing effects of the sport, and how the equipment can be adjusted to meet the physical capabilities of almost anyone. The brochure discusses the importance of a good conditioning program and, for beginners, the wisdom of taking lessons at a local golf course. Also described are many other suggestions for making golf more enjoyable and preventing injury. The brochure also provides information on the Arthritis Foundation.
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Diet and Your Arthritis Source: Atlanta, GA: Arthritis Foundation. 1997. 20 p. Contact: Available from Arthritis Foundation. P.O. Box 1616, Alpharetta, GA 300091616. (800) 207-8633. Fax (credit card orders only) (770) 442-9742. http://www.arthritis.org. PRICE: Single copy free from local Arthritis Foundation chapter (call 800-283-7800 for closest local chapter); bulk orders may be purchased from address above. Summary: This brochure for people with arthritis uses a question and answer format to examine the role that diet may have in arthritis. It states that studies have found an association between food and certain forms of arthritis or arthritis-related conditions. For example, vitamin and mineral deficiencies, gastrointestinal infections, being overweight, and food allergies may initiate or worsen certain conditions and symptoms. The brochure discusses other dietary factors, that may have positive effects on the body's immune system, and the importance of a good diet and healthy weight. The brochure also provides information on the Arthritis Foundation and its services. 4 figures.
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Arthritis in Children Source: Atlanta, GA: Arthritis Foundation. 1997. 28 p. Contact: Available from Arthritis Foundation. P.O. Box 1616, Alpharetta, GA 300091616. (800) 207-8633. Fax (credit card orders only) (770) 442-9742. http://www.arthritis.org. PRICE: Single copy free from local Arthritis Foundation
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chapter (call 800-283-7800 for closest local chapter); bulk orders may be purchased from address above. Summary: This brochure for parents who have a child with arthritis or a related condition provides information about juvenile arthritis. Although the most common form is juvenile rheumatoid arthritis, children are also affected by arthritis as a feature of more than 100 other diseases. The brochure describes the types of juvenile arthritis and related conditions, as well as juvenile noninflammatory disorders such as growing pains and chronic pain syndromes. It outlines the processes involved in diagnosing and treating juvenile arthritis and describes modes of treatment. Treatment usually includes medication, therapeutic and recreational exercise, and healthy eating practices, although surgery may be used to treat special long-term problems. The brochure also offers guidelines for dealing with the emotional effects of arthritis, identifies additional sources of information, and provides information on the Arthritis Foundation. ·
Your Podiatric Physician Talks About Arthritis Source: Bethesda, MD: American Podiatric Medical Association. 1997. 6 p. Contact: Available from American Podiatric Medical Association. 9312 Old Georgetown Road, Bethesda, MD 20814-1698. (800) 275-2762 or (301) 581-9277. Fax (301) 530-2752. Website: www.apma.org. PRICE: Single copy free; bulk orders available at cost. Summary: This pamphlet provides people who have arthritis with information on this disease, which is characterized by inflammation of the cartilage and lining of the body's joints. Arthritis can be caused by heredity, injury, bacterial and viral infections, and drug use. In addition, arthritis can develop in conjunction with inflammatory bowel disorders, and it can be a part of a congenital autoimmune disease syndrome. The pamphlet outlines arthritis symptoms, such as swelling, pain, redness, limitation of motion, early-morning stiffness, and skin changes, and describes various forms of arthritis, such as osteoarthritis, rheumatoid arthritis, and gout. Other topics include the diagnosis and treatment of arthritis. 2 figures.
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Facts About Osteoporosis, Arthritis, and Osteoarthritis Source: Washington, DC: National Osteoporosis Foundation (NOF). 1997. 6 p. Contact: Available from National Osteoporosis Foundation. 1150 17th Street, NW, Suite 500, Washington, DC 20036-4603. (202) 223-2226. Fax (202) 223-2237. Website: www.nof.org. PRICE: Single copy free; bulk orders available at cost. Summary: This pamphlet provides people who have osteoporosis, arthritis, and osteoarthritis with information on these painful chronic diseases. Osteoporosis is characterized by a loss of bone mass and by poor bone quality, which lead to reduced bone strength and increased risk of fractures. The pamphlet lists the risk factors for osteoporosis and highlights prevention and treatment strategies. Osteoarthritis (OA), the most common form of arthritis, is a degenerative joint disease that leads to the thinning or destruction of the cartilage. The pamphlet presents the features of OA, identifies risk factors, and comments on diagnosis and treatment. Rheumatoid arthritis (RA) is an inflammatory disease of the lining of the joints that has no known cause. The pamphlet presents the warning signs of RA and provides information on diagnosis, treatment, and outcomes.
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Living With Rheumatoid Arthritis Source: San Bruno, CA: StayWell Company. 1997. 6 p.
Patient Resources 549
Contact: Available from StayWell Company. 1100 Grundy Lane, San Bruno, CA 940663030. (800) 333-3032. Website: www.staywell.com. PRICE: Call or write for current pricing on single and bulk orders. Summary: This illustrated brochure provides people who have rheumatoid arthritis (RA) with information on controlling joint pain and inflammation. RA affects the lining of the joints and causes pain, swelling, and stiffness. If untreated, RA can damage joints so badly that they no longer function. Although RA can affect most joints, common sites are the fingers, wrists, elbows, knees, and balls of the feet. Diagnosis is based on information obtained through a medical history, a physical examination, and imaging tests. The brochure outlines the symptoms, offers tips to help reduce symptoms, and provides suggestions on exercising. In addition, the brochure identifies special tools and aids, presents tips on taking medications, and briefly discusses surgery. ·
Arthritis Advice Source: Bethesda, MD: National Institute on Aging. 1996. 6 p. Contact: National Institute on Aging Information Center, P.O. Box 8057, Gaithersburg, MD 20898-8057. (800) 222-2225. (800) 224-4225 (tty). Summary: This pamphlet for individuals with arthritis presents an overview of this disease. It describes the common forms of arthritis in older individuals, including osteoarthritis, rheumatoid arthritis, and gout, and outlines common warning signs of arthritis. The pamphlet discusses treatments for arthritis, including using medications to relieve pain and reduce swelling, exercising, applying heat or cold to the areas around the joint, controlling or losing weight, and undergoing surgery, and it warns against unproven remedies. In addition, the pamphlet identifies sources of additional information.
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Arthritis Source: Chicago, IL: American Academy of Orthopaedic Surgeons. 1996. 8 p. Contact: Available from American Academy of Orthopaedic Surgeons (AAOS). P.O. Box 75838, Chicago, IL 60675-5838. (800) 626-6726. Fax (for credit card or institutional purchase orders) (800) 823-8025. http://www.aaos.org. PRICE: Single copy free; bulk prices available. Summary: This brochure uses a question and answer format to provide people with arthritis with information on this condition. First it describes the features of a joint and defines inflammation. The brochure explains how arthritis is diagnosed; highlights the characteristics of osteoarthritis and rheumatoid arthritis; and discusses the use of medications, joint protective devices, and surgery to treat it. In addition, it addresses the question of whether arthritis can be cured. 2 figures.
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Living With Arthritis: Home Health Wellness Maps Source: San Bruno, CA: StayWell Company. 199x. 12 p. Contact: Available from StayWell Company. 1100 Grundy Lane, San Bruno, CA 940663030. (800) 333-3032. Website: www.staywell.com. PRICE: Call or write for current pricing on single and bulk orders. Summary: This brochure provides people who have arthritis with information on this joint condition. Arthritis results in joint inflammation and pain, swelling, stiffness, and limited mobility. The most common types of arthritis are osteoarthritis and rheumatoid
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arthritis. Other types include juvenile rheumatoid arthritis, seronegative arthritis, ankylosing spondylitis, and gouty arthritis. A healthy lifestyle that includes exercising, using relaxation techniques, and maintaining a balanced diet will help people with arthritis improve their quality of life. Various physical therapy modalities, such as hot and cold packs, ultrasound, massage, hydrotherapy, wax dips, and splints may also help relieve symptoms. Medical treatments for arthritis include taking nonsteroidal antiinflammatory drugs, injecting cortisone or gold salts, taking gold salt capsules, and undergoing surgery. The brochure notes myths about arthritis and offers suggestions on making changes in each room of the house so that the activities of daily living will be easier. ·
Arthritis: What It Is and How To Live With It Source: Seattle, WA: Hope Heart Institute. 199x. 20 p. Contact: Available from International Health Awareness Center, Inc. 350 East Michigan, Suite 301, Kalamazoo, MI 49007-3851. (800) 334-4094 or (616) 343-0770. Website: www.hithope.com. PRICE: Single copy $4.95 plus shipping and handling; bulk orders available. Item Number: 426. Summary: This illustrated booklet provides people who have arthritis with an overview of this chronic condition. Although there are over 100 different diseases that are considered arthritis, the most common are osteoarthritis (OA), rheumatoid arthritis (RA), lupus, spondyloarthropathies, and gout. The booklet explains how normal joints work, lists the warning signs of arthritis, compares the features of OA and RA, outlines the causes and symptoms of OA, offers suggestions on preventing or minimizing OA, discusses the importance of exercise in managing OA, provides examples of range of motion exercises, and presents tips on getting the most out of exercise. Other topics include maintaining a healthy diet; working with the pain; and using treatments such as aspirin and acetaminophen, hot and cold packs, ointments and creams, and unproven remedies. In addition, the booklet offers tips on making life with arthritis easier and provides sources of additional information.
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Learning To Live With Arthritis Source: Seattle, WA: Hope Heart Institute. 199x. 8 p. Contact: Available from International Health Awareness Center, Inc. 350 East Michigan, Suite 301, Kalamazoo, MI 49007-3851. (800) 334-4094 or (616) 343-0770. Website: www.hithope.com. PRICE: Single copy $0.55 plus shipping and handling; bulk orders available. Item Number: 174. Summary: This pamphlet provides people who have arthritis with information on ways to live with this chronic condition. Although there are over 100 types of arthritis, osteoarthritis and rheumatoid arthritis are among the most common. The pamphlet describes the anatomy of a joint, compares the features of these two forms of arthritis, and provides information on gout. In addition, the pamphlet discusses the role of exercise in improving quality of life for people who have arthritis, describes the basic forms of therapeutic exercise, and offers tips on exercise. Other topics include taking charge of one's condition and watching out for fraudulent cure-alls.
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Arthritis and pregnancy Source: Atlanta, GA: Arthritis Foundation. 1992. 30 pp.
Patient Resources 551
Contact: Available from Arthritis Foundation, P.O. Box 19000, Atlanta, GA 30326. Telephone: (800) 283-7800. Available at no charge. Summary: This booklet is for women who have arthritis and are pregnant or are considering pregnancy. It discusses how arthritis may affect a pregnancy and how pregnancy may affect arthritis, offers advice on seeking medical care, and includes diet and exercise tips. The brochure also provides information on care for the new mom and her baby. It addresses specific issues concerning rheumatoid arthritis, scleroderma, and systemic lupus erthematosus which are the three most common forms of arthritis that appear in women during their childbearing years. A resource list is included. ·
Rheumatoid Arthritis of the Foot and Ankle Source: American Academy of Orthopaedic Surgeons. December 2001. 3 p. Contact: Available from American Academy of Orthopaedic Surgeons. Website: www.familydoctor.org. Summary: This fact sheet discusses the symptoms of and treatment for rheumatoid arthritis (RA) of the foot and ankle. The main symptoms of foot or ankle RA are pain, swelling, and stiffness. The appearance of these symptoms may be the first indication that a patient has RA, or they may occur as the disease spreads through the body. The symptoms often start in the toes or forefoot first, and then spread into the back of the foot. Corns, bunions, claw toe, or hammer toe may develop. Medications can be given to control pain, relieve swelling and inflammation, or help slow the spread of the disease. Special shoes with a deep toe box, arch supports, molded ankle-foot orthotics, canes, or crutches may also be needed. Surgery can be used to correct bunions and hammer toes. Foot fusion (arthrodesis) or joint replacement can be performed to help maintain function and eliminate pain.
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Treating Knee Osteoarthritis With Injections Source: American Family Physician. 62(3): 572. August 1, 2000. Contact: American Academy of Family Physicians. 11400 Tomahawk Creek Parkway, Leawood, KS 66211-2672. (800) 274-2237 or (913) 906-6000. E-mail:
[email protected]. Website: www.aafp.org. Summary: This journal article uses a question and answer format to provide people who have knee osteoarthritis (OA) with information on the use of injections to treat this painful knee problem. OA is a form of wear and tear arthritis. Although the exact cause of joint cartilage loss is unknown, OA is more common in people who are older or overweight. Diagnosis is based on a medical history, a physical examination, and x rays of the knee. Treatment may involve taking medications to relieve pain; participating in physical therapy; and having the knee injected with anesthetic agents, corticosteroids, or hyaluronic acid. In people who have OA, hyaluronic acid gets thinner, so there is not enough of it to properly protect the joint. Injections add hyaluronic acid to the joint to help protect it. However, hyaluronic acid injections are expensive, usually costing more than $600 each.
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New Arthritis Drugs for Rheumatoid Arthritis and Osteoarthritis Source: Bethesda, MD: National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Information Clearinghouse. 2000. 5 p.
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Contact: Available from National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Information Clearinghouse. 1 AMS Circle, Bethesda, MD 20892-3675. (877) 226-4267 toll-free or (301) 495-4484. Fax (301) 718-6366. TTY (301) 565-2966. E-mail:
[email protected]. Website: www.niams.nih.gov. PRICE: Single copy free. Order Number: AR-210. Summary: This information sheet provides people who have arthritis with information on new drugs that are presently available or awaiting approval for the treatment of rheumatoid arthritis (RA) and osteoarthritis (OA). Biological response modifiers for RA include Enbrel (etanercept) and Remicade (infliximab). Disease modifying antirheumatic drugs for RA include Arava (leflunomide). Nonsteroidal antiinflammatory drugs include Celebrex (celecoxib) and Vioxx (rofecoxib). Among other products are hyaluronic acid viscosupplementation products such as Hyalgan (hyaluronan) and Synvisc (hyland G-F20) and the Prosorba Column (apheresis). For each drug or product, the information sheet lists its name, how it is taken, its most common side effects, its approval status, and its manufacturer. The information sheet also lists additional resources. ·
Exercise and Arthritis Source: American College of Rheumatology. 2000. 2 p. Contact: American College of Rheumatology. 1800 Century Place, Suite 250, Atlanta, GA 30345. (404) 633-3777. Website: www.rheumatology.org. Email:
[email protected]. Summary: This fact sheet discusses the benefits of exercise for patients with arthritis. A regular exercise program helps alleviate pain and stiffness while increasing strength, flexibility, and the ability to perform activities of daily living. The appropriate level of exercise will depend on the severity of the disease and the amount of joint involvement. The patient should consult with his or her rheumatologist before beginning to exercise. Any exercise program should contain exercises for flexibility or stretching, muscle conditioning, and cardiovascular or aerobic conditioning. A low-impact exercise program including swimming and water aerobics is well tolerated by most patients with arthritis. Thirty minutes of moderate aerobic activity most days is recommended.
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Juvenile Arthritis Source: American College of Rheumatology. 2000. 2 p. Contact: American College of Rheumatology. 1800 Century Place, Suite 250, Atlanta, GA 30345. (404) 633-3777. Website: www.rheumatology.org. Email:
[email protected]. Summary: This fact sheet provides information on juvenile arthritis, a condition that causes joint inflammation and stiffness in patients younger than 16 years old. Patients are classified in one of three categories, systemic onset type, pauciarticular onset disease, or polyarticular disease, depending on symptoms and the number of joints involved. Although the cause of juvenile arthritis is unknown, a genetic origin is suspected. Diagnosis can be difficult as children will compensate for inability to use a limb and tests used to diagnose adult arthritis have negative results in children. NSAIDs and steroids are used to treat juvenile arthritis. Physical and occupational therapy can help prevent disability. Children should be encouraged to participate in school, extracurricular, and family activities.
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What You Should Know About Reactive Arthritis Source: American Family Physician. 60(2): 507. August 1999.
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Contact: American Academy of Family Physicians. 11400 Tomahawk Creek Parkway, Leawood, KS 66211-2672. (800) 274-2237 or (913) 906-6000. E-mail:
[email protected]. Website: www.aafp.org. Summary: This journal article uses a question and answer format to provide people who have reactive arthritis with information on this joint disease. Reactive arthritis is an uncommon disease that causes pain and swelling in the joints. In this disease, the body is reacting to an infection that a person already has. It occurs most frequently in men between 20 and 40 years old. Diagnosis is based on the person's symptoms and laboratory test results. Treatment involves taking medication for the pain and swelling and taking antibiotics if a sexually transmitted disease is also present. ·
Gouty Arthritis Source: Physician Assistant. 23(11): 45-46. November 1999. Summary: This information sheet uses a question and answer format to provide people who have gouty arthritis with information on this disease, which produces swelling in one or more joints as a result of deposits of uric acid. Gouty arthritis, which is commonly called gout, occurs in 2 to 2.6 per 1,000 people in the United States. In the first phase of gout, known as asymptomatic hyperuricemia, the blood has high levels of uric acid but the person has no symptoms. In the next phase, gout causes pain, stiffness, and swelling in the affected joint. The third phase, known as intercritical gout, is the phase between attacks. In the final phase, accumulations of hard crystals of uric acid, called tophi, are deposited in various areas of the body. Diagnosis is based on a physical examination, blood tests, and x rays. Acute attacks of gout may be treated with nonsteroidal anti-inflammatory drugs, colchicine, corticosteroids, and adrenocorticotropic hormones. Nonpharmacologic methods of treating acute attacks include bedrest, hot or cold compresses, and elevation of the affected joint. Preventing future attacks involves following a diet low in purine; increasing fluid intake to 3 liters per day; losing weight; and taking medications such as colchicine, indomethacin, probenecid, sulfinpyrazone, and allopurinol. 1 figure.
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Living With Arthritis Source: Journal of the American Medical Association. JAMA. 282(20): 1982. November 24, 1999. Contact: Available also online from American Medical Association at www.amaassn.org/consumer.htm. Summary: This fact sheet provides people who have arthritis with information on living with this disorder. The term arthritis, which means inflammation of the joints, refers to more than 100 diseases that can cause pain, stiffness, and swelling in the joints. Two common forms of arthritis are osteoarthritis and rheumatoid arthritis. The fact sheet outlines the common warning signs of arthritis and offers suggestions for coping with pain. In addition, the fact sheet identifies some treatment options, including physical exercise, a well balanced diet, heat and cold therapies, medications, rest and relaxation, assistive devices, and surgery. The National Institute of Arthritis and Musculoskeletal and Skin Diseases Information Clearinghouse and the Arthritis Foundation can provide more information about arthritis. 1 figure.
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Guide to Intimacy with Arthritis Source: Atlanta, GA: Arthritis Foundation. 1998. 8 p.
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Contact: Available from Arthritis Foundation. P.O. Box 1616, Alpharetta, GA 300091616. (800) 207-8633. Fax (credit card orders only) (770) 442-9742. http://www.arthritis.org. PRICE: Single copy free from local Arthritis Foundation chapter (call 800-283-7800 for closest local chapter); bulk orders may be purchased from address above. Summary: This guide for people with arthritis uses a question and answer format to address physical and emotional concerns related to sexuality. It focuses on enjoying a sexual relationship, especially after joint replacement; dealing with a decrease in desire; handling the self-concept issues raised by arthritis; and communicating with one's partner about what is possible or painful at a given time. The guide also discusses appropriate sources for help with sexual matters. In addition, it provides illustrations of alternative lovemaking positions. 7 figures. [Note: The full text of this article may be found in the article 'Sexual Healing' in Arthritis Today. 12(3): 35-40,42. May-June 1998.] ·
Well-Connected: Osteoarthritis Source: New York, NY: Nidus Information Services, Inc. 1998. 8 p. Contact: Available from Nidus Information Services, Inc. 175 Fifth Avenue, Suite 2338, New York, NY 10010. (800) 334-WELL or (212) 260-4268. Fax (212) 529-2349. E-mail:
[email protected]. Website: www.well-connected.com. PRICE: $5.95 plus shipping and handling. Summary: This fact sheet uses a question and answer format to provide people who have osteoarthritis with information on this degenerative joint disease. The fact sheet begins by describing the general features of osteoarthritis and the specific features of osteoarthritis of the fingers, knees, hips, and spine. This is followed by a discussion of the symptoms of osteoarthritis, focusing on pain. A few of the most common disorders that can be confused with osteoarthritis are then identified. These include rheumatoid arthritis, chondrocalcinosis, and Charcot's joints. Other topics include risk factors for osteoarthritis, including aging, obesity, heavy labor, and vitamin D deficiency, and causes of osteoarthritis, namely genetic factors, muscle weakness, anatomical abnormalities, trauma, and obesity. The fact sheet next outlines ways to prevent or slow the progression of osteoarthritis, including losing weight, exercising, undergoing hormone replacement therapy, and consuming adequate amounts of antioxidant vitamins and other important nutrients. This is followed by a discussion of the use of xrays, blood tests, and tests of the synovial fluid to confirm the diagnosis of osteoarthritis. Lifestyle measures for managing osteoarthritis are detailed: occupational changes, exercise, weight reduction, heat therapy, mechanical aids, alternative treatments, the arthritis self-help course, and cognitive behavioral therapy. Also discussed are the drug treatments for osteoarthritis: common pain relievers such as acetaminophen and nonsteroidal anti-inflammatory drugs; drugs derived from natural joint substances such as hyaluronic acid, glucosamine, and chondroitin sulfate; capsaicin; steroids; and gene therapy. Surgical treatments for osteoarthritis are also highlighted, including arthroscopy, resection arthroplasty, osteotomy, chondroplasty, arthrodesis, and joint replacement. The article concludes with comments on the emotional ramifications of osteoarthritis and a list of helpful organizations.
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Senior Health: Staying Active With Arthritis Source: San Bruno, CA: StayWell Company. 1997. 2 p.
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Contact: Available from StayWell Company. 1100 Grundy Lane, San Bruno, CA 940663030. (800) 333-3032. Website: www.staywell.com. PRICE: Call or write for current pricing on single and bulk orders; available in tear-off pads of 100. Summary: This fact sheet provides people who have arthritis with tips on staying active. Common symptoms of arthritis include joint pain, tenderness, or swelling; redness or warmth; pain when moving; morning stiffness; and discomfort when the weather changes. An exercise program can help reduce the pain and stiffness that accompany arthritis. A program should include stretching, strengthening, and aerobic exercise. In addition, maintaining an optimal weight can reduce the stress on joints. Tips on maintaining a healthy weight include building meals around bread, cereal, rice, and other grains; eating at least five servings of fruits and vegetables a day; and limiting fat intake. Sources of additional information are also provided. ·
Fast Facts About Arthritis Source: Atlanta, GA: Arthritis Foundation. 1996. 2 p. Contact: Available from Arthritis Foundation. P.O. Box 1616, Alpharetta, GA 300091616. (800) 207-8633. Fax (credit card orders only) (770) 442-9742. http://www.arthritis.org. PRICE: Single copy free from local Arthritis Foundation chapter (call 800-283-7800 for closest local chapter); bulk orders may be purchased from address above. Summary: This fact sheet for people with arthritis provides general information about the warning signs, types, and possible treatments for the disease. It lists some of the more than 100 different types of arthritis, noting that each has its own symptoms and treatments. It discusses diagnosis based on the medical history, a physical examination, and diagnostic tests, and management of the pain, swelling, and joint changes. The fact sheet explains that treatment of arthritis may involve more than one kind, and may change over time. It emphasizes that although finding the right treatment program can involve trial and error, the proper treatment can enable individuals with arthritis to lead active lives. Types of treatments are also discussed, including medications, exercise, rest/relaxation, heat/cold therapy, self-help aids and skills, joint protection, and surgery. The fact sheet also provides information on the Arthritis Foundation and its services.
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Arthritis and Diabetes: A Common Association Source: Baltimore, MD: National Federation of the Blind. 1992. 6 p. Contact: Available from National Federation of the Blind. 1800 Johnson Street, Baltimore, MD 21230. (410) 659-9314. Fax (410) 685-5653. E-mail:
[email protected]. PRICE: Single copy free. Order number LBA30. Summary: This article, which first appeared in Voice of the Diabetic' in 1992, discusses the association between arthritis and diabetes. Both are common conditions that affect many people. The musculoskeletal system can be affected in diabetes, and some medications used to treat arthritis can interfere with the treatment of diabetes. The most common types of arthritis are osteoarthritis, rheumatoid arthritis, crystalline induced arthropathies, and systemic lupus erythematosus. Osteoarthritis is the wear and tear form of arthritis and is usually limited to the joints. Rheumatoid arthritis can affect most of the joints of the body and is associated with morning stiffness and swelling. Other internal organs may be affected by rheumatoid arthritis. Crystalline induced arthropathies include gout and pseudogout. Systemic lupus erythematosus is a form of
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arthritis that can have extensive internal organ involvement. Several types of neuropathies can occur in diabetes, including distal sensory and sensory motor disorders, diabetic amyotrophy, radiculopathy, and autonomic neuropathies. Several forms of arthropathies occur in diabetes, including osteolysis, osteoporosis, Charcot joints, osteomyelitis, and adhesive capsulitis. Connective tissue disorders, such as diffuse idiopathic skeletal hyperostosis, flexion contractures, Dupuytren's contractures, and cheiloarthropathy, can be specifically related to diabetes. In addition, people who have diabetes can experience problems with the skin, muscles, and tendons, including tenosynovitis. The treatment of arthritis involves rest; use of hot and cold packs, protective splints, and analgesics; and surgery. ·
Targeting Arthritis: Public Health Takes Action: At-a-Glance 2002 Source: Atlanta, GA, U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, 4 p., 2002. Contact: National Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control and Prevention, Mail Stop K-45, 4770 Buford Highway NE., Atlanta, GA 30341-3717. (770) 488-5464. INTERNET/EMAIL:
[email protected]; http://www.cdc.gov/nccdphp/arthritis; http://www.cdc.gov/nccdphp/arthritis.pdf. Summary: Targeting Arthritis: Public Health Takes Action: At-a-Glance 2002 provides information on arthritis and describes efforts to reduce pain and disability and increase the quality of life for people with arthritis. The most common forms of arthritis are osteoarthritis, rheumatoid arthritis, fibromyalgia, and gout. Common symptoms include pain, aching, stiffness, and swelling in or around the joints. Arthritis affects nearly 43 million Americans and is the leading cause of disability among adults in the United States. Nearly three of every five people with arthritis are younger than 65 years. However, it is more common among women and older Americans. Weight control and injury prevention measures can lower the risk for osteoarthritis. Pain and disability can be decreased through early diagnosis and appropriate management. Self-management education programs are also effective in reducing both pain and costs. The primary goal of the arthritis program of the Centers for Disease Control and Prevention is to increase the quality of life of people affected by arthritis. This is accomplished through building state arthritis programs, increasing awareness, improving the science base, measuring the burden of arthritis, and implementing systems changes.
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Physical Activity and Osteoarthritis Source: Research File, no. 97-10, 1 p., 1997. Contact: Canadian Fitness and Lifestyle Research Institute, 201-185 Somerset Street West, Ottawa, Ontario K2P 0J2, Canada. (613) 233-5528. FAX: (613) 233-5536. INTERNET/EMAIL: http://www.cflri.ca/cflri/resources/pub_rf.php.
[email protected]. Summary: This article, one of a series for fitness professionals from the Canadian Fitness and Lifestyle Research Institute, discuses the relationship between physical activity and osteoarthritis. A number of short-term studies have indicated that regular moderate exercise can relieve symptoms and improve function among people with both osteoarthritis and rheumatoid arthritis. The Fitness Arthritis and Seniors Trial (FAST), performed at the University of Tennessee and Wake Forest University, evaluated the effect of exercise on knee osteoarthritis in older adults. The participants (1) were age 60 or older, (2) experienced knee pain on most days, (3) had difficulty with daily living activities, and (4) showed radiographic evidence of knee osteoarthritis. FAST researchers compared using aerobic exercise and resistance training with a health
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education program. Both exercise components consisted of a 3-month facility-based program followed by a 15-month home-based program. Aerobic exercise participants were encouraged to walk three times a week. Resistance training participants were instructed to perform sets of nine different weight training exercises three times a week. Each session lasted 1 hour. Both exercise groups reported less pain and disability than the health education comparison group over the course of the study. The aerobic exercise group had significantly better scores than the comparison group on ambulation, transfer (getting up and down), and daily living activities. They also walked a greater distance in 6 minutes. The resistance training group had better scores than the comparison group on ambulation, transfer, and on most performance measures. An analysis of compliance showed that 364 of 439 participants completed FAST. Compliance with various aspects of the program varied from 68 to 70 percent. Prior behavior was the strongest predictor of compliance; that is, those who developed a habit of exercise in the first months of the trial tended to continue being physically active in the following months. The most regular participants derived the greatest benefit from the trial. As opposed to participants who exercised less than the specified duration, those who exercised longest did not fare better than the control group with respect to knee pain and ability to perform activities of daily living. Taken together, these findings suggest that frequent bouts of physical activity of moderate duration are the best prescription for osteoarthritis. For exercise to be of long-lasting benefit, it needs to be continued indefinitely. Physicians and other health professionals must, therefore, consider issues of long-term compliance when prescribing an exercise program for persons with osteoarthritis. ·
Care of the Arthritic Foot Source: Batavia, NY: P.W. Minor and Son, Inc. 15 p. Contact: Available from P.W. Minor and Son, Inc., 3 Treadeasy Avenue, P.O. Box 678, Batavia, NY 14201-0678. (800) PW-MINOR. Summary: This booklet for individuals with arthritis presents some basic facts about arthritis and offers suggestions for living with arthritis. Helpful advice for living with arthritis of the foot includes following a proper treatment program, having a balanced diet, using the proper medications, getting regular exercise, wearing properly designed and fitted footwear, and taking proper care of feet on a daily basis. In addition, the booklet describes footwear that has been designed especially for the arthritic foot. 8 references.
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Reiter's Syndrome Source: Detroit, MI: American Autoimmune Related Diseases Association, Inc. 1994. 2 p. Contact: Available from American Autoimmune Related Diseases Association, Inc. (AARDA). Michigan National Bank Building, 15475 Gratiot Avenue, Detroit, MI 48205. (313) 371-8600. Website: www.aarda.org. PRICE: Single copy free; send self-addressed, stamped envelope. Summary: This fact sheet for people with Reiter's syndrome discusses the affected population, symptoms, and treatment of this autoimmune syndrome, which consists of arthritis, urethritis, and conjunctivitis. People with all three of these manifestations have the complete syndrome, while those patients who have an initiating infectious episode and the infectious arthritis have an incomplete one. Although Reiter's occurs mainly in men, it is also found in women. Typically, arthritis appears 2 to 6 weeks after the beginning of the initiating infectious episode. Other signs include swelling of the
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fingers, toes, Achilles tendon region, or sole of the foot; low back pain; mouth sores; urogenital problems; noninfectious conjunctivitis; and sacroiliitis. The main medication used to treat arthritis in Reiter's syndrome is nonsteroidal anti-inflammatory drugs, although methotrexate, azathioprine, and sulfasalazine may also be used. Although prognosis is usually good, recurrences are common. 2 references.
The National Guideline Clearinghouse™ The National Guideline Clearinghouse™ offers hundreds of evidence-based clinical practice guidelines published in the United States and other countries. You can search this site located at http://www.guideline.gov/ by using the keyword “arthritis” (or synonyms). The following was recently posted: ·
2002 national guideline on the management of sexually acquired reactive arthritis Source: Association for Genitourinary Medicine - Medical Specialty Society; 1999 August (revised 2002); Various pagings http://www.guideline.gov/summary/summary.aspx?doc_id=3045&nbr=2271&a mp;string=joint+AND+inflammation
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Clinical practice guideline for the management of rheumatoid arthritis Source: Advanced Research Techniques in the Health Services - Private For Profit Research Organization; 2001; 170 pages http://www.guideline.gov/summary/summary.aspx?doc_id=3683&nbr=2909&a mp;string=arthritis
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Exercise prescription for older adults with osteoarthritis pain: consensus practice recommendations Source: American Geriatrics Society - Medical Specialty Society; 2001 June; 16 pages http://www.guideline.gov/summary/summary.aspx?doc_id=3188&nbr=2414&a mp;string=joint+AND+inflammation
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Guidelines for ophthalmologic examinations in children with juvenile rheumatoid arthritis Source: American Academy of Pediatrics - Medical Specialty Society; 1993 August (reaffirmed 1999); 4 pages http://www.guideline.gov/summary/summary.aspx?doc_id=1772&nbr=998&am p;string=arthritis
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Management of early rheumatoid arthritis. A national clinical guideline Source: Scottish Intercollegiate Guidelines Network - National Government Agency [Non-U.S.]; 2000 December; 44 pages http://www.guideline.gov/summary/summary.aspx?doc_id=2914&nbr=2140&a mp;string=joint+AND+inflammation
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Pain in osteoarthritis, rheumatoid arthritis, and juvenile chronic arthritis Source: American Pain Society - Professional Association; 2002; 179 pages http://www.guideline.gov/summary/summary.aspx?doc_id=3691&nbr=2917&a mp;string=arthritis
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Recommendations for the medical management of osteoarthritis of the hip and knee: 2000 update Source: American College of Rheumatology - Medical Specialty Society; 2000 September; 11 pages http://www.guideline.gov/summary/summary.aspx?doc_id=2935&nbr=2161&a mp;string=arthritis
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Recommendations for the medical management of osteoarthritis of the hip and knee: 2000 update Source: American College of Rheumatology - Medical Specialty Society; 2000 September; 11 pages http://www.guideline.gov/summary/summary.aspx?doc_id=2935&nbr=2161&a mp;string=joint+AND+inflammation
Healthfinder™ Healthfinder™ is sponsored by the U.S. Department of Health and Human Services and offers links to hundreds of other sites that contain healthcare information. This Web site is located at http://www.healthfinder.gov. Again, keyword searches can be used to find guidelines. The following was recently found in this database: ·
Acupuncture ( Arthritis Foundation) Summary: The Chinese therapy of acupuncture has been used for millennia to treat a range of ailments. Source: Arthritis Foundation http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=7454
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Age Page - Arthritis Advice Summary: This online fact sheet addresses your concerns about your arthritis and the treatment your doctor may have prescribed. Source: National Institute on Aging, National Institutes of Health http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=2373
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Arthritis & Rheumatism (Journal) Summary: The official journal of the American College of Rheumatology, this publication contains peer-reviewed articles on diagnosis, treatment, laboratory research, and socioeconomic issues related to all Source: Nonprofit/Professional Entity--Follow the Resource URL for More Information http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=1938
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Arthritis of the Knee Summary: Also available In: Source: American Academy of Orthopaedic Surgeons http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=7231
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Arthritis Today Summary: A magazine for people who have arthritis, their family members and caregivers. Source: Arthritis Foundation http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=5638
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Arthritis: Timely Treatments for an Ageless Disease Summary: This guide explains the types of arthritis, new treatments available, unproven remedies to guard against, and more. Source: Federal Citizen Information Center, U.S. General Services Administration http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=5977
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Assess Your Risk for Arthritis Summary: To be at risk means that there is a possibility, based on certain factors known to contribute to the disease, that you may develop arthritis or a related condition. Source: Arthritis Foundation http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=7474
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Assess Your Symptoms of Arthritis Summary: The following seven questions are designed to determine if you are exhibiting the signs of arthritis. Answer them as best as you can. Source: Arthritis Foundation http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=7475
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Celebrex Summary: Celebrex is used to relieve the signs and symptoms of osteoarthritis and rheumatoid arthritis in adults. Source: Center for Drug Evaluation and Research, U.S. Food and Drug Administration http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=6975
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Chinese Thunder God Vine Gives Relief from Rheumatoid Arthritis Symptoms Summary: The roots of Thunder God Vine, a plant whose leaves and flowers are highly toxic, have been used medicinally in China for over 400 years. Source: National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=7458
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Do I Have Arthritis? Summary: Also available In: Source: National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=5651
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FAQ - About Arthritis Summary: This site offers in-depth answers to common questions about arthritis as well as provide links to related brochures, articles, news releases, newsletters and resources. Source: Arthritis Foundation http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=1425
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FDA Information for Older People Summary: FDA has numerous articles, brochures and other publications with information for older people on a wide range of health issues, including arthritis, cancer, health fraud, and nutrition. Source: U.S. Food and Drug Administration http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=2109
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Find a Rheumatologist Summary: This page will help you find specialists in arthritis care and research in your geographic area. Source: American College of Rheumatology http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=6820
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Glucosamine and Chondroitin Sulfate Summary: Facts about the dietary (nutritional) supplements glucosamine and chondroitin sulfate and their use as treatment options for arthritis. Source: Arthritis Foundation http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=6007
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Handout on Health: Osteoarthritis Summary: This guide discusses osteoarthritis -- the most common type of arthritis, especially among older individuals. Source: National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=5983
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Handout on Health: Rheumatoid Arthritis Summary: The booklet describes how rheumatoid arthritis develops, how it is diagnosed, how it is treated and what patients can do to help manage the disease. Source: National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=3779
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Help Your Arthritis Treatment Work Summary: Also available In: Source: U.S. Food and Drug Administration http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=3546
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Questions and Answers About Arthritis and Exercise Summary: This fact sheet answers general questions about arthritis and exercise and includes specific information for the patient with Rheumatoid Arthritis. Source: National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=1459
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Questions and Answers About Arthritis and Rheumatic Diseases Summary: This fact sheet answers basic questions about arthritis and rheumatic diseases. Source: National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=6694
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Questions and Answers About Arthritis Pain Summary: The purpose of this consumer health information fact sheet is to provide the arthritis pain sufferer with information on the causes and management of arthritis pain. Source: National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=3775
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Questions and Answers about Juvenile Rheumatoid Arthritis Summary: Juvenile rheumatoid arthritis is arthritis that causes joint inflammation and stiffness for more than 6 weeks in a child of 16 years of age or less. Source: National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=6724
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Questions and Answers About Reactive Arthritis Summary: General information about Reiter’s syndrome including a description and how it develops, and Reiter’s syndrome diagnosis and treatment. Source: National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=4468
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Relieving Arthritis Summary: The pain caused by arthritis can affect how a person functions in the home and workplace. Source: American Occupational Therapy Association http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=7306
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Targeting Arthritis: The Nation’s Leading Cause of Disability Summary: This site provides statistics about arthritis as the leading cause of disability among persons 15 and older, including state specific data. It also discusses the various known forms of the disease. Source: National Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control and Prevention http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=2446
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Your Podiatric Physician Talks About Arthritis Summary: Also available In: Source: American Podiatric Medical Association http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=7632
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The NIH Search Utility The NIH search utility allows you to search for documents on over 100 selected Web sites that comprise the NIH-WEB-SPACE. Each of these servers is “crawled” and indexed on an ongoing basis. Your search will produce a list of various documents, all of which will relate in some way to arthritis. The drawbacks of this approach are that the information is not organized by theme and that the references are often a mix of information for professionals and patients. Nevertheless, a large number of the listed Web sites provide useful background information. We can only recommend this route, therefore, for relatively rare or specific disorders, or when using highly targeted searches. To use the NIH search utility, visit the following Web page: http://search.nih.gov/index.html.
Additional Web Sources
A number of Web sites are available to the public that often link to government sites. These can also point you in the direction of essential information. The following is a representative sample: ·
AOL: http://search.aol.com/cat.adp?id=168&layer=&from=subcats
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Family Village: http://www.familyvillage.wisc.edu/specific.htm
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Google: http://directory.google.com/Top/Health/Conditions_and_Diseases/
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Med Help International: http://www.medhelp.org/HealthTopics/A.html
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Open Directory Project: http://dmoz.org/Health/Conditions_and_Diseases/
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Yahoo.com: http://dir.yahoo.com/Health/Diseases_and_Conditions/
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WebMDÒHealth: http://my.webmd.com/health_topics
Finding Associations There are a number of Internet directories that provide lists of medical associations with information on or resources relating to arthritis. By consulting all of associations listed in this chapter, you will have nearly exhausted all sources for patient associations concerned with arthritis.
The National Health Information Center (NHIC) The National Health Information Center (NHIC) offers a free referral service to help people find organizations that provide information about arthritis. For more information, see the NHIC’s Web site at http://www.health.gov/NHIC/ or contact an information specialist by calling 1-800-336-4797.
Directory of Health Organizations The Directory of Health Organizations, provided by the National Library of Medicine Specialized Information Services, is a comprehensive source of information on associations.
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The Directory of Health Organizations database can be accessed via the Internet at http://www.sis.nlm.nih.gov/Dir/DirMain.html. It is composed of two parts: DIRLINE and Health Hotlines. The DIRLINE database comprises some 10,000 records of organizations, research centers, and government institutes and associations that primarily focus on health and biomedicine. To access DIRLINE directly, go to the following Web site: http://dirline.nlm.nih.gov/. Simply type in “arthritis” (or a synonym), and you will receive information on all relevant organizations listed in the database. Health Hotlines directs you to toll-free numbers to over 300 organizations. You can access this database directly at http://www.sis.nlm.nih.gov/hotlines/. On this page, you are given the option to search by keyword or by browsing the subject list. When you have received your search results, click on the name of the organization for its description and contact information.
The Combined Health Information Database Another comprehensive source of information on healthcare associations is the Combined Health Information Database. Using the “Detailed Search” option, you will need to limit your search to “Organizations” and “arthritis”. Type the following hyperlink into your Web browser: http://chid.nih.gov/detail/detail.html. To find associations, use the drop boxes at the bottom of the search page where “You may refine your search by.” For publication date, select “All Years.” Then, select your preferred language and the format option “Organization Resource Sheet.” Type “arthritis” (or synonyms) into the “For these words:” box. You should check back periodically with this database since it is updated every three months. The National Organization for Rare Disorders, Inc. The National Organization for Rare Disorders, Inc. has prepared a Web site that provides, at no charge, lists of associations organized by health topic. You can access this database at the following Web site: http://www.rarediseases.org/search/orgsearch.html. Type “arthritis” (or a synonym) into the search box, and click “Submit Query.”
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APPENDIX C. RESEARCHING MEDICATIONS Overview While a number of hard copy or CD-ROM resources are available for researching medications, a more flexible method is to use Internet-based databases. Broadly speaking, there are two sources of information on approved medications: public sources and private sources. We will emphasize free-to-use public sources.
U.S. Pharmacopeia Because of historical investments by various organizations and the emergence of the Internet, it has become rather simple to learn about the medications recommended for arthritis. One such source is the United States Pharmacopeia. In 1820, eleven physicians met in Washington, D.C. to establish the first compendium of standard drugs for the United States. They called this compendium the U.S. Pharmacopeia (USP). Today, the USP is a nonprofit organization consisting of 800 volunteer scientists, eleven elected officials, and 400 representatives of state associations and colleges of medicine and pharmacy. The USP is located in Rockville, Maryland, and its home page is located at http://www.usp.org/. The USP currently provides standards for over 3,700 medications. The resulting USP DIÒ Advice for the PatientÒ can be accessed through the National Library of Medicine of the National Institutes of Health. The database is partially derived from lists of federally approved medications in the Food and Drug Administration’s (FDA) Drug Approvals database, located at http://www.fda.gov/cder/da/da.htm. While the FDA database is rather large and difficult to navigate, the Phamacopeia is both user-friendly and free to use. It covers more than 9,000 prescription and over-the-counter medications. To access this database, simply type the following hyperlink into your Web browser: http://www.nlm.nih.gov/medlineplus/druginformation.html. To view examples of a given medication (brand names, category, description, preparation, proper use, precautions, side effects, etc.), simply follow the hyperlinks indicated within the United States Pharmacopeia (USP). Below, we have compiled a list of medications associated with arthritis. If you would like more information on a particular medication, the provided hyperlinks will direct you to ample documentation (e.g. typical dosage, side effects, drug-interaction risks, etc.). The
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following drugs have been mentioned in the Pharmacopeia and other sources as being potentially applicable to arthritis: Acetaminophen and Salicylates ·
Systemic - U.S. Brands: Note: http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/203003.html
Allopurinol ·
Systemic - U.S. Brands: Aloprim; Zyloprim http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202021.html
Anti-Inflammatory Drugs, Nonsteroidal ·
Systemic - U.S. Brands: Actron; Advil; Advil Caplets; Advil, Children's; Aleve; Anaprox; Anaprox DS; Ansaid; Bayer Select Ibuprofen Pain Relief Formula Caplets; Cataflam; Clinoril; Cotylbutazone; Cramp End; Daypro; Dolgesic; Dolobid; EC-Naprosyn; Excedrin IB; Excedrin IB Caple http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202743.html
Azathioprine ·
Systemic - U.S. Brands: Imuran http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202077.html
Capsaicin ·
Topical - U.S. Brands: Zostrix; Zostrix-HP http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202626.html
Chloroquine ·
Systemic - U.S. Brands: Aralen http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202133.html
Copper Supplements ·
Systemic - U.S. Brands: Note: http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202164.html
Corticosteroids ·
Dental - U.S. Brands: Kenalog in Orabase; Orabase-HCA; Oracort; Oralone http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202010.html
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Inhalation - U.S. Brands: AeroBid; AeroBid-M; Azmacort; Beclovent; Decadron Respihaler; Pulmicort Respules; Pulmicort Turbuhaler; Vanceril; Vanceril 84 mcg Double Strength http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202011.html
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Nasal - U.S. Brands: Beconase; Beconase AQ; Dexacort Turbinaire; Flonase; Nasacort; Nasacort AQ; Nasalide; Nasarel; Nasonex; Rhinocort; Vancenase; Vancenase AQ 84 mcg; Vancenase pockethaler http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202012.html
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Ophthalmic - U.S. Brands: AK-Dex; AK-Pred; AK-Tate; Baldex; Decadron; Dexair; Dexotic; Econopred; Econopred Plus; Eflone; Flarex; Fluor-Op; FML Forte; FML Liquifilm; FML S.O.P. HMS Liquifilm; Inflamase Forte; Inflamase Mild; I-Pred; Lite Pred; Maxidex; Ocu-Dex; Ocu-Pred; Ocu-Pr http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202013.html
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Otic - U.S. Brands: Decadron http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202014.html
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Rectal - U.S. Brands: Anucort-HC; Anu-Med HC; Anuprep HC; Anusol-HC; Anutone-HC; Anuzone-HC; Cort-Dome; Cortenema; Cortifoam; Hemorrhoidal HC; Hemril-HC Uniserts; Proctocort; Proctosol-HC; Rectosol-HC http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/203366.html
Corticosteroids Glucocorticoid Effects ·
Systemic - U.S. Brands: Acetocot; A-hydroCort; Amcort; A-MethaPred; Aristocort; Aristocort Forte; Aristopak; Aristospan; Articulose-50; Articulose-L.A. Celestone; Celestone Phosphate; Celestone Soluspan; Cinalone 40; Cinonide 40; Clinacort; Clinalog; Cordrol; Cortastat; Corta http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202018.html
Cyclophosphamide ·
Systemic - U.S. Brands: Cytoxan; Neosar http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202174.html
Cyclosporine ·
Systemic - U.S. Brands: Neoral; Sandimmune; SangCya http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202176.html
Dimethyl Sulfoxide ·
Mucosal - U.S. Brands: Rimso-50 http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202196.html
http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202911.html ·
Systemic - U.S. Brands: Tetramune http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202911.html
Gold Compounds ·
Systemic - U.S. Brands: Myochrysine; Ridaura; Solganal http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202264.html
Histamine H 2 -Receptor Antagonists ·
Systemic - U.S. Brands: Axid; Axid AR; Mylanta AR Acid Reducer; Pepcid; Pepcid AC Acid Controller; Pepcid I.V. Pepcid RPD; Tagamet; Tagamet HB; Zantac; Zantac EFFERdose Granules; Zantac EFFERdose Tablets http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202283.html
Hyaluronate Sodium ·
Systemic - U.S. Brands: Hyalgan http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/203531.html
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Hyaluronate Sodium Derivative ·
Systemic - U.S. Brands: Synvisc http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/203582.html
Hydroxychloroquine ·
Systemic - U.S. Brands: Plaquenil http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202288.html
Infliximab ·
Systemic - U.S. Brands: Remicade http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/203667.html
Leflunomide ·
Systemic - U.S. Brands: Arava http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/203680.html
Meloxicam ·
Systemic - U.S. Brands: Mobic http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/500131.html
Methotrexate for Noncancerous Conditions ·
Systemic - U.S. Brands: Folex; Rheumatrex http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202356.html
Octreotide ·
Systemic - U.S. Brands: Sandostatin http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202421.html
Penicillamine ·
Systemic - U.S. Brands: Cuprimine; Depen http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202445.html
Probenecid ·
Systemic - U.S. Brands: Benemid; Probalan http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202480.html
Probenecid and Colchicine ·
Systemic - U.S. Brands: ColBenemid; Col-Probenecid; Proben-C http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202481.html
Rofecoxib ·
Systemic - U.S. Brands: Vioxx http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/203782.html
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Salicylates ·
Systemic - U.S. Brands: Acuprin 81; Amigesic; Anacin Caplets; Anacin Maximum Strength; Anacin Tablets; Anaflex 750; Arthritis Pain Ascriptin; Arthritis Pain Formula; Arthritis Strength Bufferin; Arthropan; Aspergum; Aspirin Regimen Bayer Adult Low Dose; Aspirin Regimen Bayer R http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202515.html
Sucralfate ·
Oral - U.S. Brands: Carafate http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202533.html
Sulfasalazine ·
Systemic - U.S. Brands: Azulfidine http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202537.html
Sulfinpyrazone ·
Systemic - U.S. Brands: Anturane http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202538.html
Tetracyclines ·
Systemic - U.S. Brands: Achromycin V; Declomycin; Doryx; Dynacin; Minocin; Monodox; Terramycin; Vibramycin; Vibra-Tabs http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202552.html
Vitamin D and Related Compounds ·
Systemic - U.S. Brands: Calciferol; Calciferol Drops; Calcijex; Calderol; DHT; DHT Intensol; Drisdol; Drisdol Drops; Hectorol; Hytakerol; Rocaltrol; Zemplar http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202597.html
Commercial Databases In addition to the medications listed in the USP above, a number of commercial sites are available by subscription to physicians and their institutions. Or, you may be able to access these sources from your local medical library.
Mosby’s Drug ConsultÔ Mosby’s Drug ConsultÔ database (also available on CD-ROM and book format) covers 45,000 drug products including generics and international brands. It provides prescribing information, drug interactions, and patient information. Subscription information is available at the following hyperlink: http://www.mosbysdrugconsult.com/.
PDRhealth The PDRhealth database is a free-to-use, drug information search engine that has been written for the public in layman’s terms. It contains FDA-approved drug information adapted from the Physicians’ Desk Reference (PDR) database. PDRhealth can be searched by
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brand name, generic name, or indication. It features multiple drug interactions reports. Search PDRhealth at http://www.pdrhealth.com/drug_info/index.html.
Other Web Sites Drugs.com (www.drugs.com) reproduces the information in the Pharmacopeia as well as commercial information. You may also want to consider the Web site of the Medical Letter, Inc. (http://www.medletter.com/) which allows users to download articles on various drugs and therapeutics for a nominal fee.
Researching Orphan Drugs Although the list of orphan drugs is revised on a daily basis, you can quickly research orphan drugs that might be applicable to arthritis by using the database managed by the National Organization for Rare Disorders, Inc. (NORD), at http://www.rarediseases.org/. Scroll down the page, and on the left toolbar, click on “Orphan Drug Designation Database.” On this page (http://www.rarediseases.org/search/noddsearch.html), type “arthritis” (or synonyms) into the search box, and click “Submit Query.” When you receive your results, note that not all of the drugs may be relevant, as some may have been withdrawn from orphan status. Write down or print out the name of each drug and the relevant contact information. From there, visit the Pharmacopeia Web site and type the name of each orphan drug into the search box at http://www.nlm.nih.gov/medlineplus/druginformation.html. You may need to contact the sponsor or NORD for further information. NORD conducts “early access programs for investigational new drugs (IND) under the Food and Drug Administration’s (FDA’s) approval ‘Treatment INDs’ programs which allow for a limited number of individuals to receive investigational drugs before FDA marketing approval.” If the orphan product about which you are seeking information is approved for marketing, information on side effects can be found on the product’s label. If the product is not approved, you may need to contact the sponsor. The following is a list of orphan drugs currently listed in the NORD Orphan Drug Designation Database for arthritis: ·
human gammaglobulin http://www.rarediseases.org/nord/search/nodd_full?code=1114
·
Interleukin-1 receptor antagonist, human recombina (trade name: Antril) http://www.rarediseases.org/nord/search/nodd_full?code=124
·
Methotrexate (trade name: Rheumatrex) http://www.rarediseases.org/nord/search/nodd_full?code=114
·
Immune globulin intravenous (human) (trade name: Iveegam, Immuno) http://www.rarediseases.org/nord/search/nodd_full?code=51
·
Purified type II collagen (trade name: Colloral) http://www.rarediseases.org/nord/search/nodd_full?code=448
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·
Gammalinolenic acid http://www.rarediseases.org/nord/search/nodd_full?code=716
·
Interferon Beta-1a (trade name: Avonex) http://www.rarediseases.org/nord/search/nodd_full?code=941
·
Recombinant human tumor necrosis factor receptor f (trade name: Enbrel) http://www.rarediseases.org/nord/search/nodd_full?code=945
If you have any questions about a medical treatment, the FDA may have an office near you. Look for their number in the blue pages of the phone book. You can also contact the FDA through its toll-free number, 1-888-INFO-FDA (1-888-463-6332), or on the World Wide Web at www.fda.gov.
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ONLINE GLOSSARIES The Internet provides access to a number of free-to-use medical dictionaries. The National Library of Medicine has compiled the following list of online dictionaries: ·
ADAM Medical Encyclopedia (A.D.A.M., Inc.), comprehensive medical reference: http://www.nlm.nih.gov/medlineplus/encyclopedia.html
·
MedicineNet.com Medical Dictionary (MedicineNet, Inc.): http://www.medterms.com/Script/Main/hp.asp
·
Merriam-Webster Medical Dictionary (Inteli-Health, Inc.): http://www.intelihealth.com/IH/
·
Multilingual Glossary of Technical and Popular Medical Terms in Eight European Languages (European Commission) - Danish, Dutch, English, French, German, Italian, Portuguese, and Spanish: http://allserv.rug.ac.be/~rvdstich/eugloss/welcome.html
·
On-line Medical Dictionary (CancerWEB): http://cancerweb.ncl.ac.uk/omd/
·
Rare Diseases Terms (Office of Rare Diseases): http://ord.aspensys.com/asp/diseases/diseases.asp
·
Technology Glossary (National Library of Medicine) - Health Care Technology: http://www.nlm.nih.gov/nichsr/ta101/ta10108.htm
Beyond these, MEDLINEplus contains a very patient-friendly encyclopedia covering every aspect of medicine (licensed from A.D.A.M., Inc.). The ADAM Medical Encyclopedia can be accessed at http://www.nlm.nih.gov/medlineplus/encyclopedia.html. ADAM is also available on commercial Web sites such as drkoop.com (http://www.drkoop.com/) and Web MD (http://my.webmd.com/adam/asset/adam_disease_articles/a_to_z/a). The NIH suggests the following Web sites in the ADAM Medical Encyclopedia when searching for information on arthritis: ·
Basic Guidelines for Arthritis Arthritis Web site: http://www.nlm.nih.gov/medlineplus/ency/article/001243.htm Arthritis - resources Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002183.htm Autoimmune disorders Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000816.htm Reiter's syndrome Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000440.htm
·
Signs & Symptoms for Arthritis Ankle pain Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003167.htm
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Eye pain Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003032.htm Fever Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003090.htm Heel pain Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003181.htm Hip pain Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003179.htm Incontinence Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003142.htm Joint pain Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003261.htm Joint swelling Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003262.htm Knee pain Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003187.htm Low back pain Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003108.htm Penis pain Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003166.htm Redness of the eye Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003031.htm Skin lesions Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003220.htm Skin redness or inflammation Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003220.htm Swelling Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003103.htm Unexplained weight loss Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003107.htm Urinary hesitancy Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003143.htm Urinary urgency Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003140.htm
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Weakness Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003174.htm Weight loss Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003107.htm ·
Diagnostics and Tests for Arthritis Histocompatibility antigens Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003550.htm HLA-B27 antigen Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003551.htm Joint X-rays Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003810.htm Ulcers Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003228.htm X-ray Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003337.htm
·
Surgery and Procedures for Arthritis Knee joint replacement Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002974.htm Total knee joint replacement Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002974.htm
·
Background Topics for Arthritis Analgesics Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002123.htm Chronic Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002312.htm Exercise Web site: http://www.nlm.nih.gov/medlineplus/ency/article/001941.htm Fracture Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000001.htm Pain relievers Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002123.htm Penis Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002279.htm
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Physical examination Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002274.htm Precipitating Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002275.htm
Online Dictionary Directories The following are additional online directories compiled by the National Library of Medicine, including a number of specialized medical dictionaries: ·
Medical Dictionaries: Medical & Biological (World Health Organization): http://www.who.int/hlt/virtuallibrary/English/diction.htm#Medical
·
MEL-Michigan Electronic Library List of Online Health and Medical Dictionaries (Michigan Electronic Library): http://mel.lib.mi.us/health/health-dictionaries.html
·
Patient Education: Glossaries (DMOZ Open Directory Project): http://dmoz.org/Health/Education/Patient_Education/Glossaries/
·
Web of Online Dictionaries (Bucknell University): http://www.yourdictionary.com/diction5.html#medicine
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ARTHRITIS DICTIONARY The definitions below are derived from official public sources, including the National Institutes of Health [NIH] and the European Union [EU]. 17-Hydroxyprogesterone: progesterone. [NIH]
A hydroxyprogesterone with medical uses similar to that of
Aberrant: Wandering or deviating from the usual or normal course. [EU] Ablation: The removal of an organ by surgery. [NIH] Abscess: Accumulation of purulent material in tissues, organs, or circumscribed spaces, usually associated with signs of infection. [NIH] Acanthocephala: A phylum of parasitic worms, closely related to tapeworms and containing two genera: Moniliformis, which sometimes infects man, and Macracanthorhynchus, which infects swine. [NIH] Acceptor: A substance which, while normally not oxidized by oxygen or reduced by hydrogen, can be oxidized or reduced in presence of a substance which is itself undergoing oxidation or reduction. [NIH] Acculturation: Process of cultural change in which one group or members of a group assimilates various cultural patterns from another. [NIH] Acetaminophen: Analgesic antipyretic derivative of acetanilide. It has weak antiinflammatory properties and is used as a common analgesic, but may cause liver, blood cell, and kidney damage. [NIH] Acetylcholine: A neurotransmitter. Acetylcholine in vertebrates is the major transmitter at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system. It is generally not used as an administered drug because it is broken down very rapidly by cholinesterases, but it is useful in some ophthalmological applications. [NIH] Acidosis: A pathologic condition resulting from accumulation of acid or depletion of the alkaline reserve (bicarbonate content) in the blood and body tissues, and characterized by an increase in hydrogen ion concentration. [EU] Acromion: The lateral extension of the spine of the scapula and the highest point of the shoulder. [NIH] Acrylamide: A colorless, odorless, highly water soluble vinyl monomer formed from the hydration of acrylonitrile. It is primarily used in research laboratories for electrophoresis, chromatography, and electron microscopy and in the sewage and wastewater treatment industries. [NIH] Acrylonitrile: A highly poisonous compound used widely in the manufacture of plastics, adhesives and synthetic rubber. [NIH] Actin: Essential component of the cell skeleton. [NIH] Activities of Daily Living: The performance of the basic activities of self care, such as dressing, ambulation, eating, etc., in rehabilitation. [NIH] Acupuncture Points: Designated locations along nerves or organ meridians for inserting acupuncture needles. [NIH] Acute renal: A condition in which the kidneys suddenly stop working. In most cases,
580 Arthritis
kidneys can recover from almost complete loss of function. [NIH] Acyclovir: Functional analog of the nucleoside guanosine. It acts as an antimetabolite, especially in viruses. It is used as an antiviral agent, especially in herpes infections. [NIH] Adaptability: Ability to develop some form of tolerance to conditions extremely different from those under which a living organism evolved. [NIH] Adenine: A purine base and a fundamental unit of adenine nucleotides. [NIH] Adenocarcinoma: A malignant epithelial tumor with a glandular organization. [NIH] Adenosine: A nucleoside that is composed of adenine and d-ribose. Adenosine or adenosine derivatives play many important biological roles in addition to being components of DNA and RNA. Adenosine itself is a neurotransmitter. [NIH] Adenosine Deaminase: An enzyme that catalyzes the hydrolysis of adenosine to inosine with the elimination of ammonia. Since there are wide tissue and species variations in the enzyme, it has been used as a tool in the study of human and animal genetics and in medical diagnosis. EC 3.5.4.4. [NIH] Adenovirus: A group of viruses that cause respiratory tract and eye infections. Adenoviruses used in gene therapy are altered to carry a specific tumor-fighting gene. [NIH] Adenylate Cyclase: An enzyme of the lyase class that catalyzes the formation of cyclic AMP and pyrophosphate from ATP. EC 4.6.1.1. [NIH] Adipose Tissue: Connective tissue composed of fat cells lodged in the meshes of areolar tissue. [NIH] Adjuvant: A substance which aids another, such as an auxiliary remedy; in immunology, nonspecific stimulator (e.g., BCG vaccine) of the immune response. [EU] Adolescence: The period of life beginning with the appearance of secondary sex characteristics and terminating with the cessation of somatic growth. The years usually referred to as adolescence lie between 13 and 18 years of age. [NIH] Adrenal Cortex: The outer layer of the adrenal gland. It secretes mineralocorticoids, androgens, and glucocorticoids. [NIH] Adrenal Glands: Paired glands situated in the retroperitoneal tissues at the superior pole of each kidney. [NIH] Adrenal Medulla: The inner part of the adrenal gland; it synthesizes, stores and releases catecholamines. [NIH] Adrenergic: Activated by, characteristic of, or secreting epinephrine or substances with similar activity; the term is applied to those nerve fibres that liberate norepinephrine at a synapse when a nerve impulse passes, i.e., the sympathetic fibres. [EU] Agar: A complex sulfated polymer of galactose units, extracted from Gelidium cartilagineum, Gracilaria confervoides, and related red algae. It is used as a gel in the preparation of solid culture media for microorganisms, as a bulk laxative, in making emulsions, and as a supporting medium for immunodiffusion and immunoelectrophoresis. [NIH]
Age Groups: Persons classified by age from birth (infant, newborn) to octogenarians and older (aged, 80 and over). [NIH] Age of Onset: The age or period of life at which a disease or the initial symptoms or manifestations of a disease appear in an individual. [NIH] Aged, 80 and Over: A person 80 years of age and older. [NIH] Agonists: Drugs that trigger an action from a cell or another drug. [NIH]
Dictionary 581
A-HA: First enzyme in the biosynthetic pathway of branched-chain amino acids. [NIH] Alanine: A non-essential amino acid that occurs in high levels in its free state in plasma. It is produced from pyruvate by transamination. It is involved in sugar and acid metabolism, increases immunity, and provides energy for muscle tissue, brain, and the central nervous system. [NIH] Albumin: 1. Any protein that is soluble in water and moderately concentrated salt solutions and is coagulable by heat. 2. Serum albumin; the major plasma protein (approximately 60 per cent of the total), which is responsible for much of the plasma colloidal osmotic pressure and serves as a transport protein carrying large organic anions, such as fatty acids, bilirubin, and many drugs, and also carrying certain hormones, such as cortisol and thyroxine, when their specific binding globulins are saturated. Albumin is synthesized in the liver. Low serum levels occur in protein malnutrition, active inflammation and serious hepatic and renal disease. [EU] Algorithms: A procedure consisting of a sequence of algebraic formulas and/or logical steps to calculate or determine a given task. [NIH] Alkaline: Having the reactions of an alkali. [EU] Alkaloid: A member of a large group of chemicals that are made by plants and have nitrogen in them. Some alkaloids have been shown to work against cancer. [NIH] Alkylating Agents: Highly reactive chemicals that introduce alkyl radicals into biologically active molecules and thereby prevent their proper functioning. Many are used as antineoplastic agents, but most are very toxic, with carcinogenic, mutagenic, teratogenic, and immunosuppressant actions. They have also been used as components in poison gases. [NIH]
Alleles: Mutually exclusive forms of the same gene, occupying the same locus on homologous chromosomes, and governing the same biochemical and developmental process. [NIH] Allergen: An antigenic substance capable of producing immediate-type hypersensitivity (allergy). [EU] Allo: A female hormone. [NIH] Allogeneic: Taken from different individuals of the same species. [NIH] Allopurinol: A xanthine oxidase inhibitor that decreases uric acid production. [NIH] Alopecia: Absence of hair from areas where it is normally present. [NIH] Alpha-1: A protein with the property of inactivating proteolytic enzymes such as leucocyte collagenase and elastase. [NIH] Alpha-helix: One of the secondary element of protein. [NIH] Alphavirus: A genus of Togaviridae, also known as Group A arboviruses, serologically related to each other but not to other Togaviridae. The viruses are transmitted by mosquitoes. The type species is the sindbis virus. [NIH] Alternative Splicing: A process whereby multiple protein isoforms are generated from a single gene. Alternative splicing involves the splicing together of nonconsecutive exons during the processing of some, but not all, transcripts of the gene. Thus a particular exon may be connected to any one of several alternative exons to form messenger RNA. The alternative forms produce proteins in which one part is common while the other part is different. [NIH] Alveolar Process: The thickest and spongiest part of the maxilla and mandible hollowed out into deep cavities for the teeth. [NIH]
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Alveolitis: Inflammation of an alveolus. Called also odontobothritis. [EU] Amber: A yellowish fossil resin, the gum of several species of coniferous trees, found in the alluvial deposits of northeastern Germany. It is used in molecular biology in the analysis of organic matter fossilized in amber. [NIH] Ambulatory Care: Health care services provided to patients on an ambulatory basis, rather than by admission to a hospital or other health care facility. The services may be a part of a hospital, augmenting its inpatient services, or may be provided at a free-standing facility. [NIH]
Amebiasis: Infection with any of various amebae. It is an asymptomatic carrier state in most individuals, but diseases ranging from chronic, mild diarrhea to fulminant dysentery may occur. [NIH] Ameliorated: A changeable condition which prevents the consequence of a failure or accident from becoming as bad as it otherwise would. [NIH] Ameliorating: A changeable condition which prevents the consequence of a failure or accident from becoming as bad as it otherwise would. [NIH] Amenorrhea: Absence of menstruation. [NIH] Amine: An organic compound containing nitrogen; any member of a group of chemical compounds formed from ammonia by replacement of one or more of the hydrogen atoms by organic (hydrocarbon) radicals. The amines are distinguished as primary, secondary, and tertiary, according to whether one, two, or three hydrogen atoms are replaced. The amines include allylamine, amylamine, ethylamine, methylamine, phenylamine, propylamine, and many other compounds. [EU] Amino acid: Any organic compound containing an amino (-NH2 and a carboxyl (- COOH) group. The 20 a-amino acids listed in the accompanying table are the amino acids from which proteins are synthesized by formation of peptide bonds during ribosomal translation of messenger RNA; all except glycine, which is not optically active, have the L configuration. Other amino acids occurring in proteins, such as hydroxyproline in collagen, are formed by posttranslational enzymatic modification of amino acids residues in polypeptide chains. There are also several important amino acids, such as the neurotransmitter y-aminobutyric acid, that have no relation to proteins. Abbreviated AA. [EU] Amino Acid Sequence: The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining protein conformation. [NIH] Amino Acid Substitution: The naturally occurring or experimentally induced replacement of one or more amino acids in a protein with another. If a functionally equivalent amino acid is substituted, the protein may retain wild-type activity. Substitution may also diminish or eliminate protein function. Experimentally induced substitution is often used to study enzyme activities and binding site properties. [NIH] Amino-terminal: The end of a protein or polypeptide chain that contains a free amino group (-NH2). [NIH] Amplification: The production of additional copies of a chromosomal DNA sequence, found as either intrachromosomal or extrachromosomal DNA. [NIH] Ampulla: A sac-like enlargement of a canal or duct. [NIH] Amyloid: A general term for a variety of different proteins that accumulate as extracellular fibrils of 7-10 nm and have common structural features, including a beta-pleated sheet conformation and the ability to bind such dyes as Congo red and thioflavine (Kandel, Schwartz, and Jessel, Principles of Neural Science, 3rd ed). [NIH]
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Amyloidosis: A group of diseases in which protein is deposited in specific organs (localized amyloidosis) or throughout the body (systemic amyloidosis). Amyloidosis may be either primary (with no known cause) or secondary (caused by another disease, including some types of cancer). Generally, primary amyloidosis affects the nerves, skin, tongue, joints, heart, and liver; secondary amyloidosis often affects the spleen, kidneys, liver, and adrenal glands. [NIH] Amyotrophy: A type of diabetic neuropathy that causes muscle weakness and wasting. [NIH]
Anabolic: Relating to, characterized by, or promoting anabolism. [EU] Anaemia: A reduction below normal in the number of erythrocytes per cu. mm., in the quantity of haemoglobin, or in the volume of packed red cells per 100 ml. of blood which occurs when the equilibrium between blood loss (through bleeding or destruction) and blood production is disturbed. [EU] Anaerobic: 1. Lacking molecular oxygen. 2. Growing, living, or occurring in the absence of molecular oxygen; pertaining to an anaerobe. [EU] Anaesthesia: Loss of feeling or sensation. Although the term is used for loss of tactile sensibility, or of any of the other senses, it is applied especially to loss of the sensation of pain, as it is induced to permit performance of surgery or other painful procedures. [EU] Analgesic: An agent that alleviates pain without causing loss of consciousness. [EU] Analog: In chemistry, a substance that is similar, but not identical, to another. [NIH] Analogous: Resembling or similar in some respects, as in function or appearance, but not in origin or development;. [EU] Analytes: A component of a test sample the presence of which has to be demonstrated. The term "analyte" includes where appropriate formed from the analyte during the analyses. [NIH]
Anaphylactic: Pertaining to anaphylaxis. [EU] Anaphylatoxins: The family of peptides C3a, C4a, C5a, and C5a des-arginine produced in the serum during complement activation. They produce smooth muscle contraction, mast cell histamine release, affect platelet aggregation, and act as mediators of the local inflammatory process. The order of anaphylatoxin activity from strongest to weakest is C5a, C3a, C4a, and C5a des-arginine. The latter is the so-called "classical" anaphylatoxin but shows no spasmogenic activity though it contains some chemotactic ability. [NIH] Anaphylaxis: An acute hypersensitivity reaction due to exposure to a previously encountered antigen. The reaction may include rapidly progressing urticaria, respiratory distress, vascular collapse, systemic shock, and death. [NIH] Androgens: A class of sex hormones associated with the development and maintenance of the secondary male sex characteristics, sperm induction, and sexual differentiation. In addition to increasing virility and libido, they also increase nitrogen and water retention and stimulate skeletal growth. [NIH] Anecdotal report: An incomplete description of the medical and treatment history of one or more patients. Anecdotal reports may be published in places other than peer-reviewed, scientific journals. [NIH] Anemia: A reduction in the number of circulating erythrocytes or in the quantity of hemoglobin. [NIH] Anergic: 1. Characterized by abnormal inactivity; inactive. 2. Marked by asthenia or lack of energy. 3. Pertaining to anergy. [EU] Anergy: Absence of immune response to particular substances. [NIH]
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Anesthesia: A state characterized by loss of feeling or sensation. This depression of nerve function is usually the result of pharmacologic action and is induced to allow performance of surgery or other painful procedures. [NIH] Anesthetics: Agents that are capable of inducing a total or partial loss of sensation, especially tactile sensation and pain. They may act to induce general anesthesia, in which an unconscious state is achieved, or may act locally to induce numbness or lack of sensation at a targeted site. [NIH] Angina: Chest pain that originates in the heart. [NIH] Angiogenesis: Blood vessel formation. Tumor angiogenesis is the growth of blood vessels from surrounding tissue to a solid tumor. This is caused by the release of chemicals by the tumor. [NIH] Angiogenesis inhibitor: A substance that may prevent the formation of blood vessels. In anticancer therapy, an angiogenesis inhibitor prevents the growth of blood vessels from surrounding tissue to a solid tumor. [NIH] Animal model: An animal with a disease either the same as or like a disease in humans. Animal models are used to study the development and progression of diseases and to test new treatments before they are given to humans. Animals with transplanted human cancers or other tissues are called xenograft models. [NIH] Anions: Negatively charged atoms, radicals or groups of atoms which travel to the anode or positive pole during electrolysis. [NIH] Annealing: The spontaneous alignment of two single DNA strands to form a double helix. [NIH]
Anomalies: Birth defects; abnormalities. [NIH] Anorexia: Clinical manifestation consisting of a physiopathological lack or loss of appetite accompanied by an aversion to food and the inability to eat. [NIH] Anorexia Nervosa: The chief symptoms are inability to eat, weight loss, and amenorrhea. [NIH]
Antagonism: Interference with, or inhibition of, the growth of a living organism by another living organism, due either to creation of unfavorable conditions (e. g. exhaustion of food supplies) or to production of a specific antibiotic substance (e. g. penicillin). [NIH] Anterior chamber: The space in front of the iris and behind the cornea. [NIH] Anterior Cruciate Ligament: A strong ligament of the knee that originates from the posteromedial portion of the lateral condyle of the femur, passes anteriorly and inferiorly between the condyles, and attaches to the depression in front of the intercondylar eminence of the tibia. [NIH] Anthralin: An anti-inflammatory anthracene derivative used for the treatment of dermatoses, especially psoriasis. It may cause folliculitis. [NIH] Antibiotic Prophylaxis: Use of antibiotics before, during, or after a diagnostic, therapeutic, or surgical procedure to prevent infectious complications. [NIH] Antibodies: Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the antigen that induced their synthesis in cells of the lymphoid series (especially plasma cells), or with an antigen closely related to it. [NIH] Antibody: A type of protein made by certain white blood cells in response to a foreign substance (antigen). Each antibody can bind to only a specific antigen. The purpose of this binding is to help destroy the antigen. Antibodies can work in several ways, depending on the nature of the antigen. Some antibodies destroy antigens directly. Others make it easier for white blood cells to destroy the antigen. [NIH]
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Antibody Affinity: A measure of the binding strength between antibody and a simple hapten or antigen determinant. It depends on the closeness of stereochemical fit between antibody combining sites and antigen determinants, on the size of the area of contact between them, and on the distribution of charged and hydrophobic groups. It includes the concept of "avidity," which refers to the strength of the antigen-antibody bond after formation of reversible complexes. [NIH] Antibody therapy: Treatment with an antibody, a substance that can directly kill specific tumor cells or stimulate the immune system to kill tumor cells. [NIH] Antibody-Dependent Cell Cytotoxicity: The phenomenon of antibody-mediated target cell destruction by non-sensitized effector cells. The identity of the target cell varies, but it must possess surface IgG whose Fc portion is intact. The effector cell is a "killer" cell possessing Fc receptors. It may be a lymphocyte lacking conventional B- or T-cell markers, or a monocyte, macrophage, or polynuclear leukocyte, depending on the identity of the target cell. The reaction is complement-independent. [NIH] Anticoagulant: A drug that helps prevent blood clots from forming. Also called a blood thinner. [NIH] Antidote: A remedy for counteracting a poison. [EU] Antigen: Any substance which is capable, under appropriate conditions, of inducing a specific immune response and of reacting with the products of that response, that is, with specific antibody or specifically sensitized T-lymphocytes, or both. Antigens may be soluble substances, such as toxins and foreign proteins, or particulate, such as bacteria and tissue cells; however, only the portion of the protein or polysaccharide molecule known as the antigenic determinant (q.v.) combines with antibody or a specific receptor on a lymphocyte. Abbreviated Ag. [EU] Antigen-Antibody Complex: The complex formed by the binding of antigen and antibody molecules. The deposition of large antigen-antibody complexes leading to tissue damage causes immune complex diseases. [NIH] Antigen-presenting cell: APC. A cell that shows antigen on its surface to other cells of the immune system. This is an important part of an immune response. [NIH] Anti-infective: An agent that so acts. [EU] Anti-inflammatory: Having to do with reducing inflammation. [NIH] Antilymphocyte Serum: Serum containing gamma-globulins which are antibodies for lymphocyte antigens. It is used both as a test for histocompatibility and therapeutically in transplantation. [NIH] Antimetabolite: A chemical that is very similar to one required in a normal biochemical reaction in cells. Antimetabolites can stop or slow down the reaction. [NIH] Antineoplastic: Inhibiting or preventing the development of neoplasms, checking the maturation and proliferation of malignant cells. [EU] Antineoplastic Agents: Substances that inhibit or prevent the proliferation of neoplasms. [NIH]
Antioxidant: A substance that prevents damage caused by free radicals. Free radicals are highly reactive chemicals that often contain oxygen. They are produced when molecules are split to give products that have unpaired electrons. This process is called oxidation. [NIH] Antipruritic: Relieving or preventing itching. [EU] Antipyretic: An agent that relieves or reduces fever. Called also antifebrile, antithermic and febrifuge. [EU]
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Antirheumatic Agents: Drugs that are used to treat rheumatoid arthritis. [NIH] Anuria: Inability to form or excrete urine. [NIH] Anus: The opening of the rectum to the outside of the body. [NIH] Anxiety: Persistent feeling of dread, apprehension, and impending disaster. [NIH] Aorta: The main trunk of the systemic arteries. [NIH] Aortitis: Inflammation of the wall of the aorta. [NIH] Apheresis: Components being separated out, as leukapheresis, plasmapheresis, plateletpheresis. [NIH] Apolipoproteins: The protein components of lipoproteins which remain after the lipids to which the proteins are bound have been removed. They play an important role in lipid transport and metabolism. [NIH] Aponeurosis: Tendinous expansion consisting of a fibrous or membranous sheath which serves as a fascia to enclose or bind a group of muscles. [NIH] Apoptosis: One of the two mechanisms by which cell death occurs (the other being the pathological process of necrosis). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA (DNA fragmentation) at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth. [NIH] Applicability: A list of the commodities to which the candidate method can be applied as presented or with minor modifications. [NIH] Aqueous: Having to do with water. [NIH] Arachidonate 12-Lipoxygenase: An enzyme that catalyzes the oxidation of arachidonic acid to yield 12-hydroperoxyarachidonate (12-HPETE) which is itself rapidly converted by a peroxidase to 12-hydroxy-5,8,10,14-eicosatetraenoate (12-HETE). The 12-hydroperoxides are preferentially formed in platelets. EC 1.13.11.31. [NIH] Arachidonate 15-Lipoxygenase: An enzyme that catalyzes the oxidation of arachidonic acid to yield 15-hydroperoxyarachidonate (15-HPETE) which is rapidly converted to 15-hydroxy5,8,11,13-eicosatetraenoate (15-HETE). The 15-hydroperoxides are preferentially formed in neutrophils and lymphocytes. EC 1.13.11.33. [NIH] Arachidonate Lipoxygenases: Enzymes catalyzing the oxidation of arachidonic acid to hydroperoxyarachidonates (HPETES). These products are then rapidly converted by a peroxidase to hydroxyeicosatetraenoic acids (HETES). The positional specificity of the enzyme reaction varies from tissue to tissue. The final lipoxygenase pathway leads to the leukotrienes. EC 1.13.11.- . [NIH] Arachidonic Acid: An unsaturated, essential fatty acid. It is found in animal and human fat as well as in the liver, brain, and glandular organs, and is a constituent of animal phosphatides. It is formed by the synthesis from dietary linoleic acid and is a precursor in the biosynthesis of prostaglandins, thromboxanes, and leukotrienes. [NIH] Arginase: A ureahydrolase that catalyzes the hydrolysis of arginine or canavanine to yield L-ORNITHINE and urea. Deficiency of this enzyme causes hyperargininemia. EC 3.5.3.1. [NIH]
Arginine: An essential amino acid that is physiologically active in the L-form. [NIH] Arterioles: The smallest divisions of the arteries located between the muscular arteries and
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the capillaries. [NIH] Arteriosclerosis: Thickening and loss of elasticity of arterial walls. Atherosclerosis is the most common form of arteriosclerosis and involves lipid deposition and thickening of the intimal cell layers within arteries. Additional forms of arteriosclerosis involve calcification of the media of muscular arteries (Monkeberg medial calcific sclerosis) and thickening of the walls of small arteries or arterioles due to cell proliferation or hyaline deposition (arteriolosclerosis). [NIH] Arteritis: Inflammation of an artery. [NIH] Arthralgia: Pain in the joint. [NIH] Arthropathy: Any joint disease. [EU] Arthroplasty: Surgical reconstruction of a joint to relieve pain or restore motion. [NIH] Arthroscopy: Endoscopic examination, therapy and surgery of the joint. [NIH] Arthrosis: A disease of a joint. [EU] Articular: Of or pertaining to a joint. [EU] Articulation: The relationship of two bodies by means of a moveable joint. [NIH] Aseptic: Free from infection or septic material; sterile. [EU] Aspartic: The naturally occurring substance is L-aspartic acid. One of the acidic-aminoacids is obtained by the hydrolysis of proteins. [NIH] Aspartic Acid: One of the non-essential amino acids commonly occurring in the L-form. It is found in animals and plants, especially in sugar cane and sugar beets. It may be a neurotransmitter. [NIH] Aspartic Endopeptidases: A sub-subclass of endopeptidases that depend on an aspartic acid residue for their activity. EC 3.4.23. [NIH] Aspirate: Fluid withdrawn from a lump, often a cyst, or a nipple. [NIH] Aspiration: The act of inhaling. [NIH] Assay: Determination of the amount of a particular constituent of a mixture, or of the biological or pharmacological potency of a drug. [EU] Asthenia: Clinical sign or symptom manifested as debility, or lack or loss of strength and energy. [NIH] Asymptomatic: Having no signs or symptoms of disease. [NIH] Atherogenic: Causing the formation of plaque in the lining of the arteries. [NIH] Atrial: Pertaining to an atrium. [EU] Atrioventricular: Pertaining to an atrium of the heart and to a ventricle. [EU] Atrium: A chamber; used in anatomical nomenclature to designate a chamber affording entrance to another structure or organ. Usually used alone to designate an atrium of the heart. [EU] Atrophy: Decrease in the size of a cell, tissue, organ, or multiple organs, associated with a variety of pathological conditions such as abnormal cellular changes, ischemia, malnutrition, or hormonal changes. [NIH] Attenuation: Reduction of transmitted sound energy or its electrical equivalent. [NIH] Auranofin: An oral chrysotherapeutic agent for the treatment of rheumatoid arthritis. Its exact mechanism of action is unknown, but it is believed to act via immunological mechanisms and alteration of lysosomal enzyme activity. Its efficacy is slightly less than that of injected gold salts, but it is better tolerated, and side effects which occur are potentially
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less serious. [NIH] Autacoids: A chemically diverse group of substances produced by various tissues in the body that cause slow contraction of smooth muscle; they have other intense but varied pharmacologic activities. [NIH] Autoantibodies: Antibodies that react with self-antigens (autoantigens) of the organism that produced them. [NIH] Autoantigens: Endogenous tissue constituents that have the ability to interact with autoantibodies and cause an immune response. [NIH] Autoimmune disease: A condition in which the body recognizes its own tissues as foreign and directs an immune response against them. [NIH] Autoimmune Hepatitis: A liver disease caused when the body's immune system destroys liver cells for no known reason. [NIH] Autoimmunity: Process whereby the immune system reacts against the body's own tissues. Autoimmunity may produce or be caused by autoimmune diseases. [NIH] Autologous: Taken from an individual's own tissues, cells, or DNA. [NIH] Autologous bone marrow transplantation: A procedure in which bone marrow is removed from a person, stored, and then given back to the person after intensive treatment. [NIH] Autonomic: Self-controlling; functionally independent. [EU] Autopsy: Postmortem examination of the body. [NIH] Avidity: The strength of the interaction of an antiserum with a multivalent antigen. [NIH] Axillary: Pertaining to the armpit area, including the lymph nodes that are located there. [NIH]
Axillary Artery: The continuation of the subclavian artery; it distributes over the upper limb, axilla, chest and shoulder. [NIH] Azithromycin: A semi-synthetic macrolide antibiotic structurally related to erythromycin. It has been used in the treatment of Mycobacterium avium intracellulare infections, toxoplasmosis, and cryptosporidiosis. [NIH] Backcross: A cross between a hybrid and either one of its parents. [NIH] Bacteremia: The presence of viable bacteria circulating in the blood. Fever, chills, tachycardia, and tachypnea are common acute manifestations of bacteremia. The majority of cases are seen in already hospitalized patients, most of whom have underlying diseases or procedures which render their bloodstreams susceptible to invasion. [NIH] Bacterial Infections: Infections by bacteria, general or unspecified. [NIH] Bacterial Physiology: Physiological processes and activities of bacteria. [NIH] Bactericidal: Substance lethal to bacteria; substance capable of killing bacteria. [NIH] Bacteriophage: A virus whose host is a bacterial cell; A virus that exclusively infects bacteria. It generally has a protein coat surrounding the genome (DNA or RNA). One of the coliphages most extensively studied is the lambda phage, which is also one of the most important. [NIH] Bacteriostatic: 1. Inhibiting the growth or multiplication of bacteria. 2. An agent that inhibits the growth or multiplication of bacteria. [EU] Bacterium: Microscopic organism which may have a spherical, rod-like, or spiral unicellular or non-cellular body. Bacteria usually reproduce through asexual processes. [NIH] Bacteriuria: The presence of bacteria in the urine with or without consequent urinary tract
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infection. Since bacteriuria is a clinical entity, the term does not preclude the use of urine/microbiology for technical discussions on the isolation and segregation of bacteria in the urine. [NIH] Balanitis: Inflammation of the glans penis. [NIH] Basal Ganglia: Large subcortical nuclear masses derived from the telencephalon and located in the basal regions of the cerebral hemispheres. [NIH] Basement Membrane: Ubiquitous supportive tissue adjacent to epithelium and around smooth and striated muscle cells. This tissue contains intrinsic macromolecular components such as collagen, laminin, and sulfated proteoglycans. As seen by light microscopy one of its subdivisions is the basal (basement) lamina. [NIH] Basophils: Granular leukocytes characterized by a relatively pale-staining, lobate nucleus and cytoplasm containing coarse dark-staining granules of variable size and stainable by basic dyes. [NIH] Baths: The immersion or washing of the body or any of its parts in water or other medium for cleansing or medical treatment. It includes bathing for personal hygiene as well as for medical purposes with the addition of therapeutic agents, such as alkalines, antiseptics, oil, etc. [NIH] Behavior Therapy: The application of modern theories of learning and conditioning in the treatment of behavior disorders. [NIH] Beta-pleated: Particular three-dimensional pattern of amyloidoses. [NIH] Beta-Thromboglobulin: A platelet-specific protein which is released when platelets aggregate. Elevated plasma levels have been reported after deep venous thrombosis, preeclampsia, myocardial infarction with mural thrombosis, and myeloproliferative disorders. Measurement of beta-thromboglobulin in biological fluids by radioimmunoassay is used for the diagnosis and assessment of progress of thromboembolic disorders. [NIH] Bifida: A defect in development of the vertebral column in which there is a central deficiency of the vertebral lamina. [NIH] Bilateral: Affecting both the right and left side of body. [NIH] Bile: An emulsifying agent produced in the liver and secreted into the duodenum. Its composition includes bile acids and salts, cholesterol, and electrolytes. It aids digestion of fats in the duodenum. [NIH] Bile Acids: Acids made by the liver that work with bile to break down fats. [NIH] Biliary: Having to do with the liver, bile ducts, and/or gallbladder. [NIH] Bioassays: Determination of the relative effective strength of a substance (as a vitamin, hormone, or drug) by comparing its effect on a test organism with that of a standard preparation. [NIH] Bioavailability: The degree to which a drug or other substance becomes available to the target tissue after administration. [EU] Biochemical: Relating to biochemistry; characterized by, produced by, or involving chemical reactions in living organisms. [EU] Biochemical reactions: In living cells, chemical reactions that help sustain life and allow cells to grow. [NIH] Biological response modifier: BRM. A substance that stimulates the body's response to infection and disease. [NIH] Biological therapy: Treatment to stimulate or restore the ability of the immune system to fight infection and disease. Also used to lessen side effects that may be caused by some
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cancer treatments. Also known as immunotherapy, biotherapy, or biological response modifier (BRM) therapy. [NIH] Biomarkers: Substances sometimes found in an increased amount in the blood, other body fluids, or tissues and that may suggest the presence of some types of cancer. Biomarkers include CA 125 (ovarian cancer), CA 15-3 (breast cancer), CEA (ovarian, lung, breast, pancreas, and GI tract cancers), and PSA (prostate cancer). Also called tumor markers. [NIH] Biomechanics: The study of the application of mechanical laws and the action of forces to living structures. [NIH] Biomolecular: A scientific field at the interface between advanced computing and biotechnology. [NIH] Biophysics: The science of physical phenomena and processes in living organisms. [NIH] Biopsy: Removal and pathologic examination of specimens in the form of small pieces of tissue from the living body. [NIH] Biopsy specimen: Tissue removed from the body and examined under a microscope to determine whether disease is present. [NIH] Biosynthesis: The building up of a chemical compound in the physiologic processes of a living organism. [EU] Biotechnology: Body of knowledge related to the use of organisms, cells or cell-derived constituents for the purpose of developing products which are technically, scientifically and clinically useful. Alteration of biologic function at the molecular level (i.e., genetic engineering) is a central focus; laboratory methods used include transfection and cloning technologies, sequence and structure analysis algorithms, computer databases, and gene and protein structure function analysis and prediction. [NIH] Biotransformation: The chemical alteration of an exogenous substance by or in a biological system. The alteration may inactivate the compound or it may result in the production of an active metabolite of an inactive parent compound. The alteration may be either nonsynthetic (oxidation-reduction, hydrolysis) or synthetic (glucuronide formation, sulfate conjugation, acetylation, methylation). This also includes metabolic detoxication and clearance. [NIH] Bladder: The organ that stores urine. [NIH] Blast phase: The phase of chronic myelogenous leukemia in which the number of immature, abnormal white blood cells in the bone marrow and blood is extremely high. Also called blast crisis. [NIH] Blastomyces: A genus of onygenacetous mitosporic fungi whose perfect state is Ajellomyces. The species Blastomyces dermatitidis (perfect state Ajellomyces dermatitidis) causes blastomycosis. [NIH] Blastomycosis: A fungal infection that may appear in two forms: 1) a primary lesion characterized by the formation of a small cutaneous nodule and small nodules along the lymphatics that may heal within several months; and 2) chronic granulomatous lesions characterized by thick crusts, warty growths, and unusual vascularity and infection in the middle or upper lobes of the lung. [NIH] Blind spot: (1) A small area of the retina where the optic nerve enters the eye; occurs normally in all eyes.(2) Any gap in the visual field corresponding to an area of the retina where no visual cells are present; associated with eye disease. [NIH] Blood Coagulation: The process of the interaction of blood coagulation factors that results in an insoluble fibrin clot. [NIH]
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Blood Glucose: Glucose in blood. [NIH] Blood Platelets: Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation. [NIH] Blood pressure: The pressure of blood against the walls of a blood vessel or heart chamber. Unless there is reference to another location, such as the pulmonary artery or one of the heart chambers, it refers to the pressure in the systemic arteries, as measured, for example, in the forearm. [NIH] Blood vessel: A tube in the body through which blood circulates. Blood vessels include a network of arteries, arterioles, capillaries, venules, and veins. [NIH] Blot: To transfer DNA, RNA, or proteins to an immobilizing matrix such as nitrocellulose. [NIH]
Blotting, Western: Identification of proteins or peptides that have been electrophoretically separated by blotting and transferred to strips of nitrocellulose paper. The blots are then detected by radiolabeled antibody probes. [NIH] Body Fluids: Liquid components of living organisms. [NIH] Body Mass Index: One of the anthropometric measures of body mass; it has the highest correlation with skinfold thickness or body density. [NIH] Bone Marrow: The soft tissue filling the cavities of bones. Bone marrow exists in two types, yellow and red. Yellow marrow is found in the large cavities of large bones and consists mostly of fat cells and a few primitive blood cells. Red marrow is a hematopoietic tissue and is the site of production of erythrocytes and granular leukocytes. Bone marrow is made up of a framework of connective tissue containing branching fibers with the frame being filled with marrow cells. [NIH] Bone Marrow Cells: Cells contained in the bone marrow including fat cells, stromal cells, megakaryocytes, and the immediate precursors of most blood cells. [NIH] Bone Resorption: Bone loss due to osteoclastic activity. [NIH] Bone scan: A technique to create images of bones on a computer screen or on film. A small amount of radioactive material is injected into a blood vessel and travels through the bloodstream; it collects in the bones and is detected by a scanner. [NIH] Boron: A trace element with the atomic symbol B, atomic number 5, and atomic weight 10.81. Boron-10, an isotope of boron, is used as a neutron absorber in boron neutron capture therapy. [NIH] Boron Neutron Capture Therapy: A technique for the treatment of neoplasms, especially gliomas and melanomas in which boron-10, an isotope, is introduced into the target cells followed by irradiation with thermal neutrons. [NIH] Bowel: The long tube-shaped organ in the abdomen that completes the process of digestion. There is both a small and a large bowel. Also called the intestine. [NIH] Brachial: All the nerves from the arm are ripped from the spinal cord. [NIH] Brachial Artery: The continuation of the axillary artery; it branches into the radial and ulnar arteries. [NIH] Brachytherapy: A collective term for interstitial, intracavity, and surface radiotherapy. It uses small sealed or partly-sealed sources that may be placed on or near the body surface or within a natural body cavity or implanted directly into the tissues. [NIH] Bradykinin: A nonapeptide messenger that is enzymatically produced from kallidin in the blood where it is a potent but short-lived agent of arteriolar dilation and increased capillary permeability. Bradykinin is also released from mast cells during asthma attacks, from gut
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walls as a gastrointestinal vasodilator, from damaged tissues as a pain signal, and may be a neurotransmitter. [NIH] Brain Infarction: The formation of an area of necrosis in the brain, including the cerebral hemispheres (cerebral infarction), thalami, basal ganglia, brain stem (brain stem infarctions), or cerebellum secondary to an insufficiency of arterial or venous blood flow. [NIH] Brain Stem: The part of the brain that connects the cerebral hemispheres with the spinal cord. It consists of the mesencephalon, pons, and medulla oblongata. [NIH] Brain Stem Infarctions: Infarctions that occur in the brain stem which is comprised of the midbrain, pons, and medulla. There are several named syndromes characterized by their distinctive clinical manifestations and specific sites of ischemic injury. [NIH] Bromelain: An enzyme found in pineapples that breaks down other proteins, such as collagen and muscle fiber, and has anti-inflammatory properties. It is used as a meat tenderizer in the food industry. [NIH] Bronchi: The larger air passages of the lungs arising from the terminal bifurcation of the trachea. [NIH] Bronchial: Pertaining to one or more bronchi. [EU] Bronchitis: Inflammation (swelling and reddening) of the bronchi. [NIH] Bronchoconstriction: Diminution of the caliber of a bronchus physiologically or as a result of pharmacological intervention. [NIH] Bronchoscopy: Endoscopic examination, therapy or surgery of the bronchi. [NIH] Brucellosis: Infection caused by bacteria of the genus Brucella mainly involving the reticuloendothelial system. This condition is characterized by fever, weakness, malaise, and weight loss. [NIH] Buccal: Pertaining to or directed toward the cheek. In dental anatomy, used to refer to the buccal surface of a tooth. [EU] Buffers: A chemical system that functions to control the levels of specific ions in solution. When the level of hydrogen ion in solution is controlled the system is called a pH buffer. [NIH]
Bupivacaine: A widely used local anesthetic agent. [NIH] Bursitis: Inflammation of a bursa, occasionally accompanied by a calcific deposit in the underlying supraspinatus tendon; the most common site is the subdeltoid bursa. [EU] Cadherins: A group of functionally related glycoproteins responsible for the calciumdependent cell-to-cell adhesion mechanism. They are divided into subclasses E-, P-, and Ncadherins, which are distinct in immunological specificity and tissue distribution. They promote cell adhesion via a homophilic mechanism. These compounds play a role in the construction of tissues and of the whole animal body. [NIH] Cadmium: An element with atomic symbol Cd, atomic number 48, and atomic weight 114. It is a metal and ingestion will lead to cadmium poisoning. [NIH] Cadmium Poisoning: Poisoning occurring after exposure to cadmium compounds or fumes. It may cause gastrointestinal syndromes, anemia, or pneumonitis. [NIH] Calcaneus: The largest of the tarsal bones and is situated at the lower and back part of the foot forming the heel. [NIH] Calcitonin: A peptide hormone that lowers calcium concentration in the blood. In humans, it is released by thyroid cells and acts to decrease the formation and absorptive activity of osteoclasts. Its role in regulating plasma calcium is much greater in children and in certain diseases than in normal adults. [NIH]
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Calcium Carbonate: Carbonic acid calcium salt (CaCO3). An odorless, tasteless powder or crystal that occurs in nature. It is used therapeutically as a phosphate buffer in hemodialysis patients and as a calcium supplement. [NIH] Calculi: An abnormal concretion occurring mostly in the urinary and biliary tracts, usually composed of mineral salts. Also called stones. [NIH] Callus: A callosity or hard, thick skin; the bone-like reparative substance that is formed round the edges and fragments of broken bone. [NIH] Camphor: A bicyclic monoterpene ketone found widely in plant (primarily the camphor tree, Cinnamomum camphora). Natural camphor is used topically as a skin antipruritic and as an anti-infective agent. [NIH] Campylobacter: A genus of bacteria found in the reproductive organs, intestinal tract, and oral cavity of animals and man. Some species are pathogenic. [NIH] Canaliculus: A membranous duct for tear drainage, leading from a lacrimal punctum at the eyelid margin and ending at the sinus of Maier. [NIH] Candidiasis: Infection with a fungus of the genus Candida. It is usually a superficial infection of the moist cutaneous areas of the body, and is generally caused by C. albicans; it most commonly involves the skin (dermatocandidiasis), oral mucous membranes (thrush, def. 1), respiratory tract (bronchocandidiasis), and vagina (vaginitis). Rarely there is a systemic infection or endocarditis. Called also moniliasis, candidosis, oidiomycosis, and formerly blastodendriosis. [EU] Candidosis: An infection caused by an opportunistic yeasts that tends to proliferate and become pathologic when the environment is favorable and the host resistance is weakened. [NIH]
Cannabidiol: Compound isolated from Cannabis sativa extract. [NIH] Cannabis: The hemp plant Cannabis sativa. Products prepared from the dried flowering tops of the plant include marijuana, hashish, bhang, and ganja. [NIH] Capillary: Any one of the minute vessels that connect the arterioles and venules, forming a network in nearly all parts of the body. Their walls act as semipermeable membranes for the interchange of various substances, including fluids, between the blood and tissue fluid; called also vas capillare. [EU] Capillary Fragility: The lack of resistance, or susceptibility, of capillaries to damage or disruption under conditions of increased stress. [NIH] Capillary Permeability: Property of blood capillary walls that allows for the selective exchange of substances. Small lipid-soluble molecules such as carbon dioxide and oxygen move freely by diffusion. Water and water-soluble molecules cannot pass through the endothelial walls and are dependent on microscopic pores. These pores show narrow areas (tight junctions) which may limit large molecule movement. [NIH] Capsaicin: Cytotoxic alkaloid from various species of Capsicum (pepper, paprika), of the Solanaceae. [NIH] Capsular: Cataract which is initiated by an opacification at the surface of the lens. [NIH] Carbohydrate: An aldehyde or ketone derivative of a polyhydric alcohol, particularly of the pentahydric and hexahydric alcohols. They are so named because the hydrogen and oxygen are usually in the proportion to form water, (CH2O)n. The most important carbohydrates are the starches, sugars, celluloses, and gums. They are classified into mono-, di-, tri-, polyand heterosaccharides. [EU] Carbon Dioxide: A colorless, odorless gas that can be formed by the body and is necessary for the respiration cycle of plants and animals. [NIH]
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Carboxy: Cannabinoid. [NIH] Carcinogen: Any substance that causes cancer. [NIH] Carcinogenesis: The process by which normal cells are transformed into cancer cells. [NIH] Carcinogenic: Producing carcinoma. [EU] Carcinoma: Cancer that begins in the skin or in tissues that line or cover internal organs. [NIH]
Cardiac: Having to do with the heart. [NIH] Cardiology: The study of the heart, its physiology, and its functions. [NIH] Cardiorespiratory: Relating to the heart and lungs and their function. [EU] Cardiovascular: Having to do with the heart and blood vessels. [NIH] Cardiovascular disease: Any abnormal condition characterized by dysfunction of the heart and blood vessels. CVD includes atherosclerosis (especially coronary heart disease, which can lead to heart attacks), cerebrovascular disease (e.g., stroke), and hypertension (high blood pressure). [NIH] Carotene: The general name for a group of pigments found in green, yellow, and leafy vegetables, and yellow fruits. The pigments are fat-soluble, unsaturated aliphatic hydrocarbons functioning as provitamins and are converted to vitamin A through enzymatic processes in the intestinal wall. [NIH] Carpal Tunnel Syndrome: A median nerve injury inside the carpal tunnel that results in symptoms of pain, numbness, tingling, clumsiness, and a lack of sweating, which can be caused by work with certain hand and wrist postures. [NIH] Case report: A detailed report of the diagnosis, treatment, and follow-up of an individual patient. Case reports also contain some demographic information about the patient (for example, age, gender, ethnic origin). [NIH] Case series: A group or series of case reports involving patients who were given similar treatment. Reports of case series usually contain detailed information about the individual patients. This includes demographic information (for example, age, gender, ethnic origin) and information on diagnosis, treatment, response to treatment, and follow-up after treatment. [NIH] Caspase: Enzyme released by the cell at a crucial stage in apoptosis in order to shred all cellular proteins. [NIH] Catabolism: Any destructive metabolic process by which organisms convert substances into excreted compounds. [EU] Catalytic Domain: The region of an enzyme that interacts with its substrate to cause the enzymatic reaction. [NIH] Cataract: An opacity, partial or complete, of one or both eyes, on or in the lens or capsule, especially an opacity impairing vision or causing blindness. The many kinds of cataract are classified by their morphology (size, shape, location) or etiology (cause and time of occurrence). [EU] Catecholamine: A group of chemical substances manufactured by the adrenal medulla and secreted during physiological stress. [NIH] Catheter: A flexible tube used to deliver fluids into or withdraw fluids from the body. [NIH] Catheterization: Use or insertion of a tubular device into a duct, blood vessel, hollow organ, or body cavity for injecting or withdrawing fluids for diagnostic or therapeutic purposes. It differs from intubation in that the tube here is used to restore or maintain patency in
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obstructions. [NIH] Cations: Postively charged atoms, radicals or groups of atoms which travel to the cathode or negative pole during electrolysis. [NIH] Cauda Equina: The lower part of the spinal cord consisting of the lumbar, sacral, and coccygeal nerve roots. [NIH] Caudal: Denoting a position more toward the cauda, or tail, than some specified point of reference; same as inferior, in human anatomy. [EU] Causal: Pertaining to a cause; directed against a cause. [EU] Cavernous Sinus: An irregularly shaped venous space in the dura mater at either side of the sphenoid bone. [NIH] Celecoxib: A drug that reduces pain. Celecoxib belongs to the family of drugs called nonsteroidal anti-inflammatory agents. It is being studied for cancer prevention. [NIH] Cell: The individual unit that makes up all of the tissues of the body. All living things are made up of one or more cells. [NIH] Cell Adhesion: Adherence of cells to surfaces or to other cells. [NIH] Cell Count: A count of the number of cells of a specific kind, usually measured per unit volume of sample. [NIH] Cell Cycle: The complex series of phenomena, occurring between the end of one cell division and the end of the next, by which cellular material is divided between daughter cells. [NIH] Cell Death: The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability. [NIH] Cell Differentiation: Progressive restriction of the developmental potential and increasing specialization of function which takes place during the development of the embryo and leads to the formation of specialized cells, tissues, and organs. [NIH] Cell Division: The fission of a cell. [NIH] Cell Lineage: The developmental history of cells as traced from the first division of the original cell or cells in the embryo. [NIH] Cell membrane: Cell membrane = plasma membrane. The structure enveloping a cell, enclosing the cytoplasm, and forming a selective permeability barrier; it consists of lipids, proteins, and some carbohydrates, the lipids thought to form a bilayer in which integral proteins are embedded to varying degrees. [EU] Cell proliferation: An increase in the number of cells as a result of cell growth and cell division. [NIH] Cell Size: The physical dimensions of a cell. It refers mainly to changes in dimensions correlated with physiological or pathological changes in cells. [NIH] Cell Survival: The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability. [NIH] Cell Transplantation: Transference of cells within an individual, between individuals of the same species, or between individuals of different species. [NIH] Cellular adhesion: The close adherence (bonding) to adjoining cell surfaces. [NIH] Cellulitis: An acute, diffuse, and suppurative inflammation of loose connective tissue, particularly the deep subcutaneous tissues, and sometimes muscle, which is most commonly seen as a result of infection of a wound, ulcer, or other skin lesions. [NIH]
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Cellulose: A polysaccharide with glucose units linked as in cellobiose. It is the chief constituent of plant fibers, cotton being the purest natural form of the substance. As a raw material, it forms the basis for many derivatives used in chromatography, ion exchange materials, explosives manufacturing, and pharmaceutical preparations. [NIH] Central Nervous System: The main information-processing organs of the nervous system, consisting of the brain, spinal cord, and meninges. [NIH] Central Nervous System Infections: Pathogenic infections of the brain, spinal cord, and meninges. DNA virus infections; RNA virus infections; bacterial infections; mycoplasma infections; Spirochaetales infections; fungal infections; protozoan infections; helminthiasis; and prion diseases may involve the central nervous system as a primary or secondary process. [NIH] Cerebral: Of or pertaining of the cerebrum or the brain. [EU] Cerebral Palsy: Refers to a motor disability caused by a brain dysfunction. [NIH] Cerebrospinal: Pertaining to the brain and spinal cord. [EU] Cerebrospinal fluid: CSF. The fluid flowing around the brain and spinal cord. Cerebrospinal fluid is produced in the ventricles in the brain. [NIH] Cerebrovascular: Pertaining to the blood vessels of the cerebrum, or brain. [EU] Cerebrum: The largest part of the brain. It is divided into two hemispheres, or halves, called the cerebral hemispheres. The cerebrum controls muscle functions of the body and also controls speech, emotions, reading, writing, and learning. [NIH] Cervical: Relating to the neck, or to the neck of any organ or structure. Cervical lymph nodes are located in the neck; cervical cancer refers to cancer of the uterine cervix, which is the lower, narrow end (the "neck") of the uterus. [NIH] Cervix: The lower, narrow end of the uterus that forms a canal between the uterus and vagina. [NIH] Character: In current usage, approximately equivalent to personality. The sum of the relatively fixed personality traits and habitual modes of response of an individual. [NIH] Chemokines: Class of pro-inflammatory cytokines that have the ability to attract and activate leukocytes. They can be divided into at least three structural branches: C (chemokines, C), CC (chemokines, CC), and CXC (chemokines, CXC), according to variations in a shared cysteine motif. [NIH] Chemopreventive: Natural or synthetic compound used to intervene in the early precancerous stages of carcinogenesis. [NIH] Chemotactic Factors: Chemical substances that attract or repel cells or organisms. The concept denotes especially those factors released as a result of tissue injury, invasion, or immunologic activity, that attract leukocytes, macrophages, or other cells to the site of infection or insult. [NIH] Chemotaxis: The movement of cells or organisms toward or away from a substance in response to its concentration gradient. [NIH] Chemotherapeutic agent: A drug used to treat cancer. [NIH] Chemotherapy: Treatment with anticancer drugs. [NIH] Chimera: An individual that contains cell populations derived from different zygotes. [NIH] Chiropractic: A system of treating bodily disorders by manipulation of the spine and other parts, based on the belief that the cause is the abnormal functioning of a nerve. [NIH] Chlamydia: A genus of the family Chlamydiaceae whose species cause a variety of diseases
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in vertebrates including humans, mice, and swine. Chlamydia species are gram-negative and produce glycogen. The type species is Chlamydia trachomatis. [NIH] Cholecystokinin: A 33-amino acid peptide secreted by the upper intestinal mucosa and also found in the central nervous system. It causes gallbladder contraction, release of pancreatic exocrine (or digestive) enzymes, and affects other gastrointestinal functions. Cholecystokinin may be the mediator of satiety. [NIH] Cholestasis: Impairment of biliary flow at any level from the hepatocyte to Vater's ampulla. [NIH]
Cholesterol Esters: Fatty acid esters of cholesterol which constitute about two-thirds of the cholesterol in the plasma. The accumulation of cholesterol esters in the arterial intima is a characteristic feature of atherosclerosis. [NIH] Chondrocytes: Polymorphic cells that form cartilage. [NIH] Chondroitin sulfate: The major glycosaminoglycan (a type of sugar molecule) in cartilage. [NIH]
Choroid: The thin, highly vascular membrane covering most of the posterior of the eye between the retina and sclera. [NIH] Chromatin: The material of chromosomes. It is a complex of DNA, histones, and nonhistone proteins (chromosomal proteins, non-histone) found within the nucleus of a cell. [NIH]
Chromosomal: Pertaining to chromosomes. [EU] Chromosome: Part of a cell that contains genetic information. Except for sperm and eggs, all human cells contain 46 chromosomes. [NIH] Chromosome Deletion: Actual loss of a portion of the chromosome. [NIH] Chronic: A disease or condition that persists or progresses over a long period of time. [NIH] Chronic Disease: Disease or ailment of long duration. [NIH] Chronic Fatigue Syndrome: Fatigue caused by the combined effects of different types of prolonged fatigue. [NIH] Chronic granulocytic leukemia: A slowly progressing disease in which too many white blood cells are made in the bone marrow. Also called chronic myelogenous leukemia or chronic myeloid leukemia. [NIH] Chronic myelogenous leukemia: CML. A slowly progressing disease in which too many white blood cells are made in the bone marrow. Also called chronic myeloid leukemia or chronic granulocytic leukemia. [NIH] Chronic Obstructive Pulmonary Disease: emphysema. [NIH]
Collective term for chronic bronchitis and
Chronic phase: Refers to the early stages of chronic myelogenous leukemia or chronic lymphocytic leukemia. The number of mature and immature abnormal white blood cells in the bone marrow and blood is higher than normal, but lower than in the accelerated or blast phase. [NIH] Chylomicrons: A class of lipoproteins that carry dietary cholesterol and triglycerides from the small intestines to the tissues. [NIH] Ciliary: Inflammation or infection of the glands of the margins of the eyelids. [NIH] Ciliary Body: A ring of tissue extending from the scleral spur to the ora serrata of the retina. It consists of the uveal portion and the epithelial portion. The ciliary muscle is in the uveal portion and the ciliary processes are in the epithelial portion. [NIH]
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Circadian: Repeated more or less daily, i. e. on a 23- to 25-hour cycle. [NIH] CIS: Cancer Information Service. The CIS is the National Cancer Institute's link to the public, interpreting and explaining research findings in a clear and understandable manner, and providing personalized responses to specific questions about cancer. Access the CIS by calling 1-800-4-CANCER, or by using the Web site at http://cis.nci.nih.gov. [NIH] Clavicle: A long bone of the shoulder girdle. [NIH] Climacteric: Physiologic period, characterized by endocrine, somatic, and psychic changes with the termination of ovarian function in the female. It may also accompany the normal diminution of sexual activity in the male. [NIH] Clinical Medicine: The study and practice of medicine by direct examination of the patient. [NIH]
Clinical Protocols: Precise and detailed plans for the study of a medical or biomedical problem and/or plans for a regimen of therapy. [NIH] Clinical study: A research study in which patients receive treatment in a clinic or other medical facility. Reports of clinical studies can contain results for single patients (case reports) or many patients (case series or clinical trials). [NIH] Clinical trial: A research study that tests how well new medical treatments or other interventions work in people. Each study is designed to test new methods of screening, prevention, diagnosis, or treatment of a disease. [NIH] Clone: The term "clone" has acquired a new meaning. It is applied specifically to the bits of inserted foreign DNA in the hybrid molecules of the population. Each inserted segment originally resided in the DNA of a complex genome amid millions of other DNA segment. [NIH]
Cloning: The production of a number of genetically identical individuals; in genetic engineering, a process for the efficient replication of a great number of identical DNA molecules. [NIH] Clot Retraction: Retraction of a clot resulting from contraction of platelet pseudopods attached to fibrin strands that is dependent on the contractile protein thrombosthenin. Used as a measure of platelet function. [NIH] Coagulation: 1. The process of clot formation. 2. In colloid chemistry, the solidification of a sol into a gelatinous mass; an alteration of a disperse phase or of a dissolved solid which causes the separation of the system into a liquid phase and an insoluble mass called the clot or curd. Coagulation is usually irreversible. 3. In surgery, the disruption of tissue by physical means to form an amorphous residuum, as in electrocoagulation and photocoagulation. [EU] Cod Liver Oil: Oil obtained from fresh livers of the cod family, Gadidae. It is a source of vitamins A and D. [NIH] Codon: A set of three nucleotides in a protein coding sequence that specifies individual amino acids or a termination signal (codon, terminator). Most codons are universal, but some organisms do not produce the transfer RNAs (RNA, transfer) complementary to all codons. These codons are referred to as unassigned codons (codons, nonsense). [NIH] Coenzyme: An organic nonprotein molecule, frequently a phosphorylated derivative of a water-soluble vitamin, that binds with the protein molecule (apoenzyme) to form the active enzyme (holoenzyme). [EU] Cofactor: A substance, microorganism or environmental factor that activates or enhances the action of another entity such as a disease-causing agent. [NIH] Cognitive behavior therapy:
A system of psychotherapy based on the premise that
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distorted or dysfunctional thinking, which influences a person's mood or behavior, is common to all psychosocial problems. The focus of therapy is to identify the distorted thinking and to replace it with more rational, adaptive thoughts and beliefs. [NIH] Cohort Studies: Studies in which subsets of a defined population are identified. These groups may or may not be exposed to factors hypothesized to influence the probability of the occurrence of a particular disease or other outcome. Cohorts are defined populations which, as a whole, are followed in an attempt to determine distinguishing subgroup characteristics. [NIH] Colchicine: A major alkaloid from Colchicum autumnale L. and found also in other Colchicum species. Its primary therapeutic use is in the treatment of gout, but it has been used also in the therapy of familial Mediterranean fever (periodic disease). [NIH] Coliphages: Viruses whose host is Escherichia coli. [NIH] Colitis: Inflammation of the colon. [NIH] Collagen: A polypeptide substance comprising about one third of the total protein in mammalian organisms. It is the main constituent of skin, connective tissue, and the organic substance of bones and teeth. Different forms of collagen are produced in the body but all consist of three alpha-polypeptide chains arranged in a triple helix. Collagen is differentiated from other fibrous proteins, such as elastin, by the content of proline, hydroxyproline, and hydroxylysine; by the absence of tryptophan; and particularly by the high content of polar groups which are responsible for its swelling properties. [NIH] Collagen disease: A term previously used to describe chronic diseases of the connective tissue (e.g., rheumatoid arthritis, systemic lupus erythematosus, and systemic sclerosis), but now is thought to be more appropriate for diseases associated with defects in collagen, which is a component of the connective tissue. [NIH] Collagenases: Enzymes that catalyze the degradation of collagen by acting on the peptide bonds. EC 3.4.24.-. [NIH] Collagenous Colitis: A type of colitis. Caused by an abnormal band of collagen, a threadlike protein. [NIH] Collapse: 1. A state of extreme prostration and depression, with failure of circulation. 2. Abnormal falling in of the walls of any part of organ. [EU] College Admission Test: Test designed to identify students suitable for admission into a graduate or undergraduate curriculum. [NIH] Colon: The long, coiled, tubelike organ that removes water from digested food. The remaining material, solid waste called stool, moves through the colon to the rectum and leaves the body through the anus. [NIH] Combination chemotherapy: Treatment using more than one anticancer drug. [NIH] Combination Therapy: Association of 3 drugs to treat AIDS (AZT + DDC or DDI + protease inhibitor). [NIH] Complement: A term originally used to refer to the heat-labile factor in serum that causes immune cytolysis, the lysis of antibody-coated cells, and now referring to the entire functionally related system comprising at least 20 distinct serum proteins that is the effector not only of immune cytolysis but also of other biologic functions. Complement activation occurs by two different sequences, the classic and alternative pathways. The proteins of the classic pathway are termed 'components of complement' and are designated by the symbols C1 through C9. C1 is a calcium-dependent complex of three distinct proteins C1q, C1r and C1s. The proteins of the alternative pathway (collectively referred to as the properdin system) and complement regulatory proteins are known by semisystematic or trivial names.
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Fragments resulting from proteolytic cleavage of complement proteins are designated with lower-case letter suffixes, e.g., C3a. Inactivated fragments may be designated with the suffix 'i', e.g. C3bi. Activated components or complexes with biological activity are designated by a bar over the symbol e.g. C1 or C4b,2a. The classic pathway is activated by the binding of C1 to classic pathway activators, primarily antigen-antibody complexes containing IgM, IgG1, IgG3; C1q binds to a single IgM molecule or two adjacent IgG molecules. The alternative pathway can be activated by IgA immune complexes and also by nonimmunologic materials including bacterial endotoxins, microbial polysaccharides, and cell walls. Activation of the classic pathway triggers an enzymatic cascade involving C1, C4, C2 and C3; activation of the alternative pathway triggers a cascade involving C3 and factors B, D and P. Both result in the cleavage of C5 and the formation of the membrane attack complex. Complement activation also results in the formation of many biologically active complement fragments that act as anaphylatoxins, opsonins, or chemotactic factors. [EU] Complementary and alternative medicine: CAM. Forms of treatment that are used in addition to (complementary) or instead of (alternative) standard treatments. These practices are not considered standard medical approaches. CAM includes dietary supplements, megadose vitamins, herbal preparations, special teas, massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Complementary medicine: Practices not generally recognized by the medical community as standard or conventional medical approaches and used to enhance or complement the standard treatments. Complementary medicine includes the taking of dietary supplements, megadose vitamins, and herbal preparations; the drinking of special teas; and practices such as massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Complementation: The production of a wild-type phenotype when two different mutations are combined in a diploid or a heterokaryon and tested in trans-configuration. [NIH] Complete remission: The disappearance of all signs of cancer. Also called a complete response. [NIH] Compliance: Distensibility measure of a chamber such as the lungs (lung compliance) or bladder. Compliance is expressed as a change in volume per unit change in pressure. [NIH] Compress: A plug used to occludate an orifice in the control of bleeding, or to mop up secretions; an absorbent pad. [NIH] Computational Biology: A field of biology concerned with the development of techniques for the collection and manipulation of biological data, and the use of such data to make biological discoveries or predictions. This field encompasses all computational methods and theories applicable to molecular biology and areas of computer-based techniques for solving biological problems including manipulation of models and datasets. [NIH] Computed tomography: CT scan. A series of detailed pictures of areas inside the body, taken from different angles; the pictures are created by a computer linked to an x-ray machine. Also called computerized tomography and computerized axial tomography (CAT) scan. [NIH] Computerized axial tomography: A series of detailed pictures of areas inside the body, taken from different angles; the pictures are created by a computer linked to an x-ray machine. Also called CAT scan, computed tomography (CT scan), or computerized tomography. [NIH] Computerized tomography: A series of detailed pictures of areas inside the body, taken from different angles; the pictures are created by a computer linked to an x-ray machine. Also called computerized axial tomography (CAT) scan and computed tomography (CT scan). [NIH]
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Conception: The onset of pregnancy, marked by implantation of the blastocyst; the formation of a viable zygote. [EU] Concomitant: Accompanying; accessory; joined with another. [EU] Cones: One type of specialized light-sensitive cells (photoreceptors) in the retina that provide sharp central vision and color vision. [NIH] Confidence Intervals: A range of values for a variable of interest, e.g., a rate, constructed so that this range has a specified probability of including the true value of the variable. [NIH] Confounding: Extraneous variables resulting in outcome effects that obscure or exaggerate the "true" effect of an intervention. [NIH] Congestion: Excessive or abnormal accumulation of blood in a part. [EU] Conjugated: Acting or operating as if joined; simultaneous. [EU] Conjunctiva: The mucous membrane that lines the inner surface of the eyelids and the anterior part of the sclera. [NIH] Conjunctivitis: Inflammation of the conjunctiva, generally consisting of conjunctival hyperaemia associated with a discharge. [EU] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Connective Tissue Cells: A group of cells that includes fibroblasts, cartilage cells, adipocytes, smooth muscle cells, and bone cells. [NIH] Connective Tissue Diseases: A heterogeneous group of disorders, some hereditary, others acquired, characterized by abnormal structure or function of one or more of the elements of connective tissue, i.e., collagen, elastin, or the mucopolysaccharides. [NIH] Connexin 43: A 43 kD peptide which is a member of the connexin family of gap junction proteins. Connexin 43 is a product of a gene in the alpha class of connexin genes (the alpha-1 gene). It was first isolated from mammalian heart, but is widespread in the body including the brain. [NIH] Consciousness: Sense of awareness of self and of the environment. [NIH] Constipation: Infrequent or difficult evacuation of feces. [NIH] Consultation: A deliberation between two or more physicians concerning the diagnosis and the proper method of treatment in a case. [NIH] Consumption: Pulmonary tuberculosis. [NIH] Contact dermatitis: Inflammation of the skin with varying degrees of erythema, edema and vesinculation resulting from cutaneous contact with a foreign substance or other exposure. [NIH]
Contracture: A condition of fixed high resistance to passive stretch of a muscle, resulting from fibrosis of the tissues supporting the muscles or the joints, or from disorders of the muscle fibres. [EU] Contraindications: Any factor or sign that it is unwise to pursue a certain kind of action or treatment, e. g. giving a general anesthetic to a person with pneumonia. [NIH] Contralateral: Having to do with the opposite side of the body. [NIH] Control group: In a clinical trial, the group that does not receive the new treatment being studied. This group is compared to the group that receives the new treatment, to see if the new treatment works. [NIH]
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Controlled clinical trial: A clinical study that includes a comparison (control) group. The comparison group receives a placebo, another treatment, or no treatment at all. [NIH] Controlled study: group. [NIH]
An experiment or clinical trial that includes a comparison (control)
Conventional therapy: A currently accepted and widely used treatment for a certain type of disease, based on the results of past research. Also called conventional treatment. [NIH] Conventional treatment: A currently accepted and widely used treatment for a certain type of disease, based on the results of past research. Also called conventional therapy. [NIH] Coordination: Muscular or motor regulation or the harmonious cooperation of muscles or groups of muscles, in a complex action or series of actions. [NIH] Cor: The muscular organ that maintains the circulation of the blood. c. adiposum a heart that has undergone fatty degeneration or that has an accumulation of fat around it; called also fat or fatty, heart. c. arteriosum the left side of the heart, so called because it contains oxygenated (arterial) blood. c. biloculare a congenital anomaly characterized by failure of formation of the atrial and ventricular septums, the heart having only two chambers, a single atrium and a single ventricle, and a common atrioventricular valve. c. bovinum (L. 'ox heart') a greatly enlarged heart due to a hypertrophied left ventricle; called also c. taurinum and bucardia. c. dextrum (L. 'right heart') the right atrium and ventricle. c. hirsutum, c. villosum. c. mobile (obs.) an abnormally movable heart. c. pendulum a heart so movable that it seems to be hanging by the great blood vessels. c. pseudotriloculare biatriatum a congenital cardiac anomaly in which the heart functions as a three-chambered heart because of tricuspid atresia, the right ventricle being extremely small or rudimentary and the right atrium greatly dilated. Blood passes from the right to the left atrium and thence disease due to pulmonary hypertension secondary to disease of the lung, or its blood vessels, with hypertrophy of the right ventricle. [EU] Cornea: The transparent part of the eye that covers the iris and the pupil and allows light to enter the inside. [NIH] Corneum: The superficial layer of the epidermis containing keratinized cells. [NIH] Coronary: Encircling in the manner of a crown; a term applied to vessels; nerves, ligaments, etc. The term usually denotes the arteries that supply the heart muscle and, by extension, a pathologic involvement of them. [EU] Coronary heart disease: A type of heart disease caused by narrowing of the coronary arteries that feed the heart, which needs a constant supply of oxygen and nutrients carried by the blood in the coronary arteries. When the coronary arteries become narrowed or clogged by fat and cholesterol deposits and cannot supply enough blood to the heart, CHD results. [NIH] Coronary Thrombosis: Presence of a thrombus in a coronary artery, often causing a myocardial infarction. [NIH] Corpus: The body of the uterus. [NIH] Corpuscle: A small mass or body; a sensory nerve end bulb; a cell, especially that of the blood or the lymph. [NIH] Cortex: The outer layer of an organ or other body structure, as distinguished from the internal substance. [EU] Cortical: Pertaining to or of the nature of a cortex or bark. [EU] Corticosteroid: Any of the steroids elaborated by the adrenal cortex (excluding the sex hormones of adrenal origin) in response to the release of corticotrophin (adrenocorticotropic hormone) by the pituitary gland, to any of the synthetic equivalents of these steroids, or to
Dictionary 603
angiotensin II. They are divided, according to their predominant biological activity, into three major groups: glucocorticoids, chiefly influencing carbohydrate, fat, and protein metabolism; mineralocorticoids, affecting the regulation of electrolyte and water balance; and C19 androgens. Some corticosteroids exhibit both types of activity in varying degrees, and others exert only one type of effect. The corticosteroids are used clinically for hormonal replacement therapy, for suppression of ACTH secretion by the anterior pituitary, as antineoplastic, antiallergic, and anti-inflammatory agents, and to suppress the immune response. Called also adrenocortical hormone and corticoid. [EU] Cortisol: A steroid hormone secreted by the adrenal cortex as part of the body's response to stress. [NIH] Cortisone: A natural steroid hormone produced in the adrenal gland. It can also be made in the laboratory. Cortisone reduces swelling and can suppress immune responses. [NIH] Cowpox: A mild, eruptive skin disease of milk cows caused by cowpox virus, with lesions occurring principally on the udder and teats. Human infection may occur while milking an infected animal. [NIH] Cowpox Virus: A species of orthopoxvirus that is the etiologic agent of cowpox. It is closely related to but antigenically different from vaccina virus. [NIH] Crabs: Chiefly marine, largely carnivorous crustaceans including the genera: Cancer, Uca, and Callinectes. It includes crabs as food. [NIH] Cranial: Pertaining to the cranium, or to the anterior (in animals) or superior (in humans) end of the body. [EU] Craniocerebral Trauma: Traumatic injuries involving the cranium and intracranial structures (i.e., brain; cranial nerves; meninges; and other structures). Injuries may be classified by whether or not the skull is penetrated (i.e., penetrating vs. nonpenetrating) or whether there is an associated hemorrhage. [NIH] Criterion: A standard by which something may be judged. [EU] Crossing-over: The exchange of corresponding segments between chromatids of homologous chromosomes during meiosia, forming a chiasma. [NIH] Cross-Sectional Studies: Studies in which the presence or absence of disease or other health-related variables are determined in each member of the study population or in a representative sample at one particular time. This contrasts with longitudinal studies which are followed over a period of time. [NIH] Cryptococcosis: Infection with a fungus of the species Cryptococcus neoformans. [NIH] Cryptosporidiosis: Parasitic intestinal infection with severe diarrhea caused by a protozoan, Cryptosporidium. It occurs in both animals and humans. [NIH] Curare: Plant extracts from several species, including Strychnos toxifera, S. castelnaei, S. crevauxii, and Chondodendron tomentosum, that produce paralysis of skeletal muscle and are used adjunctively with general anesthesia. These extracts are toxic and must be used with the administration of artificial respiration. [NIH] Curative: Tending to overcome disease and promote recovery. [EU] Cutaneous: Having to do with the skin. [NIH] Cyanogen Bromide: Cyanogen bromide (CNBr). A compound used in molecular biology to digest some proteins and as a coupling reagent for phosphoroamidate or pyrophosphate internucleotide bonds in DNA duplexes. [NIH] Cyclic: Pertaining to or occurring in a cycle or cycles; the term is applied to chemical compounds that contain a ring of atoms in the nucleus. [EU]
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Cyclophosphamide: Precursor of an alkylating nitrogen mustard antineoplastic and immunosuppressive agent that must be activated in the liver to form the active aldophosphamide. It is used in the treatment of lymphomas, leukemias, etc. Its side effect, alopecia, has been made use of in defleecing sheep. Cyclophosphamide may also cause sterility, birth defects, mutations, and cancer. [NIH] Cyclosporine: A drug used to help reduce the risk of rejection of organ and bone marrow transplants by the body. It is also used in clinical trials to make cancer cells more sensitive to anticancer drugs. [NIH] Cyst: A sac or capsule filled with fluid. [NIH] Cysteine: A thiol-containing non-essential amino acid that is oxidized to form cystine. [NIH] Cysteine Endopeptidases: Endopeptidases which have a cysteine involved in the catalytic process. This group of enzymes is inactivated by sulfhydryl reagents. EC 3.4.22. [NIH] Cystine: A covalently linked dimeric nonessential amino acid formed by the oxidation of cysteine. Two molecules of cysteine are joined together by a disulfide bridge to form cystine. [NIH]
Cytochrome: Any electron transfer hemoprotein having a mode of action in which the transfer of a single electron is effected by a reversible valence change of the central iron atom of the heme prosthetic group between the +2 and +3 oxidation states; classified as cytochromes a in which the heme contains a formyl side chain, cytochromes b, which contain protoheme or a closely similar heme that is not covalently bound to the protein, cytochromes c in which protoheme or other heme is covalently bound to the protein, and cytochromes d in which the iron-tetrapyrrole has fewer conjugated double bonds than the hemes have. Well-known cytochromes have been numbered consecutively within groups and are designated by subscripts (beginning with no subscript), e.g. cytochromes c, c1, C2, ... New cytochromes are named according to the wavelength in nanometres of the absorption maximum of the a-band of the iron (II) form in pyridine, e.g., c-555. [EU] Cytochrome A: One of a group of proteins involved in electron transport systems. [NIH] Cytochrome b: Cytochromes (electron-transporting proteins) with protoheme or a related heme as the prosthetic group. The prosthetic group is not covalently bound to the protein moiety. [NIH] Cytokine: Small but highly potent protein that modulates the activity of many cell types, including T and B cells. [NIH] Cytomegalovirus: A genus of the family Herpesviridae, subfamily Betaherpesvirinae, infecting the salivary glands, liver, spleen, lungs, eyes, and other organs, in which they produce characteristically enlarged cells with intranuclear inclusions. Infection with Cytomegalovirus is also seen as an opportunistic infection in AIDS. [NIH] Cytoplasm: The protoplasm of a cell exclusive of that of the nucleus; it consists of a continuous aqueous solution (cytosol) and the organelles and inclusions suspended in it (phaneroplasm), and is the site of most of the chemical activities of the cell. [EU] Cytoskeletal Proteins: Major constituent of the cytoskeleton found in the cytoplasm of eukaryotic cells. They form a flexible framework for the cell, provide attachment points for organelles and formed bodies, and make communication between parts of the cell possible. [NIH]
Cytoskeleton: The network of filaments, tubules, and interconnecting filamentous bridges which give shape, structure, and organization to the cytoplasm. [NIH] Cytotoxic: Cell-killing. [NIH] Cytotoxicity: Quality of being capable of producing a specific toxic action upon cells of
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special organs. [NIH] Cytotoxins: Substances elaborated by microorganisms, plants or animals that are specifically toxic to individual cells; they may be involved in immunity or may be contained in venoms. [NIH] Databases, Bibliographic: Extensive collections, reputedly complete, of references and citations to books, articles, publications, etc., generally on a single subject or specialized subject area. Databases can operate through automated files, libraries, or computer disks. The concept should be differentiated from factual databases which is used for collections of data and facts apart from bibliographic references to them. [NIH] Day Care: Institutional health care of patients during the day. The patients return home at night. [NIH] Decarboxylation: The removal of a carboxyl group, usually in the form of carbon dioxide, from a chemical compound. [NIH] Decision Making: The process of making a selective intellectual judgment when presented with several complex alternatives consisting of several variables, and usually defining a course of action or an idea. [NIH] Defense Mechanisms: Unconscious process used by an individual or a group of individuals in order to cope with impulses, feelings or ideas which are not acceptable at their conscious level; various types include reaction formation, projection and self reversal. [NIH]
Degenerative: Undergoing degeneration : tending to degenerate; having the character of or involving degeneration; causing or tending to cause degeneration. [EU] Deglutition: The process or the act of swallowing. [NIH] Dehydroepiandrosterone: DHEA. A substance that is being studied as a cancer prevention drug. It belongs to the family of drugs called steroids. [NIH] Deletion: A genetic rearrangement through loss of segments of DNA (chromosomes), bringing sequences, which are normally separated, into close proximity. [NIH] Delivery of Health Care: The concept concerned with all aspects of providing and distributing health services to a patient population. [NIH] Delusion: A false belief, not susceptible to argument or reason, and determined, pathologically, by some form of mental disorder. [NIH] Dementia: An acquired organic mental disorder with loss of intellectual abilities of sufficient severity to interfere with social or occupational functioning. The dysfunction is multifaceted and involves memory, behavior, personality, judgment, attention, spatial relations, language, abstract thought, and other executive functions. The intellectual decline is usually progressive, and initially spares the level of consciousness. [NIH] Denaturation: Rupture of the hydrogen bonds by heating a DNA solution and then cooling it rapidly causes the two complementary strands to separate. [NIH] Dendrites: Extensions of the nerve cell body. They are short and branched and receive stimuli from other neurons. [NIH] Dendritic: 1. Branched like a tree. 2. Pertaining to or possessing dendrites. [EU] Dendritic cell: A special type of antigen-presenting cell (APC) that activates T lymphocytes. [NIH]
Density: The logarithm to the base 10 of the opacity of an exposed and processed film. [NIH] Dental Records: Data collected during dental examination for the purpose of study, diagnosis, or treatment planning. [NIH]
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Depolarization: The process or act of neutralizing polarity. In neurophysiology, the reversal of the resting potential in excitable cell membranes when stimulated, i.e., the tendency of the cell membrane potential to become positive with respect to the potential outside the cell. [EU] Dermal: Pertaining to or coming from the skin. [NIH] Dermatitis: Any inflammation of the skin. [NIH] Dermatologic Agents: Drugs used to treat or prevent skin disorders or for the routine care of skin. [NIH] Dermatology: A medical specialty concerned with the skin, its structure, functions, diseases, and treatment. [NIH] Dermatophytosis: Any superficial fungal infection caused by a dermatophyte and involving the stratum corneum of the skin, hair, and nails. The term broadly comprises onychophytosis and the various form of tinea (ringworm), sometimes being used specifically to designate tinea pedis (athlete's foot). Called also epidermomycosis. [EU] Dermatosis: Any skin disease, especially one not characterized by inflammation. [EU] Dermis: A layer of vascular connective tissue underneath the epidermis. The surface of the dermis contains sensitive papillae. Embedded in or beneath the dermis are sweat glands, hair follicles, and sebaceous glands. [NIH] Desensitization: The prevention or reduction of immediate hypersensitivity reactions by administration of graded doses of allergen; called also hyposensitization and immunotherapy. [EU] Desquamation: The shedding of epithelial elements, chiefly of the skin, in scales or small sheets; exfoliation. [EU] Deuterium: Deuterium. The stable isotope of hydrogen. It has one neutron and one proton in the nucleus. [NIH] Dexterity: Ability to move the hands easily and skillfully. [NIH] Diabetes Mellitus: A heterogeneous group of disorders that share glucose intolerance in common. [NIH] Diabetic Ketoacidosis: Complication of diabetes resulting from severe insulin deficiency coupled with an absolute or relative increase in glucagon concentration. The metabolic acidosis is caused by the breakdown of adipose stores and resulting increased levels of free fatty acids. Glucagon accelerates the oxidation of the free fatty acids producing excess ketone bodies (ketosis). [NIH] Diagnostic Imaging: Any visual display of structural or functional patterns of organs or tissues for diagnostic evaluation. It includes measuring physiologic and metabolic responses to physical and chemical stimuli, as well as ultramicroscopy. [NIH] Diagnostic procedure: A method used to identify a disease. [NIH] Diaphragm: The musculofibrous partition that separates the thoracic cavity from the abdominal cavity. Contraction of the diaphragm increases the volume of the thoracic cavity aiding inspiration. [NIH] Diarrhea: Passage of excessively liquid or excessively frequent stools. [NIH] Diarrhoea: Abnormal frequency and liquidity of faecal discharges. [EU] Diastolic: Of or pertaining to the diastole. [EU] Diathermy: The induction of local hyperthermia by either short radio waves or highfrequency sound waves. [NIH]
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Diclofenac: A non-steroidal anti-inflammatory agent (NSAID) with antipyretic and analgesic actions. It is primarily available as the sodium salt, diclofenac sodium. [NIH] Diffusion: The tendency of a gas or solute to pass from a point of higher pressure or concentration to a point of lower pressure or concentration and to distribute itself throughout the available space; a major mechanism of biological transport. [NIH] Digestion: The process of breakdown of food for metabolism and use by the body. [NIH] Digestive system: The organs that take in food and turn it into products that the body can use to stay healthy. Waste products the body cannot use leave the body through bowel movements. The digestive system includes the salivary glands, mouth, esophagus, stomach, liver, pancreas, gallbladder, small and large intestines, and rectum. [NIH] Digestive tract: The organs through which food passes when food is eaten. These organs are the mouth, esophagus, stomach, small and large intestines, and rectum. [NIH] Dihydrotestosterone: Anabolic agent. [NIH] Dihydroxy: AMPA/Kainate antagonist. [NIH] Dilatation: The act of dilating. [NIH] Dilate: Relax; expand. [NIH] Dilation: A process by which the pupil is temporarily enlarged with special eye drops (mydriatic); allows the eye care specialist to better view the inside of the eye. [NIH] Dilator: A device used to stretch or enlarge an opening. [NIH] Dimerization: The process by which two molecules of the same chemical composition form a condensation product or polymer. [NIH] Diploid: Having two sets of chromosomes. [NIH] Disabled Persons: Persons with physical or mental disabilities that affect or limit their activities of daily living and that may require special accommodations. [NIH] Discrete: Made up of separate parts or characterized by lesions which do not become blended; not running together; separate. [NIH] Discriminant Analysis: A statistical analytic technique used with discrete dependent variables, concerned with separating sets of observed values and allocating new values. It is sometimes used instead of regression analysis. [NIH] Discrimination: The act of qualitative and/or quantitative differentiation between two or more stimuli. [NIH] Disease Progression: The worsening of a disease over time. This concept is most often used for chronic and incurable diseases where the stage of the disease is an important determinant of therapy and prognosis. [NIH] Disease Susceptibility: A constitution or condition of the body which makes the tissues react in special ways to certain extrinsic stimuli and thus tends to make the individual more than usually susceptible to certain diseases. [NIH] Disinfectant: An agent that disinfects; applied particularly to agents used on inanimate objects. [EU] Dislocation: The displacement of any part, more especially of a bone. Called also luxation. [EU]
Disparity: Failure of the two retinal images of an object to fall on corresponding retinal points. [NIH] Dissociation: 1. The act of separating or state of being separated. 2. The separation of a molecule into two or more fragments (atoms, molecules, ions, or free radicals) produced by
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the absorption of light or thermal energy or by solvation. 3. In psychology, a defense mechanism in which a group of mental processes are segregated from the rest of a person's mental activity in order to avoid emotional distress, as in the dissociative disorders (q.v.), or in which an idea or object is segregated from its emotional significance; in the first sense it is roughly equivalent to splitting, in the second, to isolation. 4. A defect of mental integration in which one or more groups of mental processes become separated off from normal consciousness and, thus separated, function as a unitary whole. [EU] Distal: Remote; farther from any point of reference; opposed to proximal. In dentistry, used to designate a position on the dental arch farther from the median line of the jaw. [EU] Diuresis: Increased excretion of urine. [EU] Diuretic: A drug that increases the production of urine. [NIH] Dizziness: An imprecise term which may refer to a sense of spatial disorientation, motion of the environment, or lightheadedness. [NIH] Dominance: In genetics, the full phenotypic expression of a gene in both heterozygotes and homozygotes. [EU] Dorsal: 1. Pertaining to the back or to any dorsum. 2. Denoting a position more toward the back surface than some other object of reference; same as posterior in human anatomy; superior in the anatomy of quadrupeds. [EU] Dorsum: A plate of bone which forms the posterior boundary of the sella turcica. [NIH] Double-blind: Pertaining to a clinical trial or other experiment in which neither the subject nor the person administering treatment knows which treatment any particular subject is receiving. [EU] Double-blinded: A clinical trial in which neither the medical staff nor the person knows which of several possible therapies the person is receiving. [NIH] Doxycycline: A synthetic tetracycline derivative with a range of antimicrobial activity and mode of action similar to that of tetracycline, but more effective against many species. Animal studies suggest that it may cause less tooth staining than other tetracyclines. [NIH] Drive: A state of internal activity of an organism that is a necessary condition before a given stimulus will elicit a class of responses; e.g., a certain level of hunger (drive) must be present before food will elicit an eating response. [NIH] Drosophila: A genus of small, two-winged flies containing approximately 900 described species. These organisms are the most extensively studied of all genera from the standpoint of genetics and cytology. [NIH] Drug Design: The molecular designing of drugs for specific purposes (such as DNAbinding, enzyme inhibition, anti-cancer efficacy, etc.) based on knowledge of molecular properties such as activity of functional groups, molecular geometry, and electronic structure, and also on information cataloged on analogous molecules. Drug design is generally computer-assisted molecular modeling and does not include pharmacokinetics, dosage analysis, or drug administration analysis. [NIH] Drug Interactions: The action of a drug that may affect the activity, metabolism, or toxicity of another drug. [NIH] Drug Tolerance: Progressive diminution of the susceptibility of a human or animal to the effects of a drug, resulting from its continued administration. It should be differentiated from drug resistance wherein an organism, disease, or tissue fails to respond to the intended effectiveness of a chemical or drug. It should also be differentiated from maximum tolerated dose and no-observed-adverse-effect level. [NIH]
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Drug Toxicity: Manifestations of the adverse effects of drugs administered therapeutically or in the course of diagnostic techniques. It does not include accidental or intentional poisoning for which specific headings are available. [NIH] Duct: A tube through which body fluids pass. [NIH] Duodenal Ulcer: An ulcer in the lining of the first part of the small intestine (duodenum). [NIH]
Duodenum: The first part of the small intestine. [NIH] Dura mater: The outermost, toughest, and most fibrous of the three membranes (meninges) covering the brain and spinal cord; called also pachymeninx. [EU] Dyes: Chemical substances that are used to stain and color other materials. The coloring may or may not be permanent. Dyes can also be used as therapeutic agents and test reagents in medicine and scientific research. [NIH] Dysentery: Any of various disorders marked by inflammation of the intestines, especially of the colon, and attended by pain in the abdomen, tenesmus, and frequent stools containing blood and mucus. Causes include chemical irritants, bacteria, protozoa, or parasitic worms. [EU]
Dyslipidemia: Disorders in the lipoprotein metabolism; classified as hypercholesterolemia, hypertriglyceridemia, combined hyperlipidemia, and low levels of high-density lipoprotein (HDL) cholesterol. All of the dyslipidemias can be primary or secondary. Both elevated levels of low-density lipoprotein (LDL) cholesterol and low levels of HDL cholesterol predispose to premature atherosclerosis. [NIH] Dysmenorrhea: Painful menstruation. [NIH] Dyspareunia: Painful sexual intercourse. [NIH] Dyspepsia: Impaired digestion, especially after eating. [NIH] Dysphonia: Difficulty or pain in speaking; impairment of the voice. [NIH] Dysplasia: Cells that look abnormal under a microscope but are not cancer. [NIH] Dyspnea: Difficult or labored breathing. [NIH] Dystrophy: Any disorder arising from defective or faulty nutrition, especially the muscular dystrophies. [EU] Eating Disorders: A group of disorders characterized by physiological and psychological disturbances in appetite or food intake. [NIH] Edema: Excessive amount of watery fluid accumulated in the intercellular spaces, most commonly present in subcutaneous tissue. [NIH] Educational Status: Educational attainment or level of education of individuals. [NIH] Effector: It is often an enzyme that converts an inactive precursor molecule into an active second messenger. [NIH] Effector cell: A cell that performs a specific function in response to a stimulus; usually used to describe cells in the immune system. [NIH] Efficacy: The extent to which a specific intervention, procedure, regimen, or service produces a beneficial result under ideal conditions. Ideally, the determination of efficacy is based on the results of a randomized control trial. [NIH] Effusion: The escape of fluid into a part or tissue, as an exudation or a transudation. [EU] Ejaculation: The release of semen through the penis during orgasm. [NIH] Elastic: Susceptible of resisting and recovering from stretching, compression or distortion applied by a force. [EU]
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Elasticity: Resistance and recovery from distortion of shape. [NIH] Elastin: The protein that gives flexibility to tissues. [NIH] Elective: Subject to the choice or decision of the patient or physician; applied to procedures that are advantageous to the patient but not urgent. [EU] Electroacupuncture: A form of acupuncture using low frequency electrically stimulated needles to produce analgesia and anesthesia and to treat disease. [NIH] Electrocardiogram: Measurement of electrical activity during heartbeats. [NIH] Electrocoagulation: Electrosurgical procedures used to treat hemorrhage (e.g., bleeding ulcers) and to ablate tumors, mucosal lesions, and refractory arrhythmias. [NIH] Electrolyte: A substance that dissociates into ions when fused or in solution, and thus becomes capable of conducting electricity; an ionic solute. [EU] Electrons: Stable elementary particles having the smallest known negative charge, present in all elements; also called negatrons. Positively charged electrons are called positrons. The numbers, energies and arrangement of electrons around atomic nuclei determine the chemical identities of elements. Beams of electrons are called cathode rays or beta rays, the latter being a high-energy biproduct of nuclear decay. [NIH] Electrophoresis: An electrochemical process in which macromolecules or colloidal particles with a net electric charge migrate in a solution under the influence of an electric current. [NIH]
Electrophysiological: Pertaining to electrophysiology, that is a branch of physiology that is concerned with the electric phenomena associated with living bodies and involved in their functional activity. [EU] Embolism: Blocking of a blood vessel by a blood clot or foreign matter that has been transported from a distant site by the blood stream. [NIH] Embolus: Bit of foreign matter which enters the blood stream at one point and is carried until it is lodged or impacted in an artery and obstructs it. It may be a blood clot, an air bubble, fat or other tissue, or clumps of bacteria. [NIH] Embryo: The prenatal stage of mammalian development characterized by rapid morphological changes and the differentiation of basic structures. [NIH] Embryo Transfer: Removal of a mammalian embryo from one environment and replacement in the same or a new environment. The embryo is usually in the pre-nidation phase, i.e., a blastocyst. The process includes embryo or blastocyst transplantation or transfer after in vitro fertilization and transfer of the inner cell mass of the blastocyst. It is not used for transfer of differentiated embryonic tissue, e.g., germ layer cells. [NIH] Emollient: Softening or soothing; called also malactic. [EU] Emphysema: A pathological accumulation of air in tissues or organs. [NIH] Empiric: Empirical; depending upon experience or observation alone, without using scientific method or theory. [EU] Empirical: A treatment based on an assumed diagnosis, prior to receiving confirmatory laboratory test results. [NIH] Emulsion: A preparation of one liquid distributed in small globules throughout the body of a second liquid. The dispersed liquid is the discontinuous phase, and the dispersion medium is the continuous phase. When oil is the dispersed liquid and an aqueous solution is the continuous phase, it is known as an oil-in-water emulsion, whereas when water or aqueous solution is the dispersed phase and oil or oleaginous substance is the continuous phase, it is known as a water-in-oil emulsion. Pharmaceutical emulsions for which official
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standards have been promulgated include cod liver oil emulsion, cod liver oil emulsion with malt, liquid petrolatum emulsion, and phenolphthalein in liquid petrolatum emulsion. [EU] Enamel: A very hard whitish substance which covers the dentine of the anatomical crown of a tooth. [NIH] Encephalitis: Inflammation of the brain due to infection, autoimmune processes, toxins, and other conditions. Viral infections (see encephalitis, viral) are a relatively frequent cause of this condition. [NIH] Encephalitis, Viral: Inflammation of brain parenchymal tissue as a result of viral infection. Encephalitis may occur as primary or secondary manifestation of Togaviridae infections; Herpesviridae infections; Adenoviridae infections; Flaviviridae infections; Bunyaviridae infections; Picornaviridae infections; Paramyxoviridae infections; Orthomyxoviridae infections; Retroviridae infections; and Arenaviridae infections. [NIH] Encephalomyelitis: A general term indicating inflammation of the brain and spinal cord, often used to indicate an infectious process, but also applicable to a variety of autoimmune and toxic-metabolic conditions. There is significant overlap regarding the usage of this term and encephalitis in the literature. [NIH] Endemic: Present or usually prevalent in a population or geographical area at all times; said of a disease or agent. Called also endemial. [EU] Endocarditis: Exudative and proliferative inflammatory alterations of the endocardium, characterized by the presence of vegetations on the surface of the endocardium or in the endocardium itself, and most commonly involving a heart valve, but sometimes affecting the inner lining of the cardiac chambers or the endocardium elsewhere. It may occur as a primary disorder or as a complication of or in association with another disease. [EU] Endocardium: The innermost layer of the heart, comprised of endothelial cells. [NIH] Endogenous: Produced inside an organism or cell. The opposite is external (exogenous) production. [NIH] Endometrial: Having to do with the endometrium (the layer of tissue that lines the uterus). [NIH]
Endometrium: The layer of tissue that lines the uterus. [NIH] Endopeptidases: A subclass of peptide hydrolases. They are classified primarily by their catalytic mechanism. Specificity is used only for identification of individual enzymes. They comprise the serine endopeptidases, EC 3.4.21; cysteine endopeptidases, EC 3.4.22; aspartic endopeptidases, EC 3.4.23, metalloendopeptidases, EC 3.4.24; and a group of enzymes yet to be assigned to any of the above sub-classes, EC 3.4.99. EC 3.4.-. [NIH] Endostatin: A drug that is being studied for its ability to prevent the growth of new blood vessels into a solid tumor. Endostatin belongs to the family of drugs called angiogenesis inhibitors. [NIH] Endothelial cell: The main type of cell found in the inside lining of blood vessels, lymph vessels, and the heart. [NIH] Endothelium: A layer of epithelium that lines the heart, blood vessels (endothelium, vascular), lymph vessels (endothelium, lymphatic), and the serous cavities of the body. [NIH] Endothelium, Lymphatic: Unbroken cellular lining (intima) of the lymph vessels (e.g., the high endothelial lymphatic venules). It is more permeable than vascular endothelium, lacking selective absorption and functioning mainly to remove plasma proteins that have filtered through the capillaries into the tissue spaces. [NIH] Endothelium, Vascular: Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components
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from interstitium to lumen; this function has been most intensively studied in the blood capillaries. [NIH] Endothelium-derived: Small molecule that diffuses to the adjacent muscle layer and relaxes it. [NIH] Endotoxin: Toxin from cell walls of bacteria. [NIH] Enteropeptidase: A specialized proteolytic enzyme secreted by intestinal cells. It converts trypsinogen into its active form trypsin by removing the N-terminal peptide. EC 3.4.21.9. [NIH]
Environmental Health: The science of controlling or modifying those conditions, influences, or forces surrounding man which relate to promoting, establishing, and maintaining health. [NIH] Enzymatic: Phase where enzyme cuts the precursor protein. [NIH] Enzyme: A protein that speeds up chemical reactions in the body. [NIH] Enzyme-Linked Immunosorbent Assay: An immunoassay utilizing an antibody labeled with an enzyme marker such as horseradish peroxidase. While either the enzyme or the antibody is bound to an immunosorbent substrate, they both retain their biologic activity; the change in enzyme activity as a result of the enzyme-antibody-antigen reaction is proportional to the concentration of the antigen and can be measured spectrophotometrically or with the naked eye. Many variations of the method have been developed. [NIH] Eosinophil: A polymorphonuclear leucocyte with large eosinophilic granules in its cytoplasm, which plays a role in hypersensitivity reactions. [NIH] Eosinophilia: Abnormal increase in eosinophils in the blood, tissues or organs. [NIH] Eosinophilic: A condition found primarily in grinding workers caused by a reaction of the pulmonary tissue, in particular the eosinophilic cells, to dust that has entered the lung. [NIH] Epidemic: Occurring suddenly in numbers clearly in excess of normal expectancy; said especially of infectious diseases but applied also to any disease, injury, or other healthrelated event occurring in such outbreaks. [EU] Epidemiologic Studies: Studies designed to examine associations, commonly, hypothesized causal relations. They are usually concerned with identifying or measuring the effects of risk factors or exposures. The common types of analytic study are case-control studies, cohort studies, and cross-sectional studies. [NIH] Epidemiological: Relating to, or involving epidemiology. [EU] Epidermal: Pertaining to or resembling epidermis. Called also epidermic or epidermoid. [EU]
Epidermal Growth Factor: A 6 kD polypeptide growth factor initially discovered in mouse submaxillary glands. Human epidermal growth factor was originally isolated from urine based on its ability to inhibit gastric secretion and called urogastrone. epidermal growth factor exerts a wide variety of biological effects including the promotion of proliferation and differentiation of mesenchymal and epithelial cells. [NIH] Epidermis: Nonvascular layer of the skin. It is made up, from within outward, of five layers: 1) basal layer (stratum basale epidermidis); 2) spinous layer (stratum spinosum epidermidis); 3) granular layer (stratum granulosum epidermidis); 4) clear layer (stratum lucidum epidermidis); and 5) horny layer (stratum corneum epidermidis). [NIH] Epidermomycosis: An infection caused by dermatophytes. [NIH] Epigastric: Having to do with the upper middle area of the abdomen. [NIH]
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Epinephrine: The active sympathomimetic hormone from the adrenal medulla in most species. It stimulates both the alpha- and beta- adrenergic systems, causes systemic vasoconstriction and gastrointestinal relaxation, stimulates the heart, and dilates bronchi and cerebral vessels. It is used in asthma and cardiac failure and to delay absorption of local anesthetics. [NIH] Epiphyseal: Pertaining to or of the nature of an epiphysis. [EU] Episcleritis: Inflammation of the episclera and/or the outer layers of the sclera itself. [NIH] Epithelial: Refers to the cells that line the internal and external surfaces of the body. [NIH] Epithelial Cells: Cells that line the inner and outer surfaces of the body. [NIH] Epithelium: One or more layers of epithelial cells, supported by the basal lamina, which covers the inner or outer surfaces of the body. [NIH] Epitope: A molecule or portion of a molecule capable of binding to the combining site of an antibody. For every given antigenic determinant, the body can construct a variety of antibody-combining sites, some of which fit almost perfectly, and others which barely fit. [NIH]
Epoprostenol: A prostaglandin that is biosynthesized enzymatically from prostaglandin endoperoxides in human vascular tissue. It is a potent inhibitor of platelet aggregation. The sodium salt has been also used to treat primary pulmonary hypertension. [NIH] Equipment and Supplies: Expendable and nonexpendable equipment, supplies, apparatus, and instruments that are used in diagnostic, surgical, therapeutic, scientific, and experimental procedures. [NIH] Ergometry: Any method of measuring the amount of work done by an organism, usually during exertion. Ergometry also includes measures of power. Some instruments used in these determinations include the hand crank and the bicycle ergometer. [NIH] Erysipeloid: An infection caused by Erysipelothrix rhusiopathiae that is almost wholly restricted to persons who in their occupation handle infected fish, shellfish, poultry, or meat. Three forms of this condition exist: a mild localized form manifested by local swelling and redness of the skin; a diffuse form that might present with fever; and a rare systemic form associated with endocarditis. [NIH] Erythema: Redness of the skin produced by congestion of the capillaries. This condition may result from a variety of causes. [NIH] Erythema Multiforme: A skin and mucous membrane disease characterized by an eruption of macules, papules, nodules, vesicles, and/or bullae with characteristic "bull's-eye" lesions usually occurring on the dorsal aspect of the hands and forearms. [NIH] Erythrocyte Membrane: The semipermeable outer portion of the red corpuscle. It is known as a 'ghost' after hemolysis. [NIH] Erythrocytes: Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing hemoglobin whose function is to transport oxygen. [NIH] Erythromycin: A bacteriostatic antibiotic substance produced by Streptomyces erythreus. Erythromycin A is considered its major active component. In sensitive organisms, it inhibits protein synthesis by binding to 50S ribosomal subunits. This binding process inhibits peptidyl transferase activity and interferes with translocation of amino acids during translation and assembly of proteins. [NIH] Escalation: Progressive use of more harmful drugs. [NIH] Esophagus: The muscular tube through which food passes from the throat to the stomach. [NIH]
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Estrogen: One of the two female sex hormones. [NIH] Estrogen receptor: ER. Protein found on some cancer cells to which estrogen will attach. [NIH]
Estrogen Replacement Therapy: The use of hormonal agents with estrogen-like activity in postmenopausal or other estrogen-deficient women to alleviate effects of hormone deficiency, such as vasomotor symptoms, dyspareunia, and progressive development of osteoporosis. This may also include the use of progestational agents in combination therapy. [NIH]
Ethanol: A clear, colorless liquid rapidly absorbed from the gastrointestinal tract and distributed throughout the body. It has bactericidal activity and is used often as a topical disinfectant. It is widely used as a solvent and preservative in pharmaceutical preparations as well as serving as the primary ingredient in alcoholic beverages. [NIH] Ethnic Groups: A group of people with a common cultural heritage that sets them apart from others in a variety of social relationships. [NIH] Etidronate: A drug that belongs to the family of drugs called bisphosphonates. Bisphosphonates are used as treatment for hypercalcemia (abnormally high levels of calcium in the blood) and for cancer that has spread to the bone (bone metastases). [NIH] Etodolac: A nonsteroidal anti-inflammatory agent with potent analgesic and antiarthritic properties. It has been shown to be effective in the treatment of osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, and in the alleviation of postoperative pain. [NIH] Etretinate: An oral retinoid used in the treatment of keratotic genodermatosis, lichen planus, and psoriasis. Beneficial effects have also been claimed in the prophylaxis of epithelial neoplasia. The compound may be teratogenic. [NIH] Eukaryotic Cells: Cells of the higher organisms, containing a true nucleus bounded by a nuclear membrane. [NIH] Evoke: The electric response recorded from the cerebral cortex after stimulation of a peripheral sense organ. [NIH] Excitation: An act of irritation or stimulation or of responding to a stimulus; the addition of energy, as the excitation of a molecule by absorption of photons. [EU] Excrete: To get rid of waste from the body. [NIH] Exercise Test: Controlled physical activity, more strenuous than at rest, which is performed in order to allow assessment of physiological functions, particularly cardiovascular and pulmonary, but also aerobic capacity. Maximal (most intense) exercise is usually required but submaximal exercise is also used. The intensity of exercise is often graded, using criteria such as rate of work done, oxygen consumption, and heart rate. Physiological data obtained from an exercise test may be used for diagnosis, prognosis, and evaluation of disease severity, and to evaluate therapy. Data may also be used in prescribing exercise by determining a person's exercise capacity. [NIH] Exocrine: Secreting outwardly, via a duct. [EU] Exocytosis: Cellular release of material within membrane-limited vesicles by fusion of the vesicles with the cell membrane. [NIH] Exogenous: Developed or originating outside the organism, as exogenous disease. [EU] Exon: The part of the DNA that encodes the information for the actual amino acid sequence of the protein. In many eucaryotic genes, the coding sequences consist of a series of exons alternating with intron sequences. [NIH] Extensor: A muscle whose contraction tends to straighten a limb; the antagonist of a flexor. [NIH]
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External-beam radiation: Radiation therapy that uses a machine to aim high-energy rays at the cancer. Also called external radiation. [NIH] Extracellular: Outside a cell or cells. [EU] Extracellular Matrix: A meshwork-like substance found within the extracellular space and in association with the basement membrane of the cell surface. It promotes cellular proliferation and provides a supporting structure to which cells or cell lysates in culture dishes adhere. [NIH] Extracellular Matrix Proteins: Macromolecular organic compounds that contain carbon, hydrogen, oxygen, nitrogen, and usually, sulfur. These macromolecules (proteins) form an intricate meshwork in which cells are embedded to construct tissues. Variations in the relative types of macromolecules and their organization determine the type of extracellular matrix, each adapted to the functional requirements of the tissue. The two main classes of macromolecules that form the extracellular matrix are: glycosaminoglycans, usually linked to proteins (proteoglycans), and fibrous proteins (e.g., collagen, elastin, fibronectins and laminin). [NIH] Extracellular Space: Interstitial space between cells, occupied by fluid as well as amorphous and fibrous substances. [NIH] Extraction: The process or act of pulling or drawing out. [EU] Extravasation: A discharge or escape, as of blood, from a vessel into the tissues. [EU] Extremity: A limb; an arm or leg (membrum); sometimes applied specifically to a hand or foot. [EU] Eye Infections: Infection, moderate to severe, caused by bacteria, fungi, or viruses, which occurs either on the external surface of the eye or intraocularly with probable inflammation, visual impairment, or blindness. [NIH] Facial: Of or pertaining to the face. [EU] Facial Nerve: The 7th cranial nerve. The facial nerve has two parts, the larger motor root which may be called the facial nerve proper, and the smaller intermediate or sensory root. Together they provide efferent innervation to the muscles of facial expression and to the lacrimal and salivary glands, and convey afferent information for taste from the anterior two-thirds of the tongue and for touch from the external ear. [NIH] Family Planning: Programs or services designed to assist the family in controlling reproduction by either improving or diminishing fertility. [NIH] Family Practice: A medical specialty concerned with the provision of continuing, comprehensive primary health care for the entire family. [NIH] Fasciitis: Inflammation of the fascia. There are three major types: 1) Eosinophilic fasciitis, an inflammatory reaction with eosinophilia, producing hard thickened skin with an orangepeel configuration suggestive of scleroderma and considered by some a variant of scleroderma; 2) Necrotizing fasciitis, a serious fulminating infection (usually by a beta hemolytic Streptococcus) causing extensive necrosis of superficial fascia; 3) Nodular/Pseudosarcomatous/Proliferative fasciitis, characterized by a rapid growth of fibroblasts with mononuclear inflammatory cells and proliferating capillaries in soft tissue, often the forearm; it is not malignant but is sometimes mistaken for fibrosarcoma. [NIH] Fat: Total lipids including phospholipids. [NIH] Fatigue: The state of weariness following a period of exertion, mental or physical, characterized by a decreased capacity for work and reduced efficiency to respond to stimuli. [NIH]
Fatty acids: A major component of fats that are used by the body for energy and tissue
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development. [NIH] Femoral: Pertaining to the femur, or to the thigh. [EU] Femoral Artery: The main artery of the thigh, a continuation of the external iliac artery. [NIH]
Femur: The longest and largest bone of the skeleton, it is situated between the hip and the knee. [NIH] Fermentation: An enzyme-induced chemical change in organic compounds that takes place in the absence of oxygen. The change usually results in the production of ethanol or lactic acid, and the production of energy. [NIH] Fertilization in Vitro: Fertilization of an egg outside the body when the egg is normally fertilized in the body. [NIH] Fetus: The developing offspring from 7 to 8 weeks after conception until birth. [NIH] Feverfew: Aromatic perennial Tanacetum parthenium used to treat migraines, arthritis, and as a febrifuge. It contains tannins, volatile oils (oils, essential), and sesquiterpene lactones, especially parthenolide. [NIH] Fibril: Most bacterial viruses have a hollow tail with specialized fibrils at its tip. The tail fibers attach to the cell wall of the host. [NIH] Fibrin: A protein derived from fibrinogen in the presence of thrombin, which forms part of the blood clot. [NIH] Fibrinogen: Plasma glycoprotein clotted by thrombin, composed of a dimer of three nonidentical pairs of polypeptide chains (alpha, beta, gamma) held together by disulfide bonds. Fibrinogen clotting is a sol-gel change involving complex molecular arrangements: whereas fibrinogen is cleaved by thrombin to form polypeptides A and B, the proteolytic action of other enzymes yields different fibrinogen degradation products. [NIH] Fibrinolysis: The natural enzymatic dissolution of fibrin. [NIH] Fibrinolytic: Pertaining to, characterized by, or causing the dissolution of fibrin by enzymatic action [EU] Fibroblast Growth Factor: Peptide isolated from the pituitary gland and from the brain. It is a potent mitogen which stimulates growth of a variety of mesodermal cells including chondrocytes, granulosa, and endothelial cells. The peptide may be active in wound healing and animal limb regeneration. [NIH] Fibroblasts: Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules. [NIH] Fibronectin: An adhesive glycoprotein. One form circulates in plasma, acting as an opsonin; another is a cell-surface protein which mediates cellular adhesive interactions. [NIH] Fibrosarcoma: A type of soft tissue sarcoma that begins in fibrous tissue, which holds bones, muscles, and other organs in place. [NIH] Fibrosis: Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury. [NIH] Fibula: The bone of the lower leg lateral to and smaller than the tibia. In proportion to its length, it is the most slender of the long bones. [NIH] Film Dosimetry: Use of a device (film badge) for measuring exposure of individuals to radiation. It is usually made of metal, plastic, or paper and loaded with one or more pieces of X-ray film. [NIH] Fine-needle aspiration: The removal of tissue or fluid with a needle for examination under
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a microscope. Also called needle biopsy. [NIH] Fish Oils: Oils high in unsaturated fats extracted from the bodies of fish or fish parts, especially the livers. Those from the liver are usually high in vitamin A. The oils are used as dietary supplements, in soaps and detergents, as protective coatings, and as a base for other food products such as vegetable shortenings. [NIH] Fistula: Abnormal communication most commonly seen between two internal organs, or between an internal organ and the surface of the body. [NIH] Fixation: 1. The act or operation of holding, suturing, or fastening in a fixed position. 2. The condition of being held in a fixed position. 3. In psychiatry, a term with two related but distinct meanings : (1) arrest of development at a particular stage, which like regression (return to an earlier stage), if temporary is a normal reaction to setbacks and difficulties but if protracted or frequent is a cause of developmental failures and emotional problems, and (2) a close and suffocating attachment to another person, especially a childhood figure, such as one's mother or father. Both meanings are derived from psychoanalytic theory and refer to 'fixation' of libidinal energy either in a specific erogenous zone, hence fixation at the oral, anal, or phallic stage, or in a specific object, hence mother or father fixation. 4. The use of a fixative (q.v.) to preserve histological or cytological specimens. 5. In chemistry, the process whereby a substance is removed from the gaseous or solution phase and localized, as in carbon dioxide fixation or nitrogen fixation. 6. In ophthalmology, direction of the gaze so that the visual image of the object falls on the fovea centralis. 7. In film processing, the chemical removal of all undeveloped salts of the film emulsion, leaving only the developed silver to form a permanent image. [EU] Flatus: Gas passed through the rectum. [NIH] Flexion: In gynaecology, a displacement of the uterus in which the organ is bent so far forward or backward that an acute angle forms between the fundus and the cervix. [EU] Flexor: Muscles which flex a joint. [NIH] Flow Cytometry: Technique using an instrument system for making, processing, and displaying one or more measurements on individual cells obtained from a cell suspension. Cells are usually stained with one or more fluorescent dyes specific to cell components of interest, e.g., DNA, and fluorescence of each cell is measured as it rapidly transverses the excitation beam (laser or mercury arc lamp). Fluorescence provides a quantitative measure of various biochemical and biophysical properties of the cell, as well as a basis for cell sorting. Other measurable optical parameters include light absorption and light scattering, the latter being applicable to the measurement of cell size, shape, density, granularity, and stain uptake. [NIH] Fluconazole: Triazole antifungal agent that is used to treat oropharyngeal candidiasis and cryptococcal meningitis in AIDS. [NIH] Fludarabine: An anticancer drug that belongs to the family of drugs called antimetabolites. [NIH]
Fluorescein Angiography: Visualization of a vascular system after intravenous injection of a fluorescein solution. The images may be photographed or televised. It is used especially in studying the retinal and uveal vasculature. [NIH] Fluorescence: The property of emitting radiation while being irradiated. The radiation emitted is usually of longer wavelength than that incident or absorbed, e.g., a substance can be irradiated with invisible radiation and emit visible light. X-ray fluorescence is used in diagnosis. [NIH] Fluorescent Antibody Technique: Test for tissue antigen using either a direct method by conjugation of antibody with fluorescent dye or an indirect method by formation of antigen-
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antibody complex which is then labeled with fluorescein-conjugated anti-immunoglobulin antibody. The tissue is then examined by fluorescence microscopy. [NIH] Fluorescent Dyes: Dyes that emit light when exposed to light. The wave length of the emitted light is usually longer than that of the incident light. Fluorochromes are substances that cause fluorescence in other substances, i.e., dyes used to mark or label other compounds with fluorescent tags. They are used as markers in biochemistry and immunology. [NIH] Fluoroimmunoassay: The use of fluorescence spectrometry to obtain quantitative results for the fluorescent antibody technique. One advantage over the other methods (e.g., radioimmunoassay) is its extreme sensitivity, with a detection limit on the order of tenths of microgram/liter. [NIH] Focus Groups: A method of data collection and a qualitative research tool in which a small group of individuals are brought together and allowed to interact in a discussion of their opinions about topics, issues, or questions. [NIH] Folate: A B-complex vitamin that is being studied as a cancer prevention agent. Also called folic acid. [NIH] Fold: A plication or doubling of various parts of the body. [NIH] Folic Acid: N-(4-(((2-Amino-1,4-dihydro-4-oxo-6-pteridinyl)methyl)amino)benzoyl)-Lglutamic acid. A member of the vitamin B family that stimulates the hematopoietic system. It is present in the liver and kidney and is found in mushrooms, spinach, yeast, green leaves, and grasses. Folic acid is used in the treatment and prevention of folate deficiencies and megaloblastic anemia. [NIH] Folliculitis: Inflammation of follicles, primarily hair follicles. [NIH] Food Technology: The application of knowledge to the food industry. [NIH] Forearm: The part between the elbow and the wrist. [NIH] Fovea: The central part of the macula that provides the sharpest vision. [NIH] Frameshift: A type of mutation which causes out-of-phase transcription of the base sequence; such mutations arise from the addition or delection of nucleotide(s) in numbers other than 3 or multiples of 3. [NIH] Frameshift Mutation: A type of mutation in which a number of nucleotides not divisible by three is deleted from or inserted into a coding sequence, thereby causing an alteration in the reading frame of the entire sequence downstream of the mutation. These mutations may be induced by certain types of mutagens or may occur spontaneously. [NIH] Fraud: Exploitation through misrepresentation of the facts or concealment of the purposes of the exploiter. [NIH] Free Radicals: Highly reactive molecules with an unsatisfied electron valence pair. Free radicals are produced in both normal and pathological processes. They are proven or suspected agents of tissue damage in a wide variety of circumstances including radiation, damage from environment chemicals, and aging. Natural and pharmacological prevention of free radical damage is being actively investigated. [NIH] Freeze-dried: A method used to dry substances, such as food, to make them last longer. The substance is frozen and then dried in a vacuum. [NIH] Friction: Surface resistance to the relative motion of one body against the rubbing, sliding, rolling, or flowing of another with which it is in contact. [NIH] Fructose: A type of sugar found in many fruits and vegetables and in honey. Fructose is used to sweeten some diet foods. It is considered a nutritive sweetener because it has calories. [NIH]
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Fundus: The larger part of a hollow organ that is farthest away from the organ's opening. The bladder, gallbladder, stomach, uterus, eye, and cavity of the middle ear all have a fundus. [NIH] Gadolinium: An element of the rare earth family of metals. It has the atomic symbol Gd, atomic number 64, and atomic weight 157.25. Its oxide is used in the control rods of some nuclear reactors. [NIH] Gait: Manner or style of walking. [NIH] Gallate: Antioxidant present in tea. [NIH] Gallbladder: The pear-shaped organ that sits below the liver. Bile is concentrated and stored in the gallbladder. [NIH] Gamma-interferon: Interferon produced by T-lymphocytes in response to various mitogens and antigens. Gamma interferon appears to have potent antineoplastic, immunoregulatory and antiviral activity. [NIH] Ganglia: Clusters of multipolar neurons surrounded by a capsule of loosely organized connective tissue located outside the central nervous system. [NIH] Ganglion: 1. A knot, or knotlike mass. 2. A general term for a group of nerve cell bodies located outside the central nervous system; occasionally applied to certain nuclear groups within the brain or spinal cord, e.g. basal ganglia. 3. A benign cystic tumour occurring on a aponeurosis or tendon, as in the wrist or dorsum of the foot; it consists of a thin fibrous capsule enclosing a clear mucinous fluid. [EU] Gas: Air that comes from normal breakdown of food. The gases are passed out of the body through the rectum (flatus) or the mouth (burp). [NIH] Gastric: Having to do with the stomach. [NIH] Gastric Acid: Hydrochloric acid present in gastric juice. [NIH] Gastric Juices: Liquids produced in the stomach to help break down food and kill bacteria. [NIH]
Gastric Mucosa: Surface epithelium in the stomach that invaginates into the lamina propria, forming gastric pits. Tubular glands, characteristic of each region of the stomach (cardiac, gastric, and pyloric), empty into the gastric pits. The gastric mucosa is made up of several different kinds of cells. [NIH] Gastrin: A hormone released after eating. Gastrin causes the stomach to produce more acid. [NIH]
Gastroduodenal: Pertaining to or communicating with the stomach and duodenum, as a gastroduodenal fistula. [EU] Gastroenteritis: An acute inflammation of the lining of the stomach and intestines, characterized by anorexia, nausea, diarrhoea, abdominal pain, and weakness, which has various causes, including food poisoning due to infection with such organisms as Escherichia coli, Staphylococcus aureus, and Salmonella species; consumption of irritating food or drink; or psychological factors such as anger, stress, and fear. Called also enterogastritis. [EU] Gastrointestinal: Refers to the stomach and intestines. [NIH] Gastrointestinal tract: The stomach and intestines. [NIH] Gelatin: A product formed from skin, white connective tissue, or bone collagen. It is used as a protein food adjuvant, plasma substitute, hemostatic, suspending agent in pharmaceutical preparations, and in the manufacturing of capsules and suppositories. [NIH] Gene: The functional and physical unit of heredity passed from parent to offspring. Genes
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are pieces of DNA, and most genes contain the information for making a specific protein. [NIH]
Gene Expression: The phenotypic manifestation of a gene or genes by the processes of gene action. [NIH] Gene Therapy: The introduction of new genes into cells for the purpose of treating disease by restoring or adding gene expression. Techniques include insertion of retroviral vectors, transfection, homologous recombination, and injection of new genes into the nuclei of single cell embryos. The entire gene therapy process may consist of multiple steps. The new genes may be introduced into proliferating cells in vivo (e.g., bone marrow) or in vitro (e.g., fibroblast cultures) and the modified cells transferred to the site where the gene expression is required. Gene therapy may be particularly useful for treating enzyme deficiency diseases, hemoglobinopathies, and leukemias and may also prove useful in restoring drug sensitivity, particularly for leukemia. [NIH] General practitioner: A medical practitioner who does not specialize in a particular branch of medicine or limit his practice to a specific class of diseases. [NIH] Genetic Code: The specifications for how information, stored in nucleic acid sequence (base sequence), is translated into protein sequence (amino acid sequence). The start, stop, and order of amino acids of a protein is specified by consecutive triplets of nucleotides called codons (codon). [NIH] Genetic Engineering: Directed modification of the gene complement of a living organism by such techniques as altering the DNA, substituting genetic material by means of a virus, transplanting whole nuclei, transplanting cell hybrids, etc. [NIH] Genetic Markers: A phenotypically recognizable genetic trait which can be used to identify a genetic locus, a linkage group, or a recombination event. [NIH] Genetic testing: Analyzing DNA to look for a genetic alteration that may indicate an increased risk for developing a specific disease or disorder. [NIH] Genetics: The biological science that deals with the phenomena and mechanisms of heredity. [NIH] Genital: Pertaining to the genitalia. [EU] Genitourinary: Pertaining to the genital and urinary organs; urogenital; urinosexual. [EU] Genomics: The systematic study of the complete DNA sequences (genome) of organisms. [NIH]
Genotype: The genetic constitution of the individual; the characterization of the genes. [NIH] Gestation: The period of development of the young in viviparous animals, from the time of fertilization of the ovum until birth. [EU] Giardiasis: An infection of the small intestine caused by the flagellated protozoan Giardia lamblia. It is spread via contaminated food and water and by direct person-to-person contact. [NIH] Ginger: Deciduous plant rich in volatile oil (oils, volatile). It is used as a flavoring agent and has many other uses both internally and topically. [NIH] Ginseng: An araliaceous genus of plants that contains a number of pharmacologically active agents used as stimulants, sedatives, and tonics, especially in traditional medicine. [NIH]
Gland: An organ that produces and releases one or more substances for use in the body. Some glands produce fluids that affect tissues or organs. Others produce hormones or participate in blood production. [NIH]
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Glomerular: Pertaining to or of the nature of a glomerulus, especially a renal glomerulus. [EU]
Glomerulus: A tiny set of looping blood vessels in the nephron where blood is filtered in the kidney. [NIH] Glucocorticoid: A compound that belongs to the family of compounds called corticosteroids (steroids). Glucocorticoids affect metabolism and have anti-inflammatory and immunosuppressive effects. They may be naturally produced (hormones) or synthetic (drugs). [NIH] Glucose: D-Glucose. A primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used therapeutically in fluid and nutrient replacement. [NIH] Glucose Intolerance: A pathological state in which the fasting plasma glucose level is less than 140 mg per deciliter and the 30-, 60-, or 90-minute plasma glucose concentration following a glucose tolerance test exceeds 200 mg per deciliter. This condition is seen frequently in diabetes mellitus but also occurs with other diseases. [NIH] Glucose tolerance: The power of the normal liver to absorb and store large quantities of glucose and the effectiveness of intestinal absorption of glucose. The glucose tolerance test is a metabolic test of carbohydrate tolerance that measures active insulin, a hepatic function based on the ability of the liver to absorb glucose. The test consists of ingesting 100 grams of glucose into a fasting stomach; blood sugar should return to normal in 2 to 21 hours after ingestion. [NIH] Glucose Tolerance Test: Determination of whole blood or plasma sugar in a fasting state before and at prescribed intervals (usually 1/2 hr, 1 hr, 3 hr, 4 hr) after taking a specified amount (usually 100 gm orally) of glucose. [NIH] Glucose-6-Phosphate Isomerase: An enzyme that catalyzes the reversible interconversion of glucose 6-phosphate and fructose 6-phosphate, and is a part of the glycolytic and gluconeogenic pathways. Deficiency of the enzyme, an autosomal recessive trait, results in liver glycogenesis and hemolytic anemia. EC 5.3.1.9. [NIH] Glucuronic Acid: Derivatives of uronic acid found throughout the plant and animal kingdoms. They detoxify drugs and toxins by conjugating with them to form glucuronides in the liver which are more water-soluble metabolites that can be easily eliminated from the body. [NIH] Glutamate: Excitatory neurotransmitter of the brain. [NIH] Glutamic Acid: A non-essential amino acid naturally occurring in the L-form. Glutamic acid (glutamate) is the most common excitatory neurotransmitter in the central nervous system. [NIH] Glutathione Peroxidase: An enzyme catalyzing the oxidation of 2 moles of glutathione in the presence of hydrogen peroxide to yield oxidized glutathione and water. EC 1.11.1.9. [NIH]
Gluten: The protein of wheat and other grains which gives to the dough its tough elastic character. [EU] Glycine: A non-essential amino acid. It is found primarily in gelatin and silk fibroin and used therapeutically as a nutrient. It is also a fast inhibitory neurotransmitter. [NIH] Glycogen: A sugar stored in the liver and muscles. It releases glucose into the blood when cells need it for energy. Glycogen is the chief source of stored fuel in the body. [NIH] Glycoprotein: A protein that has sugar molecules attached to it. [NIH] Glycosaminoglycan:
A
type
of
long,
unbranched
polysaccharide
molecule.
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Glycosaminoglycans are major structural components of cartilage and are also found in the cornea of the eye. [NIH] Goats: Any of numerous agile, hollow-horned ruminants of the genus Capra, closely related to the sheep. [NIH] Gold Compounds: molecule. [NIH]
Inorganic compounds that contain gold as an integral part of the
Gonad: A sex organ, such as an ovary or a testicle, which produces the gametes in most multicellular animals. [NIH] Gonadal: Pertaining to a gonad. [EU] Gonorrhea: Acute infectious disease characterized by primary invasion of the urogenital tract. The etiologic agent, Neisseria gonorrhoeae, was isolated by Neisser in 1879. [NIH] Gonorrhoea: Infection due to Neisseria gonorrhoeae transmitted sexually in most cases, but also by contact with infected exudates in neonatal children at birth, or by infants in households with infected inhabitants. It is marked in males by urethritis with pain and purulent discharge, but is commonly asymptomatic in females, although it may extend to produce suppurative salpingitis, oophoritis, tubo-ovarian abscess, and peritonitis. Bacteraemia occurs in both sexes, resulting in cutaneous lesions, arthritis, and rarely meningitis or endocarditis. Formerly called blennorrhagia and blennorrhoea. [EU] Gout: Hereditary metabolic disorder characterized by recurrent acute arthritis, hyperuricemia and deposition of sodium urate in and around the joints, sometimes with formation of uric acid calculi. [NIH] Governing Board: The group in which legal authority is vested for the control of healthrelated institutions and organizations. [NIH] Government Agencies: Administrative units of government responsible for policy making and management of governmental activities in the U.S. and abroad. [NIH] Grade: The grade of a tumor depends on how abnormal the cancer cells look under a microscope and how quickly the tumor is likely to grow and spread. Grading systems are different for each type of cancer. [NIH] Graft Rejection: An immune response with both cellular and humoral components, directed against an allogeneic transplant, whose tissue antigens are not compatible with those of the recipient. [NIH] Grafting: The operation of transfer of tissue from one site to another. [NIH] Gram-negative: Losing the stain or decolorized by alcohol in Gram's method of staining, a primary characteristic of bacteria having a cell wall composed of a thin layer of peptidoglycan covered by an outer membrane of lipoprotein and lipopolysaccharide. [EU] Gram-positive: Retaining the stain or resisting decolorization by alcohol in Gram's method of staining, a primary characteristic of bacteria whose cell wall is composed of a thick layer of peptidologlycan with attached teichoic acids. [EU] Granule: A small pill made from sucrose. [EU] Granulocyte: A type of white blood cell that fights bacterial infection. Neutrophils, eosinophils, and basophils are granulocytes. [NIH] Granulocyte-Macrophage Colony-Stimulating Factor: An acidic glycoprotein of MW 23 kDa with internal disulfide bonds. The protein is produced in response to a number of inflammatory mediators by mesenchymal cells present in the hemopoietic environment and at peripheral sites of inflammation. GM-CSF is able to stimulate the production of neutrophilic granulocytes, macrophages, and mixed granulocyte-macrophage colonies from
Dictionary 623
bone marrow cells and can stimulate the formation of eosinophil colonies from fetal liver progenitor cells. GM-CSF can also stimulate some functional activities in mature granulocytes and macrophages. [NIH] Granuloma: A relatively small nodular inflammatory lesion containing grouped mononuclear phagocytes, caused by infectious and noninfectious agents. [NIH] Granulomatous Disease, Chronic: A recessive X-linked defect of leukocyte function in which phagocytic cells ingest but fail to digest bacteria, resulting in recurring bacterial infections with granuloma formation. [NIH] Grasses: A large family, Gramineae, of narrow-leaved herbaceous monocots. Many grasses produce highly allergenic pollens and are hosts to cattle parasites and toxic fungi. [NIH] Gravis: Eruption of watery blisters on the skin among those handling animals and animal products. [NIH] Growth: The progressive development of a living being or part of an organism from its earliest stage to maturity. [NIH] Growth factors: Substances made by the body that function to regulate cell division and cell survival. Some growth factors are also produced in the laboratory and used in biological therapy. [NIH] Guanine: One of the four DNA bases. [NIH] Guanylate Cyclase: An enzyme that catalyzes the conversion of GTP to 3',5'-cyclic GMP and pyrophosphate. It also acts on ITP and dGTP. (From Enzyme Nomenclature, 1992) EC 4.6.1.2. [NIH] Habitat: An area considered in terms of its environment, particularly as this determines the type and quality of the vegetation the area can carry. [NIH] Hair follicles: Shafts or openings on the surface of the skin through which hair grows. [NIH] Half-Life: The time it takes for a substance (drug, radioactive nuclide, or other) to lose half of its pharmacologic, physiologic, or radiologic activity. [NIH] Hallux Rigidus: A condition caused by degenerative arthritis (osteoarthritis) of the metatarsophalangeal joint of the great toe and characterized by pain and limited dorsiflexion, but relatively unrestricted plantar flexion. [NIH] Hammer: The largest of the three ossicles of the ear. [NIH] Hand Deformities: Alterations or deviations from normal shape or size which result in a disfigurement of the hand. [NIH] Haploid: An organism with one basic chromosome set, symbolized by n; the normal condition of gametes in diploids. [NIH] Haplotypes: The genetic constitution of individuals with respect to one member of a pair of allelic genes, or sets of genes that are closely linked and tend to be inherited together such as those of the major histocompatibility complex. [NIH] Haptens: Small antigenic determinants capable of eliciting an immune response only when coupled to a carrier. Haptens bind to antibodies but by themselves cannot elicit an antibody response. [NIH] Headache: Pain in the cranial region that may occur as an isolated and benign symptom or as a manifestation of a wide variety of conditions including subarachnoid hemorrhage; craniocerebral trauma; central nervous system infections; intracranial hypertension; and other disorders. In general, recurrent headaches that are not associated with a primary disease process are referred to as headache disorders (e.g., migraine). [NIH] Headache Disorders:
Common conditions characterized by persistent or recurrent
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headaches. Headache syndrome classification systems may be based on etiology (e.g., vascular headache, post-traumatic headaches, etc.), temporal pattern (e.g., cluster headache, paroxysmal hemicrania, etc.), and precipitating factors (e.g., cough headache). [NIH] Health Behavior: Behaviors expressed by individuals to protect, maintain or promote their health status. For example, proper diet, and appropriate exercise are activities perceived to influence health status. Life style is closely associated with health behavior and factors influencing life style are socioeconomic, educational, and cultural. [NIH] Health Care Costs: The actual costs of providing services related to the delivery of health care, including the costs of procedures, therapies, and medications. It is differentiated from health expenditures, which refers to the amount of money paid for the services, and from fees, which refers to the amount charged, regardless of cost. [NIH] Health Education: Education that increases the awareness and favorably influences the attitudes and knowledge relating to the improvement of health on a personal or community basis. [NIH] Health Expenditures: The amounts spent by individuals, groups, nations, or private or public organizations for total health care and/or its various components. These amounts may or may not be equivalent to the actual costs (health care costs) and may or may not be shared among the patient, insurers, and/or employers. [NIH] Health Promotion: Encouraging consumer behaviors most likely to optimize health potentials (physical and psychosocial) through health information, preventive programs, and access to medical care. [NIH] Health Services: Services for the diagnosis and treatment of disease and the maintenance of health. [NIH] Health Surveys: A systematic collection of factual data pertaining to health and disease in a human population within a given geographic area. [NIH] Heart attack: A seizure of weak or abnormal functioning of the heart. [NIH] Heart failure: Loss of pumping ability by the heart, often accompanied by fatigue, breathlessness, and excess fluid accumulation in body tissues. [NIH] Heartburn: Substernal pain or burning sensation, usually associated with regurgitation of gastric juice into the esophagus. [NIH] Helminths: Commonly known as parasitic worms, this group includes the acanthocephala, nematoda, and platyhelminths. Some authors consider certain species of leeches that can become temporarily parasitic as helminths. [NIH] Hematogenous: Originating in the blood or spread through the bloodstream. [NIH] Hematopoiesis: The development and formation of various types of blood cells. [NIH] Hematopoietic Stem Cell Transplantation: The transference of stem cells from one animal or human to another (allogeneic), or within the same individual (autologous). The source for the stem cells may be the bone marrow or peripheral blood. Stem cell transplantation has been used as an alternative to autologous bone marrow transplantation in the treatment of a variety of neoplasms. [NIH] Heme: The color-furnishing portion of hemoglobin. It is found free in tissues and as the prosthetic group in many hemeproteins. [NIH] Hemodialysis: The use of a machine to clean wastes from the blood after the kidneys have failed. The blood travels through tubes to a dialyzer, which removes wastes and extra fluid. The cleaned blood then flows through another set of tubes back into the body. [NIH] Hemoglobin:
One of the fractions of glycosylated hemoglobin A1c. Glycosylated
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hemoglobin is formed when linkages of glucose and related monosaccharides bind to hemoglobin A and its concentration represents the average blood glucose level over the previous several weeks. HbA1c levels are used as a measure of long-term control of plasma glucose (normal, 4 to 6 percent). In controlled diabetes mellitus, the concentration of glycosylated hemoglobin A is within the normal range, but in uncontrolled cases the level may be 3 to 4 times the normal conentration. Generally, complications are substantially lower among patients with Hb levels of 7 percent or less than in patients with HbA1c levels of 9 percent or more. [NIH] Hemoglobinopathies: A group of inherited disorders characterized by structural alterations within the hemoglobin molecule. [NIH] Hemolysis: The destruction of erythrocytes by many different causal agents such as antibodies, bacteria, chemicals, temperature, and changes in tonicity. [NIH] Hemolytic: A disease that affects the blood and blood vessels. It destroys red blood cells, cells that cause the blood to clot, and the lining of blood vessels. HUS is often caused by the Escherichia coli bacterium in contaminated food. People with HUS may develop acute renal failure. [NIH] Hemorrhage: Bleeding or escape of blood from a vessel. [NIH] Hemosiderin: Molecule which can bind large numbers of iron atoms. [NIH] Hemosiderosis: Conditions in which there is a generalized increase in the iron stores of body tissues, particularly of liver and the reticuloendothelial system, without demonstrable tissue damage. The name refers to the presence of stainable iron in the tissue in the form of hemosiderin. [NIH] Hemostasis: The process which spontaneously arrests the flow of blood from vessels carrying blood under pressure. It is accomplished by contraction of the vessels, adhesion and aggregation of formed blood elements, and the process of blood or plasma coagulation. [NIH]
Heparin: Heparinic acid. A highly acidic mucopolysaccharide formed of equal parts of sulfated D-glucosamine and D-glucuronic acid with sulfaminic bridges. The molecular weight ranges from six to twenty thousand. Heparin occurs in and is obtained from liver, lung, mast cells, etc., of vertebrates. Its function is unknown, but it is used to prevent blood clotting in vivo and vitro, in the form of many different salts. [NIH] Hepatic: Refers to the liver. [NIH] Hepatitis: Inflammation of the liver and liver disease involving degenerative or necrotic alterations of hepatocytes. [NIH] Hepatobiliary: Pertaining to the liver and the bile or the biliary ducts. [EU] Hepatocyte: A liver cell. [NIH] Hepatotoxicity: How much damage a medicine or other substance does to the liver. [NIH] Hereditary: Of, relating to, or denoting factors that can be transmitted genetically from one generation to another. [NIH] Heredity: 1. The genetic transmission of a particular quality or trait from parent to offspring. 2. The genetic constitution of an individual. [EU] Herpes: Any inflammatory skin disease caused by a herpesvirus and characterized by the formation of clusters of small vesicles. When used alone, the term may refer to herpes simplex or to herpes zoster. [EU] Herpes Zoster: Acute vesicular inflammation. [NIH] Hesperidin: Predominant flavonoid in lemons and sweet oranges. [NIH]
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Heterogeneity: The property of one or more samples or populations which implies that they are not identical in respect of some or all of their parameters, e. g. heterogeneity of variance. [NIH] Heterotrophic: Pertaining to organisms that are consumers and dependent on other organisms for their source of energy (food). [NIH] Heterozygotes: Having unlike alleles at one or more corresponding loci on homologous chromosomes. [NIH] Histamine: 1H-Imidazole-4-ethanamine. A depressor amine derived by enzymatic decarboxylation of histidine. It is a powerful stimulant of gastric secretion, a constrictor of bronchial smooth muscle, a vasodilator, and also a centrally acting neurotransmitter. [NIH] Histidine: An essential amino acid important in a number of metabolic processes. It is required for the production of histamine. [NIH] Homeostasis: The processes whereby the internal environment of an organism tends to remain balanced and stable. [NIH] Homodimer: Protein-binding "activation domains" always combine with identical proteins. [NIH]
Homologous: Corresponding in structure, position, origin, etc., as (a) the feathers of a bird and the scales of a fish, (b) antigen and its specific antibody, (c) allelic chromosomes. [EU] Homozygotes: An individual having a homozygous gene pair. [NIH] Hormonal: Pertaining to or of the nature of a hormone. [EU] Hormone: A substance in the body that regulates certain organs. Hormones such as gastrin help in breaking down food. Some hormones come from cells in the stomach and small intestine. [NIH] Hormone Replacement Therapy: Therapeutic use of hormones to alleviate the effects of hormone deficiency. [NIH] Horny layer: The superficial layer of the epidermis containing keratinized cells. [NIH] Horseradish Peroxidase: An enzyme isolated from horseradish which is able to act as an antigen. It is frequently used as a histochemical tracer for light and electron microscopy. Its antigenicity has permitted its use as a combined antigen and marker in experimental immunology. [NIH] Host: Any animal that receives a transplanted graft. [NIH] Human Genome Project: A coordinated effort of researchers to map and sequence the human genome. [NIH] Humoral: Of, relating to, proceeding from, or involving a bodily humour - now often used of endocrine factors as opposed to neural or somatic. [EU] Humour: 1. A normal functioning fluid or semifluid of the body (as the blood, lymph or bile) especially of vertebrates. 2. A secretion that is itself an excitant of activity (as certain hormones). [EU] Hyalin: A clear, homogenous, structureless, eosinophilic substance occurring in pathological degeneration of tissues. [NIH] Hybrid: Cross fertilization between two varieties or, more usually, two species of vines, see also crossing. [NIH] Hybridomas: Cells artificially created by fusion of activated lymphocytes with neoplastic cells. The resulting hybrid cells are cloned and produce pure or "monoclonal" antibodies or T-cell products, identical to those produced by the immunologically competent parent, and
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continually grow and divide as the neoplastic parent. [NIH] Hydration: Combining with water. [NIH] Hydroalcoholic: Of or relating to water and alcohol. [EU] Hydrogel: A network of cross-linked hydrophilic macromolecules used in biomedical applications. [NIH] Hydrolysis: The process of cleaving a chemical compound by the addition of a molecule of water. [NIH] Hydrophilic: Readily absorbing moisture; hygroscopic; having strongly polar groups that readily interact with water. [EU] Hydrophobic: Not readily absorbing water, or being adversely affected by water, as a hydrophobic colloid. [EU] Hydroxylysine: A hydroxylated derivative of the amino acid lysine that is present in certain collagens. [NIH] Hydroxyproline: A hydroxylated form of the imino acid proline. A deficiency in ascorbic acid can result in impaired hydroxyproline formation. [NIH] Hyperaemia: An excess of blood in a part; engorgement. [EU] Hypercalcemia: Abnormally high level of calcium in the blood. [NIH] Hypercholesterolemia: Abnormally high levels of cholesterol in the blood. [NIH] Hyperglycemia: Abnormally high blood sugar. [NIH] Hyperlipidemia: An excess of lipids in the blood. [NIH] Hyperlipoproteinemia: Metabolic disease characterized by elevated plasma cholesterol and/or triglyceride levels. The inherited form is attributed to a single gene mechanism. [NIH] Hyperostosis: Increase in the mass of bone per unit volume. [NIH] Hyperplasia: An increase in the number of cells in a tissue or organ, not due to tumor formation. It differs from hypertrophy, which is an increase in bulk without an increase in the number of cells. [NIH] Hypersensitivity: Altered reactivity to an antigen, which can result in pathologic reactions upon subsequent exposure to that particular antigen. [NIH] Hypertension: Persistently high arterial blood pressure. Currently accepted threshold levels are 140 mm Hg systolic and 90 mm Hg diastolic pressure. [NIH] Hyperthermia: A type of treatment in which body tissue is exposed to high temperatures to damage and kill cancer cells or to make cancer cells more sensitive to the effects of radiation and certain anticancer drugs. [NIH] Hyperthyroidism: Excessive functional activity of the thyroid gland. [NIH] Hypertriglyceridemia: Condition of elevated triglyceride concentration in the blood; an inherited form occurs in familial hyperlipoproteinemia IIb and hyperlipoproteinemia type IV. It has been linked to higher risk of heart disease and arteriosclerosis. [NIH] Hypertrophy: General increase in bulk of a part or organ, not due to tumor formation, nor to an increase in the number of cells. [NIH] Hyperuricemia: A buildup of uric acid (a byproduct of metabolism) in the blood; a side effect of some anticancer drugs. [NIH] Hypoglycemia: Abnormally low blood sugar [NIH] Hypothalamic: Of or involving the hypothalamus. [EU]
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Hypothalamus: Ventral part of the diencephalon extending from the region of the optic chiasm to the caudal border of the mammillary bodies and forming the inferior and lateral walls of the third ventricle. [NIH] Hypoxia: Reduction of oxygen supply to tissue below physiological levels despite adequate perfusion of the tissue by blood. [EU] Hypoxic: Having too little oxygen. [NIH] Ibuprofen: A nonsteroidal anti-inflammatory agent with analgesic properties used in the therapy of rheumatism and arthritis. [NIH] Id: The part of the personality structure which harbors the unconscious instinctive desires and strivings of the individual. [NIH] Idiopathic: Describes a disease of unknown cause. [NIH] Ileus: Obstruction of the intestines. [EU] Iliac Artery: Either of two large arteries originating from the abdominal aorta; they supply blood to the pelvis, abdominal wall and legs. [NIH] Iloprost: An eicosanoid, derived from the cyclooxygenase pathway of arachidonic acid metabolism. It is a stable and synthetic analog of epoprostenol, but with a longer half-life than the parent compound. Its actions are similar to prostacyclin. Iloprost produces vasodilation and inhibits platelet aggregation. [NIH] Imaging procedures: Methods of producing pictures of areas inside the body. [NIH] Immersion: The placing of a body or a part thereof into a liquid. [NIH] Immune function: Production and action of cells that fight disease or infection. [NIH] Immune response: (antigens). [NIH]
The activity of the immune system against foreign substances
Immune Sera: Serum that contains antibodies. It is obtained from an animal that has been immunized either by antigen injection or infection with microorganisms containing the antigen. [NIH] Immune system: The organs, cells, and molecules responsible for the recognition and disposal of foreign ("non-self") material which enters the body. [NIH] Immune Tolerance: The specific failure of a normally responsive individual to make an immune response to a known antigen. It results from previous contact with the antigen by an immunologically immature individual (fetus or neonate) or by an adult exposed to extreme high-dose or low-dose antigen, or by exposure to radiation, antimetabolites, antilymphocytic serum, etc. [NIH] Immunity: Nonsusceptibility to the invasive or pathogenic effects of foreign microorganisms or to the toxic effect of antigenic substances. [NIH] Immunization: Deliberate stimulation of the host's immune response. Active immunization involves administration of antigens or immunologic adjuvants. Passive immunization involves administration of immune sera or lymphocytes or their extracts (e.g., transfer factor, immune RNA) or transplantation of immunocompetent cell producing tissue (thymus or bone marrow). [NIH] Immunoassay: Immunochemical assay or detection of a substance by serologic or immunologic methods. Usually the substance being studied serves as antigen both in antibody production and in measurement of antibody by the test substance. [NIH] Immunoblotting: Immunologic methods for isolating and quantitatively measuring immunoreactive substances. When used with immune reagents such as monoclonal antibodies, the process is known generically as western blot analysis (blotting, western).
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[NIH]
Immunocompromised: Having a weakened immune system caused by certain diseases or treatments. [NIH] Immunodeficiency: The decreased ability of the body to fight infection and disease. [NIH] Immunogenetics: A branch of genetics which deals with the genetic basis of the immune response. [NIH] Immunogenic: Producing immunity; evoking an immune response. [EU] Immunoglobulin: A protein that acts as an antibody. [NIH] Immunohistochemistry: Histochemical localization of immunoreactive substances using labeled antibodies as reagents. [NIH] Immunologic: The ability of the antibody-forming system to recall a previous experience with an antigen and to respond to a second exposure with the prompt production of large amounts of antibody. [NIH] Immunologic Factors: Biologically active substances whose activities affect or play a role in the functioning of the immune system. [NIH] Immunology: The study of the body's immune system. [NIH] Immunosuppressant: An agent capable of suppressing immune responses. [EU] Immunosuppression: Deliberate prevention or diminution of the host's immune response. It may be nonspecific as in the administration of immunosuppressive agents (drugs or radiation) or by lymphocyte depletion or may be specific as in desensitization or the simultaneous administration of antigen and immunosuppressive drugs. [NIH] Immunosuppressive: Describes the ability to lower immune system responses. [NIH] Immunosuppressive Agents: Agents that suppress immune function by one of several mechanisms of action. Classical cytotoxic immunosuppressants act by inhibiting DNA synthesis. Others may act through activation of suppressor T-cell populations or by inhibiting the activation of helper cells. While immunosuppression has been brought about in the past primarily to prevent rejection of transplanted organs, new applications involving mediation of the effects of interleukins and other cytokines are emerging. [NIH] Immunosuppressive therapy: Therapy used to decrease the body's immune response, such as drugs given to prevent transplant rejection. [NIH] Immunotherapy: Manipulation of the host's immune system in treatment of disease. It includes both active and passive immunization as well as immunosuppressive therapy to prevent graft rejection. [NIH] Immunotoxin: An antibody linked to a toxic substance. Some immmunotoxins can bind to cancer cells and kill them. [NIH] Impairment: In the context of health experience, an impairment is any loss or abnormality of psychological, physiological, or anatomical structure or function. [NIH] Implant radiation: A procedure in which radioactive material sealed in needles, seeds, wires, or catheters is placed directly into or near the tumor. Also called [NIH] Impotence: The inability to perform sexual intercourse. [NIH] In situ: In the natural or normal place; confined to the site of origin without invasion of neighbouring tissues. [EU] In Situ Hybridization: A technique that localizes specific nucleic acid sequences within intact chromosomes, eukaryotic cells, or bacterial cells through the use of specific nucleic acid-labeled probes. [NIH]
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In vitro: In the laboratory (outside the body). The opposite of in vivo (in the body). [NIH] In vivo: In the body. The opposite of in vitro (outside the body or in the laboratory). [NIH] Incidental: 1. Small and relatively unimportant, minor; 2. Accompanying, but not a major part of something; 3. (To something) Liable to occur because of something or in connection with something (said of risks, responsibilities, ...) [EU] Incision: A cut made in the body during surgery. [NIH] Incontinence: Inability to control the flow of urine from the bladder (urinary incontinence) or the escape of stool from the rectum (fecal incontinence). [NIH] Incubation: The development of an infectious disease from the entrance of the pathogen to the appearance of clinical symptoms. [EU] Incubation period: The period of time likely to elapse between exposure to the agent of the disease and the onset of clinical symptoms. [NIH] Indolent: A type of cancer that grows slowly. [NIH] Indomethacin: A non-steroidal anti-inflammatory agent (NSAID) that inhibits the enzyme cyclooxygenase necessary for the formation of prostaglandins and other autacoids. It also inhibits the motility of polymorphonuclear leukocytes. [NIH] Induction: The act or process of inducing or causing to occur, especially the production of a specific morphogenetic effect in the developing embryo through the influence of evocators or organizers, or the production of anaesthesia or unconsciousness by use of appropriate agents. [EU] Infancy: The period of complete dependency prior to the acquisition of competence in walking, talking, and self-feeding. [NIH] Infant, Newborn: An infant during the first month after birth. [NIH] Infantile: Pertaining to an infant or to infancy. [EU] Infarction: A pathological process consisting of a sudden insufficient blood supply to an area, which results in necrosis of that area. It is usually caused by a thrombus, an embolus, or a vascular torsion. [NIH] Infection: 1. Invasion and multiplication of microorganisms in body tissues, which may be clinically unapparent or result in local cellular injury due to competitive metabolism, toxins, intracellular replication, or antigen-antibody response. The infection may remain localized, subclinical, and temporary if the body's defensive mechanisms are effective. A local infection may persist and spread by extension to become an acute, subacute, or chronic clinical infection or disease state. A local infection may also become systemic when the microorganisms gain access to the lymphatic or vascular system. 2. An infectious disease. [EU]
Infectious Mononucleosis: A common, acute infection usually caused by the Epstein-Barr virus (Human herpesvirus 4). There is an increase in mononuclear white blood cells and other atypical lymphocytes, generalized lymphadenopathy, splenomegaly, and occasionally hepatomegaly with hepatitis. [NIH] Infiltration: The diffusion or accumulation in a tissue or cells of substances not normal to it or in amounts of the normal. Also, the material so accumulated. [EU] Inflammation: A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function. [NIH] Inflammatory bowel disease: A general term that refers to the inflammation of the colon and rectum. Inflammatory bowel disease includes ulcerative colitis and Crohn's disease.
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[NIH]
Influenza: An acute viral infection involving the respiratory tract. It is marked by inflammation of the nasal mucosa, the pharynx, and conjunctiva, and by headache and severe, often generalized, myalgia. [NIH] Informed Consent: Voluntary authorization, given to the physician by the patient, with full comprehension of the risks involved, for diagnostic or investigative procedures and medical and surgical treatment. [NIH] Infusion: A method of putting fluids, including drugs, into the bloodstream. Also called intravenous infusion. [NIH] Ingestion: Taking into the body by mouth [NIH] Inhalation: The drawing of air or other substances into the lungs. [EU] Initiation: Mutation induced by a chemical reactive substance causing cell changes; being a step in a carcinogenic process. [NIH] Initiator: A chemically reactive substance which may cause cell changes if ingested, inhaled or absorbed into the body; the substance may thus initiate a carcinogenic process. [NIH] Inlay: In dentistry, a filling first made to correspond with the form of a dental cavity and then cemented into the cavity. [NIH] Inorganic: Pertaining to substances not of organic origin. [EU] Inpatients: Persons admitted to health facilities which provide board and room, for the purpose of observation, care, diagnosis or treatment. [NIH] Insight: The capacity to understand one's own motives, to be aware of one's own psychodynamics, to appreciate the meaning of symbolic behavior. [NIH] Insulator: Material covering the metal conductor of the lead. It is usually polyurethane or silicone. [NIH] Insulin: A protein hormone secreted by beta cells of the pancreas. Insulin plays a major role in the regulation of glucose metabolism, generally promoting the cellular utilization of glucose. It is also an important regulator of protein and lipid metabolism. Insulin is used as a drug to control insulin-dependent diabetes mellitus. [NIH] Insulin-dependent diabetes mellitus: A disease characterized by high levels of blood glucose resulting from defects in insulin secretion, insulin action, or both. Autoimmune, genetic, and environmental factors are involved in the development of type I diabetes. [NIH] Insulin-like: Muscular growth factor. [NIH] Intensive Care: Advanced and highly specialized care provided to medical or surgical patients whose conditions are life-threatening and require comprehensive care and constant monitoring. It is usually administered in specially equipped units of a health care facility. [NIH]
Intercellular Adhesion Molecule-1: A cell-surface ligand with a role in leukocyte adhesion and inflammation. Its production is induced by gamma-interferon and it is required for neutrophil migration into inflamed tissue. [NIH] Interferon: A biological response modifier (a substance that can improve the body's natural response to disease). Interferons interfere with the division of cancer cells and can slow tumor growth. There are several types of interferons, including interferon-alpha, -beta, and gamma. These substances are normally produced by the body. They are also made in the laboratory for use in treating cancer and other diseases. [NIH] Interferon-alpha: One of the type I interferons produced by peripheral blood leukocytes or lymphoblastoid cells when exposed to live or inactivated virus, double-stranded RNA, or
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bacterial products. It is the major interferon produced by virus-induced leukocyte cultures and, in addition to its pronounced antiviral activity, it causes activation of NK cells. [NIH] Interleukin-1: A soluble factor produced by monocytes, macrophages, and other cells which activates T-lymphocytes and potentiates their response to mitogens or antigens. IL-1 consists of two distinct forms, IL-1 alpha and IL-1 beta which perform the same functions but are distinct proteins. The biological effects of IL-1 include the ability to replace macrophage requirements for T-cell activation. The factor is distinct from interleukin-2. [NIH] Interleukin-10: Factor that is a coregulator of mast cell growth. It is produced by T-cells and B-cells and shows extensive homology with the Epstein-Barr virus BCRFI gene. [NIH] Interleukin-11: Lymphohematopoietic cytokine that has the ability to modulate antigenspecific antibody responses, potentiate megakaryocytes, and regulate bone marrow adipogenesis. [NIH] Interleukin-12: A heterodimeric cytokine that stimulates the production of interferon gamma from T-cells and natural killer cells, and also induces differentiation of Th1 helper cells. It is an initiator of cell-mediated immunity. [NIH] Interleukin-17: Proinflammatory cytokine produced primarily by T-lymphocytes or their precursors. IL-17 is homologous to an open reading frame found in Herpesvirus saimiri. [NIH]
Interleukin-18: Cytokine which resembles IL-1 structurally and IL-12 functionally. It enhances the cytotoxic activity of NK cells and CTLs, and appears to play a role both as neuroimmunomodulator and in the induction of mucosal immunity. [NIH] Interleukin-2: Chemical mediator produced by activated T lymphocytes and which regulates the proliferation of T cells, as well as playing a role in the regulation of NK cell activity. [NIH] Interleukin-4: Soluble factor produced by activated T-lymphocytes that causes proliferation and differentiation of B-cells. Interleukin-4 induces the expression of class II major histocompatibility complex and Fc receptors on B-cells. It also acts on T-lymphocytes, mast cell lines, and several other hematopoietic lineage cells including granulocyte, megakaryocyte, and erythroid precursors, as well as macrophages. [NIH] Interleukin-6: Factor that stimulates the growth and differentiation of human B-cells and is also a growth factor for hybridomas and plasmacytomas. It is produced by many different cells including T-cells, monocytes, and fibroblasts. [NIH] Interleukin-8: A cytokine that activates neutrophils and attracts neutrophils and Tlymphocytes. It is released by several cell types including monocytes, macrophages, Tlymphocytes, fibroblasts, endothelial cells, and keratinocytes by an inflammatory stimulus. IL-8 is a member of the beta-thromboglobulin superfamily and structurally related to platelet factor 4. [NIH] Interleukins: Soluble factors which stimulate growth-related activities of leukocytes as well as other cell types. They enhance cell proliferation and differentiation, DNA synthesis, secretion of other biologically active molecules and responses to immune and inflammatory stimuli. [NIH] Intermittent: Occurring at separated intervals; having periods of cessation of activity. [EU] Internal Medicine: A medical specialty concerned with the diagnosis and treatment of diseases of the internal organ systems of adults. [NIH] Internal radiation: A procedure in which radioactive material sealed in needles, seeds, wires, or catheters is placed directly into or near the tumor. Also called brachytherapy, implant radiation, or interstitial radiation therapy. [NIH]
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Interpersonal Relations: The reciprocal interaction of two or more persons. [NIH] Interstitial: Pertaining to or situated between parts or in the interspaces of a tissue. [EU] Intervention Studies: Epidemiologic investigations designed to test a hypothesized causeeffect relation by modifying the supposed causal factor(s) in the study population. [NIH] Intervertebral: Situated between two contiguous vertebrae. [EU] Intervertebral Disk Displacement: An intervertebral disk in which the nucleus pulposus has protruded through surrounding fibrocartilage. This occurs most frequently in the lower lumbar region. [NIH] Intestinal: Having to do with the intestines. [NIH] Intestinal Mucosa: The surface lining of the intestines where the cells absorb nutrients. [NIH]
Intestine: A long, tube-shaped organ in the abdomen that completes the process of digestion. There is both a large intestine and a small intestine. Also called the bowel. [NIH] Intoxication: Poisoning, the state of being poisoned. [EU] Intracellular: Inside a cell. [NIH] Intraindividual: Being or occurring within the individual. [EU] Intramuscular: IM. Within or into muscle. [NIH] Intramuscular injection: IM. Injection into a muscle. [NIH] Intravenous: IV. Into a vein. [NIH] Intrinsic: Situated entirely within or pertaining exclusively to a part. [EU] Intubation: Introduction of a tube into a hollow organ to restore or maintain patency if obstructed. It is differentiated from catheterization in that the insertion of a catheter is usually performed for the introducing or withdrawing of fluids from the body. [NIH] Invasive: 1. Having the quality of invasiveness. 2. Involving puncture or incision of the skin or insertion of an instrument or foreign material into the body; said of diagnostic techniques. [EU]
Involuntary: Reaction occurring without intention or volition. [NIH] Iodine: A nonmetallic element of the halogen group that is represented by the atomic symbol I, atomic number 53, and atomic weight of 126.90. It is a nutritionally essential element, especially important in thyroid hormone synthesis. In solution, it has anti-infective properties and is used topically. [NIH] Ions: An atom or group of atoms that have a positive or negative electric charge due to a gain (negative charge) or loss (positive charge) of one or more electrons. Atoms with a positive charge are known as cations; those with a negative charge are anions. [NIH] Iridocyclitis: Acute or chronic inflammation of the iris and ciliary body characterized by exudates into the anterior chamber, discoloration of the iris, and constricted, sluggish pupil. Symptoms include radiating pain, photophobia, lacrimation, and interference with vision. [NIH]
Iris: The most anterior portion of the uveal layer, separating the anterior chamber from the posterior. It consists of two layers - the stroma and the pigmented epithelium. Color of the iris depends on the amount of melanin in the stroma on reflection from the pigmented epithelium. [NIH] Iritis: Inflammation of the iris characterized by circumcorneal injection, aqueous flare, keratotic precipitates, and constricted and sluggish pupil along with discoloration of the iris. [NIH]
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Irradiation: The use of high-energy radiation from x-rays, neutrons, and other sources to kill cancer cells and shrink tumors. Radiation may come from a machine outside the body (external-beam radiation therapy) or from materials called radioisotopes. Radioisotopes produce radiation and can be placed in or near the tumor or in the area near cancer cells. This type of radiation treatment is called internal radiation therapy, implant radiation, interstitial radiation, or brachytherapy. Systemic radiation therapy uses a radioactive substance, such as a radiolabeled monoclonal antibody, that circulates throughout the body. Irradiation is also called radiation therapy, radiotherapy, and x-ray therapy. [NIH] Ischemia: Deficiency of blood in a part, due to functional constriction or actual obstruction of a blood vessel. [EU] Isoenzymes: One of various structurally related forms of an enzyme, each having the same mechanism but with differing chemical, physical, or immunological characteristics. [NIH] Isopropyl: A gene mutation inducer. [NIH] Isotonic: A biological term denoting a solution in which body cells can be bathed without a net flow of water across the semipermeable cell membrane. Also, denoting a solution having the same tonicity as some other solution with which it is compared, such as physiologic salt solution and the blood serum. [EU] Joint: The point of contact between elements of an animal skeleton with the parts that surround and support it. [NIH] Joint Capsule: The sac enclosing a joint. It is composed of an outer fibrous articular capsule and an inner synovial membrane. [NIH] Joint Instability: Lack of stability of a joint or joint prosthesis. Factors involved are intraarticular disease and integrity of extra-articular structures such as joint capsule, ligaments, and muscles. [NIH] Kallidin: A decapeptide bradykinin homolog produced by the action of tissue and glandular kallikreins on low-molecular-weight kininogen. It is a smooth-muscle stimulant and hypotensive agent that functions through vasodilatation. [NIH] Kb: A measure of the length of DNA fragments, 1 Kb = 1000 base pairs. The largest DNA fragments are up to 50 kilobases long. [NIH] Keratin: A class of fibrous proteins or scleroproteins important both as structural proteins and as keys to the study of protein conformation. The family represents the principal constituent of epidermis, hair, nails, horny tissues, and the organic matrix of tooth enamel. Two major conformational groups have been characterized, alpha-keratin, whose peptide backbone forms an alpha-helix, and beta-keratin, whose backbone forms a zigzag or pleated sheet structure. [NIH] Keratinocytes: Epidermal cells which synthesize keratin and undergo characteristic changes as they move upward from the basal layers of the epidermis to the cornified (horny) layer of the skin. Successive stages of differentiation of the keratinocytes forming the epidermal layers are basal cell, spinous or prickle cell, and the granular cell. [NIH] Keratoconjunctivitis: Simultaneous inflammation of the cornea and conjunctiva. [NIH] Keratoconjunctivitis Sicca: Drying and inflammation of the conjunctiva as a result of insufficient lacrimal secretion. When found in association with xerostomia and polyarthritis, it is called Sjogren's syndrome. [NIH] Keratolytic: An agent that promotes keratolysis. [EU] Keratolytic Agents: Agents that soften, separate, and cause desquamation of the cornified epithelium or horny layer of skin. They are used to expose mycelia of infecting fungi or to treat corns, warts, and certain other skin diseases. [NIH]
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Ketone Bodies: Chemicals that the body makes when there is not enough insulin in the blood and it must break down fat for its energy. Ketone bodies can poison and even kill body cells. When the body does not have the help of insulin, the ketones build up in the blood and then "spill" over into the urine so that the body can get rid of them. The body can also rid itself of one type of ketone, called acetone, through the lungs. This gives the breath a fruity odor. Ketones that build up in the body for a long time lead to serious illness and coma. [NIH] Ketosis: A condition of having ketone bodies build up in body tissues and fluids. The signs of ketosis are nausea, vomiting, and stomach pain. Ketosis can lead to ketoacidosis. [NIH] Kidney Disease: Any one of several chronic conditions that are caused by damage to the cells of the kidney. People who have had diabetes for a long time may have kidney damage. Also called nephropathy. [NIH] Kidney Failure: The inability of a kidney to excrete metabolites at normal plasma levels under conditions of normal loading, or the inability to retain electrolytes under conditions of normal intake. In the acute form (kidney failure, acute), it is marked by uremia and usually by oliguria or anuria, with hyperkalemia and pulmonary edema. The chronic form (kidney failure, chronic) is irreversible and requires hemodialysis. [NIH] Kidney Failure, Acute: A clinical syndrome characterized by a sudden decrease in glomerular filtration rate, often to values of less than 1 to 2 ml per minute. It is usually associated with oliguria (urine volumes of less than 400 ml per day) and is always associated with biochemical consequences of the reduction in glomerular filtration rate such as a rise in blood urea nitrogen (BUN) and serum creatinine concentrations. [NIH] Kidney Failure, Chronic: An irreversible and usually progressive reduction in renal function in which both kidneys have been damaged by a variety of diseases to the extent that they are unable to adequately remove the metabolic products from the blood and regulate the body's electrolyte composition and acid-base balance. Chronic kidney failure requires hemodialysis or surgery, usually kidney transplantation. [NIH] Kidney stone: A stone that develops from crystals that form in urine and build up on the inner surfaces of the kidney, in the renal pelvis, or in the ureters. [NIH] Killer Cells: Lymphocyte-like effector cells which mediate antibody-dependent cell cytotoxicity. They kill antibody-coated target cells which they bind with their Fc receptors. [NIH]
Kinetics: The study of rate dynamics in chemical or physical systems. [NIH] Kringles: Triple-looped protein domains linked by disulfide bonds. These common structural domains, so-named for their resemblance to Danish pastries known as kringlers, play a role in binding membranes, proteins, and phospholipids as well as in regulating proteolysis. Kringles are also present in coagulation-related and fibrinolytic proteins and other plasma proteinases. [NIH] Labile: 1. Gliding; moving from point to point over the surface; unstable; fluctuating. 2. Chemically unstable. [EU] Labyrinth: The internal ear; the essential part of the organ of hearing. It consists of an osseous and a membranous portion. [NIH] Lacrimal: Pertaining to the tears. [EU] Lactation: The period of the secretion of milk. [EU] Lag: The time elapsing between application of a stimulus and the resulting reaction. [NIH] Laminin: Large, noncollagenous glycoprotein with antigenic properties. It is localized in the basement membrane lamina lucida and functions to bind epithelial cells to the basement
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membrane. Evidence suggests that the protein plays a role in tumor invasion. [NIH] Large Intestine: The part of the intestine that goes from the cecum to the rectum. The large intestine absorbs water from stool and changes it from a liquid to a solid form. The large intestine is 5 feet long and includes the appendix, cecum, colon, and rectum. Also called colon. [NIH] Latency: The period of apparent inactivity between the time when a stimulus is presented and the moment a response occurs. [NIH] Latent: Phoria which occurs at one distance or another and which usually has no troublesome effect. [NIH] Lavage: A cleaning of the stomach and colon. Uses a special drink and enemas. [NIH] Least-Squares Analysis: A principle of estimation in which the estimates of a set of parameters in a statistical model are those quantities minimizing the sum of squared differences between the observed values of a dependent variable and the values predicted by the model. [NIH] Lectin: A complex molecule that has both protein and sugars. Lectins are able to bind to the outside of a cell and cause biochemical changes in it. Lectins are made by both animals and plants. [NIH] Leflunomide: An anticancer drug that works by inhibiting a cancer cell growth factor. Also called SU101. [NIH] Leg Ulcer: Ulceration of the skin and underlying structures of the lower extremity. About 90% of the cases are due to venous insufficiency (varicose ulcer), 5% to arterial disease, and the remaining 5% to other causes. [NIH] Lens: The transparent, double convex (outward curve on both sides) structure suspended between the aqueous and vitreous; helps to focus light on the retina. [NIH] Lentivirus: A genus of the family Retroviridae consisting of non-oncogenic retroviruses that produce multi-organ diseases characterized by long incubation periods and persistent infection. Lentiviruses are unique in that they contain open reading frames (ORFs) between the pol and env genes and in the 3' env region. Five serogroups are recognized, reflecting the mammalian hosts with which they are associated. HIV-1 is the type species. [NIH] Leprosy: A chronic granulomatous infection caused by Mycobacterium leprae. The granulomatous lesions are manifested in the skin, the mucous membranes, and the peripheral nerves. Two polar or principal types are lepromatous and tuberculoid. [NIH] Lesion: An area of abnormal tissue change. [NIH] Leucovorin: The active metabolite of folic acid. Leucovorin is used principally as its calcium salt as an antidote to folic acid antagonists which block the conversion of folic acid to folinic acid. [NIH] Leukapheresis: The preparation of leukocyte concentrates with the return of red cells and leukocyte-poor plasma to the donor. [NIH] Leukemia: Cancer of blood-forming tissue. [NIH] Leukocytes: White blood cells. These include granular leukocytes (basophils, eosinophils, and neutrophils) as well as non-granular leukocytes (lymphocytes and monocytes). [NIH] Leukopenia: A condition in which the number of leukocytes (white blood cells) in the blood is reduced. [NIH] Leukotrienes: A family of biologically active compounds derived from arachidonic acid by oxidative metabolism through the 5-lipoxygenase pathway. They participate in host defense reactions and pathophysiological conditions such as immediate hypersensitivity and
Dictionary 637
inflammation. They have potent actions on many essential organs and systems, including the cardiovascular, pulmonary, and central nervous system as well as the gastrointestinal tract and the immune system. [NIH] Libido: The psychic drive or energy associated with sexual instinct in the broad sense (pleasure and love-object seeking). It may also connote the psychic energy associated with instincts in general that motivate behavior. [NIH] Library Services: circulation. [NIH]
Services offered to the library user. They include reference and
Lichen Planus: An inflammatory, pruritic disease of the skin and mucous membranes, which can be either generalized or localized. It is characterized by distinctive purplish, flattopped papules having a predilection for the trunk and flexor surfaces. The lesions may be discrete or coalesce to form plaques. Histologically, there is a "saw-tooth" pattern of epidermal hyperplasia and vacuolar alteration of the basal layer of the epidermis along with an intense upper dermal inflammatory infiltrate composed predominantly of T-cells. Etiology is unknown. [NIH] Lidocaine: A local anesthetic and cardiac depressant used as an antiarrhythmia agent. Its actions are more intense and its effects more prolonged than those of procaine but its duration of action is shorter than that of bupivacaine or prilocaine. [NIH] Life cycle: The successive stages through which an organism passes from fertilized ovum or spore to the fertilized ovum or spore of the next generation. [NIH] Life Expectancy: A figure representing the number of years, based on known statistics, to which any person of a given age may reasonably expect to live. [NIH] Ligament: A band of fibrous tissue that connects bones or cartilages, serving to support and strengthen joints. [EU] Ligands: A RNA simulation method developed by the MIT. [NIH] Ligation: Application of a ligature to tie a vessel or strangulate a part. [NIH] Likelihood Functions: Functions constructed from a statistical model and a set of observed data which give the probability of that data for various values of the unknown model parameters. Those parameter values that maximize the probability are the maximum likelihood estimates of the parameters. [NIH] Linear Models: Statistical models in which the value of a parameter for a given value of a factor is assumed to be equal to a + bx, where a and b are constants. The models predict a linear regression. [NIH] Linkage: The tendency of two or more genes in the same chromosome to remain together from one generation to the next more frequently than expected according to the law of independent assortment. [NIH] Lip: Either of the two fleshy, full-blooded margins of the mouth. [NIH] Lipid: Fat. [NIH] Lipid Peroxidation: Peroxidase catalyzed oxidation of lipids using hydrogen peroxide as an electron acceptor. [NIH] Lipopolysaccharide: Substance consisting of polysaccaride and lipid. [NIH] Lipoprotein: Any of the lipid-protein complexes in which lipids are transported in the blood; lipoprotein particles consist of a spherical hydrophobic core of triglycerides or cholesterol esters surrounded by an amphipathic monolayer of phospholipids, cholesterol, and apolipoproteins; the four principal classes are high-density, low-density, and very-lowdensity lipoproteins and chylomicrons. [EU]
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Lipoprotein Lipase: An enzyme of the hydrolase class that catalyzes the reaction of triacylglycerol and water to yield diacylglycerol and a fatty acid anion. The enzyme hydrolyzes triacylglycerols in chylomicrons, very-low-density lipoproteins, low-density lipoproteins, and diacylglycerols. It occurs on capillary endothelial surfaces, especially in mammary, muscle, and adipose tissue. Genetic deficiency of the enzyme causes familial hyperlipoproteinemia Type I. (Dorland, 27th ed) EC 3.1.1.34. [NIH] Liposomal: A drug preparation that contains the active drug in very tiny fat particles. This fat-encapsulated drug is absorbed better, and its distribution to the tumor site is improved. [NIH]
Liposomes: Artificial, single or multilaminar vesicles (made from lecithins or other lipids) that are used for the delivery of a variety of biological molecules or molecular complexes to cells, for example, drug delivery and gene transfer. They are also used to study membranes and membrane proteins. [NIH] Lipoxygenase: An enzyme of the oxidoreductase class that catalyzes reactions between linoleate and other fatty acids and oxygen to form hydroperoxy-fatty acid derivatives. Related enzymes in this class include the arachidonate lipoxygenases, arachidonate 5lipoxygenase, arachidonate 12-lipoxygenase, and arachidonate 15-lipoxygenase. EC 1.13.11.12. [NIH] Liquor: 1. A liquid, especially an aqueous solution containing a medicinal substance. 2. A general term used in anatomical nomenclature for certain fluids of the body. [EU] Liver: A large, glandular organ located in the upper abdomen. The liver cleanses the blood and aids in digestion by secreting bile. [NIH] Liver scan: An image of the liver created on a computer screen or on film. A radioactive substance is injected into a blood vessel and travels through the bloodstream. It collects in the liver, especially in abnormal areas, and can be detected by the scanner. [NIH] Living will: A health care directive that tells others how a person would like to be treated if they lose their capacity to make decisions about health care; it contains instructions about the person's choices of medical treatment and it is prepared in advance. [NIH] Localization: The process of determining or marking the location or site of a lesion or disease. May also refer to the process of keeping a lesion or disease in a specific location or site. [NIH] Localized: Cancer which has not metastasized yet. [NIH] Locomotion: Movement or the ability to move from one place or another. It can refer to humans, vertebrate or invertebrate animals, and microorganisms. [NIH] Logistic Models: Statistical models which describe the relationship between a qualitative dependent variable (that is, one which can take only certain discrete values, such as the presence or absence of a disease) and an independent variable. A common application is in epidemiology for estimating an individual's risk (probability of a disease) as a function of a given risk factor. [NIH] Longitudinal study: Also referred to as a "cohort study" or "prospective study"; the analytic method of epidemiologic study in which subsets of a defined population can be identified who are, have been, or in the future may be exposed or not exposed, or exposed in different degrees, to a factor or factors hypothesized to influence the probability of occurrence of a given disease or other outcome. The main feature of this type of study is to observe large numbers of subjects over an extended time, with comparisons of incidence rates in groups that differ in exposure levels. [NIH] Lovastatin: A fungal metabolite isolated from cultures of Aspergillus terreus. The compound is a potent anticholesteremic agent. It inhibits 3-hydroxy-3-methylglutaryl
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coenzyme A reductase (hydroxymethylglutaryl CoA reductases), which is the rate-limiting enzyme in cholesterol biosynthesis. It also stimulates the production of low-density lipoprotein receptors in the liver. [NIH] Low Back Pain: Acute or chronic pain in the lumbar or sacral regions, which may be associated with musculo-ligamentous sprains and strains; intervertebral disk displacement; and other conditions. [NIH] Low-density lipoprotein: Lipoprotein that contains most of the cholesterol in the blood. LDL carries cholesterol to the tissues of the body, including the arteries. A high level of LDL increases the risk of heart disease. LDL typically contains 60 to 70 percent of the total serum cholesterol and both are directly correlated with CHD risk. [NIH] Lubricants: Oily or slippery substances. [NIH] Lubrication: The application of a substance to diminish friction between two surfaces. It may refer to oils, greases, and similar substances for the lubrication of medical equipment but it can be used for the application of substances to tissue to reduce friction, such as lotions for skin and vaginal lubricants. [NIH] Lumbago: Pain in the lumbar region. [EU] Lumbar: Pertaining to the loins, the part of the back between the thorax and the pelvis. [EU] Lung Transplantation: The transference of either one or both of the lungs from one human or animal to another. [NIH] Lupus: A form of cutaneous tuberculosis. It is seen predominantly in women and typically involves the nasal, buccal, and conjunctival mucosa. [NIH] Lutein Cells: The cells of the corpus luteum which are derived from the granulosa cells and the theca cells of the Graafian follicle. [NIH] Luxation: The displacement of the particular surface of a bone from its normal joint, without fracture. [NIH] Lymph: The almost colorless fluid that travels through the lymphatic system and carries cells that help fight infection and disease. [NIH] Lymph node: A rounded mass of lymphatic tissue that is surrounded by a capsule of connective tissue. Also known as a lymph gland. Lymph nodes are spread out along lymphatic vessels and contain many lymphocytes, which filter the lymphatic fluid (lymph). [NIH]
Lymphatic: The tissues and organs, including the bone marrow, spleen, thymus, and lymph nodes, that produce and store cells that fight infection and disease. [NIH] Lymphatic system: The tissues and organs that produce, store, and carry white blood cells that fight infection and other diseases. This system includes the bone marrow, spleen, thymus, lymph nodes and a network of thin tubes that carry lymph and white blood cells. These tubes branch, like blood vessels, into all the tissues of the body. [NIH] Lymphocyte: A white blood cell. Lymphocytes have a number of roles in the immune system, including the production of antibodies and other substances that fight infection and diseases. [NIH] Lymphocyte Depletion: Immunosuppression by reduction of circulating lymphocytes or by T-cell depletion of bone marrow. The former may be accomplished in vivo by thoracic duct drainage or administration of antilymphocyte serum. The latter is performed ex vivo on bone marrow before its transplantation. [NIH] Lymphocyte Subsets: A classification of lymphocytes based on structurally or functionally different populations of cells. [NIH]
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Lymphocytic: Referring to lymphocytes, a type of white blood cell. [NIH] Lymphoid: Referring to lymphocytes, a type of white blood cell. Also refers to tissue in which lymphocytes develop. [NIH] Lymphokine: A soluble protein produced by some types of white blood cell that stimulates other white blood cells to kill foreign invaders. [NIH] Lymphoma: A general term for various neoplastic diseases of the lymphoid tissue. [NIH] Lymphopenia: Reduction in the number of lymphocytes. [NIH] Lymphoproliferative: Disorders characterized by proliferation of lymphoid tissue, general or unspecified. [NIH] Lymphotoxin: Soluble substance released by lymphocytes activated by antigens or T-cell mitogens, that is cytotoxic to other cells. It is involved in allergies and chronic inflammatory diseases. Lymphotoxin is antigenically distinct from tumor necrosis factor-alpha (tumor necrosis factor), though they both share a common receptor, biological activities, and significant amino acid sequences. [NIH] Lysine: An essential amino acid. It is often added to animal feed. [NIH] Lytic: 1. Pertaining to lysis or to a lysin. 2. Producing lysis. [EU] Macrophage: A type of white blood cell that surrounds and kills microorganisms, removes dead cells, and stimulates the action of other immune system cells. [NIH] Macrophage Activation: The process of altering the morphology and functional activity of macrophages so that they become avidly phagocytic. It is initiated by lymphokines, such as the macrophage activation factor (MAF) and the macrophage migration-inhibitory factor (MMIF), immune complexes, C3b, and various peptides, polysaccharides, and immunologic adjuvants. [NIH] Macrophage Colony-Stimulating Factor: A mononuclear phagocyte colony-stimulating factor synthesized by mesenchymal cells. The compound stimulates the survival, proliferation, and differentiation of hematopoietic cells of the monocyte-macrophage series. M-CSF is a disulfide-bonded glycoprotein dimer with a MW of 70 kDa. It binds to a specific high affinity receptor (receptor, macrophage colony-stimulating factor). [NIH] Magnetic Resonance Imaging: Non-invasive method of demonstrating internal anatomy based on the principle that atomic nuclei in a strong magnetic field absorb pulses of radiofrequency energy and emit them as radiowaves which can be reconstructed into computerized images. The concept includes proton spin tomographic techniques. [NIH] Major Histocompatibility Complex: The genetic region which contains the loci of genes which determine the structure of the serologically defined (SD) and lymphocyte-defined (LD) transplantation antigens, genes which control the structure of the immune responseassociated (Ia) antigens, the immune response (Ir) genes which control the ability of an animal to respond immunologically to antigenic stimuli, and genes which determine the structure and/or level of the first four components of complement. [NIH] Malaise: A vague feeling of bodily discomfort. [EU] Malformation: A morphologic defect resulting from an intrinsically abnormal developmental process. [EU] Malignancy: A cancerous tumor that can invade and destroy nearby tissue and spread to other parts of the body. [NIH] Malignant: Cancerous; a growth with a tendency to invade and destroy nearby tissue and spread to other parts of the body. [NIH] Malignant tumor: A tumor capable of metastasizing. [NIH]
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Malnutrition: A condition caused by not eating enough food or not eating a balanced diet. [NIH]
Malondialdehyde: The dialdehyde of malonic acid. [NIH] Mammary: Pertaining to the mamma, or breast. [EU] Mandible: The largest and strongest bone of the face constituting the lower jaw. It supports the lower teeth. [NIH] Marital Status: A demographic parameter indicating a person's status with respect to marriage, divorce, widowhood, singleness, etc. [NIH] Mastication: The act and process of chewing and grinding food in the mouth. [NIH] Mastitis: Inflammatory disease of the breast, or mammary gland. [NIH] Matrix metalloproteinase: A member of a group of enzymes that can break down proteins, such as collagen, that are normally found in the spaces between cells in tissues (i.e., extracellular matrix proteins). Because these enzymes need zinc or calcium atoms to work properly, they are called metalloproteinases. Matrix metalloproteinases are involved in wound healing, angiogenesis, and tumor cell metastasis. [NIH] Meat: The edible portions of any animal used for food including domestic mammals (the major ones being cattle, swine, and sheep) along with poultry, fish, shellfish, and game. [NIH]
Medial: Lying near the midsaggital plane of the body; opposed to lateral. [NIH] Median Nerve: A major nerve of the upper extremity. In humans, the fibers of the median nerve originate in the lower cervical and upper thoracic spinal cord (usually C6 to T1), travel via the brachial plexus, and supply sensory and motor innervation to parts of the forearm and hand. [NIH] Mediate: Indirect; accomplished by the aid of an intervening medium. [EU] Mediator: An object or substance by which something is mediated, such as (1) a structure of the nervous system that transmits impulses eliciting a specific response; (2) a chemical substance (transmitter substance) that induces activity in an excitable tissue, such as nerve or muscle; or (3) a substance released from cells as the result of the interaction of antigen with antibody or by the action of antigen with a sensitized lymphocyte. [EU] Medical Records: illnesses. [NIH]
Recording of pertinent information concerning patient's illness or
Medical Staff: Professional medical personnel who provide care to patients in an organized facility, institution or agency. [NIH] MEDLINE: An online database of MEDLARS, the computerized bibliographic Medical Literature Analysis and Retrieval System of the National Library of Medicine. [NIH] Megaloblastic: anaemia. [EU]
A large abnormal red blood cell appearing in the blood in pernicious
Meiosis: A special method of cell division, occurring in maturation of the germ cells, by means of which each daughter nucleus receives half the number of chromosomes characteristic of the somatic cells of the species. [NIH] Melanin: The substance that gives the skin its color. [NIH] Melanocytes: Epidermal dendritic pigment cells which control long-term morphological color changes by alteration in their number or in the amount of pigment they produce and store in the pigment containing organelles called melanosomes. Melanophores are larger cells which do not exist in mammals. [NIH] Melanoma:
A form of skin cancer that arises in melanocytes, the cells that produce
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pigment. Melanoma usually begins in a mole. [NIH] Membrane: A very thin layer of tissue that covers a surface. [NIH] Membrane Proteins: Proteins which are found in membranes including cellular and intracellular membranes. They consist of two types, peripheral and integral proteins. They include most membrane-associated enzymes, antigenic proteins, transport proteins, and drug, hormone, and lectin receptors. [NIH] Memory: Complex mental function having four distinct phases: (1) memorizing or learning, (2) retention, (3) recall, and (4) recognition. Clinically, it is usually subdivided into immediate, recent, and remote memory. [NIH] Menarche: The establishment or beginning of the menstrual function. [EU] Meninges: The three membranes that cover and protect the brain and spinal cord. [NIH] Meningitis: Inflammation of the meninges. When it affects the dura mater, the disease is termed pachymeningitis; when the arachnoid and pia mater are involved, it is called leptomeningitis, or meningitis proper. [EU] Menopause: Permanent cessation of menstruation. [NIH] Menstruation: The normal physiologic discharge through the vagina of blood and mucosal tissues from the nonpregnant uterus. [NIH] Mental: Pertaining to the mind; psychic. 2. (L. mentum chin) pertaining to the chin. [EU] Mental Disorders: Psychiatric illness or diseases manifested by breakdowns in the adaptational process expressed primarily as abnormalities of thought, feeling, and behavior producing either distress or impairment of function. [NIH] Mental Health: The state wherein the person is well adjusted. [NIH] Mental Processes: Conceptual functions or thinking in all its forms. [NIH] Mentors: Senior professionals who provide guidance, direction and support to those persons desirous of improvement in academic positions, administrative positions or other career development situations. [NIH] Mercury: A silver metallic element that exists as a liquid at room temperature. It has the atomic symbol Hg (from hydrargyrum, liquid silver), atomic number 80, and atomic weight 200.59. Mercury is used in many industrial applications and its salts have been employed therapeutically as purgatives, antisyphilitics, disinfectants, and astringents. It can be absorbed through the skin and mucous membranes which leads to mercury poisoning. Because of its toxicity, the clinical use of mercury and mercurials is diminishing. [NIH] Mesenchymal: Refers to cells that develop into connective tissue, blood vessels, and lymphatic tissue. [NIH] Meta-Analysis: A quantitative method of combining the results of independent studies (usually drawn from the published literature) and synthesizing summaries and conclusions which may be used to evaluate therapeutic effectiveness, plan new studies, etc., with application chiefly in the areas of research and medicine. [NIH] Metabolic acidosis: (met-ah-BOL-ik as-id-O-sis): A condition in which the blood is too acidic. It may be caused by severe illness or sepsis (bacteria in the bloodstream). [NIH] Metabolic disorder: A condition in which normal metabolic processes are disrupted, usually because of a missing enzyme. [NIH] Metabolite: Any substance produced by metabolism or by a metabolic process. [EU] Metacarpophalangeal Joint: The articulation between a metacarpal bone and a phalanx. [NIH]
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Metalloendopeptidases: Endopeptidases which use a metal, normally zinc, in the catalytic mechanism. This group of enzymes is inactivated by metal chelators. EC 3.4.24. [NIH] Metastasis: The spread of cancer from one part of the body to another. Tumors formed from cells that have spread are called "secondary tumors" and contain cells that are like those in the original (primary) tumor. The plural is metastases. [NIH] Metatarsophalangeal Joint: The articulation between a metatarsal bone and a phalanx. [NIH]
Methotrexate: An antineoplastic antimetabolite with immunosuppressant properties. It is an inhibitor of dihydrofolate reductase and prevents the formation of tetrahydrofolate, necessary for synthesis of thymidylate, an essential component of DNA. [NIH] Methyltransferase: A drug-metabolizing enzyme. [NIH] Metronidazole: Antiprotozoal used in amebiasis, trichomoniasis, giardiasis, and as treponemacide in livestock. It has also been proposed as a radiation sensitizer for hypoxic cells. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985, p133), this substance may reasonably be anticipated to be a carcinogen (Merck, 11th ed). [NIH] MI: Myocardial infarction. Gross necrosis of the myocardium as a result of interruption of the blood supply to the area; it is almost always caused by atherosclerosis of the coronary arteries, upon which coronary thrombosis is usually superimposed. [NIH] Mice Minute Virus: The type species of parvovirus prevalent in mouse colonies and found as a contaminant of many transplanted tumors or leukemias. [NIH] Microbe: An organism which cannot be observed with the naked eye; e. g. unicellular animals, lower algae, lower fungi, bacteria. [NIH] Microgram: A unit of mass (weight) of the metric system, being one-millionth of a gram (10-6 gm.) or one one-thousandth of a milligram (10-3 mg.). [EU] Micronuclei: Nuclei, separate from and additional to the main nucleus of a cell, produced during the telophase of mitosis or meiosis by lagging chromosomes or chromosome fragments derived from spontaneous or experimentally induced chromosomal structural changes. This concept also includes the smaller, reproductive nuclei found in multinucleate protozoans. [NIH] Micronutrients: Essential dietary elements or organic compounds that are required in only small quantities for normal physiologic processes to occur. [NIH] Microorganism: An organism that can be seen only through a microscope. Microorganisms include bacteria, protozoa, algae, and fungi. Although viruses are not considered living organisms, they are sometimes classified as microorganisms. [NIH] Microscopy: The application of microscope magnification to the study of materials that cannot be properly seen by the unaided eye. [NIH] Microtubules: Slender, cylindrical filaments found in the cytoskeleton of plant and animal cells. They are composed of the protein tubulin. [NIH] Migrans: Infestation of the dermis by various larvae, characterized by bizarre red irregular lines which are broad at one end and fade at the other, produced by burrowing larvae. [NIH] Migration: The systematic movement of genes between populations of the same species, geographic race, or variety. [NIH] Millimeter: A measure of length. A millimeter is approximately 26-times smaller than an inch. [NIH] Mineralization: The action of mineralizing; the state of being mineralized. [EU] Mineralocorticoids: A group of corticosteroids primarily associated with the regulation of
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water and electrolyte balance. This is accomplished through the effect on ion transport in renal tubules, resulting in retention of sodium and loss of potassium. Mineralocorticoid secretion is itself regulated by plasma volume, serum potassium, and angiotensin II. [NIH] Minocycline: A semisynthetic staphylococcus infections. [NIH]
antibiotic
effective
against
tetracycline-resistant
Minority Groups: A subgroup having special characteristics within a larger group, often bound together by special ties which distinguish it from the larger group. [NIH] Misoprostol: A synthetic analog of natural prostaglandin E1. It produces a dose-related inhibition of gastric acid and pepsin secretion, and enhances mucosal resistance to injury. It is an effective anti-ulcer agent and also has oxytocic properties. [NIH] Mitochondrial Swelling: Increase in volume of mitochondria due to an influx of fluid; it occurs in hypotonic solutions due to osmotic pressure and in isotonic solutions as a result of altered permeability of the membranes of respiring mitochondria. [NIH] Mobility: Capability of movement, of being moved, or of flowing freely. [EU] Mobilization: The process of making a fixed part or stored substance mobile, as by separating a part from surrounding structures to make it accessible for an operative procedure or by causing release into the circulation for body use of a substance stored in the body. [EU] Modeling: A treatment procedure whereby the therapist presents the target behavior which the learner is to imitate and make part of his repertoire. [NIH] Modification: A change in an organism, or in a process in an organism, that is acquired from its own activity or environment. [NIH] Modulator: A specific inductor that brings out characteristics peculiar to a definite region. [EU]
Molecular: Of, pertaining to, or composed of molecules : a very small mass of matter. [EU] Molecular Structure: The location of the atoms, groups or ions relative to one another in a molecule, as well as the number, type and location of covalent bonds. [NIH] Molecule: A chemical made up of two or more atoms. The atoms in a molecule can be the same (an oxygen molecule has two oxygen atoms) or different (a water molecule has two hydrogen atoms and one oxygen atom). Biological molecules, such as proteins and DNA, can be made up of many thousands of atoms. [NIH] Monitor: An apparatus which automatically records such physiological signs as respiration, pulse, and blood pressure in an anesthetized patient or one undergoing surgical or other procedures. [NIH] Monoclonal: An antibody produced by culturing a single type of cell. It therefore consists of a single species of immunoglobulin molecules. [NIH] Monoclonal antibodies: Laboratory-produced substances that can locate and bind to cancer cells wherever they are in the body. Many monoclonal antibodies are used in cancer detection or therapy; each one recognizes a different protein on certain cancer cells. Monoclonal antibodies can be used alone, or they can be used to deliver drugs, toxins, or radioactive material directly to a tumor. [NIH] Monocyte: A type of white blood cell. [NIH] Mononuclear: A cell with one nucleus. [NIH] Mononucleosis: The presence of an abnormally large number of mononuclear leucocytes (monocytes) in the blood. The term is often used alone to refer to infectious mononucleosis. [EU]
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Monotherapy: A therapy which uses only one drug. [EU] Morphine: The principal alkaloid in opium and the prototype opiate analgesic and narcotic. Morphine has widespread effects in the central nervous system and on smooth muscle. [NIH] Morphological: Relating to the configuration or the structure of live organs. [NIH] Motility: The ability to move spontaneously. [EU] Motion Sickness: Sickness caused by motion, as sea sickness, train sickness, car sickness, and air sickness. [NIH] Motor nerve: An efferent nerve conveying an impulse that excites muscular contraction. [NIH]
Mucinous: Containing or resembling mucin, the main compound in mucus. [NIH] Mucocutaneous: Pertaining to or affecting the mucous membrane and the skin. [EU] Mucosa: A mucous membrane, or tunica mucosa. [EU] Multidrug resistance: Adaptation of tumor cells to anticancer drugs in ways that make the drugs less effective. [NIH] Multigene Family: The progeny of a single open-pollinated parent or of a single cross between two individuals. [NIH] Multiple Myeloma: A malignant tumor of plasma cells usually arising in the bone marrow; characterized by diffuse involvement of the skeletal system, hyperglobulinemia, Bence-Jones proteinuria, and anemia. [NIH] Multiple sclerosis: A disorder of the central nervous system marked by weakness, numbness, a loss of muscle coordination, and problems with vision, speech, and bladder control. Multiple sclerosis is thought to be an autoimmune disease in which the body's immune system destroys myelin. Myelin is a substance that contains both protein and fat (lipid) and serves as a nerve insulator and helps in the transmission of nerve signals. [NIH] Multivariate Analysis: A set of techniques used when variation in several variables has to be studied simultaneously. In statistics, multivariate analysis is interpreted as any analytic method that allows simultaneous study of two or more dependent variables. [NIH] Muscle relaxant: An agent that specifically aids in reducing muscle tension, as those acting at the polysynaptic neurons of motor nerves (e.g. meprobamate) or at the myoneural junction (curare and related compounds). [EU] Muscle tension: A force in a material tending to produce extension; the state of being stretched. [NIH] Muscular Dystrophies: A general term for a group of inherited disorders which are characterized by progressive degeneration of skeletal muscles. [NIH] Musculoskeletal Diseases: Diseases of the muscles and their associated ligaments and other connective tissue and of the bones and cartilage viewed collectively. [NIH] Musculoskeletal System: Themuscles, bones, and cartilage of the body. [NIH] Mutagenesis: Process of generating genetic mutations. It may occur spontaneously or be induced by mutagens. [NIH] Mutagenic: Inducing genetic mutation. [EU] Mutagens: Chemical agents that increase the rate of genetic mutation by interfering with the function of nucleic acids. A clastogen is a specific mutagen that causes breaks in chromosomes. [NIH] Myalgia: Pain in a muscle or muscles. [EU]
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Mycobacterium: A genus of gram-positive, aerobic bacteria. Most species are free-living in soil and water, but the major habitat for some is the diseased tissue of warm-blooded hosts. [NIH]
Mycobacterium avium: A bacterium causing tuberculosis in domestic fowl and other birds. In pigs, it may cause localized and sometimes disseminated disease. The organism occurs occasionally in sheep and cattle. It should be distinguished from the M. avium complex, which infects primarily humans. [NIH] Mycobacterium leprae: A species of gram-positive, aerobic bacteria that causes leprosy in man. Its organisms are generally arranged in clumps, rounded masses, or in groups of bacilli side by side. [NIH] Mycobacterium tuberculosis: A species of gram-positive, aerobic bacteria that produces tuberculosis in man, other primates, dogs, and some animals which have contact with man. Growth tends to be in serpentine, cordlike masses in which the bacilli show a parallel orientation. [NIH] Mycoplasma: A genus of gram-negative, facultatively anaerobic bacteria bounded by a plasma membrane only. Its organisms are parasites and pathogens, found on the mucous membranes of humans, animals, and birds. [NIH] Mycosis: Any disease caused by a fungus. [EU] Myelin: The fatty substance that covers and protects nerves. [NIH] Myelogenous: Produced by, or originating in, the bone marrow. [NIH] Myeloid Cells: Cells which include the monocytes and the granulocytes. [NIH] Myocardial infarction: Gross necrosis of the myocardium as a result of interruption of the blood supply to the area; it is almost always caused by atherosclerosis of the coronary arteries, upon which coronary thrombosis is usually superimposed. [NIH] Myocardium: The muscle tissue of the heart composed of striated, involuntary muscle known as cardiac muscle. [NIH] Myopathy: Any disease of a muscle. [EU] Myosin: Chief protein in muscle and the main constituent of the thick filaments of muscle fibers. In conjunction with actin, it is responsible for the contraction and relaxation of muscles. [NIH] Myositis: Inflammation of a voluntary muscle. [EU] Naive: Used to describe an individual who has never taken a certain drug or class of drugs (e. g., AZT-naive, antiretroviral-naive), or to refer to an undifferentiated immune system cell. [NIH] Naproxen: An anti-inflammatory agent with analgesic and antipyretic properties. Both the acid and its sodium salt are used in the treatment of rheumatoid arthritis and other rheumatic or musculoskeletal disorders, dysmenorrhea, and acute gout. [NIH] Narcosis: A general and nonspecific reversible depression of neuronal excitability, produced by a number of physical and chemical aspects, usually resulting in stupor. [NIH] Narcotic: 1. Pertaining to or producing narcosis. 2. An agent that produces insensibility or stupor, applied especially to the opioids, i.e. to any natural or synthetic drug that has morphine-like actions. [EU] Nasal Mucosa: The mucous membrane lining the nasal cavity. [NIH] Natural killer cells: NK cells. A type of white blood cell that contains granules with enzymes that can kill tumor cells or microbial cells. Also called large granular lymphocytes (LGL). [NIH]
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Nausea: An unpleasant sensation in the stomach usually accompanied by the urge to vomit. Common causes are early pregnancy, sea and motion sickness, emotional stress, intense pain, food poisoning, and various enteroviruses. [NIH] NCI: National Cancer Institute. NCI, part of the National Institutes of Health of the United States Department of Health and Human Services, is the federal government's principal agency for cancer research. NCI conducts, coordinates, and funds cancer research, training, health information dissemination, and other programs with respect to the cause, diagnosis, prevention, and treatment of cancer. Access the NCI Web site at http://cancer.gov. [NIH] Necrosis: A pathological process caused by the progressive degradative action of enzymes that is generally associated with severe cellular trauma. It is characterized by mitochondrial swelling, nuclear flocculation, uncontrolled cell lysis, and ultimately cell death. [NIH] Need: A state of tension or dissatisfaction felt by an individual that impels him to action toward a goal he believes will satisfy the impulse. [NIH] Needle biopsy: The removal of tissue or fluid with a needle for examination under a microscope. Also called fine-needle aspiration. [NIH] Nematoda: A class of unsegmented helminths with fundamental bilateral symmetry and secondary triradiate symmetry of the oral and esophageal structures. Many species are parasites. [NIH] Neomycin: Antibiotic complex produced by Streptomyces fradiae. It is composed of neomycins A, B, and C. It acts by inhibiting translation during protein synthesis. [NIH] Neonatal: Pertaining to the first four weeks after birth. [EU] Neoplasia: Abnormal and uncontrolled cell growth. [NIH] Neoplasm: A new growth of benign or malignant tissue. [NIH] Neoplastic: Pertaining to or like a neoplasm (= any new and abnormal growth); pertaining to neoplasia (= the formation of a neoplasm). [EU] Nephritis: Inflammation of the kidney; a focal or diffuse proliferative or destructive process which may involve the glomerulus, tubule, or interstitial renal tissue. [EU] Nephropathy: Disease of the kidneys. [EU] Nephrosis: Descriptive histopathologic term for renal disease without an inflammatory component. [NIH] Nephrotic: Pertaining to, resembling, or caused by nephrosis. [EU] Nephrotic Syndrome: Clinical association of heavy proteinuria, hypoalbuminemia, and generalized edema. [NIH] Nerve: A cordlike structure of nervous tissue that connects parts of the nervous system with other tissues of the body and conveys nervous impulses to, or away from, these tissues. [NIH]
Nerve Growth Factor: Nerve growth factor is the first of a series of neurotrophic factors that were found to influence the growth and differentiation of sympathetic and sensory neurons. It is comprised of alpha, beta, and gamma subunits. The beta subunit is responsible for its growth stimulating activity. [NIH] Nervous System: The entire nerve apparatus composed of the brain, spinal cord, nerves and ganglia. [NIH] Networks: Pertaining to a nerve or to the nerves, a meshlike structure of interlocking fibers or strands. [NIH] Neural: 1. Pertaining to a nerve or to the nerves. 2. Situated in the region of the spinal axis,
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as the neutral arch. [EU] Neurologic: Having to do with nerves or the nervous system. [NIH] Neurology: A medical specialty concerned with the study of the structures, functions, and diseases of the nervous system. [NIH] Neuromuscular: Pertaining to muscles and nerves. [EU] Neurons: The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the nervous system. [NIH] Neuropathy: A problem in any part of the nervous system except the brain and spinal cord. Neuropathies can be caused by infection, toxic substances, or disease. [NIH] Neurotic: 1. Pertaining to or characterized by neurosis. 2. A person affected with a neurosis. [EU]
Neurotransmitter: Any of a group of substances that are released on excitation from the axon terminal of a presynaptic neuron of the central or peripheral nervous system and travel across the synaptic cleft to either excite or inhibit the target cell. Among the many substances that have the properties of a neurotransmitter are acetylcholine, norepinephrine, epinephrine, dopamine, glycine, y-aminobutyrate, glutamic acid, substance P, enkephalins, endorphins, and serotonin. [EU] Neutrons: Electrically neutral elementary particles found in all atomic nuclei except light hydrogen; the mass is equal to that of the proton and electron combined and they are unstable when isolated from the nucleus, undergoing beta decay. Slow, thermal, epithermal, and fast neutrons refer to the energy levels with which the neutrons are ejected from heavier nuclei during their decay. [NIH] Neutropenia: An abnormal decrease in the number of neutrophils, a type of white blood cell. [NIH] Neutrophil: A type of white blood cell. [NIH] Nitric Oxide: A free radical gas produced endogenously by a variety of mammalian cells. It is synthesized from arginine by a complex reaction, catalyzed by nitric oxide synthase. Nitric oxide is endothelium-derived relaxing factor. It is released by the vascular endothelium and mediates the relaxation induced by some vasodilators such as acetylcholine and bradykinin. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic guanylate cyclase and thus elevates intracellular levels of cyclic GMP. [NIH]
Nitric-Oxide Synthase: An enzyme that catalyzes the conversion of L-arginine, NADPH, and oxygen to citrulline, nitric oxide, and NADP+. The enzyme found in brain, but not that induced in lung or liver by endotoxin, requires calcium. (From Enzyme Nomenclature, 1992) EC 1.14.13.39. [NIH] Nitrogen: An element with the atomic symbol N, atomic number 7, and atomic weight 14. Nitrogen exists as a diatomic gas and makes up about 78% of the earth's atmosphere by volume. It is a constituent of proteins and nucleic acids and found in all living cells. [NIH] Nitroglycerin: A highly volatile organic nitrate that acts as a dilator of arterial and venous smooth muscle and is used in the treatment of angina. It provides relief through improvement of the balance between myocardial oxygen supply and demand. Although total coronary blood flow is not increased, there is redistribution of blood flow in the heart when partial occlusion of coronary circulation is effected. [NIH] Nonmalignant: Not cancerous. [NIH]
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Norepinephrine: Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic. [NIH] Nuclear: A test of the structure, blood flow, and function of the kidneys. The doctor injects a mildly radioactive solution into an arm vein and uses x-rays to monitor its progress through the kidneys. [NIH] Nuclear Medicine: A specialty field of radiology concerned with diagnostic, therapeutic, and investigative use of radioactive compounds in a pharmaceutical form. [NIH] Nuclei: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Nucleic acid: Either of two types of macromolecule (DNA or RNA) formed by polymerization of nucleotides. Nucleic acids are found in all living cells and contain the information (genetic code) for the transfer of genetic information from one generation to the next. [NIH] Nucleus: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Nursing Care: Care given to patients by nursing service personnel. [NIH] Nutritional Status: State of the body in relation to the consumption and utilization of nutrients. [NIH] Observational study: An epidemiologic study that does not involve any intervention, experimental or otherwise. Such a study may be one in which nature is allowed to take its course, with changes in one characteristic being studied in relation to changes in other characteristics. Analytical epidemiologic methods, such as case-control and cohort study designs, are properly called observational epidemiology because the investigator is observing without intervention other than to record, classify, count, and statistically analyze results. [NIH] Occipital Lobe: Posterior part of the cerebral hemisphere. [NIH] Occult: Obscure; concealed from observation, difficult to understand. [EU] Occupational Therapy: The field concerned with utilizing craft or work activities in the rehabilitation of patients. Occupational therapy can also refer to the activities themselves. [NIH]
Ocular: 1. Of, pertaining to, or affecting the eye. 2. Eyepiece. [EU] Odds Ratio: The ratio of two odds. The exposure-odds ratio for case control data is the ratio of the odds in favor of exposure among cases to the odds in favor of exposure among noncases. The disease-odds ratio for a cohort or cross section is the ratio of the odds in favor of disease among the exposed to the odds in favor of disease among the unexposed. The prevalence-odds ratio refers to an odds ratio derived cross-sectionally from studies of prevalent cases. [NIH] Ointments: Semisolid preparations used topically for protective emollient effects or as a vehicle for local administration of medications. Ointment bases are various mixtures of fats, waxes, animal and plant oils and solid and liquid hydrocarbons. [NIH] Oligopeptides: Peptides composed of between two and twelve amino acids. [NIH] Oliguria: Clinical manifestation of the urinary system consisting of a decrease in the amount of urine secreted. [NIH]
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Omeprazole: A highly effective inhibitor of gastric acid secretion used in the therapy of gastric ulcers and Zollinger-Ellison syndrome. The drug inhibits the H(+)-K(+)-ATPase (H(+)-K(+)-exchanging ATPase) in a pH-dependent manner. This ATPase is considered the proton pump in the secretory membrane of the parietal cell. [NIH] Oncogenic: Chemical, viral, radioactive or other agent that causes cancer; carcinogenic. [NIH]
Oophoritis: Inflammation of an ovary. [NIH] Opacity: Degree of density (area most dense taken for reading). [NIH] Open Reading Frames: Reading frames where successive nucleotide triplets can be read as codons specifying amino acids and where the sequence of these triplets is not interrupted by stop codons. [NIH] Operon: The genetic unit consisting of a feedback system under the control of an operator gene, in which a structural gene transcribes its message in the form of mRNA upon blockade of a repressor produced by a regulator gene. Included here is the attenuator site of bacterial operons where transcription termination is regulated. [NIH] Ophthalmic: Pertaining to the eye. [EU] Ophthalmologic: Pertaining to ophthalmology (= the branch of medicine dealing with the eye). [EU] Ophthalmology: A surgical specialty concerned with the structure and function of the eye and the medical and surgical treatment of its defects and diseases. [NIH] Opportunistic Infections: An infection caused by an organism which becomes pathogenic under certain conditions, e.g., during immunosuppression. [NIH] Opsin: A protein formed, together with retinene, by the chemical breakdown of metarhodopsin. [NIH] Optic Nerve: The 2nd cranial nerve. The optic nerve conveys visual information from the retina to the brain. The nerve carries the axons of the retinal ganglion cells which sort at the optic chiasm and continue via the optic tracts to the brain. The largest projection is to the lateral geniculate nuclei; other important targets include the superior colliculi and the suprachiasmatic nuclei. Though known as the second cranial nerve, it is considered part of the central nervous system. [NIH] Oral Health: The optimal state of the mouth and normal functioning of the organs of the mouth without evidence of disease. [NIH] Oral Hygiene: The practice of personal hygiene of the mouth. It includes the maintenance of oral cleanliness, tissue tone, and general preservation of oral health. [NIH] Oral Manifestations: Disorders of the mouth attendant upon non-oral disease or injury. [NIH]
Orbit: One of the two cavities in the skull which contains an eyeball. Each eye is located in a bony socket or orbit. [NIH] Orbital: Pertaining to the orbit (= the bony cavity that contains the eyeball). [EU] Organelles: Specific particles of membrane-bound organized living substances present in eukaryotic cells, such as the mitochondria; the golgi apparatus; endoplasmic reticulum; lysomomes; plastids; and vacuoles. [NIH] Organogenesis: Clonal propagation which involves culturing explants from roots, leaves, or stems to form undifferentiated callus tissue; after the cells form shoots, they are separated and rooted. Alternatively, if the callus is put in liquid culture, somatic embryos form. [NIH] Orthodontics: A dental specialty concerned with the prevention and correction of dental
Dictionary 651
and oral anomalies (malocclusion). [NIH] Orthopaedic: Pertaining to the correction of deformities of the musculoskeletal system; pertaining to orthopaedics. [EU] Orthotic Devices: Apparatus used to support, align, prevent, or correct deformities or to improve the function of movable parts of the body. [NIH] Ossicles: The hammer, anvil and stirrup, the small bones of the middle ear, which transmit the vibrations from the tympanic membrane to the oval window. [NIH] Ossification: The formation of bone or of a bony substance; the conversion of fibrous tissue or of cartilage into bone or a bony substance. [EU] Osteoarthritis: A progressive, degenerative joint disease, the most common form of arthritis, especially in older persons. The disease is thought to result not from the aging process but from biochemical changes and biomechanical stresses affecting articular cartilage. In the foreign literature it is often called osteoarthrosis deformans. [NIH] Osteoblasts: Bone-forming cells which secrete an extracellular matrix. Hydroxyapatite crystals are then deposited into the matrix to form bone. [NIH] Osteocalcin: Vitamin K-dependent calcium-binding protein synthesized by osteoblasts and found primarily in bone. Serum osteocalcin measurements provide a noninvasive specific marker of bone metabolism. The protein contains three residues of the amino acid gammacarboxyglutamic acid (GLA), which, in the presence of calcium, promotes binding to hydroxyapatite and subsequent accumulation in bone matrix. [NIH] Osteoclasts: A large multinuclear cell associated with the absorption and removal of bone. An odontoclast, also called cementoclast, is cytomorphologically the same as an osteoclast and is involved in cementum resorption. [NIH] Osteolysis: Dissolution of bone that particularly involves the removal or loss of calcium. [NIH]
Osteomalacia: A condition marked by softening of the bones (due to impaired mineralization, with excess accumulation of osteoid), with pain, tenderness, muscular weakness, anorexia, and loss of weight, resulting from deficiency of vitamin D and calcium. [EU]
Osteomyelitis: Inflammation of bone caused by a pyogenic organism. It may remain localized or may spread through the bone to involve the marrow, cortex, cancellous tissue, and periosteum. [EU] Osteonecrosis: Death of a bone or part of a bone, either atraumatic or posttraumatic. [NIH] Osteonectin: Non-collagenous, calcium-binding glycoprotein of developing bone. It links collagen to mineral in the bone matrix. In the synonym SPARC glycoprotein, the acronym stands for secreted protein, acidic and rich in cysteine. [NIH] Osteoporosis: Reduction of bone mass without alteration in the composition of bone, leading to fractures. Primary osteoporosis can be of two major types: postmenopausal osteoporosis and age-related (or senile) osteoporosis. [NIH] Osteotomy: The surgical cutting of a bone. [EU] Outpatient: A patient who is not an inmate of a hospital but receives diagnosis or treatment in a clinic or dispensary connected with the hospital. [NIH] Ovary: Either of the paired glands in the female that produce the female germ cells and secrete some of the female sex hormones. [NIH] Overweight: An excess of body weight but not necessarily body fat; a body mass index of 25 to 29.9 kg/m2. [NIH]
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Ovum: A female germ cell extruded from the ovary at ovulation. [NIH] Oxidation: The act of oxidizing or state of being oxidized. Chemically it consists in the increase of positive charges on an atom or the loss of negative charges. Most biological oxidations are accomplished by the removal of a pair of hydrogen atoms (dehydrogenation) from a molecule. Such oxidations must be accompanied by reduction of an acceptor molecule. Univalent o. indicates loss of one electron; divalent o., the loss of two electrons. [EU]
Oxidative metabolism: A chemical process in which oxygen is used to make energy from carbohydrates (sugars). Also known as aerobic respiration, cell respiration, or aerobic metabolism. [NIH] Oxidative Stress: A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi). [NIH] Oxygen Consumption: The oxygen consumption is determined by calculating the difference between the amount of oxygen inhaled and exhaled. [NIH] Oxygenase: Enzyme which breaks down heme, the iron-containing oxygen-carrying constituent of the red blood cells. [NIH] Oxygenation: The process of supplying, treating, or mixing with oxygen. No:1245 oxygenation the process of supplying, treating, or mixing with oxygen. [EU] Oxytocic: 1. Pertaining to, characterized by, or promoting oxytocia (= rapid labor). 2. An agent that hastens evacuation of the uterus by stimulating contractions of the myometrium. [EU]
Pachymeningitis: Inflammation of the dura mater of the brain, the spinal cord or the optic nerve. [NIH] Paclitaxel: Antineoplastic agent isolated from the bark of the Pacific yew tree, Taxus brevifolia. Paclitaxel stabilizes microtubules in their polymerized form and thus mimics the action of the proto-oncogene proteins c-mos. [NIH] Palate: The structure that forms the roof of the mouth. It consists of the anterior hard palate and the posterior soft palate. [NIH] Palliative: 1. Affording relief, but not cure. 2. An alleviating medicine. [EU] Palsy: Disease of the peripheral nervous system occurring usually after many years of increased lead absorption. [NIH] Pancreas: A mixed exocrine and endocrine gland situated transversely across the posterior abdominal wall in the epigastric and hypochondriac regions. The endocrine portion is comprised of the Islets of Langerhans, while the exocrine portion is a compound acinar gland that secretes digestive enzymes. [NIH] Pancreas Transplant: A surgical procedure that involves replacing the pancreas of a person who has diabetes with a healthy pancreas that can make insulin. The healthy pancreas comes from a donor who has just died or from a living relative. A person can donate half a pancreas and still live normally. [NIH] Pancreas Transplantation: The transference of a pancreas from one human or animal to another. [NIH] Pancreatic: Having to do with the pancreas. [NIH] Pancytopenia: Deficiency of all three cell elements of the blood, erythrocytes, leukocytes and platelets. [NIH]
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Paracoccidioidomycosis: A mycosis affecting the skin, mucous membranes, lymph nodes, and internal organs. It is caused by Paracoccidioides brasiliensis. It is also called paracoccidioidal granuloma. Superficial resemblance of P. brasiliensis to Blastomyces brasiliensis (blastomyces) may cause misdiagnosis. [NIH] Paralysis: Loss of ability to move all or part of the body. [NIH] Parasite: An animal or a plant that lives on or in an organism of another species and gets at least some of its nutrition from that other organism. [NIH] Parasitic: Having to do with or being a parasite. A parasite is an animal or a plant that lives on or in an organism of another species and gets at least some of its nutrients from it. [NIH] Parasitic Diseases: Infections or infestations with parasitic organisms. They are often contracted through contact with an intermediate vector, but may occur as the result of direct exposure. [NIH] Parathyroid: 1. Situated beside the thyroid gland. 2. One of the parathyroid glands. 3. A sterile preparation of the water-soluble principle(s) of the parathyroid glands, ad-ministered parenterally as an antihypocalcaemic, especially in the treatment of acute hypoparathyroidism with tetany. [EU] Parathyroid Glands: Two small paired endocrine glands in the region of the thyroid gland. They secrete parathyroid hormone and are concerned with the metabolism of calcium and phosphorus. [NIH] Parenteral: Not through the alimentary canal but rather by injection through some other route, as subcutaneous, intramuscular, intraorbital, intracapsular, intraspinal, intrasternal, intravenous, etc. [EU] Paresthesia: Subjective cutaneous sensations (e.g., cold, warmth, tingling, pressure, etc.) that are experienced spontaneously in the absence of stimulation. [NIH] Parietal: 1. Of or pertaining to the walls of a cavity. 2. Pertaining to or located near the parietal bone, as the parietal lobe. [EU] Parotid: The space that contains the parotid gland, the facial nerve, the external carotid artery, and the retromandibular vein. [NIH] Partial remission: The shrinking, but not complete disappearance, of a tumor in response to therapy. Also called partial response. [NIH] Partial response: A decrease in the size of a tumor, or in the extent of cancer in the body, in response to treatment. [NIH] Particle: A tiny mass of material. [EU] Partnership Practice: A voluntary contract between two or more doctors who may or may not share responsibility for the care of patients, with proportional sharing of profits and losses. [NIH] Parturition: The act or process of given birth to a child. [EU] Parvovirus: A genus of the family Parvoviridae, subfamily Parvovirinae, infecting a variety of vertebrates including humans. Parvoviruses are responsible for a number of important diseases but also can be non-pathogenic in certain hosts. The type species is mice minute virus. [NIH] Patch: A piece of material used to cover or protect a wound, an injured part, etc.: a patch over the eye. [NIH] Pathogen: Any disease-producing microorganism. [EU] Pathogenesis: The cellular events and reactions that occur in the development of disease. [NIH]
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Pathologic: 1. Indicative of or caused by a morbid condition. 2. Pertaining to pathology (= branch of medicine that treats the essential nature of the disease, especially the structural and functional changes in tissues and organs of the body caused by the disease). [EU] Pathologic Processes: The abnormal mechanisms and forms involved in the dysfunctions of tissues and organs. [NIH] Pathologies: The study of abnormality, especially the study of diseases. [NIH] Pathophysiology: Altered functions in an individual or an organ due to disease. [NIH] Peer Review: An organized procedure carried out by a select committee of professionals in evaluating the performance of other professionals in meeting the standards of their specialty. Review by peers is used by editors in the evaluation of articles and other papers submitted for publication. Peer review is used also in the evaluation of grant applications. It is applied also in evaluating the quality of health care provided to patients. [NIH] Penicillamine: 3-Mercapto-D-valine. The most characteristic degradation product of the penicillin antibiotics. It is used as an antirheumatic and as a chelating agent in Wilson's disease. [NIH] Penicillin: An antibiotic drug used to treat infection. [NIH] Pepsin: An enzyme made in the stomach that breaks down proteins. [NIH] Pepsin A: Formed from pig pepsinogen by cleavage of one peptide bond. The enzyme is a single polypeptide chain and is inhibited by methyl 2-diaazoacetamidohexanoate. It cleaves peptides preferentially at the carbonyl linkages of phenylalanine or leucine and acts as the principal digestive enzyme of gastric juice. [NIH] Peptic: Pertaining to pepsin or to digestion; related to the action of gastric juices. [EU] Peptic Ulcer: Ulcer that occurs in those portions of the alimentary tract which come into contact with gastric juice containing pepsin and acid. It occurs when the amount of acid and pepsin is sufficient to overcome the gastric mucosal barrier. [NIH] Peptide: Any compound consisting of two or more amino acids, the building blocks of proteins. Peptides are combined to make proteins. [NIH] Peptide Fragments: Partial proteins formed by partial hydrolysis of complete proteins. [NIH] Peptide Hydrolases: A subclass of enzymes from the hydrolase class that catalyze the hydrolysis of peptide bonds. Exopeptidases and endopeptidases make up the sub-subclasses for this group. EC 3.4. [NIH] Perceived risk: Estimate or evaluation of risk as observed through personal experience or personal study, and personal evaluation of consequences. [NIH] Perception: The ability quickly and accurately to recognize similarities and differences among presented objects, whether these be pairs of words, pairs of number series, or multiple sets of these or other symbols such as geometric figures. [NIH] Percutaneous: Performed through the skin, as injection of radiopacque material in radiological examination, or the removal of tissue for biopsy accomplished by a needle. [EU] Perennial: Lasting through the year of for several years. [EU] Perfusion: Bathing an organ or tissue with a fluid. In regional perfusion, a specific area of the body (usually an arm or a leg) receives high doses of anticancer drugs through a blood vessel. Such a procedure is performed to treat cancer that has not spread. [NIH] Periarthritis: Inflammation of the tissues around a joint. [EU] Pericarditis: Inflammation of the pericardium. [EU] Perinatal: Pertaining to or occurring in the period shortly before and after birth; variously
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defined as beginning with completion of the twentieth to twenty-eighth week of gestation and ending 7 to 28 days after birth. [EU] Periodic Acid: Periodic acid (H5IO6). A strong oxidizing agent. [NIH] Periodontal disease: Disease involving the supporting structures of the teeth (as the gums and periodontal membranes). [NIH] Periodontal disease: Disease involving the supporting structures of the teeth (as the gums and periodontal membranes). [NIH] Peripheral blood: Blood circulating throughout the body. [NIH] Peripheral Nerves: The nerves outside of the brain and spinal cord, including the autonomic, cranial, and spinal nerves. Peripheral nerves contain non-neuronal cells and connective tissue as well as axons. The connective tissue layers include, from the outside to the inside, the epineurium, the perineurium, and the endoneurium. [NIH] Peripheral Nervous System: The nervous system outside of the brain and spinal cord. The peripheral nervous system has autonomic and somatic divisions. The autonomic nervous system includes the enteric, parasympathetic, and sympathetic subdivisions. The somatic nervous system includes the cranial and spinal nerves and their ganglia and the peripheral sensory receptors. [NIH] Peripheral Neuropathy: Nerve damage, usually affecting the feet and legs; causing pain, numbness, or a tingling feeling. Also called "somatic neuropathy" or "distal sensory polyneuropathy." [NIH] Peritoneal: Having to do with the peritoneum (the tissue that lines the abdominal wall and covers most of the organs in the abdomen). [NIH] Peritoneum: Endothelial lining of the abdominal cavity, the parietal peritoneum covering the inside of the abdominal wall and the visceral peritoneum covering the bowel, the mesentery, and certain of the organs. The portion that covers the bowel becomes the serosal layer of the bowel wall. [NIH] Peritonitis: Inflammation of the peritoneum; a condition marked by exudations in the peritoneum of serum, fibrin, cells, and pus. It is attended by abdominal pain and tenderness, constipation, vomiting, and moderate fever. [EU] Perivascular: Situated around a vessel. [EU] Peroxide: Chemical compound which contains an atom group with two oxygen atoms tied to each other. [NIH] P-Glycoprotein: A 170 kD transmembrane glycoprotein from the superfamily of ABC transporters. It serves as an ATP-dependent efflux pump for a variety of chemicals, including many antineoplastic agents. Overexpression of this glycoprotein is associated with multidrug resistance. [NIH] Phagocyte: An immune system cell that can surround and kill microorganisms and remove dead cells. Phagocytes include macrophages. [NIH] Phallic: Pertaining to the phallus, or penis. [EU] Phantom: Used to absorb and/or scatter radiation equivalently to a patient, and hence to estimate radiation doses and test imaging systems without actually exposing a patient. It may be an anthropomorphic or a physical test object. [NIH] Pharmacogenetics: A branch of genetics which deals with the genetic components of variability in individual responses to and metabolism (biotransformation) of drugs. [NIH] Pharmacokinetic: The mathematical analysis of the time courses of absorption, distribution, and elimination of drugs. [NIH]
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Pharmacologic: Pertaining to pharmacology or to the properties and reactions of drugs. [EU] Pharynx: The hollow tube about 5 inches long that starts behind the nose and ends at the top of the trachea (windpipe) and esophagus (the tube that goes to the stomach). [NIH] Phenotype: The outward appearance of the individual. It is the product of interactions between genes and between the genotype and the environment. This includes the killer phenotype, characteristic of yeasts. [NIH] Phenyl: Ingredient used in cold and flu remedies. [NIH] Phenylalanine: An aromatic amino acid that is essential in the animal diet. It is a precursor of melanin, dopamine, noradrenalin, and thyroxine. [NIH] Phospholipases: A class of enzymes that catalyze the hydrolysis of phosphoglycerides or glycerophosphatidates. EC 3.1.-. [NIH] Phospholipids: Lipids containing one or more phosphate groups, particularly those derived from either glycerol (phosphoglycerides; glycerophospholipids) or sphingosine (sphingolipids). They are polar lipids that are of great importance for the structure and function of cell membranes and are the most abundant of membrane lipids, although not stored in large amounts in the system. [NIH] Phosphorus: A non-metallic element that is found in the blood, muscles, nevers, bones, and teeth, and is a component of adenosine triphosphate (ATP; the primary energy source for the body's cells.) [NIH] Phosphorylation: The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety. [NIH] Photochemotherapy: Therapy using oral or topical photosensitizing agents with subsequent exposure to light. [NIH] Photocoagulation: Using a special strong beam of light (laser) to seal off bleeding blood vessels such as in the eye. The laser can also burn away blood vessels that should not have grown in the eye. This is the main treatment for diabetic retinopathy. [NIH] Photophobia: Abnormal sensitivity to light. This may occur as a manifestation of eye diseases; migraine; subarachnoid hemorrhage; meningitis; and other disorders. Photophobia may also occur in association with depression and other mental disorders. [NIH] Photosensitizing Agents: Drugs that are pharmacologically inactive but when exposed to ultraviolet radiation or sunlight are converted to their active metabolite to produce a beneficial reaction affecting the diseased tissue. These compounds can be administered topically or systemically and have been used therapeutically to treat psoriasis and various types of neoplasms. [NIH] Physical Examination: Systematic and thorough inspection of the patient for physical signs of disease or abnormality. [NIH] Physical Fitness: A state of well-being in which performance is optimal, often as a result of physical conditioning which may be prescribed for disease therapy. [NIH] Physical Therapy: The restoration of function and the prevention of disability following disease or injury with the use of light, heat, cold, water, electricity, ultrasound, and exercise. [NIH]
Physician-Patient Relations: The interactions between physician and patient. [NIH] Physiologic: Having to do with the functions of the body. When used in the phrase "physiologic age," it refers to an age assigned by general health, as opposed to calendar age. [NIH]
Physiology: The science that deals with the life processes and functions of organismus,
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their cells, tissues, and organs. [NIH] Pigment: A substance that gives color to tissue. Pigments are responsible for the color of skin, eyes, and hair. [NIH] Pilot study: The initial study examining a new method or treatment. [NIH] Pituitary Gland: A small, unpaired gland situated in the sella turcica tissue. It is connected to the hypothalamus by a short stalk. [NIH] Placebo Effect: An effect usually, but not necessarily, beneficial that is attributable to an expectation that the regimen will have an effect, i.e., the effect is due to the power of suggestion. [NIH] Plana: The radiographic term applied to a vertebral body crushed to a thin plate. [NIH] Plaque: A clear zone in a bacterial culture grown on an agar plate caused by localized destruction of bacterial cells by a bacteriophage. The concentration of infective virus in a fluid can be estimated by applying the fluid to a culture and counting the number of. [NIH] Plasma: The clear, yellowish, fluid part of the blood that carries the blood cells. The proteins that form blood clots are in plasma. [NIH] Plasma cells: A type of white blood cell that produces antibodies. [NIH] Plasma protein: One of the hundreds of different proteins present in blood plasma, including carrier proteins ( such albumin, transferrin, and haptoglobin), fibrinogen and other coagulation factors, complement components, immunoglobulins, enzyme inhibitors, precursors of substances such as angiotension and bradykinin, and many other types of proteins. [EU] Plasmapheresis: Procedure whereby plasma is separated and extracted from anticoagulated whole blood and the red cells retransfused to the donor. Plasmapheresis is also employed for therapeutic use. [NIH] Plasmid: An autonomously replicating, extra-chromosomal DNA molecule found in many bacteria. Plasmids are widely used as carriers of cloned genes. [NIH] Plasmin: A product of the lysis of plasminogen (profibrinolysin) by plasminogen activators. It is composed of two polypeptide chains, light (B) and heavy (A), with a molecular weight of 75,000. It is the major proteolytic enzyme involved in blood clot retraction or the lysis of fibrin and quickly inactivated by antiplasmins. EC 3.4.21.7. [NIH] Plasminogen: Precursor of fibrinolysin (plasmin). It is a single-chain beta-globulin of molecular weight 80-90,000 found mostly in association with fibrinogen in plasma; plasminogen activators change it to fibrinolysin. It is used in wound debriding and has been investigated as a thrombolytic agent. [NIH] Plasminogen Activators: A heterogeneous group of proteolytic enzymes that convert plasminogen to plasmin. They are concentrated in the lysosomes of most cells and in the vascular endothelium, particularly in the vessels of the microcirculation. EC 3.4.21.-. [NIH] Platelet Activating Factor: A phospholipid derivative formed by platelets, basophils, neutrophils, monocytes, and macrophages. It is a potent platelet aggregating agent and inducer of systemic anaphylactic symptoms, including hypotension, thrombocytopenia, neutropenia, and bronchoconstriction. [NIH] Platelet Activation: A series of progressive, overlapping events triggered by exposure of the platelets to subendothelial tissue. These events include shape change, adhesiveness, aggregation, and release reactions. When carried through to completion, these events lead to the formation of a stable hemostatic plug. [NIH] Platelet Aggregation: The attachment of platelets to one another. This clumping together
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can be induced by a number of agents (e.g., thrombin, collagen) and is part of the mechanism leading to the formation of a thrombus. [NIH] Platelet Factor 4: A high-molecular-weight proteoglycan-platelet factor complex which is released from blood platelets by thrombin. It acts as a mediator in the heparin-neutralizing capacity of the blood and plays a role in platelet aggregation. At high ionic strength (I=0.75), the complex dissociates into the active component (molecular weight 29,000) and the proteoglycan carrier (chondroitin 4-sulfate, molecular weight 350,000). The molecule exists in the form of a dimer consisting of 8 moles of platelet factor 4 and 2 moles of proteoglycan. [NIH]
Platelet-Derived Growth Factor: Mitogenic peptide growth hormone carried in the alphagranules of platelets. It is released when platelets adhere to traumatized tissues. Connective tissue cells near the traumatized region respond by initiating the process of replication. [NIH] Plateletpheresis: The preparation of platelet concentrates with the return of red cells and platelet-poor plasma to the donor. [NIH] Platelets: A type of blood cell that helps prevent bleeding by causing blood clots to form. Also called thrombocytes. [NIH] Platyhelminths: A phylum of acoelomate, bilaterally symmetrical flatworms, without a definite anus. It includes three classes: Cestoda, Turbellaria, and Trematoda. [NIH] Pleated: Particular three-dimensional pattern of amyloidoses. [NIH] Pleura: The thin serous membrane enveloping the lungs and lining the thoracic cavity. [NIH] Pleural: A circumscribed area of hyaline whorled fibrous tissue which appears on the surface of the parietal pleura, on the fibrous part of the diaphragm or on the pleura in the interlobar fissures. [NIH] Pleural cavity: A space enclosed by the pleura (thin tissue covering the lungs and lining the interior wall of the chest cavity). It is bound by thin membranes. [NIH] Pleural Effusion: Presence of fluid in the pleural cavity resulting from excessive transudation or exudation from the pleural surfaces. It is a sign of disease and not a diagnosis in itself. [NIH] Pneumoconiosis: Condition characterized by permanent deposition of substantial amounts of particulate matter in the lungs, usually of occupational or environmental origin, and by the tissue reaction to its presence. [NIH] Pneumonia: Inflammation of the lungs. [NIH] Pneumonitis: A disease caused by inhaling a wide variety of substances such as dusts and molds. Also called "farmer's disease". [NIH] Podiatry: A specialty concerned with the diagnosis and treatment of foot disorders and injuries and anatomic defects of the foot. [NIH] Poisoning: A condition or physical state produced by the ingestion, injection or inhalation of, or exposure to a deleterious agent. [NIH] Policy Making: The decision process by which individuals, groups or institutions establish policies pertaining to plans, programs or procedures. [NIH] Poliomyelitis: An acute viral disease, occurring sporadically and in epidemics, and characterized clinically by fever, sore throat, headache, and vomiting, often with stiffness of the neck and back. In the minor illness these may be the only symptoms. The major illness, which may or may not be preceded by the minor illness, is characterized by involvement of the central nervous system, stiff neck, pleocytosis in the spinal fluid, and perhaps paralysis. There may be subsequent atrophy of groups of muscles, ending in contraction and
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permanent deformity. The major illness is called acute anterior p., infantile paralysis and Heine-Medin disease. The disease is now largely controlled by vaccines. [EU] Polyarthritis: An inflammation of several joints together. [EU] Polymerase: An enzyme which catalyses the synthesis of DNA using a single DNA strand as a template. The polymerase copies the template in the 5'-3'direction provided that sufficient quantities of free nucleotides, dATP and dTTP are present. [NIH] Polymerase Chain Reaction: In vitro method for producing large amounts of specific DNA or RNA fragments of defined length and sequence from small amounts of short oligonucleotide flanking sequences (primers). The essential steps include thermal denaturation of the double-stranded target molecules, annealing of the primers to their complementary sequences, and extension of the annealed primers by enzymatic synthesis with DNA polymerase. The reaction is efficient, specific, and extremely sensitive. Uses for the reaction include disease diagnosis, detection of difficult-to-isolate pathogens, mutation analysis, genetic testing, DNA sequencing, and analyzing evolutionary relationships. [NIH] Polymers: Compounds formed by the joining of smaller, usually repeating, units linked by covalent bonds. These compounds often form large macromolecules (e.g., polypeptides, proteins, plastics). [NIH] Polymorphic: Occurring in several or many forms; appearing in different forms at different stages of development. [EU] Polymorphism: The occurrence together of two or more distinct forms in the same population. [NIH] Polymyalgia Rheumatica: A syndrome in the elderly characterized by proximal joint and muscle pain, high erythrocyte sedimentation rate, and a self-limiting course. Pain is usually accompanied by evidence of an inflammatory reaction. Women are affected twice as commonly as men and Caucasians more frequently than other groups. The condition is frequently associated with temporal arteritis and some theories pose the possibility that the two diseases arise from a single etiology or even that they are the same entity. [NIH] Polypeptide: A peptide which on hydrolysis yields more than two amino acids; called tripeptides, tetrapeptides, etc. according to the number of amino acids contained. [EU] Polyposis: The development of numerous polyps (growths that protrude from a mucous membrane). [NIH] Polysaccharide: A type of carbohydrate. It contains sugar molecules that are linked together chemically. [NIH] Polyunsaturated fat: An unsaturated fat found in greatest amounts in foods derived from plants, including safflower, sunflower, corn, and soybean oils. [NIH] Posterior: Situated in back of, or in the back part of, or affecting the back or dorsal surface of the body. In lower animals, it refers to the caudal end of the body. [EU] Postmenopausal: Refers to the time after menopause. Menopause is the time in a woman's life when menstrual periods stop permanently; also called "change of life." [NIH] Postnatal: Occurring after birth, with reference to the newborn. [EU] Postoperative: After surgery. [NIH] Postsynaptic: Nerve potential generated by an inhibitory hyperpolarizing stimulation. [NIH] Post-translational: The cleavage of signal sequence that directs the passage of the protein through a cell or organelle membrane. [NIH] Post-traumatic: Occurring as a result of or after injury. [EU] Postural: Pertaining to posture or position. [EU]
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Potentiate: A degree of synergism which causes the exposure of the organism to a harmful substance to worsen a disease already contracted. [NIH] Potentiation: An overall effect of two drugs taken together which is greater than the sum of the effects of each drug taken alone. [NIH] Practice Guidelines: Directions or principles presenting current or future rules of policy for the health care practitioner to assist him in patient care decisions regarding diagnosis, therapy, or related clinical circumstances. The guidelines may be developed by government agencies at any level, institutions, professional societies, governing boards, or by the convening of expert panels. The guidelines form a basis for the evaluation of all aspects of health care and delivery. [NIH] Precancerous: A term used to describe a condition that may (or is likely to) become cancer. Also called premalignant. [NIH] Preclinical: Before a disease becomes clinically recognizable. [EU] Precursor: Something that precedes. In biological processes, a substance from which another, usually more active or mature substance is formed. In clinical medicine, a sign or symptom that heralds another. [EU] Predictive factor: A situation or condition that may increase a person's risk of developing a certain disease or disorder. [NIH] Predisposition: A latent susceptibility to disease which may be activated under certain conditions, as by stress. [EU] Prednisolone: A glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [NIH] Prednisone: A synthetic anti-inflammatory glucocorticoid derived from cortisone. It is biologically inert and converted to prednisolone in the liver. [NIH] Pregnancy Outcome: Results of conception and ensuing pregnancy, including live birth, stillbirth, spontaneous abortion, induced abortion. The outcome may follow natural or artificial insemination or any of the various reproduction techniques, such as embryo transfer or fertilization in vitro. [NIH] Pregnenolone: Steroid hormone. [NIH] Premenopausal: Refers to the time before menopause. Menopause is the time of life when a women's menstrual periods stop permanently; also called "change of life." [NIH] Prevalence: The total number of cases of a given disease in a specified population at a designated time. It is differentiated from incidence, which refers to the number of new cases in the population at a given time. [NIH] Primary endpoint: The main result that is measured at the end of a study to see if a given treatment worked (e.g., the number of deaths or the difference in survival between the treatment group and the control group). What the primary endpoint will be is decided before the study begins. [NIH] Private Practice: Practice of a health profession by an individual, offering services on a person-to-person basis, as opposed to group or partnership practice. [NIH] Probe: An instrument used in exploring cavities, or in the detection and dilatation of strictures, or in demonstrating the potency of channels; an elongated instrument for exploring or sounding body cavities. [NIH] Probenecid: The prototypical uricosuric agent. It inhibits the renal excretion of organic anions and reduces tubular reabsorption of urate. Probenecid has also been used to treat
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patients with renal impairment, and, because it reduces the renal tubular excretion of other drugs, has been used as an adjunct to antibacterial therapy. [NIH] Procaine: A local anesthetic of the ester type that has a slow onset and a short duration of action. It is mainly used for infiltration anesthesia, peripheral nerve block, and spinal block. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1016). [NIH] Progeny: The offspring produced in any generation. [NIH] Progesterone: Pregn-4-ene-3,20-dione. The principal progestational hormone of the body, secreted by the corpus luteum, adrenal cortex, and placenta. Its chief function is to prepare the uterus for the reception and development of the fertilized ovum. It acts as an antiovulatory agent when administered on days 5-25 of the menstrual cycle. [NIH] Prognostic factor: A situation or condition, or a characteristic of a patient, that can be used to estimate the chance of recovery from a disease, or the chance of the disease recurring (coming back). [NIH] Progression: Increase in the size of a tumor or spread of cancer in the body. [NIH] Progressive: Advancing; going forward; going from bad to worse; increasing in scope or severity. [EU] Progressive disease: Cancer that is increasing in scope or severity. [NIH] Projection: A defense mechanism, operating unconsciously, whereby that which is emotionally unacceptable in the self is rejected and attributed (projected) to others. [NIH] Prolactin: Pituitary lactogenic hormone. A polypeptide hormone with a molecular weight of about 23,000. It is essential in the induction of lactation in mammals at parturition and is synergistic with estrogen. The hormone also brings about the release of progesterone from lutein cells, which renders the uterine mucosa suited for the embedding of the ovum should fertilization occur. [NIH] Proline: A non-essential amino acid that is synthesized from glutamic acid. It is an essential component of collagen and is important for proper functioning of joints and tendons. [NIH] Promoter: A chemical substance that increases the activity of a carcinogenic process. [NIH] Prophylaxis: An attempt to prevent disease. [NIH] Proportional: Being in proportion : corresponding in size, degree, or intensity, having the same or a constant ratio; of, relating to, or used in determining proportions. [EU] Proprioception: The mechanism involved in the self-regulation of posture and movement through stimuli originating in the receptors imbedded in the joints, tendons, muscles, and labyrinth. [NIH] Prospective study: An epidemiologic study in which a group of individuals (a cohort), all free of a particular disease and varying in their exposure to a possible risk factor, is followed over a specific amount of time to determine the incidence rates of the disease in the exposed and unexposed groups. [NIH] Prostaglandin: Any of a group of components derived from unsaturated 20-carbon fatty acids, primarily arachidonic acid, via the cyclooxygenase pathway that are extremely potent mediators of a diverse group of physiologic processes. The abbreviation for prostaglandin is PG; specific compounds are designated by adding one of the letters A through I to indicate the type of substituents found on the hydrocarbon skeleton and a subscript (1, 2 or 3) to indicate the number of double bonds in the hydrocarbon skeleton e.g., PGE2. The predominant naturally occurring prostaglandins all have two double bonds and are synthesized from arachidonic acid (5,8,11,14-eicosatetraenoic acid) by the pathway shown in the illustration. The 1 series and 3 series are produced by the same pathway with fatty acids
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having one fewer double bond (8,11,14-eicosatrienoic acid or one more double bond (5,8,11,14,17-eicosapentaenoic acid) than arachidonic acid. The subscript a or ß indicates the configuration at C-9 (a denotes a substituent below the plane of the ring, ß, above the plane). The naturally occurring PGF's have the a configuration, e.g., PGF2a. All of the prostaglandins act by binding to specific cell-surface receptors causing an increase in the level of the intracellular second messenger cyclic AMP (and in some cases cyclic GMP also). The effect produced by the cyclic AMP increase depends on the specific cell type. In some cases there is also a positive feedback effect. Increased cyclic AMP increases prostaglandin synthesis leading to further increases in cyclic AMP. [EU] Prostaglandins A: (13E,15S)-15-Hydroxy-9-oxoprosta-10,13-dien-1-oic acid (PGA(1)); (5Z,13E,15S)-15-hydroxy-9-oxoprosta-5,10,13-trien-1-oic acid (PGA(2)); (5Z,13E,15S,17Z)-15hydroxy-9-oxoprosta-5,10,13,17-tetraen-1-oic acid (PGA(3)). A group of naturally occurring secondary prostaglandins derived from PGE. PGA(1) and PGA(2) as well as their 19hydroxy derivatives are found in many organs and tissues. [NIH] Prostaglandins D: Physiologically active prostaglandins found in many tissues and organs. They show pressor activity, are mediators of inflammation, and have potential antithrombotic effects. [NIH] Prostate: A gland in males that surrounds the neck of the bladder and the urethra. It secretes a substance that liquifies coagulated semen. It is situated in the pelvic cavity behind the lower part of the pubic symphysis, above the deep layer of the triangular ligament, and rests upon the rectum. [NIH] Prosthesis: An artificial replacement of a part of the body. [NIH] Protease: Proteinase (= any enzyme that catalyses the splitting of interior peptide bonds in a protein). [EU] Protease Inhibitors: Compounds which inhibit or antagonize biosynthesis or actions of proteases (endopeptidases). [NIH] Protective Devices: Devices designed to provide personal protection against injury to individuals exposed to hazards in industry, sports, aviation, or daily activities. [NIH] Protein Binding: The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific proteinbinding measures are often used as assays in diagnostic assessments. [NIH] Protein C: A vitamin-K dependent zymogen present in the blood, which, upon activation by thrombin and thrombomodulin exerts anticoagulant properties by inactivating factors Va and VIIIa at the rate-limiting steps of thrombin formation. [NIH] Protein Conformation: The characteristic 3-dimensional shape of a protein, including the secondary, supersecondary (motifs), tertiary (domains) and quaternary structure of the peptide chain. Quaternary protein structure describes the conformation assumed by multimeric proteins (aggregates of more than one polypeptide chain). [NIH] Protein Isoforms: Different forms of a protein that may be produced from different genes, or from the same gene by alternative splicing. [NIH] Protein Kinases: A family of enzymes that catalyze the conversion of ATP and a protein to ADP and a phosphoprotein. EC 2.7.1.37. [NIH] Protein S: The vitamin K-dependent cofactor of activated protein C. Together with protein C, it inhibits the action of factors VIIIa and Va. A deficiency in protein S can lead to recurrent venous and arterial thrombosis. [NIH] Proteins: Polymers of amino acids linked by peptide bonds. The specific sequence of amino acids determines the shape and function of the protein. [NIH]
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Proteinuria: The presence of protein in the urine, indicating that the kidneys are not working properly. [NIH] Proteoglycan: A molecule that contains both protein and glycosaminoglycans, which are a type of polysaccharide. Proteoglycans are found in cartilage and other connective tissues. [NIH]
Proteolytic: 1. Pertaining to, characterized by, or promoting proteolysis. 2. An enzyme that promotes proteolysis (= the splitting of proteins by hydrolysis of the peptide bonds with formation of smaller polypeptides). [EU] Proteome: The protein complement of an organism coded for by its genome. [NIH] Proton Pump: Integral membrane proteins that transport protons across a membrane against a concentration gradient. This transport is driven by hydrolysis of ATP by H(+)transporting ATP synthase. [NIH] Protons: Stable elementary particles having the smallest known positive charge, found in the nuclei of all elements. The proton mass is less than that of a neutron. A proton is the nucleus of the light hydrogen atom, i.e., the hydrogen ion. [NIH] Proto-Oncogene Proteins: Products of proto-oncogenes. Normally they do not have oncogenic or transforming properties, but are involved in the regulation or differentiation of cell growth. They often have protein kinase activity. [NIH] Proto-Oncogene Proteins c-mos: Cellular proteins encoded by the c-mos genes. They function in the cell cycle to maintain maturation promoting factor in the active state and have protein-serine/threonine kinase activity. Oncogenic transformation can take place when c-mos proteins are expressed at the wrong time. [NIH] Protozoa: A subkingdom consisting of unicellular organisms that are the simplest in the animal kingdom. Most are free living. They range in size from submicroscopic to macroscopic. Protozoa are divided into seven phyla: Sarcomastigophora, Labyrinthomorpha, Apicomplexa, Microspora, Ascetospora, Myxozoa, and Ciliophora. [NIH] Protozoan: 1. Any individual of the protozoa; protozoon. 2. Of or pertaining to the protozoa; protozoal. [EU] Proximal: Nearest; closer to any point of reference; opposed to distal. [EU] Psoriasis: A common genetically determined, chronic, inflammatory skin disease characterized by rounded erythematous, dry, scaling patches. The lesions have a predilection for nails, scalp, genitalia, extensor surfaces, and the lumbosacral region. Accelerated epidermopoiesis is considered to be the fundamental pathologic feature in psoriasis. [NIH] Psychiatric: Pertaining to or within the purview of psychiatry. [EU] Psychiatry: The medical science that deals with the origin, diagnosis, prevention, and treatment of mental disorders. [NIH] Psychic: Pertaining to the psyche or to the mind; mental. [EU] Psychoactive: Those drugs which alter sensation, mood, consciousness or other psychological or behavioral functions. [NIH] Psychogenic: Produced or caused by psychic or mental factors rather than organic factors. [EU]
Psychological Adaptation: The alteration of the selective response of a neural unit due to the received signals. [NIH] Psychology: The science dealing with the study of mental processes and behavior in man and animals. [NIH]
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Psychosomatic: Pertaining to the mind-body relationship; having bodily symptoms of psychic, emotional, or mental origin; called also psychophysiologic. [EU] Psychotherapy: A generic term for the treatment of mental illness or emotional disturbances primarily by verbal or nonverbal communication. [NIH] Public Health: Branch of medicine concerned with the prevention and control of disease and disability, and the promotion of physical and mental health of the population on the international, national, state, or municipal level. [NIH] Publication Bias: The influence of study results on the chances of publication and the tendency of investigators, reviewers, and editors to submit or accept manuscripts for publication based on the direction or strength of the study findings. Publication bias has an impact on the interpretation of clinical trials and meta-analyses. Bias can be minimized by insistence by editors on high-quality research, thorough literature reviews, acknowledgement of conflicts of interest, modification of peer review practices, etc. [NIH] Publishing: "The business or profession of the commercial production and issuance of literature" (Webster's 3d). It includes the publisher, publication processes, editing and editors. Production may be by conventional printing methods or by electronic publishing. [NIH]
Pulmonary: Relating to the lungs. [NIH] Pulmonary Artery: The short wide vessel arising from the conus arteriosus of the right ventricle and conveying unaerated blood to the lungs. [NIH] Pulmonary Edema: An accumulation of an excessive amount of watery fluid in the lungs, may be caused by acute exposure to dangerous concentrations of irritant gasses. [NIH] Pulmonary Fibrosis: Chronic inflammation and progressive fibrosis of the pulmonary alveolar walls, with steadily progressive dyspnea, resulting finally in death from oxygen lack or right heart failure. [NIH] Pulmonary hypertension: Abnormally high blood pressure in the arteries of the lungs. [NIH]
Pulse: The rhythmical expansion and contraction of an artery produced by waves of pressure caused by the ejection of blood from the left ventricle of the heart as it contracts. [NIH]
Pupil: The aperture in the iris through which light passes. [NIH] Purines: A series of heterocyclic compounds that are variously substituted in nature and are known also as purine bases. They include adenine and guanine, constituents of nucleic acids, as well as many alkaloids such as caffeine and theophylline. Uric acid is the metabolic end product of purine metabolism. [NIH] Purulent: Consisting of or containing pus; associated with the formation of or caused by pus. [EU] Pustular: Pertaining to or of the nature of a pustule; consisting of pustules (= a visible collection of pus within or beneath the epidermis). [EU] Pyogenic: Producing pus; pyopoietic (= liquid inflammation product made up of cells and a thin fluid called liquor puris). [EU] Pyridoxal: 3-Hydroxy-5-(hydroxymethyl)-2-methyl-4- pyridinecarboxaldehyde. [NIH] Pyrimidines: A family of 6-membered heterocyclic compounds occurring in nature in a wide variety of forms. They include several nucleic acid constituents (cytosine, thymine, and uracil) and form the basic structure of the barbiturates. [NIH] Quality of Health Care: The levels of excellence which characterize the health service or
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health care provided based on accepted standards of quality. [NIH] Quality of Life: A generic concept reflecting concern with the modification and enhancement of life attributes, e.g., physical, political, moral and social environment. [NIH] Quercetin: Aglucon of quercetrin, rutin, and other glycosides. It is widely distributed in the plant kingdom, especially in rinds and barks, clover blossoms, and ragweed pollen. [NIH] Race: A population within a species which exhibits general similarities within itself, but is both discontinuous and distinct from other populations of that species, though not sufficiently so as to achieve the status of a taxon. [NIH] Radiation: Emission or propagation of electromagnetic energy (waves/rays), or the waves/rays themselves; a stream of electromagnetic particles (electrons, neutrons, protons, alpha particles) or a mixture of these. The most common source is the sun. [NIH] Radiation therapy: The use of high-energy radiation from x-rays, gamma rays, neutrons, and other sources to kill cancer cells and shrink tumors. Radiation may come from a machine outside the body (external-beam radiation therapy), or it may come from radioactive material placed in the body in the area near cancer cells (internal radiation therapy, implant radiation, or brachytherapy). Systemic radiation therapy uses a radioactive substance, such as a radiolabeled monoclonal antibody, that circulates throughout the body. Also called radiotherapy. [NIH] Radicular: Having the character of or relating to a radicle or root. [NIH] Radiculopathy: Disease involving a spinal nerve root (see spinal nerve roots) which may result from compression related to intervertebral disk displacement; spinal cord injuries; spinal diseases; and other conditions. Clinical manifestations include radicular pain, weakness, and sensory loss referable to structures innervated by the involved nerve root. [NIH]
Radio Waves: That portion of the electromagnetic spectrum beyond the microwaves, with wavelengths as high as 30 KM. They are used in communications, including television. Short Wave or HF (high frequency), UHF (ultrahigh frequency) and VHF (very high frequency) waves are used in citizen's band communication. [NIH] Radioactive: Giving off radiation. [NIH] Radiography: Examination of any part of the body for diagnostic purposes by means of roentgen rays, recording the image on a sensitized surface (such as photographic film). [NIH] Radioimmunoassay: Classic quantitative assay for detection of antigen-antibody reactions using a radioactively labeled substance (radioligand) either directly or indirectly to measure the binding of the unlabeled substance to a specific antibody or other receptor system. Nonimmunogenic substances (e.g., haptens) can be measured if coupled to larger carrier proteins (e.g., bovine gamma-globulin or human serum albumin) capable of inducing antibody formation. [NIH] Radiolabeled: Any compound that has been joined with a radioactive substance. [NIH] Radiological: Pertaining to radiodiagnostic and radiotherapeutic procedures, and interventional radiology or other planning and guiding medical radiology. [NIH] Radiology: A specialty concerned with the use of x-ray and other forms of radiant energy in the diagnosis and treatment of disease. [NIH] Radiotherapy: The use of ionizing radiation to treat malignant neoplasms and other benign conditions. The most common forms of ionizing radiation used as therapy are x-rays, gamma rays, and electrons. A special form of radiotherapy, targeted radiotherapy, links a cytotoxic radionuclide to a molecule that targets the tumor. When this molecule is an antibody or other immunologic molecule, the technique is called radioimmunotherapy. [NIH]
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Randomized: Describes an experiment or clinical trial in which animal or human subjects are assigned by chance to separate groups that compare different treatments. [NIH] Randomized clinical trial: A study in which the participants are assigned by chance to separate groups that compare different treatments; neither the researchers nor the participants can choose which group. Using chance to assign people to groups means that the groups will be similar and that the treatments they receive can be compared objectively. At the time of the trial, it is not known which treatment is best. It is the patient's choice to be in a randomized trial. [NIH] Randomized Controlled Trials: Clinical trials that involve at least one test treatment and one control treatment, concurrent enrollment and follow-up of the test- and control-treated groups, and in which the treatments to be administered are selected by a random process, such as the use of a random-numbers table. Treatment allocations using coin flips, odd-even numbers, patient social security numbers, days of the week, medical record numbers, or other such pseudo- or quasi-random processes, are not truly randomized and trials employing any of these techniques for patient assignment are designated simply controlled clinical trials. [NIH] Rarefaction: The reduction of the density of a substance; the attenuation of a gas. [NIH] Reabsorption: 1. The act or process of absorbing again, as the selective absorption by the kidneys of substances (glucose, proteins, sodium, etc.) already secreted into the renal tubules, and their return to the circulating blood. 2. Resorption. [EU] Reactivation: The restoration of activity to something that has been inactivated. [EU] Reactive Oxygen Species: Reactive intermediate oxygen species including both radicals and non-radicals. These substances are constantly formed in the human body and have been shown to kill bacteria and inactivate proteins, and have been implicated in a number of diseases. Scientific data exist that link the reactive oxygen species produced by inflammatory phagocytes to cancer development. [NIH] Reagent: A substance employed to produce a chemical reaction so as to detect, measure, produce, etc., other substances. [EU] Receptor: A molecule inside or on the surface of a cell that binds to a specific substance and causes a specific physiologic effect in the cell. [NIH] Receptors, Serotonin: Cell-surface proteins that bind serotonin and trigger intracellular changes which influence the behavior of cells. Several types of serotonin receptors have been recognized which differ in their pharmacology, molecular biology, and mode of action. [NIH] Receptors, Tumor Necrosis Factor: Cell surface receptors that bind tumor necrosis factor and trigger changes which influence the behavior of cells. The two recognized tumor necrosis factor receptors are designated alpha and beta receptors. Both receptors bind both alpha and beta tumor necrosis factors with high affinity, and both are members of the nerve growth factor receptor family. [NIH] Recombinant: A cell or an individual with a new combination of genes not found together in either parent; usually applied to linked genes. [EU] Recombination: The formation of new combinations of genes as a result of segregation in crosses between genetically different parents; also the rearrangement of linked genes due to crossing-over. [NIH] Reconstitution: 1. A type of regeneration in which a new organ forms by the rearrangement of tissues rather than from new formation at an injured surface. 2. The restoration to original form of a substance previously altered for preservation and storage, as the restoration to a liquid state of blood serum or plasma that has been dried and stored. [EU]
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Rectum: The last 8 to 10 inches of the large intestine. [NIH] Red blood cells: RBCs. Cells that carry oxygen to all parts of the body. Also called erythrocytes. [NIH] Reductase: Enzyme converting testosterone to dihydrotestosterone. [NIH] Refer: To send or direct for treatment, aid, information, de decision. [NIH] Reflective: Capable of throwing back light, images, sound waves : reflecting. [EU] Reflux: The term used when liquid backs up into the esophagus from the stomach. [NIH] Refraction: A test to determine the best eyeglasses or contact lenses to correct a refractive error (myopia, hyperopia, or astigmatism). [NIH] Refractory: Not readily yielding to treatment. [EU] Regeneration: The natural renewal of a structure, as of a lost tissue or part. [EU] Regimen: A treatment plan that specifies the dosage, the schedule, and the duration of treatment. [NIH] Regression Analysis: Procedures for finding the mathematical function which best describes the relationship between a dependent variable and one or more independent variables. In linear regression (see linear models) the relationship is constrained to be a straight line and least-squares analysis is used to determine the best fit. In logistic regression (see logistic models) the dependent variable is qualitative rather than continuously variable and likelihood functions are used to find the best relationship. In multiple regression the dependent variable is considered to depend on more than a single independent variable. [NIH]
Regurgitation: A backward flowing, as the casting up of undigested food, or the backward flowing of blood into the heart, or between the chambers of the heart when a valve is incompetent. [EU] Rehabilitation Centers: Facilities which provide programs for rehabilitating the mentally or physically disabled individuals. [NIH] Rehabilitative: Instruction of incapacitated individuals or of those affected with some mental disorder, so that some or all of their lost ability may be regained. [NIH] Relapse: The return of signs and symptoms of cancer after a period of improvement. [NIH] Relative risk: The ratio of the incidence rate of a disease among individuals exposed to a specific risk factor to the incidence rate among unexposed individuals; synonymous with risk ratio. Alternatively, the ratio of the cumulative incidence rate in the exposed to the cumulative incidence rate in the unexposed (cumulative incidence ratio). The term relative risk has also been used synonymously with odds ratio. This is because the odds ratio and relative risk approach each other if the disease is rare ( 5 percent of population) and the number of subjects is large. [NIH] Relaxant: 1. Lessening or reducing tension. 2. An agent that lessens tension. [EU] Relaxation Techniques: The use of muscular relaxation techniques in treatment. [NIH] Reliability: Used technically, in a statistical sense, of consistency of a test with itself, i. e. the extent to which we can assume that it will yield the same result if repeated a second time. [NIH]
Remission: A decrease in or disappearance of signs and symptoms of cancer. In partial remission, some, but not all, signs and symptoms of cancer have disappeared. In complete remission, all signs and symptoms of cancer have disappeared, although there still may be cancer in the body. [NIH] Renal amyloidosis:
A disease of unknown etiology characterized by the abnormal
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deposition of amyloid, a translucent homogenous glycoprotein, in various organs and tissues of the body. [NIH] Renal failure: Progressive renal insufficiency and uremia, due to irreversible and progressive renal glomerular tubular or interstitial disease. [NIH] Renal tubular: A defect in the kidneys that hinders their normal excretion of acids. Failure to excrete acids can lead to weak bones, kidney stones, and poor growth in children. [NIH] Renal tubular acidosis: A rare disorder in which structures in the kidney that filter the blood are impaired, producing using that is more acid than normal. [NIH] Repressor: Any of the specific allosteric protein molecules, products of regulator genes, which bind to the operator of operons and prevent RNA polymerase from proceeding into the operon to transcribe messenger RNA. [NIH] Reproduction Techniques: Methods pertaining to the generation of new individuals. [NIH] Research Design: A plan for collecting and utilizing data so that desired information can be obtained with sufficient precision or so that an hypothesis can be tested properly. [NIH] Research Support: Financial support of research activities. [NIH] Resection: Removal of tissue or part or all of an organ by surgery. [NIH] Resorption: The loss of substance through physiologic or pathologic means, such as loss of dentin and cementum of a tooth, or of the alveolar process of the mandible or maxilla. [EU] Respiration: The act of breathing with the lungs, consisting of inspiration, or the taking into the lungs of the ambient air, and of expiration, or the expelling of the modified air which contains more carbon dioxide than the air taken in (Blakiston's Gould Medical Dictionary, 4th ed.). This does not include tissue respiration (= oxygen consumption) or cell respiration (= cell respiration). [NIH] Respiratory Burst: A large increase in oxygen uptake by neutrophils and most types of tissue macrophages through activation of an NADPH-cytochrome b-dependent oxidase that reduces oxygen to a superoxide. Individuals with an inherited defect in which the oxidase that reduces oxygen to superoxide is decreased or absent (granulomatous disease, chronic) often die as a result of recurrent bacterial infections. [NIH] Response rate: treatment. [NIH]
The percentage of patients whose cancer shrinks or disappears after
Restoration: Broad term applied to any inlay, crown, bridge or complete denture which restores or replaces loss of teeth or oral tissues. [NIH] Retina: The ten-layered nervous tissue membrane of the eye. It is continuous with the optic nerve and receives images of external objects and transmits visual impulses to the brain. Its outer surface is in contact with the choroid and the inner surface with the vitreous body. The outer-most layer is pigmented, whereas the inner nine layers are transparent. [NIH] Retinal: 1. Pertaining to the retina. 2. The aldehyde of retinol, derived by the oxidative enzymatic splitting of absorbed dietary carotene, and having vitamin A activity. In the retina, retinal combines with opsins to form visual pigments. One isomer, 11-cis retinal combines with opsin in the rods (scotopsin) to form rhodopsin, or visual purple. Another, all-trans retinal (trans-r.); visual yellow; xanthopsin) results from the bleaching of rhodopsin by light, in which the 11-cis form is converted to the all-trans form. Retinal also combines with opsins in the cones (photopsins) to form the three pigments responsible for colour vision. Called also retinal, and retinene1. [EU] Retinal Vein: Central retinal vein and its tributaries. It runs a short course within the optic nerve and then leaves and empties into the superior ophthalmic vein or cavernous sinus. [NIH]
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Retinal Vein Occlusion: Occlusion of the retinal vein. Those at high risk for this condition include patients with hypertension, diabetes mellitus, arteriosclerosis, and other cardiovascular diseases. [NIH] Retinoid: Vitamin A or a vitamin A-like compound. [NIH] Retinol: Vitamin A. It is essential for proper vision and healthy skin and mucous membranes. Retinol is being studied for cancer prevention; it belongs to the family of drugs called retinoids. [NIH] Retreatment: The therapy of the same disease in a patient, with the same agent or procedure repeated after initial treatment, or with an additional or alternate measure or follow-up. It does not include therapy which requires more than one administration of a therapeutic agent or regimen. Retreatment is often used with reference to a different modality when the original one was inadequate, harmful, or unsuccessful. [NIH] Retrospective: Looking back at events that have already taken place. [NIH] Retrospective study: A study that looks backward in time, usually using medical records and interviews with patients who already have or had a disease. [NIH] Retroviral vector: RNA from a virus that is used to insert genetic material into cells. [NIH] Retrovirus: A member of a group of RNA viruses, the RNA of which is copied during viral replication into DNA by reverse transcriptase. The viral DNA is then able to be integrated into the host chromosomal DNA. [NIH] Reverse Transcriptase Polymerase Chain Reaction: A variation of the PCR technique in which cDNA is made from RNA via reverse transcription. The resultant cDNA is then amplified using standard PCR protocols. [NIH] Reversion: A return to the original condition, e. g. the reappearance of the normal or wild type in previously mutated cells, tissues, or organisms. [NIH] Rheumatic Diseases: Disorders of connective tissue, especially the joints and related structures, characterized by inflammation, degeneration, or metabolic derangement. [NIH] Rheumatism: A group of disorders marked by inflammation or pain in the connective tissue structures of the body. These structures include bone, cartilage, and fat. [NIH] Rheumatoid: Resembling rheumatism. [EU] Rheumatoid arthritis: A form of arthritis, the cause of which is unknown, although infection, hypersensitivity, hormone imbalance and psychologic stress have been suggested as possible causes. [NIH] Rheumatoid Nodule: Subcutaneous nodules seen in 20-30% of rheumatoid arthritis patients. They may arise anywhere on the body, but are most frequently found over the bony prominences. The nodules are characterized histologically by dense areas of fibrinoid necrosis with basophilic streaks and granules, surrounded by a palisade of cells, mainly fibroblasts and histiocytes. [NIH] Rheumatology: A subspecialty of internal medicine concerned with the study of inflammatory or degenerative processes and metabolic derangement of connective tissue structures which pertain to a variety of musculoskeletal disorders, such as arthritis. [NIH] Rhodopsin: A photoreceptor protein found in retinal rods. It is a complex formed by the binding of retinal, the oxidized form of retinol, to the protein opsin and undergoes a series of complex reactions in response to visible light resulting in the transmission of nerve impulses to the brain. [NIH] Rhusiopathiae: Causal agent of the anthropozoonosis called erysipeloid. [NIH] Ribose: A pentose active in biological systems usually in its D-form. [NIH]
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Ribosomal Proteins: Proteins found in ribosomes. They are believed to have a catalytic function in reconstituting biologically active ribosomal subunits. [NIH] Ribosome: A granule of protein and RNA, synthesized in the nucleolus and found in the cytoplasm of cells. Ribosomes are the main sites of protein synthesis. Messenger RNA attaches to them and there receives molecules of transfer RNA bearing amino acids. [NIH] Rickets: A condition caused by deficiency of vitamin D, especially in infancy and childhood, with disturbance of normal ossification. The disease is marked by bending and distortion of the bones under muscular action, by the formation of nodular enlargements on the ends and sides of the bones, by delayed closure of the fontanelles, pain in the muscles, and sweating of the head. Vitamin D and sunlight together with an adequate diet are curative, provided that the parathyroid glands are functioning properly. [EU] Rigidity: Stiffness or inflexibility, chiefly that which is abnormal or morbid; rigor. [EU] Risk factor: A habit, trait, condition, or genetic alteration that increases a person's chance of developing a disease. [NIH] Rituximab: A type of monoclonal antibody used in cancer detection or therapy. Monoclonal antibodies are laboratory-produced substances that can locate and bind to cancer cells. [NIH] Rod: A reception for vision, located in the retina. [NIH] Rotator: A muscle by which a part can be turned circularly. [NIH] Rotator Cuff: The musculotendinous sheath formed by the supraspinatus, infraspinatus, subscapularis, and teres minor muscles. These help stabilize the head of the humerus in the glenoid fossa and allow for rotation of the shoulder joint about its longitudinal axis. [NIH] Rubella: An acute, usually benign, infectious disease caused by a togavirus and most often affecting children and nonimmune young adults, in which the virus enters the respiratory tract via droplet nuclei and spreads to the lymphatic system. It is characterized by a slight cold, sore throat, and fever, followed by enlargement of the postauricular, suboccipital, and cervical lymph nodes, and the appearances of a fine pink rash that begins on the head and spreads to become generalized. Called also German measles, roetln, röteln, and three-day measles, and rubeola in French and Spanish. [EU] Ruminants: A suborder of the order Artiodactyla whose members have the distinguishing feature of a four-chambered stomach. Horns or antlers are usually present, at least in males. [NIH]
Rutin: 3-((6-O-(6-Deoxy-alpha-L-mannopyranosyl)-beta-D-glucopyranosyl)oxy)-2-(3,4dihydroxyphenyl)-5,7-dihydroxy-4H-1-benzopyran-4-one. Found in many plants, including buckwheat, tobacco, forsythia, hydrangea, pansies, etc. It has been used therapeutically to decrease capillary fragility. [NIH] Sacroiliac Joint: The immovable joint formed by the lateral surfaces of the sacrum and ilium. [NIH] Saimiri: A genus of the family Cebidae consisting of four species: S. boliviensis, S. orstedii (red-backed squirrel monkey), S. sciureus (common squirrel monkey), and S. ustus. They inhabit tropical rain forests in Central and South America. S. sciureus is used extensively in research studies. [NIH] Salivary: The duct that convey saliva to the mouth. [NIH] Salivary glands: Glands in the mouth that produce saliva. [NIH] Salmonella: A genus of gram-negative, facultatively anaerobic, rod-shaped bacteria that utilizes citrate as a sole carbon source. It is pathogenic for humans, causing enteric fevers, gastroenteritis, and bacteremia. Food poisoning is the most common clinical manifestation. Organisms within this genus are separated on the basis of antigenic characteristics, sugar
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fermentation patterns, and bacteriophage susceptibility. [NIH] Salpingitis: 1. Inflammation of the uterine tube. 2. Inflammation of the auditory tube. [EU] Salvage Therapy: A therapeutic approach, involving chemotherapy, radiation therapy, or surgery, after initial regimens have failed to lead to improvement in a patient's condition. Salvage therapy is most often used for neoplastic diseases. [NIH] Saponins: Sapogenin glycosides. A type of glycoside widely distributed in plants. Each consists of a sapogenin as the aglycon moiety, and a sugar. The sapogenin may be a steroid or a triterpene and the sugar may be glucose, galactose, a pentose, or a methylpentose. Sapogenins are poisonous towards the lower forms of life and are powerful hemolytics when injected into the blood stream able to dissolve red blood cells at even extreme dilutions. [NIH] Sarcoma: A connective tissue neoplasm formed by proliferation of mesodermal cells; it is usually highly malignant. [NIH] Scatter: The extent to which relative success and failure are divergently manifested in qualitatively different tests. [NIH] Schizoid: Having qualities resembling those found in greater degree in schizophrenics; a person of schizoid personality. [NIH] Schizophrenia: A severe emotional disorder of psychotic depth characteristically marked by a retreat from reality with delusion formation, hallucinations, emotional disharmony, and regressive behavior. [NIH] Schizotypal Personality Disorder: A personality disorder in which there are oddities of thought (magical thinking, paranoid ideation, suspiciousness), perception (illusions, depersonalization), speech (digressive, vague, overelaborate), and behavior (inappropriate affect in social interactions, frequently social isolation) that are not severe enough to characterize schizophrenia. [NIH] Sciatica: A condition characterized by pain radiating from the back into the buttock and posterior/lateral aspects of the leg. Sciatica may be a manifestation of sciatic neuropathy; radiculopathy (involving the L4, L5, S1 or S2 spinal nerve roots; often associated with intervertebral disk displacement); or lesions of the cauda equina. [NIH] Sclera: The tough white outer coat of the eyeball, covering approximately the posterior fivesixths of its surface, and continuous anteriorly with the cornea and posteriorly with the external sheath of the optic nerve. [EU] Scleritis: Refers to any inflammation of the sclera including episcleritis, a benign condition affecting only the episclera, which is generally short-lived and easily treated. Classic scleritis, on the other hand, affects deeper tissue and is characterized by higher rates of visual acuity loss and even mortality, particularly in necrotizing form. Its characteristic symptom is severe and general head pain. Scleritis has also been associated with systemic collagen disease. Etiology is unknown but is thought to involve a local immune response. Treatment is difficult and includes administration of anti-inflammatory and immunosuppressive agents such as corticosteroids. Inflammation of the sclera may also be secondary to inflammation of adjacent tissues, such as the conjunctiva. [NIH] Scleroderma: A chronic disorder marked by hardening and thickening of the skin. Scleroderma can be localized or it can affect the entire body (systemic). [NIH] Scleroproteins: Simple proteins characterized by their insolubility and fibrous structure. Within the body, they perform a supportive or protective function. [NIH] Sclerosis: A pathological process consisting of hardening or fibrosis of an anatomical structure, often a vessel or a nerve. [NIH]
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Screening: Checking for disease when there are no symptoms. [NIH] Sebaceous: Gland that secretes sebum. [NIH] Sebaceous gland: Gland that secretes sebum. [NIH] Secretion: 1. The process of elaborating a specific product as a result of the activity of a gland; this activity may range from separating a specific substance of the blood to the elaboration of a new chemical substance. 2. Any substance produced by secretion. [EU] Secretory: Secreting; relating to or influencing secretion or the secretions. [NIH] Sedative: 1. Allaying activity and excitement. 2. An agent that allays excitement. [EU] Sedentary: 1. Sitting habitually; of inactive habits. 2. Pertaining to a sitting posture. [EU] Sediment: A precipitate, especially one that is formed spontaneously. [EU] Sedimentation: The act of causing the deposit of sediment, especially by the use of a centrifugal machine. [EU] Segregation: The separation in meiotic cell division of homologous chromosome pairs and their contained allelomorphic gene pairs. [NIH] Selenium: An element with the atomic symbol Se, atomic number 34, and atomic weight 78.96. It is an essential micronutrient for mammals and other animals but is toxic in large amounts. Selenium protects intracellular structures against oxidative damage. It is an essential component of glutathione peroxidase. [NIH] Self Care: Performance of activities or tasks traditionally performed by professional health care providers. The concept includes care of oneself or one's family and friends. [NIH] Self Tolerance: The normal lack of the ability to produce an immunological response to autologous (self) antigens. A breakdown of self tolerance leads to autoimmune diseases. The ability to recognize the difference between self and non-self is the prime function of the immune system. [NIH] Sella: A deep depression in the shape of a Turkish saddle in the upper surface of the body of the sphenoid bone in the deepest part of which is lodged the hypophysis cerebri. [NIH] Sella Turcica: A bony prominence situated on the upper surface of the body of the sphenoid bone. It houses the pituitary gland. [NIH] Semen: The thick, yellowish-white, viscid fluid secretion of male reproductive organs discharged upon ejaculation. In addition to reproductive organ secretions, it contains spermatozoa and their nutrient plasma. [NIH] Semisynthetic: Produced by chemical manipulation of naturally occurring substances. [EU] Senile: Relating or belonging to old age; characteristic of old age; resulting from infirmity of old age. [NIH] Sensory loss: A disease of the nerves whereby the myelin or insulating sheath of myelin on the nerves does not stay intact and the messages from the brain to the muscles through the nerves are not carried properly. [NIH] Sepsis: The presence of bacteria in the bloodstream. [NIH] Septic: Produced by or due to decomposition by microorganisms; putrefactive. [EU] Septicemia: Systemic disease associated with the presence and persistence of pathogenic microorganisms or their toxins in the blood. Called also blood poisoning. [EU] Sequela: Any lesion or affection following or caused by an attack of disease. [EU] Sequencing: The determination of the order of nucleotides in a DNA or RNA chain. [NIH] Sequester: A portion of dead bone which has become detached from the healthy bone
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tissue, as occurs in necrosis. [NIH] Serine: A non-essential amino acid occurring in natural form as the L-isomer. It is synthesized from glycine or threonine. It is involved in the biosynthesis of purines, pyrimidines, and other amino acids. [NIH] Serine Endopeptidases: Any member of the group of endopeptidases containing at the active site a serine residue involved in catalysis. EC 3.4.21. [NIH] Serologic: Analysis of a person's serum, especially specific immune or lytic serums. [NIH] Serology: The study of serum, especially of antigen-antibody reactions in vitro. [NIH] Serositis: Inflammation of a serous membrane. [NIH] Serotonin: A biochemical messenger and regulator, synthesized from the essential amino acid L-tryptophan. In humans it is found primarily in the central nervous system, gastrointestinal tract, and blood platelets. Serotonin mediates several important physiological functions including neurotransmission, gastrointestinal motility, hemostasis, and cardiovascular integrity. Multiple receptor families (receptors, serotonin) explain the broad physiological actions and distribution of this biochemical mediator. [NIH] Serous: Having to do with serum, the clear liquid part of blood. [NIH] Serrata: The serrated anterior border of the retina located approximately 8.5 mm from the limbus and adjacent to the pars plana of the ciliary body. [NIH] Serrated: Having notches or teeth on the edge as a saw has. [NIH] Serum Globulins: The amber-colored fluid which exudes from coagulated blood as the clot shrinks and then no longer contain fibrinogen. [NIH] Sex Characteristics: Those characteristics that distinguish one sex from the other. The primary sex characteristics are the ovaries and testes and their related hormones. Secondary sex characteristics are those which are masculine or feminine but not directly related to reproduction. [NIH] Sexually Transmitted Diseases: Diseases due to or propagated by sexual contact. [NIH] Sharpness: The apparent blurring of the border between two adjacent areas of a radiograph having different optical densities. [NIH] Shedding: Release of infectious particles (e. g., bacteria, viruses) into the environment, for example by sneezing, by fecal excretion, or from an open lesion. [NIH] Shigella: A genus of gram-negative, facultatively anaerobic, rod-shaped bacteria that ferments sugar without gas production. Its organisms are intestinal pathogens of man and other primates and cause bacillary dysentery. [NIH] Shock: The general bodily disturbance following a severe injury; an emotional or moral upset occasioned by some disturbing or unexpected experience; disruption of the circulation, which can upset all body functions: sometimes referred to as circulatory shock. [NIH]
Shoulder Impingement Syndrome: Tenosinovitis in the shoulders and arms of persons having a poor posture while working with visual display terminals. [NIH] Shunt: A surgically created diversion of fluid (e.g., blood or cerebrospinal fluid) from one area of the body to another area of the body. [NIH] Sicca: Failure of lacrimal secretion, keratoconjunctivitis sicca, failure of secretion of the salivary glands and mucous glands of the upper respiratory tract and polyarthritis. [NIH] Side effect: A consequence other than the one(s) for which an agent or measure is used, as the adverse effects produced by a drug, especially on a tissue or organ system other than the
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one sought to be benefited by its administration. [EU] Signal Transduction: The intercellular or intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GABA-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptormediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway. [NIH] Signs and Symptoms: Clinical manifestations that can be either objective when observed by a physician, or subjective when perceived by the patient. [NIH] Silicosis: A type of pneumoconiosis caused by inhalation of particles of silica, quartz, ganister or slate. [NIH] Simvastatin: A derivative of lovastatin and potent competitive inhibitor of 3-hydroxy-3methylglutaryl coenzyme A reductase (hydroxymethylglutaryl CoA reductases), which is the rate-limiting enzyme in cholesterol biosynthesis. It may also interfere with steroid hormone production. Due to the induction of hepatic LDL receptors, it increases breakdown of LDL-cholesterol (lipoproteins, LDL cholesterol). [NIH] Sindbis Virus: The type species of alphavirus normally transmitted to birds by Culex mosquitoes in Egypt, South Africa, India, Malaya, the Philippines, and Australia. It may be associated with fever in humans. [NIH] Skeletal: Having to do with the skeleton (boney part of the body). [NIH] Skeleton: The framework that supports the soft tissues of vertebrate animals and protects many of their internal organs. The skeletons of vertebrates are made of bone and/or cartilage. [NIH] Skull: The skeleton of the head including the bones of the face and the bones enclosing the brain. [NIH] Small intestine: The part of the digestive tract that is located between the stomach and the large intestine. [NIH] Smallpox: A generalized virus infection with a vesicular rash. [NIH] Smooth muscle: Muscle that performs automatic tasks, such as constricting blood vessels. [NIH]
Social Environment: The aggregate of social and cultural institutions, forms, patterns, and processes that influence the life of an individual or community. [NIH] Social Perception: The perceiving of attributes, characteristics, and behaviors of one's associates or social groups. [NIH] Soft tissue: Refers to muscle, fat, fibrous tissue, blood vessels, or other supporting tissue of the body. [NIH] Solid tumor: Cancer of body tissues other than blood, bone marrow, or the lymphatic system. [NIH] Solvent: 1. Dissolving; effecting a solution. 2. A liquid that dissolves or that is capable of dissolving; the component of a solution that is present in greater amount. [EU]
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Soma: The body as distinct from the mind; all the body tissue except the germ cells; all the axial body. [NIH] Somatic: 1. Pertaining to or characteristic of the soma or body. 2. Pertaining to the body wall in contrast to the viscera. [EU] Sound wave: An alteration of properties of an elastic medium, such as pressure, particle displacement, or density, that propagates through the medium, or a superposition of such alterations. [NIH] Soybean Oil: Oil from soybean or soybean plant. [NIH] Spasm: An involuntary contraction of a muscle or group of muscles. Spasms may involve skeletal muscle or smooth muscle. [NIH] Spatial disorientation: Loss of orientation in space where person does not know which way is up. [NIH] Specialist: In medicine, one who concentrates on 1 special branch of medical science. [NIH] Species: A taxonomic category subordinate to a genus (or subgenus) and superior to a subspecies or variety, composed of individuals possessing common characters distinguishing them from other categories of individuals of the same taxonomic level. In taxonomic nomenclature, species are designated by the genus name followed by a Latin or Latinized adjective or noun. [EU] Specificity: Degree of selectivity shown by an antibody with respect to the number and types of antigens with which the antibody combines, as well as with respect to the rates and the extents of these reactions. [NIH] Spectroscopic: The recognition of elements through their emission spectra. [NIH] Spectrum: A charted band of wavelengths of electromagnetic vibrations obtained by refraction and diffraction. By extension, a measurable range of activity, such as the range of bacteria affected by an antibiotic (antibacterial s.) or the complete range of manifestations of a disease. [EU] Sperm: The fecundating fluid of the male. [NIH] Spermatozoa: Mature male germ cells that develop in the seminiferous tubules of the testes. Each consists of a head, a body, and a tail that provides propulsion. The head consists mainly of chromatin. [NIH] Spinal cord: The main trunk or bundle of nerves running down the spine through holes in the spinal bone (the vertebrae) from the brain to the level of the lower back. [NIH] Spinal Cord Injuries: Penetrating and non-penetrating injuries to the spinal cord resulting from traumatic external forces (e.g., wounds, gunshot; whiplash injuries; etc.). [NIH] Spinal Nerve Roots: The paired bundles of nerve fibers entering and leaving the spinal cord at each segment. The dorsal and ventral nerve roots join to form the mixed segmental spinal nerves. The dorsal roots are generally afferent, formed by the central projections of the spinal (dorsal root) ganglia sensory cells, and the ventral roots efferent, comprising the axons of spinal motor and autonomic preganglionic neurons. There are, however, some exceptions to this afferent/efferent rule. [NIH] Spirochete: Lyme disease. [NIH] Spleen: An organ that is part of the lymphatic system. The spleen produces lymphocytes, filters the blood, stores blood cells, and destroys old blood cells. It is located on the left side of the abdomen near the stomach. [NIH] Splint: A rigid appliance used for the immobilization of a part or for the correction of deformity. [NIH]
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Spondylarthritis: A condition occurring most commonly in children by narrowing of intervertebral disc spaces and some destruction of adjacent vertebrae, followed by slow healing over a period of months. [NIH] Spondylitis: Inflammation of the vertebrae. [EU] Spontaneous Abortion: The non-induced birth of an embryo or of fetus prior to the stage of viability at about 20 weeks of gestation. [NIH] Sporotrichosis: The commonest and least serious of the deep mycoses, characterized by nodular lesions of the cutaneous and subcutaneous tissues. It is caused by inhalation of contaminated dust or by infection of a wound. [NIH] Sports Medicine: The field of medicine concerned with physical fitness and the diagnosis and treatment of injuries sustained in sports activities. [NIH] Sprains and Strains: A collective term for muscle and ligament injuries without dislocation or fracture. A sprain is a joint injury in which some of the fibers of a supporting ligament are ruptured but the continuity of the ligament remains intact. A strain is an overstretching or overexertion of some part of the musculature. [NIH] Stabilization: The creation of a stable state. [EU] Staging: Performing exams and tests to learn the extent of the cancer within the body, especially whether the disease has spread from the original site to other parts of the body. [NIH]
Standard therapy: A currently accepted and widely used treatment for a certain type of cancer, based on the results of past research. [NIH] Staphylococcus: A genus of gram-positive, facultatively anaerobic, coccoid bacteria. Its organisms occur singly, in pairs, and in tetrads and characteristically divide in more than one plane to form irregular clusters. Natural populations of Staphylococcus are membranes of warm-blooded animals. Some species are opportunistic pathogens of humans and animals. [NIH] Stasis: A word termination indicating the maintenance of (or maintaining) a constant level; preventing increase or multiplication. [EU] Statistically significant: Describes a mathematical measure of difference between groups. The difference is said to be statistically significant if it is greater than what might be expected to happen by chance alone. [NIH] Stem cell transplantation: A method of replacing immature blood-forming cells that were destroyed by cancer treatment. The stem cells are given to the person after treatment to help the bone marrow recover and continue producing healthy blood cells. [NIH] Stem Cells: Relatively undifferentiated cells of the same lineage (family type) that retain the ability to divide and cycle throughout postnatal life to provide cells that can become specialized and take the place of those that die or are lost. [NIH] Stenosis: Narrowing or stricture of a duct or canal. [EU] Sterile: Unable to produce children. [NIH] Steroid: A group name for lipids that contain a hydrogenated cyclopentanoperhydrophenanthrene ring system. Some of the substances included in this group are progesterone, adrenocortical hormones, the gonadal hormones, cardiac aglycones, bile acids, sterols (such as cholesterol), toad poisons, saponins, and some of the carcinogenic hydrocarbons. [EU] Steroid therapy: Treatment with corticosteroid drugs to reduce swelling, pain, and other symptoms of inflammation. [NIH]
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Stillbirth: The birth of a dead fetus or baby. [NIH] Stimulant: 1. Producing stimulation; especially producing stimulation by causing tension on muscle fibre through the nervous tissue. 2. An agent or remedy that produces stimulation. [EU] Stimulus: That which can elicit or evoke action (response) in a muscle, nerve, gland or other excitable issue, or cause an augmenting action upon any function or metabolic process. [NIH]
Stoma: A surgically created opening from an area inside the body to the outside. [NIH] Stomach: An organ of digestion situated in the left upper quadrant of the abdomen between the termination of the esophagus and the beginning of the duodenum. [NIH] Stomachic: Medicine that acts like a tonic on the stomach. [NIH] Stomatitis: Inflammation of the oral mucosa, due to local or systemic factors which may involve the buccal and labial mucosa, palate, tongue, floor of the mouth, and the gingivae. [EU]
Stomatognathic System: The mouth, teeth, jaws, pharynx, and related structures as they relate to mastication, deglutition, and speech. [NIH] Stool: The waste matter discharged in a bowel movement; feces. [NIH] Strand: DNA normally exists in the bacterial nucleus in a helix, in which two strands are coiled together. [NIH] Streptococcal: Caused by infection due to any species of streptococcus. [NIH] Streptococcus: A genus of gram-positive, coccoid bacteria whose organisms occur in pairs or chains. No endospores are produced. Many species exist as commensals or parasites on man or animals with some being highly pathogenic. A few species are saprophytes and occur in the natural environment. [NIH] Stress: Forcibly exerted influence; pressure. Any condition or situation that causes strain or tension. Stress may be either physical or psychologic, or both. [NIH] Stroke: Sudden loss of function of part of the brain because of loss of blood flow. Stroke may be caused by a clot (thrombosis) or rupture (hemorrhage) of a blood vessel to the brain. [NIH]
Stroma: The middle, thickest layer of tissue in the cornea. [NIH] Stromal: Large, veil-like cell in the bone marrow. [NIH] Stromal Cells: Connective tissue cells of an organ found in the loose connective tissue. These are most often associated with the uterine mucosa and the ovary as well as the hematopoietic system and elsewhere. [NIH] Stupor: Partial or nearly complete unconsciousness, manifested by the subject's responding only to vigorous stimulation. Also, in psychiatry, a disorder marked by reduced responsiveness. [EU] Subacute: Somewhat acute; between acute and chronic. [EU] Subarachnoid: Situated or occurring between the arachnoid and the pia mater. [EU] Subcapsular: Situated below a capsule. [EU] Subclinical: Without clinical manifestations; said of the early stage(s) of an infection or other disease or abnormality before symptoms and signs become apparent or detectable by clinical examination or laboratory tests, or of a very mild form of an infection or other disease or abnormality. [EU] Subcutaneous: Beneath the skin. [NIH]
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Submaxillary: Four to six lymph glands, located between the lower jaw and the submandibular salivary gland. [NIH] Subspecies: A category intermediate in rank between species and variety, based on a smaller number of correlated characters than are used to differentiate species and generally conditioned by geographical and/or ecological occurrence. [NIH] Substance P: An eleven-amino acid neurotransmitter that appears in both the central and peripheral nervous systems. It is involved in transmission of pain, causes rapid contractions of the gastrointestinal smooth muscle, and modulates inflammatory and immune responses. [NIH]
Substrate: A substance upon which an enzyme acts. [EU] Substrate Specificity: A characteristic feature of enzyme activity in relation to the kind of substrate on which the enzyme or catalytic molecule reacts. [NIH] Sulfinpyrazone: A uricosuric drug that is used to reduce the serum urate levels in gout therapy. It lacks anti-inflammatory, analgesic, and diuretic properties. [NIH] Sulfur: An element that is a member of the chalcogen family. It has an atomic symbol S, atomic number 16, and atomic weight 32.066. It is found in the amino acids cysteine and methionine. [NIH] Superantigens: Microbial antigens that have in common an extremely potent activating effect on T-cells that bear a specific variable region. Superantigens cross-link the variable region with class II MHC proteins regardless of the peptide binding in the T-cell receptor's pocket. The result is a transient expansion and subsequent death and anergy of the T-cells with the appropriate variable regions. [NIH] Superoxide: Derivative of molecular oxygen that can damage cells. [NIH] Superoxide Dismutase: An oxidoreductase that catalyzes the reaction between superoxide anions and hydrogen to yield molecular oxygen and hydrogen peroxide. The enzyme protects the cell against dangerous levels of superoxide. EC 1.15.1.1. [NIH] Supplementation: Adding nutrients to the diet. [NIH] Support group: A group of people with similar disease who meet to discuss how better to cope with their cancer and treatment. [NIH] Suppressive: Tending to suppress : effecting suppression; specifically : serving to suppress activity, function, symptoms. [EU] Suppurative: Consisting of, containing, associated with, or identified by the formation of pus. [NIH] Survival Rate: The proportion of survivors in a group, e.g., of patients, studied and followed over a period, or the proportion of persons in a specified group alive at the beginning of a time interval who survive to the end of the interval. It is often studied using life table methods. [NIH] Sympathomimetic: 1. Mimicking the effects of impulses conveyed by adrenergic postganglionic fibres of the sympathetic nervous system. 2. An agent that produces effects similar to those of impulses conveyed by adrenergic postganglionic fibres of the sympathetic nervous system. Called also adrenergic. [EU] Symphysis: A secondary cartilaginous joint. [NIH] Symptomatic: Having to do with symptoms, which are signs of a condition or disease. [NIH] Symptomatology: 1. That branch of medicine with treats of symptoms; the systematic discussion of symptoms. 2. The combined symptoms of a disease. [EU] Synaptic: Pertaining to or affecting a synapse (= site of functional apposition between
Dictionary 679
neurons, at which an impulse is transmitted from one neuron to another by electrical or chemical means); pertaining to synapsis (= pairing off in point-for-point association of homologous chromosomes from the male and female pronuclei during the early prophase of meiosis). [EU] Syncope: A temporary suspension of consciousness due to generalized cerebral schemia, a faint or swoon. [EU] Synergistic: Acting together; enhancing the effect of another force or agent. [EU] Synovial: Of pertaining to, or secreting synovia. [EU] Synovial Fluid: The clear, viscous fluid secreted by the synovial membrane. It contains mucin, albumin, fat, and mineral salts and serves to lubricate joints. [NIH] Synovial Membrane: The inner membrane of a joint capsule surrounding a freely movable joint. It is loosely attached to the external fibrous capsule and secretes synovial fluid. [NIH] Synovitis: Inflammation of a synovial membrane. It is usually painful, particularly on motion, and is characterized by a fluctuating swelling due to effusion within a synovial sac. Synovitis is qualified as fibrinous, gonorrhoeal, hyperplastic, lipomatous, metritic, puerperal, rheumatic, scarlatinal, syphilitic, tuberculous, urethral, etc. [EU] Syphilis: A contagious venereal disease caused by the spirochete Treponema pallidum. [NIH]
Systemic: Affecting the entire body. [NIH] Systemic disease: Disease that affects the whole body. [NIH] Systemic lupus erythematosus: SLE. A chronic inflammatory connective tissue disease marked by skin rashes, joint pain and swelling, inflammation of the kidneys, inflammation of the fibrous tissue surrounding the heart (i.e., the pericardium), as well as other problems. Not all affected individuals display all of these problems. May be referred to as lupus. [NIH] Systolic: Indicating the maximum arterial pressure during contraction of the left ventricle of the heart. [EU] Systolic blood pressure: The maximum pressure in the artery produced as the heart contracts and blood begins to flow. [NIH] Tachycardia: Excessive rapidity in the action of the heart, usually with a heart rate above 100 beats per minute. [NIH] Tachypnea: Rapid breathing. [NIH] Tacrolimus: A macrolide isolated from the culture broth of a strain of Streptomyces tsukubaensis that has strong immunosuppressive activity in vivo and prevents the activation of T-lymphocytes in response to antigenic or mitogenic stimulation in vitro. [NIH] Talus: The second largest of the tarsal bones and occupies the middle and upper part of the tarsus. [NIH] Tarsal Bones: The seven bones which form the tarsus - namely, calcaneus, talus, cuboid, navicular, and first, second and third cuneiforms. The tarsus is a skeletal part of the foot. [NIH]
Taurine: 2-Aminoethanesulfonic acid. A conditionally essential nutrient, important during mammalian development. It is present in milk but is isolated mostly from ox bile and strongly conjugates bile acids. [NIH] Telophase: The final phase of cell division, in which two daughter nuclei are formed, the cytoplasm divides, and the chromosomes lose their distinctness and are transformed into chromatin networks. [NIH] Temporal: One of the two irregular bones forming part of the lateral surfaces and base of
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the skull, and containing the organs of hearing. [NIH] Temporal Lobe: Lower lateral part of the cerebral hemisphere. [NIH] Tendinitis: Inflammation of tendons and of tendon-muscle attachments. [EU] Tendon: A discrete band of connective tissue mainly composed of parallel bundles of collagenous fibers by which muscles are attached, or two muscles bellies joined. [NIH] Tendonitis: Inflammation of tendons attached to the biceps muscle, i. e. the main flexor muscle of the upper arm. [NIH] Tenosynovitis: Inflammation of a tendon sheath. [EU] Teratogenic: Tending to produce anomalies of formation, or teratism (= anomaly of formation or development : condition of a monster). [EU] Teratogenicity: The power to cause abnormal development. [NIH] Terminator: A DNA sequence sited at the end of a transcriptional unit that signals the end of transcription. [NIH] Testicle: The male gonad where, in adult life, spermatozoa develop; the testis. [NIH] Testicular: Pertaining to a testis. [EU] Testis: Either of the paired male reproductive glands that produce the male germ cells and the male hormones. [NIH] Testosterone: A hormone that promotes the development and maintenance of male sex characteristics. [NIH] Tetracycline: An antibiotic originally produced by Streptomyces viridifaciens, but used mostly in synthetic form. It is an inhibitor of aminoacyl-tRNA binding during protein synthesis. [NIH] Thalamus: Paired bodies containing mostly gray substance and forming part of the lateral wall of the third ventricle of the brain. The thalamus represents the major portion of the diencephalon and is commonly divided into cellular aggregates known as nuclear groups. [NIH]
Theophylline: Alkaloid obtained from Thea sinensis (tea) and others. It stimulates the heart and central nervous system, dilates bronchi and blood vessels, and causes diuresis. The drug is used mainly in bronchial asthma and for myocardial stimulation. Among its more prominent cellular effects are inhibition of cyclic nucleotide phosphodiesterases and antagonism of adenosine receptors. [NIH] Therapeutics: The branch of medicine which is concerned with the treatment of diseases, palliative or curative. [NIH] Thermal: Pertaining to or characterized by heat. [EU] Thigh: A leg; in anatomy, any elongated process or part of a structure more or less comparable to a leg. [NIH] Thoracic: Having to do with the chest. [NIH] Thorax: A part of the trunk between the neck and the abdomen; the chest. [NIH] Threonine: An essential amino acid occurring naturally in the L-form, which is the active form. It is found in eggs, milk, gelatin, and other proteins. [NIH] Threshold: For a specified sensory modality (e. g. light, sound, vibration), the lowest level (absolute threshold) or smallest difference (difference threshold, difference limen) or intensity of the stimulus discernible in prescribed conditions of stimulation. [NIH] Thrombocytopenia: A decrease in the number of blood platelets. [NIH]
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Thrombocytosis: Increased numbers of platelets in the peripheral blood. [EU] Thromboembolism: Obstruction of a vessel by a blood clot that has been transported from a distant site by the blood stream. [NIH] Thrombolytic: 1. Dissolving or splitting up a thrombus. 2. A thrombolytic agent. [EU] Thrombomodulin: A cell surface glycoprotein of endothelial cells that binds thrombin and serves as a cofactor in the activation of protein C and its regulation of blood coagulation. [NIH]
Thrombophlebitis: Inflammation of a vein associated with thrombus formation. [NIH] Thrombopoietin: A humoral factor that controls blood platelet production through stimulation of megakaryocyte populations. Bone marrow megakaryocytes increase in both size and number in response to exposure to thrombopoietin. [NIH] Thrombosis: The formation or presence of a blood clot inside a blood vessel. [NIH] Thromboxanes: Physiologically active compounds found in many organs of the body. They are formed in vivo from the prostaglandin endoperoxides and cause platelet aggregation, contraction of arteries, and other biological effects. Thromboxanes are important mediators of the actions of polyunsaturated fatty acids transformed by cyclooxygenase. [NIH] Thrombus: An aggregation of blood factors, primarily platelets and fibrin with entrapment of cellular elements, frequently causing vascular obstruction at the point of its formation. Some authorities thus differentiate thrombus formation from simple coagulation or clot formation. [EU] Thrush: A disease due to infection with species of fungi of the genus Candida. [NIH] Thymus: An organ that is part of the lymphatic system, in which T lymphocytes grow and multiply. The thymus is in the chest behind the breastbone. [NIH] Thyroid: A gland located near the windpipe (trachea) that produces thyroid hormone, which helps regulate growth and metabolism. [NIH] Thyroid Gland: A highly vascular endocrine gland consisting of two lobes, one on either side of the trachea, joined by a narrow isthmus; it produces the thyroid hormones which are concerned in regulating the metabolic rate of the body. [NIH] Thyroiditis: Inflammation of the thyroid gland. [NIH] Tibia: The second longest bone of the skeleton. It is located on the medial side of the lower leg, articulating with the fibula laterally, the talus distally, and the femur proximally. [NIH] Ticks: Blood-sucking arachnids of the order Acarina. [NIH] Tin: A trace element that is required in bone formation. It has the atomic symbol Sn, atomic number 50, and atomic weight 118.71. [NIH] Tinea Pedis: Dermatological pruritic lesion in the feet, caused by Trichophyton rubrum, T. mentagrophytes, or Epidermophyton floccosum. [NIH] Tissue: A group or layer of cells that are alike in type and work together to perform a specific function. [NIH] Tissue Distribution: Accumulation of a drug or chemical substance in various organs (including those not relevant to its pharmacologic or therapeutic action). This distribution depends on the blood flow or perfusion rate of the organ, the ability of the drug to penetrate organ membranes, tissue specificity, protein binding. The distribution is usually expressed as tissue to plasma ratios. [NIH] Tissue Extracts: Preparations made from animal tissues or organs; they usually contain many components, any one of which may be pharmacologically or physiologically active;
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extracts may contain specific, but uncharacterized factors or proteins with specific actions. [NIH]
Tolerance: 1. The ability to endure unusually large doses of a drug or toxin. 2. Acquired drug tolerance; a decreasing response to repeated constant doses of a drug or the need for increasing doses to maintain a constant response. [EU] Tome: A zone produced by a number of irregular spaces contained in the outermost layer of denture of the root of a tooth. [NIH] Tomography: Imaging methods that result in sharp images of objects located on a chosen plane and blurred images located above or below the plane. [NIH] Tone: 1. The normal degree of vigour and tension; in muscle, the resistance to passive elongation or stretch; tonus. 2. A particular quality of sound or of voice. 3. To make permanent, or to change, the colour of silver stain by chemical treatment, usually with a heavy metal. [EU] Tonicity: The normal state of muscular tension. [NIH] Tooth Preparation: Procedures carried out with regard to the teeth or tooth structures preparatory to specified dental therapeutic and surgical measures. [NIH] Tophus: A chalky deposit of sodium urate occurring in gout; tophi form most often around joints in cartilage, bone, bursae, and subcutaneous tissue and in the external ear, producing a chronic foreign-body inflammatory response. [EU] Topical: On the surface of the body. [NIH] Torsion: A twisting or rotation of a bodily part or member on its axis. [NIH] Tourniquet: A device, band or elastic tube applied temporarily to press upon an artery to stop bleeding; a device to compress a blood vessel in order to stop bleeding. [NIH] Toxic: Having to do with poison or something harmful to the body. Toxic substances usually cause unwanted side effects. [NIH] Toxicity: The quality of being poisonous, especially the degree of virulence of a toxic microbe or of a poison. [EU] Toxicodendron: A genus (formerly Rhus) of shrubs, vines, or trees that yields a highly allergenic oleoresin which causes a severe contact dermatitis. The most toxic species are Toxicodendron vernix (poison sumac), T. diversilobum (poison oak), and T. radicans (poison ivy). T. vernicifera yields a useful varnish from which certain enzymes (laccases) are obtained. [NIH] Toxicology: The science concerned with the detection, chemical composition, and pharmacologic action of toxic substances or poisons and the treatment and prevention of toxic manifestations. [NIH] Toxin: A poison; frequently used to refer specifically to a protein produced by some higher plants, certain animals, and pathogenic bacteria, which is highly toxic for other living organisms. Such substances are differentiated from the simple chemical poisons and the vegetable alkaloids by their high molecular weight and antigenicity. [EU] Toxoplasmosis: The acquired form of infection by Toxoplasma gondii in animals and man. [NIH]
Trace element: Substance or element essential to plant or animal life, but present in extremely small amounts. [NIH] Trachea: The cartilaginous and membranous tube descending from the larynx and branching into the right and left main bronchi. [NIH] Traction: The act of pulling. [NIH]
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Transcriptase: An enzyme which catalyses the synthesis of a complementary mRNA molecule from a DNA template in the presence of a mixture of the four ribonucleotides (ATP, UTP, GTP and CTP). [NIH] Transcription Factors: Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process. [NIH] Transcutaneous: Transdermal. [EU] Transdermal: Entering through the dermis, or skin, as in administration of a drug applied to the skin in ointment or patch form. [EU] Transduction: The transfer of genes from one cell to another by means of a viral (in the case of bacteria, a bacteriophage) vector or a vector which is similar to a virus particle (pseudovirion). [NIH] Transfection: The uptake of naked or purified DNA into cells, usually eukaryotic. It is analogous to bacterial transformation. [NIH] Transfer Factor: Factor derived from leukocyte lysates of immune donors which can transfer both local and systemic cellular immunity to nonimmune recipients. [NIH] Transforming Growth Factor beta: A factor synthesized in a wide variety of tissues. It acts synergistically with TGF-alpha in inducing phenotypic transformation and can also act as a negative autocrine growth factor. TGF-beta has a potential role in embryonal development, cellular differentiation, hormone secretion, and immune function. TGF-beta is found mostly as homodimer forms of separate gene products TGF-beta1, TGF-beta2 or TGF-beta3. Heterodimers composed of TGF-beta1 and 2 (TGF-beta1.2) or of TGF-beta2 and 3 (TGFbeta2.3) have been isolated. The TGF-beta proteins are synthesized as precursor proteins. [NIH]
Transgenes: Genes that are introduced into an organism using gene transfer techniques. [NIH]
Translation: The process whereby the genetic information present in the linear sequence of ribonucleotides in mRNA is converted into a corresponding sequence of amino acids in a protein. It occurs on the ribosome and is unidirectional. [NIH] Translational: The cleavage of signal sequence that directs the passage of the protein through a cell or organelle membrane. [NIH] Translocation: The movement of material in solution inside the body of the plant. [NIH] Transmitter: A chemical substance which effects the passage of nerve impulses from one cell to the other at the synapse. [NIH] Transplantation: Transference of a tissue or organ, alive or dead, within an individual, between individuals of the same species, or between individuals of different species. [NIH] Trauma: Any injury, wound, or shock, must frequently physical or structural shock, producing a disturbance. [NIH] Trees: Woody, usually tall, perennial higher plants (Angiosperms, Gymnosperms, and some Pterophyta) having usually a main stem and numerous branches. [NIH] Triage: The sorting out and classification of patients or casualties to determine priority of need and proper place of treatment. [NIH] Trichomoniasis: An infection with the protozoan parasite Trichomonas vaginalis. [NIH] Tricuspid Atresia: Absence of the orifice between the right atrium and ventricle, with the presence of an atrial defect through which all the systemic venous return reaches the left heart. As a result, there is left ventricular hypertrophy because the right ventricle is absent or not functional. [NIH]
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Tricyclic: Containing three fused rings or closed chains in the molecular structure. [EU] Triglyceride: A lipid carried through the blood stream to tissues. Most of the body's fat tissue is in the form of triglycerides, stored for use as energy. Triglycerides are obtained primarily from fat in foods. [NIH] Tropomyosin: A protein found in the thin filaments of muscle fibers. It inhibits contraction of the muscle unless its position is modified by troponin. [NIH] Troponin: One of the minor protein components of skeletal muscle. Its function is to serve as the calcium-binding component in the troponin-tropomyosin B-actin-myosin complex by conferring calcium sensitivity to the cross-linked actin and myosin filaments. [NIH] Trypsin: A serine endopeptidase that is formed from trypsinogen in the pancreas. It is converted into its active form by enteropeptidase in the small intestine. It catalyzes hydrolysis of the carboxyl group of either arginine or lysine. EC 3.4.21.4. [NIH] Trypsin Inhibitors: Serine proteinase inhibitors which inhibit trypsin. They may be endogenous or exogenous compounds. [NIH] Tryptophan: An essential amino acid that is necessary for normal growth in infants and for nitrogen balance in adults. It is a precursor serotonin and niacin. [NIH] Tuberculosis: Any of the infectious diseases of man and other animals caused by species of Mycobacterium. [NIH] Tumor marker: A substance sometimes found in an increased amount in the blood, other body fluids, or tissues and which may mean that a certain type of cancer is in the body. Examples of tumor markers include CA 125 (ovarian cancer), CA 15-3 (breast cancer), CEA (ovarian, lung, breast, pancreas, and gastrointestinal tract cancers), and PSA (prostate cancer). Also called biomarker. [NIH] Tumor Necrosis Factor: Serum glycoprotein produced by activated macrophages and other mammalian mononuclear leukocytes which has necrotizing activity against tumor cell lines and increases ability to reject tumor transplants. It mimics the action of endotoxin but differs from it. It has a molecular weight of less than 70,000 kDa. [NIH] Tumor suppressor gene: Genes in the body that can suppress or block the development of cancer. [NIH] Tumour: 1. Swelling, one of the cardinal signs of inflammations; morbid enlargement. 2. A new growth of tissue in which the multiplication of cells is uncontrolled and progressive; called also neoplasm. [EU] Typhimurium: Microbial assay which measures his-his+ reversion by chemicals which cause base substitutions or frameshift mutations in the genome of this organism. [NIH] Tyrosine: A non-essential amino acid. In animals it is synthesized from phenylalanine. It is also the precursor of epinephrine, thyroid hormones, and melanin. [NIH] Ulcer: A localized necrotic lesion of the skin or a mucous surface. [NIH] Ulceration: 1. The formation or development of an ulcer. 2. An ulcer. [EU] Ulcerative colitis: Chronic inflammation of the colon that produces ulcers in its lining. This condition is marked by abdominal pain, cramps, and loose discharges of pus, blood, and mucus from the bowel. [NIH] Ulna: The long and medial bone of the forearm. [NIH] Ultrasonography: The visualization of deep structures of the body by recording the reflections of echoes of pulses of ultrasonic waves directed into the tissues. Use of ultrasound for imaging or diagnostic purposes employs frequencies ranging from 1.6 to 10 megahertz. [NIH]
Dictionary 685
Unconscious: Experience which was once conscious, but was subsequently rejected, as the "personal unconscious". [NIH] Uncontrolled study: A clinical study that lacks a comparison (i.e., a control) group. [NIH] Unsaturated Fats: A type of fat. [NIH] Urea: A compound (CO(NH2)2), formed in the liver from ammonia produced by the deamination of amino acids. It is the principal end product of protein catabolism and constitutes about one half of the total urinary solids. [NIH] Uremia: The illness associated with the buildup of urea in the blood because the kidneys are not working effectively. Symptoms include nausea, vomiting, loss of appetite, weakness, and mental confusion. [NIH] Ureters: Tubes that carry urine from the kidneys to the bladder. [NIH] Urethra: The tube through which urine leaves the body. It empties urine from the bladder. [NIH]
Urethritis: Inflammation of the urethra. [EU] Uric: A kidney stone that may result from a diet high in animal protein. When the body breaks down this protein, uric acid levels rise and can form stones. [NIH] Uricosuric: 1. Pertaining to, characterized by, or promoting uricosuria (= the excretion of uric acid in the urine). 2. An agent that promotes uricosuria. [EU] Uricosuric Agents: Gout suppressants that act directly on the renal tubule to increase the excretion of uric acid, thus reducing its concentrations in plasma. [NIH] Urinalysis: Examination of urine by chemical, physical, or microscopic means. Routine urinalysis usually includes performing chemical screening tests, determining specific gravity, observing any unusual color or odor, screening for bacteriuria, and examining the sediment microscopically. [NIH] Urinary: Having to do with urine or the organs of the body that produce and get rid of urine. [NIH] Urinary Retention: Inability to urinate. The etiology of this disorder includes obstructive, neurogenic, pharmacologic, and psychogenic causes. [NIH] Urinary tract: The organs of the body that produce and discharge urine. These include the kidneys, ureters, bladder, and urethra. [NIH] Urinary tract infection: An illness caused by harmful bacteria growing in the urinary tract. [NIH]
Urokinase: A drug that dissolves blood clots or prevents them from forming. [NIH] Urticaria: A vascular reaction of the skin characterized by erythema and wheal formation due to localized increase of vascular permeability. The causative mechanism may be allergy, infection, or stress. [NIH] Uterus: The small, hollow, pear-shaped organ in a woman's pelvis. This is the organ in which a fetus develops. Also called the womb. [NIH] Vaccination: Administration of vaccines to stimulate the host's immune response. This includes any preparation intended for active immunological prophylaxis. [NIH] Vaccine: A substance or group of substances meant to cause the immune system to respond to a tumor or to microorganisms, such as bacteria or viruses. [NIH] Vaccinia: The cutaneous and occasional systemic reactions associated with vaccination using smallpox (variola) vaccine. [NIH] Vaccinia Virus: The type species of Orthopoxvirus, related to cowpox virus, but whose true
686 Arthritis
origin is unknown. It has been used as a live vaccine against smallpox. It is also used as a vector for inserting foreign DNA into animals. Rabbitpox virus is a subspecies of vaccinia virus. [NIH] Vagina: The muscular canal extending from the uterus to the exterior of the body. Also called the birth canal. [NIH] Vaginal: Of or having to do with the vagina, the birth canal. [NIH] Vaginitis: Inflammation of the vagina characterized by pain and a purulent discharge. [NIH] Valerian: Valeriana officinale, an ancient, sedative herb of the large family Valerianaceae. The roots were formerly used to treat hysterias and other neurotic states and are presently used to treat sleep disorders. [NIH] Valine: A branched-chain essential amino acid that has stimulant activity. It promotes muscle growth and tissue repair. It is a precursor in the penicillin biosynthetic pathway. [NIH]
Varicella: Chicken pox. [EU] Varicose: The common ulcer in the lower third of the leg or near the ankle. [NIH] Varicose Ulcer: Ulcer due to varicose veins. Chronic venous insufficiency in the deep veins of the legs leads to shunting the venous return into the superficial veins, in which pressure and flow rate, as well as oxygen content, are increased. [NIH] Variola: A generalized virus infection with a vesicular rash. [NIH] Vascular: Pertaining to blood vessels or indicative of a copious blood supply. [EU] Vascular endothelial growth factor: VEGF. A substance made by cells that stimulates new blood vessel formation. [NIH] Vasculitis: Inflammation of a blood vessel. [NIH] Vasoconstriction: Narrowing of the blood vessels without anatomic change, for which constriction, pathologic is used. [NIH] Vasodilation: Physiological dilation of the blood vessels without anatomic change. For dilation with anatomic change, dilatation, pathologic or aneurysm (or specific aneurysm) is used. [NIH] Vasodilator: An agent that widens blood vessels. [NIH] Vasomotor: 1. Affecting the calibre of a vessel, especially of a blood vessel. 2. Any element or agent that effects the calibre of a blood vessel. [EU] VE: The total volume of gas either inspired or expired in one minute. [NIH] Vector: Plasmid or other self-replicating DNA molecule that transfers DNA between cells in nature or in recombinant DNA technology. [NIH] Vein: Vessel-carrying blood from various parts of the body to the heart. [NIH] Venereal: Pertaining or related to or transmitted by sexual contact. [EU] Venom: That produced by the poison glands of the mouth and injected by the fangs of poisonous snakes. [NIH] Venous: Of or pertaining to the veins. [EU] Ventricle: One of the two pumping chambers of the heart. The right ventricle receives oxygen-poor blood from the right atrium and pumps it to the lungs through the pulmonary artery. The left ventricle receives oxygen-rich blood from the left atrium and pumps it to the body through the aorta. [NIH] Ventricular: Pertaining to a ventricle. [EU]
Dictionary 687
Venules: The minute vessels that collect blood from the capillary plexuses and join together to form veins. [NIH] Vertebrae: A bony unit of the segmented spinal column. [NIH] Vertebral: Of or pertaining to a vertebra. [EU] Vertebrobasilar Insufficiency: Localized or diffuse reduction in blood flow through the vertebrobasilar arterial system, which supplies the brain stem; cerebellum; occipital lobe; medial temporal lobe; and thalamus. Characteristic clinical features include syncope; lightheadedness; visual disturbances; and vertigo. brain stem infarctions or other brain infarction may be associated. [NIH] Vertigo: An illusion of movement; a sensation as if the external world were revolving around the patient (objective vertigo) or as if he himself were revolving in space (subjective vertigo). The term is sometimes erroneously used to mean any form of dizziness. [EU] Vesicoureteral: An abnormal condition in which urine backs up into the ureters, and occasionally into the kidneys, raising the risk of infection. [NIH] Vesicular: 1. Composed of or relating to small, saclike bodies. 2. Pertaining to or made up of vesicles on the skin. [EU] Veterinary Medicine: The medical science concerned with the prevention, diagnosis, and treatment of diseases in animals. [NIH] Video Recording: The storing or preserving of video signals for television to be played back later via a transmitter or receiver. Recordings may be made on magnetic tape or discs (videodisc recording). [NIH] Videodisc Recording: The storing of visual and usually sound signals on discs for later reproduction on a television screen or monitor. [NIH] Viral: Pertaining to, caused by, or of the nature of virus. [EU] Viral vector: A type of virus used in cancer therapy. The virus is changed in the laboratory and cannot cause disease. Viral vectors produce tumor antigens (proteins found on a tumor cell) and can stimulate an antitumor immune response in the body. Viral vectors may also be used to carry genes that can change cancer cells back to normal cells. [NIH] Virulence: The degree of pathogenicity within a group or species of microorganisms or viruses as indicated by case fatality rates and/or the ability of the organism to invade the tissues of the host. [NIH] Virulent: A virus or bacteriophage capable only of lytic growth, as opposed to temperate phages establishing the lysogenic response. [NIH] Virus: Submicroscopic organism that causes infectious disease. In cancer therapy, some viruses may be made into vaccines that help the body build an immune response to, and kill, tumor cells. [NIH] Viscera: Any of the large interior organs in any one of the three great cavities of the body, especially in the abdomen. [NIH] Visceral: , from viscus a viscus) pertaining to a viscus. [EU] Visual Acuity: Acuteness or clearness of vision, especially of form vision, which is dependent mainly on the sharpness of the retinal focus. [NIH] Visual field: The entire area that can be seen when the eye is forward, including peripheral vision. [NIH] Vitamin A: A substance used in cancer prevention; it belongs to the family of drugs called retinoids. [NIH]
688 Arthritis
Vitamin D: The vitamin that mediates intestinal calcium absorption, bone calcium metabolism, and probably muscle activity. It usually acts as a hormone precursor, requiring 2 stages of metabolism before reaching actual hormonal form. It is isolated from fish liver oils and used in the treatment and prevention of rickets. [NIH] Vitamin K: A substance that promotes the clotting of blood. [NIH] Vitreous: Glasslike or hyaline; often used alone to designate the vitreous body of the eye (corpus vitreum). [EU] Vitreous Body: The transparent, semigelatinous substance that fills the cavity behind the crystalline lens of the eye and in front of the retina. It is contained in a thin hyoid membrane and forms about four fifths of the optic globe. [NIH] Vitro: Descriptive of an event or enzyme reaction under experimental investigation occurring outside a living organism. Parts of an organism or microorganism are used together with artificial substrates and/or conditions. [NIH] Vivo: Outside of or removed from the body of a living organism. [NIH] Vocational Education: Education for specific trades or occupations. [NIH] Void: To urinate, empty the bladder. [NIH] Volition: Voluntary activity without external compulsion. [NIH] Vulgaris: An affection of the skin, especially of the face, the back and the chest, due to chronic inflammation of the sebaceous glands and the hair follicles. [NIH] Windpipe: A rigid tube, 10 cm long, extending from the cricoid cartilage to the upper border of the fifth thoracic vertebra. [NIH] Withdrawal: 1. A pathological retreat from interpersonal contact and social involvement, as may occur in schizophrenia, depression, or schizoid avoidant and schizotypal personality disorders. 2. (DSM III-R) A substance-specific organic brain syndrome that follows the cessation of use or reduction in intake of a psychoactive substance that had been regularly used to induce a state of intoxication. [EU] Wound Healing: Restoration of integrity to traumatized tissue. [NIH] Xanthine: An urinary calculus. [NIH] Xanthine Oxidase: An iron-molybdenum flavoprotein containing FAD that oxidizes hypoxanthine, some other purines and pterins, and aldehydes. Deficiency of the enzyme, an autosomal recessive trait, causes xanthinuria. EC 1.1.3.22. [NIH] Xenograft: The cells of one species transplanted to another species. [NIH] Xerostomia: Decreased salivary flow. [NIH] X-ray: High-energy radiation used in low doses to diagnose diseases and in high doses to treat cancer. [NIH] X-ray therapy: The use of high-energy radiation from x-rays to kill cancer cells and shrink tumors. Radiation may come from a machine outside the body (external-beam radiation therapy) or from materials called radioisotopes. Radioisotopes produce radiation and can be placed in or near the tumor or in the area near cancer cells. This type of radiation treatment is called internal radiation therapy, implant radiation, interstitial radiation, or brachytherapy. Systemic radiation therapy uses a radioactive substance, such as a radiolabeled monoclonal antibody, that circulates throughout the body. X-ray therapy is also called radiation therapy, radiotherapy, and irradiation. [NIH] Yeasts: A general term for single-celled rounded fungi that reproduce by budding. Brewers' and bakers' yeasts are Saccharomyces cerevisiae; therapeutic dried yeast is dried yeast. [NIH]
Dictionary 689
Yersinia: A genus of gram-negative, facultatively anaerobic rod- to coccobacillus-shaped bacteria that occurs in a broad spectrum of habitats. [NIH] Yttrium: An element of the rare earth family of metals. It has the atomic symbol Y, atomic number 39, and atomic weight 88.91. In conjunction with other rare earths, yttrium is used as a phosphor in television receivers and is a component of the yttrium-aluminum garnet (YAG) lasers. [NIH] Zoster: A virus infection of the Gasserian ganglion and its nerve branches, characterized by discrete areas of vesiculation of the epithelium of the forehead, the nose, the eyelids, and the cornea together with subepithelial infiltration. [NIH] Zymogen: Inactive form of an enzyme which can then be converted to the active form, usually by excision of a polypeptide, e. g. trypsinogen is the zymogen of trypsin. [NIH]
690
INDEX 1 17-Hydroxyprogesterone, 579 A Abdomen, 591, 609, 612, 633, 638, 655, 675, 677, 680, 687 Abdominal, 37, 606, 619, 628, 652, 655, 684 Abdominal Pain, 37, 619, 655, 684 Aberrant, 43, 70, 579 Ablation, 62, 66, 579 Abortion, 660 Abrasion, 9 Abscess, 579, 622 Acanthocephala, 579, 624 Acceptor, 579, 637, 652 Acculturation, 45, 579 Acetaminophen, 10, 20, 27, 243, 505, 511, 535, 536, 550, 554, 568, 579 Acetylcholine, 579, 648 Acidosis, 579 Acne, 463 Acromion, 22, 579 Acrylamide, 579 Acrylonitrile, 579 Actin, 579, 646, 684 Activities of Daily Living, 5, 45, 550, 552, 557, 579, 607 Acupuncture Points, 213, 231, 579 Acute renal, 579, 625 Acyclovir, 580 Adaptability, 261, 580, 595 Adaptation, 5, 46, 260, 261, 645 Adenine, 580, 664 Adenocarcinoma, 195, 580 Adenosine, 33, 580, 656, 680 Adenosine Deaminase, 580 Adenovirus, 71, 74, 479, 483, 580 Adenylate Cyclase, 580 Adipose Tissue, 580, 638 Adjustment, 260, 262, 488 Adjuvant, 63, 67, 71, 76, 80, 82, 84, 192, 193, 197, 209, 213, 215, 216, 218, 220, 222, 224, 229, 231, 232, 283, 580, 619 Adolescence, 509, 580 Adrenal Cortex, 580, 602, 603, 661 Adrenal Glands, 580, 583 Adrenal Medulla, 580, 594, 613, 649 Adrenergic, 580, 613, 678 Adverse Effect, 6, 11, 18, 21, 36, 285, 512, 609, 673 Aerobic, 13, 52, 452, 453, 489, 511, 537, 552, 555, 556, 614, 646, 652
Aerobic Exercise, 13, 52, 453, 489, 537, 555, 556 Affinity, 51, 640, 666 Agar, 580, 657 Age Groups, 34, 580 Age of Onset, 580 Aged, 80 and Over, 580 Aggravation, 512 Agonists, 52, 192, 482, 580 A-HA, 219, 581 Alanine, 581 Albumin, 581, 657, 665, 679 Alcoholic Beverages, 614 Algorithms, 581, 590 Alkaline, 579, 581 Alkaloid, 226, 581, 593, 599, 645, 680 Alkylating Agents, 484, 581 Alleles, 10, 581, 626 Allergen, 581, 606 Allo, 581 Allogeneic, 62, 581, 622, 624 Allopurinol, 20, 553, 568, 581 Alopecia, 581, 604 Alpha-1, 581, 601 Alpha-helix, 581, 634 Alphavirus, 479, 581, 674 Alternative medicine, 17, 209, 212, 500 Alternative Splicing, 581, 662 Aluminum, 689 Alveolar Process, 581, 668 Alveolitis, 582 Amber, 582, 673 Ambulatory Care, 23, 582 Amebiasis, 582, 643 Ameliorated, 582 Ameliorating, 582 Amenorrhea, 582, 584 Amine, 582, 626 Amino Acid Sequence, 582, 584, 614, 620, 640 Amino Acid Substitution, 582 Amino-terminal, 32, 582 Ammonia, 580, 582, 685 Amplification, 58, 582 Ampulla, 582, 597 Amyloid, 9, 66, 481, 582, 668 Amyloidosis, 9, 481, 484, 485, 583 Amyotrophy, 556, 583 Anabolic, 41, 583, 607 Anaemia, 583, 641 Anaerobic, 583, 646, 670, 673, 676, 689 Anaesthesia, 583, 630
Index 691
Anal, 34, 46, 607, 612, 617, 638, 645 Analgesic, 209, 212, 229, 511, 579, 583, 607, 614, 628, 645, 646, 678 Analog, 31, 191, 283, 285, 580, 583, 628, 644 Analogous, 583, 608, 683 Analytes, 532, 583 Anaphylactic, 583, 657 Anaphylatoxins, 583, 600 Anaphylaxis, 51, 583 Anatomical, 53, 76, 554, 587, 611, 629, 638, 671 Androgens, 34, 580, 583, 603 Anecdotal report, 57, 583 Anemia, 476, 481, 583, 592, 618, 621, 645 Anergic, 583 Anergy, 583, 678 Anesthesia, 31, 514, 584, 603, 610, 661 Anesthetics, 584, 613 Angina, 584, 648 Angiogenesis, 35, 86, 285, 496, 584, 611, 641 Angiogenesis inhibitor, 35, 86, 584, 611 Animal model, 34, 53, 59, 67, 86, 195, 197, 535, 584 Anions, 581, 584, 633, 660, 678 Ankle, 27, 40, 463, 512, 532, 540, 551, 575, 686 Annealing, 584, 659 Anomalies, 584, 651, 680 Anorexia, 584, 619, 651 Anorexia Nervosa, 584 Antagonism, 468, 584, 680 Antecedent, 5 Anterior chamber, 290, 584, 633 Anterior Cruciate Ligament, 584 Anthralin, 478, 584 Antiallergic, 603 Antibacterial, 36, 661, 675 Antibiotic Prophylaxis, 502, 584 Antibody, 26, 32, 43, 66, 67, 68, 80, 86, 87, 192, 265, 267, 271, 275, 288, 532, 584, 585, 591, 599, 612, 613, 617, 623, 626, 628, 629, 630, 632, 634, 635, 641, 644, 665, 670, 673, 675, 688 Antibody Affinity, 32, 585 Antibody therapy, 585 Antibody-Dependent Cell Cytotoxicity, 585, 635 Anticoagulant, 585, 662 Antidote, 585, 636 Antifungal, 479, 617 Antigen-Antibody Complex, 585, 600, 618 Antigen-presenting cell, 585, 605 Anti-infective, 585, 593, 633 Anti-Inflammatory Agents, 33, 595, 603 Antilymphocyte Serum, 585, 639 Antimetabolite, 580, 585, 643
Antineoplastic, 581, 585, 603, 604, 619, 643, 652, 655 Antineoplastic Agents, 581, 585, 655 Antioxidant, 210, 214, 554, 585, 619, 652 Antipruritic, 585, 593 Antipyretic, 579, 585, 607, 646 Antirheumatic Agents, 478, 586 Antiviral, 491, 580, 619, 632 Anuria, 586, 635 Anus, 586, 599, 658 Anxiety, 58, 586 Aorta, 586, 628, 686 Aortitis, 481, 586 Apheresis, 552, 586 Apolipoproteins, 586, 637 Aponeurosis, 586, 619 Applicability, 502, 586 Aqueous, 220, 586, 604, 610, 633, 636, 638 Arachidonate 12-Lipoxygenase, 586, 638 Arachidonate 15-Lipoxygenase, 586, 638 Arachidonate Lipoxygenases, 586, 638 Arachidonic Acid, 193, 210, 586, 628, 636, 661 Arginase, 586 Arginine, 244, 583, 586, 648, 684 Arterial, 587, 592, 597, 602, 627, 636, 648, 662, 679, 687 Arteries, 586, 587, 591, 602, 628, 639, 643, 646, 664, 681 Arteriolar, 591 Arterioles, 586, 587, 591, 593 Arteriosclerosis, 587, 627, 669 Arteritis, 29, 587, 659 Artery, 278, 587, 588, 602, 610, 616, 653, 664, 679, 682 Arthralgia, 479, 587 Arthritis, Adjuvant, 483 Arthritis, Psoriatic, 274, 283, 284, 480, 536 Arthritis, Reactive, 287, 290, 536 Arthritis, Rheumatoid, 5, 234, 285, 287, 288, 290 Arthropathy, 5, 20, 41, 287, 504, 587 Arthroscopy, 18, 284, 554, 587 Arthrosis, 587 Articulation, 587, 642, 643 Aseptic, 4, 587 Aspartic, 587, 611 Aspartic Acid, 587 Aspartic Endopeptidases, 587, 611 Aspirate, 5, 587 Aspiration, 21, 277, 284, 478, 513, 587 Aspirin, 13, 18, 26, 243, 244, 461, 474, 508, 542, 544, 545, 550, 571 Assay, 38, 194, 587, 628, 665, 684 Asthenia, 583, 587 Asymptomatic, 20, 491, 553, 582, 587, 622
692 Arthritis
Atherogenic, 496, 587 Atrial, 587, 602, 683 Atrioventricular, 587, 602 Atrium, 587, 602, 683, 686 Atrophy, 587, 658 Attenuation, 587, 666 Atypical, 20, 479, 630 Auranofin, 461, 484, 587 Autacoids, 588, 630 Autoantibodies, 70, 83, 588 Autoantigens, 59, 62, 588 Autoimmune Hepatitis, 588 Autologous, 62, 213, 274, 275, 588, 624, 672 Autologous bone marrow transplantation, 588, 624 Autonomic, 556, 579, 588, 649, 655, 675 Autopsy, 46, 276, 588 Avidity, 585, 588 Axillary, 588, 591 Axillary Artery, 588, 591 Azithromycin, 36, 76, 588 B Back Pain, 468, 576 Backcross, 588 Bacteremia, 66, 83, 588, 670 Bacterial Infections, 482, 513, 588, 596, 623, 668 Bacterial Physiology, 588 Bactericidal, 588, 614 Bacteriophage, 588, 657, 671, 683, 687 Bacteriostatic, 588, 613 Bacterium, 536, 588, 625, 646 Bacteriuria, 588, 685 Balanitis, 481, 589 Basal Ganglia, 589, 592, 619 Base, 84, 539, 556, 580, 605, 617, 618, 620, 634, 635, 679, 684 Basement Membrane, 61, 589, 615, 635 Basophils, 589, 622, 636, 657 Baths, 214, 589 Behavior Therapy, 60, 589 Beta-pleated, 582, 589 Beta-Thromboglobulin, 589, 632 Bicycling, 13 Bifida, 589 Bilateral, 79, 589, 647 Bile, 589, 619, 625, 626, 638, 676, 679 Bile Acids, 589, 676, 679 Biliary, 589, 593, 597, 625 Bioassays, 44, 589 Bioavailability, 589 Biochemical, 17, 36, 41, 53, 192, 224, 284, 581, 585, 589, 617, 635, 636, 651, 673 Biochemical reactions, 284, 589 Biological response modifier, 552, 589, 590, 631
Biological therapy, 589, 623 Biomarkers, 50, 590 Biomechanics, 23, 26, 52, 590 Biomolecular, 590 Biophysics, 193, 590 Biopsy, 17, 276, 277, 284, 286, 479, 590, 654 Biopsy specimen, 479, 590 Biosynthesis, 21, 586, 590, 639, 662, 673, 674 Biotechnology, 65, 87, 475, 500, 521, 590 Biotransformation, 590, 655 Bladder, 590, 600, 619, 630, 645, 662, 685, 688 Blast phase, 590, 597 Blastomyces, 22, 590, 653 Blastomycosis, 479, 483, 590 Blind spot, 590 Blood Coagulation, 590, 591, 681 Blood Glucose, 455, 491, 591, 625, 631 Blood Platelets, 591, 658, 673, 680 Blood pressure, 277, 278, 512, 591, 594, 627, 644, 664 Blot, 591, 628 Blotting, Western, 591, 628 Body Fluids, 590, 591, 609, 684 Body Mass Index, 591, 651 Bone Marrow Cells, 62, 591, 623 Bone Resorption, 8, 79, 591 Bone scan, 591 Boron, 79, 201, 591 Boron Neutron Capture Therapy, 79, 591 Bowel, 82, 481, 485, 548, 591, 607, 630, 633, 655, 677, 684 Bowel Movement, 607, 677 Brachial, 278, 591, 641 Brachial Artery, 278, 591 Brachytherapy, 591, 632, 634, 665, 688 Bradykinin, 79, 82, 195, 591, 634, 648, 657 Brain Infarction, 592, 687 Brain Stem, 592, 687 Brain Stem Infarctions, 592, 687 Branch, 197, 610, 620, 629, 639, 650, 654, 655, 664, 675, 678, 680 Breakdown, 44, 509, 545, 606, 607, 619, 650, 672, 674 Bromelain, 17, 245, 592 Bronchi, 592, 613, 680, 682 Bronchial, 477, 592, 626, 680 Bronchitis, 455, 592, 597 Bronchoconstriction, 592, 657 Bronchoscopy, 274, 276, 592 Brucellosis, 483, 592 Buccal, 281, 592, 639, 677 Buffers, 38, 592 Bupivacaine, 592, 637 Bursitis, 465, 478, 482, 536, 592
Index 693
C Cadherins, 61, 592 Cadmium, 592 Cadmium Poisoning, 592 Caffeine, 664 Calcaneus, 592, 679 Calcitonin, 211, 215, 592 Calcium, 19, 48, 201, 272, 280, 546, 592, 593, 599, 614, 627, 636, 641, 648, 651, 653, 674, 684, 688 Calcium Carbonate, 280, 593 Calculi, 593, 622 Callus, 593, 650 Camphor, 208, 593 Campylobacter, 4, 536, 593 Canaliculus, 593 Candidiasis, 479, 593, 617 Candidosis, 593 Cannabidiol, 86, 593 Cannabis, 86, 593 Capillary, 591, 593, 638, 670, 687 Capillary Fragility, 593, 670 Capillary Permeability, 591, 593 Capsaicin, 17, 246, 554, 568, 593 Capsular, 18, 593 Capsules, 279, 550, 619 Carbohydrate, 593, 603, 621, 659 Carbon Dioxide, 593, 605, 617, 668 Carboxy, 594 Carcinogen, 594, 643 Carcinogenesis, 594, 596 Carcinogenic, 581, 594, 631, 650, 661, 676 Carcinoma, 594 Cardiac, 39, 64, 594, 602, 611, 613, 619, 637, 646, 676 Cardiology, 39, 594 Cardiorespiratory, 594 Cardiovascular disease, 55, 64, 594, 669 Carotene, 244, 594, 668 Carpal Tunnel Syndrome, 474, 594 Case series, 42, 594, 598 Caspase, 44, 594 Catabolism, 9, 594 Catalytic Domain, 594 Cataract, 593, 594 Catecholamine, 594 Catheter, 36, 273, 286, 594, 633 Catheterization, 594, 633 Cations, 595, 633 Cauda Equina, 595, 671 Caudal, 595, 628, 659 Causal, 595, 612, 625, 633, 669 Cavernous Sinus, 595, 668 Celecoxib, 10, 18, 26, 73, 246, 497, 506, 552, 595 Cell Adhesion, 592, 595
Cell Count, 478, 501, 595 Cell Cycle, 44, 595, 663 Cell Death, 43, 586, 595, 647 Cell Differentiation, 595, 674 Cell Division, 595, 623, 641, 672, 679 Cell Lineage, 483, 595 Cell membrane, 21, 595, 606, 614, 634, 656 Cell proliferation, 36, 61, 587, 595, 632, 674 Cell Size, 595, 617 Cell Survival, 595, 623 Cell Transplantation, 62, 595 Cellular adhesion, 9, 595 Cellulitis, 595 Cellulose, 596 Central Nervous System, 579, 581, 596, 597, 619, 621, 623, 637, 645, 650, 658, 673, 680 Central Nervous System Infections, 596, 623 Cerebral, 589, 592, 596, 613, 614, 649, 679, 680 Cerebral Palsy, 596 Cerebrospinal, 596, 673 Cerebrospinal fluid, 596, 673 Cerebrovascular, 39, 594, 596 Cerebrum, 596 Cervical, 16, 26, 27, 212, 484, 596, 641, 670 Cervix, 596, 617 Character, 596, 605, 621, 665 Chemokines, 596 Chemopreventive, 36, 596 Chemotactic Factors, 596, 600 Chemotaxis, 9, 54, 596 Chemotherapeutic agent, 268, 596 Chemotherapy, 247, 479, 596, 671 Chewing Gum, 3 Chimera, 596 Chin, 192, 197, 209, 212, 216, 223, 227, 231, 642 Chiropractic, 235, 596 Chlamydia, 4, 6, 74, 480, 536, 596 Cholecystokinin, 196, 597 Cholestasis, 207, 597 Cholesterol Esters, 597, 637 Chondrocytes, 9, 41, 48, 56, 217, 597, 616 Chondroitin sulfate, 9, 15, 17, 21, 201, 208, 218, 508, 509, 511, 554, 562, 597 Choroid, 597, 668 Chromatin, 586, 597, 675, 679 Chromosomal, 79, 582, 597, 643, 657, 669 Chromosome, 597, 623, 637, 643, 672 Chromosome Deletion, 597 Chronic Fatigue Syndrome, 597 Chronic granulocytic leukemia, 597 Chronic myelogenous leukemia, 590, 597 Chronic Obstructive Pulmonary Disease, 597 Chronic phase, 53, 597 Chylomicrons, 597, 637, 638
694 Arthritis
Ciliary, 597, 633, 673 Ciliary Body, 597, 633, 673 Circadian, 598 CIS, 598, 668 Clavicle, 22, 598 Climacteric, 598 Clinical Medicine, 598, 660 Clinical Protocols, 59, 598 Clinical study, 231, 268, 598, 602, 685 Clone, 598 Cloning, 265, 590, 598 Clot Retraction, 598, 657 Coagulation, 73, 590, 598, 625, 635, 657, 681 Cod Liver Oil, 214, 598, 611 Codon, 598, 620 Coenzyme, 598, 639, 674 Cofactor, 598, 662, 681 Cognitive behavior therapy, 60, 598 Cohort Studies, 599, 612 Colchicine, 20, 553, 570, 599 Coliphages, 588, 599 Colitis, 599 Collagen, 9, 32, 33, 36, 49, 51, 54, 59, 62, 66, 67, 68, 69, 71, 73, 74, 76, 77, 78, 79, 80, 81, 85, 86, 192, 193, 211, 215, 216, 227, 228, 231, 265, 282, 290, 483, 572, 582, 589, 592, 599, 601, 615, 616, 619, 641, 651, 658, 661, 671 Collagen disease, 599, 671 Collagenases, 599 Collagenous Colitis, 599 Collapse, 583, 599 College Admission Test, 543, 599 Colon, 599, 609, 630, 636, 684 Combination chemotherapy, 479, 599 Combination Therapy, 35, 285, 510, 599, 614 Complement, 190, 583, 585, 599, 600, 620, 640, 657 Complementary and alternative medicine, 17, 207, 208, 232, 258, 600 Complementary medicine, 208, 600 Complementation, 600 Complete remission, 600, 667 Compliance, 5, 18, 45, 265, 557, 600 Compress, 600, 682 Computational Biology, 521, 600 Computed tomography, 272, 479, 600 Computerized axial tomography, 600 Computerized tomography, 600 Conception, 601, 616, 660 Concomitant, 282, 601 Cones, 601, 668 Confidence Intervals, 7, 601 Confounding, 28, 601 Congestion, 601, 613 Conjugated, 601, 604, 618
Conjunctiva, 601, 631, 634, 671 Conjunctivitis, 480, 557, 601 Connective Tissue Cells, 601 Connective Tissue Diseases, 601 Connexin 43, 48, 601 Consciousness, 583, 601, 605, 608, 663, 679 Constipation, 601, 655 Consultation, 601 Consumption, 601, 619, 649, 652 Contact dermatitis, 601, 682 Contracture, 454, 601 Contraindications, ii, 8, 21, 601 Contralateral, 601 Control group, 25, 46, 58, 477, 557, 601, 660 Controlled clinical trial, 36, 42, 52, 57, 58, 502, 509, 602, 666 Controlled study, 11, 214, 221, 228, 268, 283, 602 Conventional therapy, 481, 602 Conventional treatment, 18, 545, 602 Coordination, 602, 645 Cor, 20, 602 Cornea, 584, 602, 622, 634, 671, 677, 689 Corneum, 602, 606, 612 Coronary, 46, 594, 602, 643, 646, 648 Coronary heart disease, 46, 594, 602 Coronary Thrombosis, 602, 643, 646 Corpus, 602, 639, 661, 688 Corpuscle, 602, 613 Cortex, 238, 241, 602, 614, 651 Cortical, 602 Corticosteroid, 21, 25, 26, 64, 192, 512, 536, 602, 660, 676 Cortisol, 262, 498, 581, 603 Cortisone, 3, 550, 603, 660 Cowpox, 603, 685 Cowpox Virus, 603, 685 Crabs, 506, 603 Cranial, 16, 603, 615, 623, 650, 655 Craniocerebral Trauma, 603, 623 Criterion, 603 Crossing-over, 603, 666 Cross-Sectional Studies, 603, 612 Cryptococcosis, 479, 483, 603 Cryptosporidiosis, 491, 588, 603 Curare, 603, 645 Curative, 57, 603, 670, 680 Cutaneous, 22, 590, 593, 601, 603, 622, 639, 653, 676, 685 Cyanogen Bromide, 603 Cyclic, 56, 76, 580, 603, 623, 648, 662, 680 Cyclophosphamide, 26, 57, 274, 275, 569, 604 Cyclosporine, 11, 22, 542, 569, 604 Cyst, 587, 604 Cysteine, 44, 596, 604, 611, 651, 678
Index 695
Cysteine Endopeptidases, 604, 611 Cystine, 604 Cytochrome, 604, 668 Cytochrome A, 604 Cytochrome b, 604, 668 Cytomegalovirus, 483, 604 Cytoplasm, 586, 589, 595, 604, 612, 670, 679 Cytoskeletal Proteins, 604 Cytoskeleton, 604, 643 Cytotoxic, 26, 476, 593, 604, 629, 632, 640, 665, 674 Cytotoxicity, 604 Cytotoxins, 605 D Databases, Bibliographic, 521, 605 Day Care, 77, 605 Decarboxylation, 605, 626 Decision Making, 543, 605 Defense Mechanisms, 483, 605 Deglutition, 605, 677 Dehydroepiandrosterone, 17, 75, 248, 605 Deletion, 44, 80, 586, 605 Delivery of Health Care, 605, 624 Delusion, 605, 671 Dementia, 4, 605 Denaturation, 605, 659 Dendrites, 605, 648 Dendritic, 59, 605, 641 Dendritic cell, 59, 605 Dental Care, 29, 533 Dental Records, 3, 605 Depolarization, 606, 674 Dermal, 606, 637 Dermatitis, 606 Dermatologic Agents, 606 Dermatology, 606 Dermatophytosis, 606 Dermatosis, 606 Dermis, 606, 643, 683 Desensitization, 51, 606, 629 Desquamation, 606, 634 Detergents, 617 Deuterium, 606 Dexterity, 45, 606 Diabetes Mellitus, 606, 621, 625, 669 Diabetic Ketoacidosis, 491, 606 Diagnostic Imaging, 11, 545, 606 Diagnostic procedure, 293, 500, 538, 606 Diaphragm, 606, 658 Diarrhea, 11, 37, 582, 603, 606 Diarrhoea, 606, 619 Diastolic, 606, 627 Diathermy, 522, 606 Diclofenac, 18, 248, 607 Diffusion, 593, 607, 630
Digestion, 14, 589, 591, 607, 609, 633, 638, 654, 677 Digestive system, 292, 607 Digestive tract, 536, 607, 674 Dihydrotestosterone, 607, 667 Dihydroxy, 607, 670 Dilatation, 607, 660, 686 Dilate, 278, 607 Dilation, 591, 607, 686 Dilator, 607, 648 Dimerization, 195, 607 Diploid, 600, 607 Direct, iii, 28, 44, 71, 72, 567, 598, 617, 620, 653, 667 Disabled Persons, 38, 607 Discrete, 34, 480, 607, 637, 638, 680, 689 Discriminant Analysis, 607 Discrimination, 607 Disease Progression, 12, 20, 28, 36, 52, 544, 607 Disease Susceptibility, 9, 48, 607 Disinfectant, 607, 614 Dislocation, 22, 484, 493, 607, 676 Disparity, 607 Dissociation, 607 Distal, 71, 542, 556, 608, 655, 663 Diuresis, 608, 680 Diuretic, 30, 608, 678 Dizziness, 3, 37, 608, 687 Dominance, 608 Dorsal, 52, 79, 608, 613, 659, 675 Dorsum, 608, 619 Double-blinded, 608 Doxycycline, 36, 608 Drive, ii, vii, 32, 37, 189, 452, 455, 513, 608, 637 Drosophila, 608 Drug Design, 572, 608 Drug Interactions, 571, 572, 608 Drug Tolerance, 608, 682 Drug Toxicity, 609 Duct, 582, 593, 594, 609, 614, 639, 670, 676 Duodenal Ulcer, 487, 609 Duodenum, 589, 609, 619, 677 Dura mater, 595, 609, 642, 652 Dyes, 582, 589, 609, 618 Dysentery, 582, 609, 673 Dyslipidemia, 72, 609 Dysmenorrhea, 10, 609, 646 Dyspareunia, 609, 614 Dyspepsia, 11, 609 Dysphonia, 609 Dysplasia, 213, 609 Dyspnea, 609, 664 Dystrophy, 609
696 Arthritis
E Eating Disorders, 609 Edema, 11, 18, 19, 601, 609, 647 Educational Status, 487, 609 Effector, 35, 48, 68, 70, 74, 579, 585, 599, 609, 635 Effector cell, 585, 609, 635 Effusion, 609, 679 Ejaculation, 609, 672 Elastic, 13, 511, 609, 621, 675, 682 Elasticity, 587, 610 Elastin, 599, 601, 610, 615 Elective, 610 Electroacupuncture, 610 Electrocardiogram, 277, 278, 610 Electrocoagulation, 598, 610 Electrolyte, 603, 610, 635, 644 Electrons, 585, 610, 633, 652, 665 Electrophoresis, 87, 579, 610 Electrophysiological, 53, 610 Embolism, 610 Embolus, 610, 630 Embryo, 595, 610, 630, 660, 676 Embryo Transfer, 610, 660 Emollient, 610, 649 Emphysema, 455, 597, 610 Empiric, 58, 610 Empirical, 56, 610 Emulsion, 610, 617 Enamel, 611, 634 Encephalitis, 69, 75, 78, 79, 81, 84, 87, 265, 611 Encephalitis, Viral, 611 Encephalomyelitis, 611 Endemic, 611 Endocarditis, 22, 593, 611, 613, 622 Endocardium, 611 Endogenous, 20, 49, 73, 588, 611, 662, 683, 684 Endometrial, 195, 611 Endometrium, 611 Endopeptidases, 32, 587, 604, 611, 643, 654, 662, 673 Endostatin, 35, 498, 611 Endothelial cell, 14, 35, 611, 616, 632, 681 Endothelium, 61, 611, 612, 648, 657 Endothelium, Lymphatic, 611 Endothelium, Vascular, 611 Endothelium-derived, 612, 648 Endotoxin, 33, 612, 648, 684 Enteropeptidase, 612, 684 Environmental Health, 520, 522, 612 Enzymatic, 17, 582, 594, 600, 612, 616, 626, 659, 668 Enzyme-Linked Immunosorbent Assay, 69, 79, 84, 612
Eosinophil, 612, 623 Eosinophilia, 612, 615 Eosinophilic, 612, 615, 626 Epidemic, 8, 612 Epidemiologic Studies, 33, 612 Epidemiological, 612 Epidermal, 612, 634, 637, 641 Epidermal Growth Factor, 612 Epidermis, 602, 606, 612, 626, 634, 637, 664 Epidermomycosis, 606, 612 Epigastric, 612, 652 Epinephrine, 580, 613, 648, 649, 684 Epiphyseal, 613 Episcleritis, 613, 671 Epithelial, 61, 580, 597, 606, 612, 613, 614, 635 Epithelial Cells, 612, 613, 635 Epithelium, 61, 589, 611, 613, 619, 633, 634, 689 Epoprostenol, 613, 628 Equipment and Supplies, 491, 613 Ergometry, 613 Erysipeloid, 613, 669 Erythema, 601, 613, 685 Erythema Multiforme, 613 Erythrocyte Membrane, 613 Erythrocytes, 476, 583, 591, 613, 625, 652, 667 Erythromycin, 76, 588, 613 Escalation, 613 Esophagus, 607, 613, 624, 656, 667, 677 Estrogen, 7, 23, 216, 487, 614, 661 Estrogen receptor, 7, 614 Estrogen Replacement Therapy, 216, 487, 614 Ethanol, 228, 614, 616 Ethnic Groups, 614 Etidronate, 614 Etodolac, 10, 249, 614 Etretinate, 11, 614 Eukaryotic Cells, 604, 614, 629, 650 Evoke, 614, 677 Excitation, 614, 617, 648 Excrete, 586, 614, 635, 668 Exercise Test, 274, 614 Exocrine, 597, 614, 652 Exocytosis, 614 Exogenous, 8, 46, 590, 611, 614, 662, 684 Exon, 581, 614 Extensor, 614, 663 External-beam radiation, 615, 634, 665, 688 Extracellular, 32, 41, 48, 582, 601, 615, 616, 641, 651 Extracellular Matrix, 32, 601, 615, 616, 641, 651 Extracellular Matrix Proteins, 615, 641 Extracellular Space, 615
Index 697
Extraction, 16, 44, 615 Extravasation, 52, 82, 615 Extremity, 27, 45, 615, 636, 641 Eye Infections, 580, 615 F Facial, 615, 653 Facial Nerve, 615, 653 Family Planning, 521, 615 Family Practice, 60, 217, 227, 615 Fasciitis, 26, 195, 615 Fatigue, 37, 269, 278, 451, 452, 455, 473, 475, 506, 597, 615, 624 Fatty acids, 17, 25, 190, 205, 581, 606, 615, 638, 661 Femoral, 616 Femoral Artery, 616 Femur, 503, 584, 616, 681 Fermentation, 616, 671 Fertilization in Vitro, 616, 660 Fetus, 616, 628, 676, 677, 685 Feverfew, 17, 250, 256, 616 Fibril, 38, 616 Fibrin, 193, 590, 598, 616, 655, 657, 681 Fibrinogen, 616, 657, 673 Fibrinolysis, 73, 616 Fibrinolytic, 616, 635 Fibroblast Growth Factor, 616 Fibronectin, 616 Fibrosarcoma, 615, 616 Fibrosis, 271, 274, 276, 486, 601, 616, 664, 671 Fibula, 616, 681 Film Dosimetry, 616 Fine-needle aspiration, 616, 647 Fish Oils, 190, 230, 617 Fistula, 617, 619 Fixation, 617 Flatus, 617, 619 Flexion, 556, 617, 623 Flexor, 614, 617, 637, 680 Flow Cytometry, 617 Fluconazole, 617 Fludarabine, 283, 285, 617 Fluorescein Angiography, 291, 617 Fluorescence, 617, 618 Fluorescent Antibody Technique, 617, 618 Fluorescent Dyes, 617, 618 Fluoroimmunoassay, 618 Focus Groups, 523, 618 Folate, 56, 194, 200, 202, 218, 618 Fold, 47, 618 Folic Acid, 199, 200, 202, 219, 220, 272, 283, 618, 636 Folliculitis, 584, 618 Food Technology, 190, 618 Forearm, 591, 615, 618, 641, 684
Fovea, 617, 618 Frameshift, 618, 684 Frameshift Mutation, 618, 684 Fraud, 561, 618 Free Radicals, 515, 585, 607, 618 Freeze-dried, 216, 618 Friction, 22, 618, 639 Fructose, 618, 621 Fundus, 617, 619 Fungi, 483, 590, 615, 623, 634, 643, 681, 688 Fungus, 593, 603, 646 G Gadolinium, 272, 286, 619 Gait, 52, 619 Gallate, 217, 619 Gallbladder, 589, 597, 607, 619 Gamma-interferon, 619, 631 Ganglia, 579, 619, 647, 655, 675 Ganglion, 79, 619, 650, 689 Gas, 593, 607, 617, 619, 648, 666, 673, 686 Gastric, 612, 619, 624, 626, 644, 650, 654 Gastric Acid, 619, 644, 650 Gastric Juices, 619, 654 Gastric Mucosa, 619, 654 Gastrin, 619, 626 Gastroduodenal, 619 Gastroenteritis, 480, 619, 670 Gastrointestinal tract, 5, 614, 619, 637, 673, 684 Gelatin, 619, 621, 680 Gene Expression, 37, 51, 53, 54, 74, 503, 620 Gene Therapy, 35, 74, 228, 265, 452, 554, 580, 620 General practitioner, 620 Genetic Code, 620, 649 Genetic Engineering, 590, 598, 620 Genetic Markers, 271, 620 Genetic testing, 620, 659 Genital, 620 Genitourinary, 5, 504, 558, 620 Genomics, 620 Genotype, 45, 620, 656 Gestation, 288, 620, 655, 676 Giardiasis, 620, 643 Ginger, 215, 221, 250, 257, 620 Ginseng, 255, 620 Gland, 580, 603, 620, 639, 641, 652, 653, 657, 662, 672, 677, 678, 681 Glomerular, 621, 635, 668 Glomerulus, 621, 647 Glucocorticoid, 30, 81, 194, 502, 569, 621, 660 Glucose, 455, 491, 512, 591, 596, 606, 621, 625, 631, 666, 671 Glucose Intolerance, 606, 621 Glucose tolerance, 512, 621
698 Arthritis
Glucose Tolerance Test, 621 Glucose-6-Phosphate Isomerase, 621 Glucuronic Acid, 621, 625 Glutamate, 52, 621 Glutamic Acid, 618, 621, 648, 661 Glutathione Peroxidase, 621, 672 Gluten, 205, 209, 621 Glycine, 71, 213, 582, 621, 648, 673 Glycogen, 597, 621 Glycoprotein, 79, 87, 616, 621, 622, 635, 640, 651, 655, 668, 681, 684 Glycosaminoglycan, 597, 621 Goats, 81, 622 Gold Compounds, 26, 569, 622 Gonad, 622, 680 Gonadal, 622, 676 Gonorrhea, 622 Gonorrhoea, 482, 622 Gout, 5, 19, 21, 30, 48, 459, 462, 465, 472, 492, 505, 513, 514, 532, 536, 548, 549, 550, 553, 555, 556, 599, 622, 646, 678, 682, 685 Governing Board, 622, 660 Government Agencies, 622, 660 Grade, 274, 487, 622 Graft Rejection, 622, 629 Grafting, 622 Gram-negative, 597, 622, 646, 670, 673, 689 Gram-positive, 478, 622, 646, 676, 677 Granule, 622, 670 Granulocyte, 68, 75, 622, 632 Granulocyte-Macrophage Colony-Stimulating Factor, 68, 75, 622 Granuloma, 623, 653 Granulomatous Disease, Chronic, 623, 668 Grasses, 15, 618, 623 Gravis, 623 Growth factors, 48, 623 Guanine, 623, 664 Guanylate Cyclase, 623, 648 H Habitat, 623, 646 Hair follicles, 606, 618, 623, 688 Half-Life, 623, 628 Hallux Rigidus, 623 Hammer, 551, 623, 651 Hand Deformities, 454, 623 Haploid, 623 Haplotypes, 48, 623 Haptens, 623, 665 Headache, 37, 83, 278, 623, 631, 658 Headache Disorders, 623 Health Behavior, 624 Health Care Costs, 523, 624 Health Education, 557, 624 Health Expenditures, 624
Health Promotion, 524, 556, 563, 624 Health Services, 558, 605, 624 Health Surveys, 624 Heart attack, 506, 594, 624 Heart failure, 624, 664 Heartburn, 10, 624 Helminths, 479, 624, 647 Hematogenous, 513, 624 Hematopoiesis, 624 Hematopoietic Stem Cell Transplantation, 624 Heme, 604, 624, 652 Hemodialysis, 593, 624, 635 Hemoglobin, 583, 613, 624, 625 Hemoglobinopathies, 620, 625 Hemolysis, 613, 625 Hemolytic, 66, 476, 615, 621, 625 Hemorrhage, 603, 610, 623, 625, 656, 677 Hemosiderin, 625 Hemosiderosis, 625 Hemostasis, 30, 625, 673 Heparin, 625, 658 Hepatic, 581, 621, 625, 674 Hepatitis, 479, 483, 625, 630 Hepatobiliary, 625 Hepatocyte, 597, 625 Hepatotoxicity, 19, 625 Hereditary, 281, 601, 622, 625 Heredity, 47, 538, 544, 548, 619, 620, 625 Herpes, 483, 580, 625 Herpes Zoster, 625 Hesperidin, 625 Heterogeneity, 16, 34, 78, 82, 626 Heterotrophic, 626 Heterozygotes, 608, 626 Histamine, 210, 216, 569, 583, 626 Histidine, 251, 626 Homeostasis, 73, 85, 626 Homodimer, 626, 683 Homologous, 262, 581, 603, 620, 626, 632, 672, 679 Homozygotes, 608, 626 Hormonal, 7, 19, 288, 290, 587, 603, 614, 626, 688 Hormone Replacement Therapy, 554, 626 Horny layer, 612, 626, 634 Horseradish Peroxidase, 612, 626 Human Genome Project, 626 Humoral, 265, 486, 622, 626, 681 Humour, 626 Hyalin, 626 Hybrid, 588, 598, 626 Hybridomas, 59, 626, 632 Hydration, 579, 627 Hydroalcoholic, 227, 627 Hydrogel, 627
Index 699
Hydrogen, 579, 582, 592, 593, 605, 606, 615, 621, 637, 644, 648, 652, 663, 678 Hydrogen Peroxide, 621, 637, 678 Hydrolysis, 580, 586, 587, 590, 627, 654, 656, 659, 663, 684 Hydrophilic, 627 Hydrophobic, 585, 627, 637 Hydroxylysine, 599, 627 Hydroxyproline, 582, 599, 627 Hyperaemia, 601, 627 Hypercalcemia, 614, 627 Hypercholesterolemia, 609, 627 Hyperglycemia, 455, 627 Hyperlipidemia, 46, 609, 627 Hyperlipoproteinemia, 627, 638 Hyperostosis, 556, 627 Hyperplasia, 50, 80, 485, 627, 637 Hypersensitivity, 581, 583, 606, 612, 627, 636, 669 Hypertension, 10, 477, 487, 594, 623, 627, 669 Hyperthermia, 606, 627 Hyperthyroidism, 627 Hypertriglyceridemia, 609, 627 Hypertrophy, 602, 627, 683 Hyperuricemia, 20, 553, 622, 627 Hypoglycemia, 455, 491, 627 Hypothalamic, 627 Hypothalamus, 627, 628, 657 Hypoxia, 87, 628 Hypoxic, 628, 643 I Ibuprofen, 10, 18, 25, 191, 252, 506, 568, 628 Id, 198, 233, 558, 559, 564, 628, 642 Ileus, 628 Iliac Artery, 616, 628 Iloprost, 191, 628 Imaging procedures, 286, 628 Immersion, 589, 628 Immune function, 628, 629, 683 Immune Sera, 628 Immune Tolerance, 282, 628 Immunization, 43, 628, 629 Immunoassay, 612, 628 Immunoblotting, 38, 628 Immunocompromised, 629 Immunodeficiency, 491, 629 Immunogenetics, 484, 629 Immunogenic, 629, 665 Immunoglobulin, 6, 86, 479, 584, 618, 629, 644 Immunohistochemistry, 53, 629 Immunologic, 20, 22, 62, 284, 290, 477, 596, 628, 629, 640, 665 Immunologic Factors, 284, 477, 629 Immunosuppressant, 581, 629, 643
Immunosuppression, 629, 639, 650 Immunosuppressive, 22, 23, 26, 30, 31, 285, 536, 604, 621, 629, 671, 679 Immunosuppressive Agents, 26, 629, 671 Immunosuppressive therapy, 22, 629 Immunotherapy, 62, 84, 590, 606, 629 Immunotoxin, 629 Impairment, 45, 58, 597, 609, 615, 629, 642, 661 Implant radiation, 629, 632, 634, 665, 688 Impotence, 629 In situ, 629 In Situ Hybridization, 629 Incidental, 20, 630 Incision, 507, 630, 633 Incontinence, 16, 576, 630 Incubation, 630, 636 Incubation period, 630, 636 Indolent, 479, 630 Indomethacin, 252, 553, 630 Infancy, 630, 670 Infant, Newborn, 580, 630 Infantile, 630, 659 Infarction, 64, 463, 592, 630 Infectious Mononucleosis, 630, 644 Infiltration, 6, 14, 37, 59, 630, 661, 689 Inflammatory bowel disease, 480, 481, 485, 486, 630 Influenza, 631 Informed Consent, 63, 631 Infusion, 37, 272, 273, 631 Ingestion, 592, 621, 631, 658 Inhalation, 568, 631, 658, 674, 676 Initiation, 9, 29, 45, 53, 282, 482, 501, 631, 683 Initiator, 631, 632 Inlay, 631, 668 Inorganic, 48, 622, 631 Inpatients, 631 Insight, 468, 631 Insulator, 631, 645 Insulin, 48, 69, 72, 75, 278, 455, 491, 606, 621, 631, 635, 652 Insulin-dependent diabetes mellitus, 631 Insulin-like, 48, 75, 631 Intensive Care, 631 Intercellular Adhesion Molecule-1, 631 Interferon, 40, 71, 73, 74, 573, 619, 631, 632 Interferon-alpha, 631 Interleukin-10, 26, 72, 74, 82, 632 Interleukin-11, 82, 632 Interleukin-12, 66, 632 Interleukin-17, 74, 632 Interleukin-18, 632 Interleukin-2, 265, 632 Interleukin-4, 73, 74, 77, 81, 228, 632
700 Arthritis
Interleukin-6, 83, 632 Interleukin-8, 632 Interleukins, 629, 632 Intermittent, 32, 283, 508, 632 Internal radiation, 632, 634, 665, 688 Interpersonal Relations, 540, 633 Interstitial, 591, 615, 632, 633, 634, 647, 668, 688 Intervention Studies, 633 Intervertebral, 633, 639, 665, 671, 676 Intervertebral Disk Displacement, 633, 639, 665, 671 Intestinal, 4, 194, 593, 594, 597, 603, 612, 621, 633, 673, 688 Intestinal Mucosa, 597, 633 Intestine, 591, 633, 636 Intoxication, 633, 688 Intraindividual, 4, 633 Intramuscular, 25, 28, 40, 196, 633, 653 Intramuscular injection, 40, 633 Intravenous, 57, 268, 572, 617, 631, 633, 653 Intrinsic, 589, 633 Intubation, 594, 633 Invasive, 36, 38, 40, 57, 66, 288, 628, 633, 640 Involuntary, 16, 633, 646, 675 Iodine, 633 Ions, 592, 607, 610, 633, 644 Iridocyclitis, 13, 192, 633 Iris, 29, 584, 602, 633, 664 Iritis, 29, 633 Irradiation, 274, 275, 591, 634, 688 Ischemia, 587, 634 Isoenzymes, 634 Isopropyl, 634 Isotonic, 8, 13, 634, 644 J Joint Capsule, 545, 634, 679 Joint Instability, 454, 634 K Kallidin, 591, 634 Kb, 520, 634 Keratin, 634 Keratinocytes, 632, 634 Keratoconjunctivitis, 634, 673 Keratoconjunctivitis Sicca, 634, 673 Keratolytic, 478, 634 Keratolytic Agents, 478, 634 Ketone Bodies, 606, 635 Ketosis, 606, 635 Kidney Disease, 292, 520, 635 Kidney Failure, 30, 491, 635 Kidney Failure, Acute, 635 Kidney Failure, Chronic, 635 Kidney stone, 635, 668, 685 Killer Cells, 66, 635
Kinetics, 50, 263, 635 Kringles, 86, 635 L Labile, 599, 635 Labyrinth, 635, 661 Lacrimal, 593, 615, 634, 635, 673 Lactation, 635, 661 Lag, 45, 635 Laminin, 589, 615, 635 Large Intestine, 607, 633, 636, 667, 674 Latency, 4, 636 Latent, 636, 660 Lavage, 7, 31, 636 Least-Squares Analysis, 636, 667 Lectin, 636, 642 Leg Ulcer, 636 Lens, 593, 594, 636, 688 Lentivirus, 75, 636 Leprosy, 210, 636, 646 Lesion, 288, 590, 623, 636, 638, 672, 673, 681, 684 Leucovorin, 31, 636 Leukapheresis, 277, 586, 636 Leukemia, 597, 620, 636 Leukocytes, 224, 589, 591, 596, 630, 631, 632, 636, 652, 684 Leukopenia, 491, 636 Leukotrienes, 51, 586, 636 Libido, 583, 637 Library Services, 637 Lichen Planus, 614, 637 Lidocaine, 637 Life cycle, 637 Life Expectancy, 40, 55, 637 Ligament, 463, 484, 584, 637, 662, 676 Ligands, 33, 224, 637 Ligation, 637 Likelihood Functions, 637, 667 Linear Models, 637, 667 Linkage, 79, 504, 620, 637 Lip, 17, 637 Lipid, 84, 192, 214, 496, 586, 587, 593, 631, 637, 645, 652, 684 Lipid Peroxidation, 637, 652 Lipopolysaccharide, 622, 637 Lipoprotein, 69, 609, 622, 637, 638, 639 Lipoprotein Lipase, 638 Liposomal, 228, 638 Liposomes, 79, 638 Lipoxygenase, 213, 586, 636, 638 Liquor, 638, 664 Liver scan, 638 Living will, 638 Localization, 51, 61, 78, 629, 638 Locomotion, 638 Logistic Models, 638, 667
Index 701
Longitudinal study, 638 Lovastatin, 638, 674 Low Back Pain, 213, 453, 487, 558, 639 Low-density lipoprotein, 609, 637, 638, 639 Lubricants, 639 Lubrication, 492, 639 Lumbago, 639 Lumbar, 595, 633, 639 Lung Transplantation, 276, 639 Lutein Cells, 639, 661 Luxation, 607, 639 Lymph, 12, 82, 481, 588, 596, 602, 611, 626, 630, 639, 653, 670, 678 Lymph node, 12, 481, 588, 596, 639, 653, 670 Lymphatic, 611, 630, 639, 642, 670, 674, 675, 681 Lymphatic system, 639, 670, 674, 675, 681 Lymphocyte, 51, 61, 585, 629, 635, 639, 640, 641 Lymphocyte Depletion, 629, 639 Lymphocyte Subsets, 639 Lymphocytic, 14, 597, 640 Lymphoid, 584, 640 Lymphokine, 640 Lymphoma, 72, 640 Lymphopenia, 640 Lymphoproliferative, 7, 640 Lymphotoxin, 640 Lysine, 627, 640, 684 Lytic, 640, 673, 687 M Macrophage Activation, 640 Macrophage Colony-Stimulating Factor, 640 Malaise, 592, 640 Malformation, 514, 640 Malignancy, 5, 61, 640 Malignant, 580, 585, 615, 640, 645, 647, 665, 671 Malignant tumor, 640, 645 Malnutrition, 581, 587, 641 Malondialdehyde, 641 Mammary, 638, 641 Mandible, 581, 641, 668 Marital Status, 488, 641 Mastication, 641, 677 Mastitis, 641 Meat, 6, 592, 613, 641 Medial, 26, 587, 641, 681, 684, 687 Median Nerve, 594, 641 Mediate, 51, 57, 61, 288, 635, 641 Mediator, 53, 224, 278, 597, 632, 641, 658, 673 Medical Records, 269, 281, 454, 492, 641, 669 Medical Staff, 608, 641 MEDLINE, 15, 28, 29, 521, 641
Megaloblastic, 618, 641 Meiosis, 641, 643, 679 Melanin, 633, 641, 656, 684 Melanocytes, 641 Melanoma, 591, 641 Membrane Proteins, 638, 642, 663 Memory, 4, 70, 605, 642 Menarche, 642 Meninges, 596, 603, 609, 642 Meningitis, 14, 617, 622, 642, 656 Menopause, 642, 659, 660 Menstruation, 582, 609, 642 Mental, v, 31, 60, 292, 453, 520, 525, 605, 607, 608, 615, 642, 656, 663, 664, 667, 685 Mental Disorders, 292, 642, 656, 663 Mental Health, v, 31, 60, 292, 520, 525, 642, 664 Mental Processes, 608, 642, 663 Mentors, 55, 642 Mercury, 617, 642 Mesenchymal, 612, 622, 640, 642 Meta-Analysis, 225, 227, 642 Metabolic acidosis, 606, 642 Metabolic disorder, 622, 642 Metabolite, 590, 636, 638, 642, 656 Metacarpophalangeal Joint, 642 Metalloendopeptidases, 611, 643 Metastasis, 641, 643 Metatarsophalangeal Joint, 11, 623, 643 Methyltransferase, 643 Metronidazole, 643 MI, 46, 87, 540, 541, 542, 550, 557, 578, 643 Mice Minute Virus, 643, 653 Microbe, 643, 682 Microgram, 618, 643 Micronuclei, 194, 643 Micronutrients, 643 Microorganism, 22, 478, 501, 504, 598, 643, 653, 688 Microscopy, 51, 478, 579, 589, 618, 626, 643 Microtubules, 643, 652 Migrans, 643 Millimeter, 29, 231, 643 Mineralization, 643, 651 Mineralocorticoids, 580, 603, 643 Minocycline, 30, 644 Minority Groups, 644 Misoprostol, 282, 644 Mitochondrial Swelling, 644, 647 Mobility, 5, 8, 13, 454, 455, 468, 489, 549, 644 Mobilization, 536, 537, 644 Modeling, 504, 608, 644 Modification, 502, 507, 582, 620, 644, 664, 665 Modulator, 644
702 Arthritis
Molecular Structure, 644, 684 Monitor, 50, 644, 649, 687 Monoclonal antibodies, 26, 68, 71, 486, 628, 644, 670 Monocyte, 25, 61, 585, 640, 644 Mononuclear, 476, 615, 623, 630, 640, 644, 684 Mononucleosis, 14, 644 Monotherapy, 6, 63, 482, 645 Morphine, 645, 646 Morphological, 193, 610, 641, 645 Motility, 630, 645, 673 Motion Sickness, 645, 647 Motor nerve, 645 Mucinous, 619, 645 Mucocutaneous, 481, 645 Mucosa, 619, 639, 645, 661, 677 Multidrug resistance, 645, 655 Multigene Family, 645 Multiple Myeloma, 645 Multiple sclerosis, 14, 645 Multivariate Analysis, 645 Muscle relaxant, 453, 645 Muscle tension, 455, 511, 645 Muscular Dystrophies, 609, 645 Musculoskeletal Diseases, 55, 284, 455, 645 Musculoskeletal System, 502, 555, 645, 651 Mutagenesis, 645 Mutagenic, 581, 645 Mutagens, 618, 645 Myalgia, 465, 479, 631, 645 Mycobacterium, 71, 479, 491, 588, 636, 646, 684 Mycobacterium avium, 491, 588, 646 Mycobacterium leprae, 479, 636, 646 Mycobacterium tuberculosis, 71, 479, 646 Mycoplasma, 70, 73, 75, 76, 79, 81, 596, 646 Mycosis, 646, 653 Myelin, 645, 646, 672 Myelogenous, 646 Myeloid Cells, 53, 646 Myocardial infarction, 64, 589, 602, 643, 646 Myocardium, 643, 646 Myopathy, 512, 646 Myosin, 646, 684 Myositis, 646 N Naive, 62, 646 Naproxen, 203, 506, 646 Narcosis, 646 Narcotic, 17, 535, 645, 646 Nasal Mucosa, 631, 646 Natural killer cells, 632, 646 Nausea, 11, 37, 619, 635, 647, 685 NCI, 1, 292, 519, 598, 647 Needle biopsy, 277, 284, 617, 647
Nematoda, 624, 647 Neomycin, 647 Neonatal, 482, 622, 647 Neoplasia, 614, 647 Neoplasm, 647, 671, 684 Neoplastic, 57, 626, 640, 647, 671 Nephritis, 647 Nephropathy, 635, 647 Nephrosis, 647 Nephrotic, 647 Nephrotic Syndrome, 647 Nerve Growth Factor, 196, 647, 666 Nervous System, 15, 596, 641, 647, 648, 655, 678 Networks, 647, 679 Neural, 16, 582, 626, 647, 663 Neurologic, 27, 37, 504, 648 Neurology, 39, 648 Neuromuscular, 264, 502, 579, 648 Neurons, 79, 605, 619, 645, 647, 648, 675, 679 Neuropathy, 583, 648, 655, 671 Neurotic, 648, 686 Neurotransmitter, 579, 580, 582, 587, 592, 621, 626, 648, 649, 674, 678 Neutrons, 591, 634, 648, 665 Neutropenia, 6, 648, 657 Neutrophil, 51, 53, 71, 631, 648 Nitric Oxide, 36, 41, 193, 195, 503, 648 Nitric-Oxide Synthase, 195, 648 Nitrogen, 34, 581, 582, 583, 604, 615, 617, 635, 648, 684 Nitroglycerin, 278, 648 Nonmalignant, 648 Norepinephrine, 580, 648, 649 Nuclear, 56, 274, 589, 610, 614, 619, 647, 649, 680 Nuclear Medicine, 274, 649 Nuclei, 610, 620, 640, 643, 648, 649, 650, 663, 670, 679 Nucleic acid, 56, 620, 629, 645, 648, 649, 664 Nucleus, 56, 586, 589, 597, 603, 604, 606, 614, 633, 641, 643, 644, 648, 649, 663, 677 Nursing Care, 649 Nutritional Status, 263, 649 O Observational study, 215, 649 Occipital Lobe, 649, 687 Occult, 649 Occupational Therapy, 14, 22, 83, 454, 478, 552, 563, 649 Ocular, 480, 484, 649 Odds Ratio, 649, 667 Ointments, 550, 649 Oligopeptides, 649 Oliguria, 635, 649
Index 703
Omeprazole, 650 Oncogenic, 636, 650, 663 Oophoritis, 622, 650 Opacity, 594, 605, 650 Open Reading Frames, 636, 650 Operon, 650, 668 Ophthalmic, 290, 569, 650, 668 Ophthalmologic, 558, 650 Ophthalmology, 192, 617, 650 Opportunistic Infections, 491, 650 Opsin, 650, 668, 669 Optic Nerve, 590, 650, 652, 668, 671 Oral Health, 29, 55, 650 Oral Hygiene, 30, 650 Oral Manifestations, 30, 650 Orbit, 650 Orbital, 650 Organelles, 604, 641, 650 Organogenesis, 650 Orthodontics, 650 Orthotic Devices, 536, 651 Ossicles, 623, 651 Ossification, 651, 670 Osteoblasts, 34, 651 Osteocalcin, 651 Osteoclasts, 54, 592, 651 Osteolysis, 556, 651 Osteomalacia, 226, 651 Osteomyelitis, 67, 483, 556, 651 Osteonecrosis, 5, 651 Osteonectin, 651 Osteotomy, 554, 651 Outpatient, 11, 28, 651 Ovary, 622, 650, 651, 652, 677 Overweight, 8, 26, 198, 547, 551, 651 Ovum, 620, 637, 652, 661 Oxidation, 579, 585, 586, 590, 604, 606, 621, 637, 652 Oxidative metabolism, 636, 652 Oxidative Stress, 210, 652 Oxygen Consumption, 614, 652, 668 Oxygenase, 26, 652 Oxygenation, 652 Oxytocic, 644, 652 P Pachymeningitis, 642, 652 Paclitaxel, 216, 268, 652 Palate, 652, 677 Palliative, 9, 652, 680 Palsy, 652 Pancreas, 491, 590, 607, 631, 652, 684 Pancreas Transplant, 491, 652 Pancreas Transplantation, 491, 652 Pancreatic, 597, 652 Pancytopenia, 504, 652 Paracoccidioidomycosis, 483, 653
Paralysis, 603, 653, 658 Parasite, 653, 683 Parasitic, 479, 579, 603, 609, 624, 653 Parasitic Diseases, 653 Parathyroid, 653, 670 Parathyroid Glands, 653, 670 Parenteral, 196, 491, 653 Paresthesia, 479, 653 Parietal, 650, 653, 655, 658 Parotid, 653 Partial remission, 653, 667 Partial response, 283, 653 Particle, 653, 675, 683 Partnership Practice, 653, 660 Parturition, 653, 661 Parvovirus, 75, 479, 482, 643, 653 Patch, 653, 683 Pathogen, 69, 630, 653 Pathologic Processes, 35, 586, 654 Pathologies, 56, 654 Pathophysiology, 7, 29, 35, 51, 482, 486, 654 Patient Education, 5, 7, 39, 260, 274, 279, 285, 490, 535, 578 Pediatrics, 50, 197, 533, 558 Peer Review, 189, 654, 664 Pelvic, 662 Pelvis, 503, 628, 635, 639, 685 Penicillamine, 30, 254, 484, 570, 654 Penicillin, 76, 584, 654, 686 Penis, 576, 577, 589, 609, 655 Pepsin, 644, 654 Pepsin A, 654 Peptic, 7, 477, 654 Peptic Ulcer, 7, 477, 654 Peptide Fragments, 654 Peptide Hydrolases, 611, 654 Perceived risk, 491, 654 Perception, 227, 511, 654, 671 Percutaneous, 654 Perennial, 616, 654, 683 Perfusion, 628, 654, 681 Periarthritis, 212, 654 Pericarditis, 654 Perinatal, 81, 491, 654 Periodic Acid, 481, 655 Periodontal disease, 55, 655 Peripheral Nerves, 636, 655 Peripheral Nervous System, 648, 652, 655, 678 Peripheral Neuropathy, 491, 655 Peritoneal, 655 Peritoneum, 655 Peritonitis, 622, 655 Perivascular, 14, 655 Peroxide, 214, 655 P-Glycoprotein, 48, 655
704 Arthritis
Phagocyte, 640, 655 Phallic, 617, 655 Phantom, 655 Pharmacogenetics, 655 Pharmacokinetic, 33, 655 Pharmacologic, 6, 9, 20, 21, 25, 42, 224, 480, 584, 588, 623, 656, 681, 682, 685 Pharynx, 631, 656, 677 Phenotype, 56, 63, 600, 656 Phenyl, 229, 656 Phenylalanine, 254, 654, 656, 684 Phospholipases, 656, 674 Phospholipids, 615, 635, 637, 656 Phosphorus, 254, 653, 656 Phosphorylation, 51, 656 Photochemotherapy, 11, 542, 656 Photocoagulation, 598, 656 Photophobia, 633, 656 Photosensitizing Agents, 656 Physical Fitness, 452, 489, 496, 656, 676 Physical Therapy, 3, 26, 27, 468, 507, 522, 539, 542, 544, 545, 550, 551, 656 Physician-Patient Relations, 454, 656 Physiologic, 13, 31, 42, 60, 590, 598, 606, 623, 634, 642, 643, 656, 661, 666, 668 Physiology, 594, 610, 656 Pigment, 641, 642, 657 Pilot study, 40, 72, 219, 221, 290, 657 Pituitary Gland, 602, 616, 657, 672 Placebo Effect, 510, 657 Plana, 657, 673 Plant Oils, 649 Plants, 210, 547, 581, 587, 593, 605, 620, 621, 636, 649, 659, 670, 671, 682, 683 Plaque, 478, 587, 657 Plasma cells, 584, 645, 657 Plasma protein, 581, 611, 635, 657 Plasmapheresis, 586, 657 Plasmid, 228, 657, 686 Plasmin, 657 Plasminogen, 32, 657 Plasminogen Activators, 657 Platelet Activating Factor, 657 Platelet Activation, 657, 674 Platelet Aggregation, 583, 613, 628, 648, 657, 658, 681 Platelet Factor 4, 632, 658 Platelet-Derived Growth Factor, 658 Plateletpheresis, 586, 658 Platelets, 586, 589, 648, 652, 657, 658, 681 Platyhelminths, 624, 658 Pleated, 634, 658 Pleura, 658 Pleural, 196, 658 Pleural cavity, 658 Pleural Effusion, 196, 658
Pneumoconiosis, 658, 674 Pneumonia, 491, 601, 658 Pneumonitis, 592, 658 Podiatry, 492, 658 Poisoning, 592, 609, 619, 633, 642, 647, 658, 670, 672 Policy Making, 622, 658 Poliomyelitis, 476, 658 Pollen, 254, 665 Polymerase, 38, 659, 668 Polymerase Chain Reaction, 38, 659 Polymers, 82, 659, 662 Polymorphic, 597, 659 Polymyalgia Rheumatica, 19, 29, 659 Polypeptide, 582, 599, 612, 616, 654, 657, 659, 661, 662, 689 Polyposis, 10, 659 Polysaccharide, 71, 86, 213, 585, 596, 621, 659, 663 Polyunsaturated fat, 190, 659, 681 Posterior, 27, 512, 597, 608, 633, 649, 652, 659, 671 Postmenopausal, 16, 263, 498, 614, 651, 659 Postnatal, 659, 676 Postoperative, 21, 614, 659 Postsynaptic, 659, 674 Post-translational, 659 Post-traumatic, 624, 659 Postural, 659 Potassium, 644 Potentiate, 632, 660 Potentiation, 660, 674 Practice Guidelines, 525, 558, 660 Precancerous, 596, 660 Preclinical, 63, 481, 660 Precursor, 9, 586, 604, 609, 612, 649, 656, 657, 660, 683, 684, 686, 688 Predictive factor, 660 Predisposition, 76, 501, 660 Prednisolone, 61, 79, 512, 660 Prednisone, 11, 29, 197, 269, 270, 272, 282, 291, 502, 512, 660 Pregnancy Outcome, 660 Pregnenolone, 254, 660 Premenopausal, 197, 278, 288, 660 Primary endpoint, 37, 660 Private Practice, 660 Probe, 660 Probenecid, 553, 570, 660 Procaine, 637, 661 Progeny, 645, 661 Progesterone, 579, 661, 676 Prognostic factor, 661 Progressive disease, 58, 661 Projection, 605, 649, 650, 661 Prolactin, 661
Index 705
Proline, 599, 627, 661 Promoter, 54, 661 Prophylaxis, 18, 478, 614, 661, 685 Proportional, 612, 653, 661 Proprioception, 661 Prospective study, 64, 638, 661 Prostaglandin, 41, 86, 195, 222, 481, 613, 644, 661, 681 Prostaglandins A, 506, 630, 661, 662 Prostaglandins D, 662 Prostate, 464, 590, 662, 684 Prosthesis, 634, 662 Protease, 49, 86, 599, 662 Protease Inhibitors, 49, 662 Protective Devices, 549, 662 Protein Binding, 662, 681 Protein C, 51, 273, 581, 582, 586, 588, 598, 634, 637, 651, 662, 663, 684, 685 Protein Conformation, 582, 634, 662 Protein Isoforms, 581, 662 Protein Kinases, 662 Protein S, 475, 590, 613, 620, 647, 651, 662, 670, 680 Proteinuria, 645, 647, 663 Proteoglycan, 21, 36, 43, 49, 86, 216, 481, 658, 663 Proteolytic, 254, 581, 600, 612, 616, 657, 663 Proteome, 663 Proton Pump, 650, 663 Protons, 663, 665 Proto-Oncogene Proteins, 652, 663 Proto-Oncogene Proteins c-mos, 652, 663 Protozoa, 479, 609, 643, 663 Protozoan, 596, 603, 620, 663, 683 Proximal, 19, 492, 608, 659, 663 Psychiatric, 271, 642, 663 Psychiatry, 42, 617, 663, 677 Psychic, 598, 637, 642, 663, 664 Psychoactive, 663, 688 Psychogenic, 663, 685 Psychological Adaptation, 41, 663 Psychology, 60, 608, 663 Psychosomatic, 477, 664 Psychotherapy, 598, 664 Publication Bias, 16, 664 Publishing, 65, 452, 453, 454, 455, 664 Pulmonary Artery, 591, 664, 686 Pulmonary Edema, 635, 664 Pulmonary Fibrosis, 271, 274, 276, 664 Pulmonary hypertension, 602, 613, 664 Pulse, 57, 221, 512, 644, 664 Pupil, 602, 607, 633, 664 Purines, 30, 664, 673, 688 Purulent, 579, 622, 664, 686 Pustular, 664 Pyogenic, 482, 651, 664
Pyridoxal, 664 Pyrimidines, 664, 673 Q Quality of Health Care, 654, 664 Quercetin, 203, 665 R Race, 488, 643, 665 Radiation, 615, 616, 617, 618, 627, 628, 629, 632, 634, 643, 655, 656, 665, 671, 688 Radiation therapy, 615, 632, 634, 665, 671, 688 Radicular, 665 Radiculopathy, 26, 556, 665, 671 Radio Waves, 606, 665 Radioactive, 286, 591, 623, 629, 632, 634, 638, 644, 649, 650, 665, 688 Radiography, 26, 522, 665 Radioimmunoassay, 589, 618, 665 Radiolabeled, 591, 634, 665, 688 Radiology, 195, 649, 665 Radiotherapy, 591, 634, 665, 688 Randomized clinical trial, 216, 666 Randomized Controlled Trials, 225, 666 Rarefaction, 666 Reabsorption, 660, 666 Reactivation, 82, 666 Reactive Oxygen Species, 666 Reagent, 482, 603, 666 Receptor, 8, 26, 33, 43, 51, 52, 54, 61, 68, 70, 71, 72, 73, 75, 78, 82, 85, 86, 192, 211, 217, 265, 482, 499, 503, 569, 572, 573, 585, 640, 665, 666, 673, 674, 678 Receptors, Serotonin, 666, 673 Receptors, Tumor Necrosis Factor, 666 Recombinant, 8, 72, 82, 573, 666, 686 Recombination, 620, 666 Reconstitution, 62, 666 Rectum, 586, 599, 607, 617, 619, 630, 636, 662, 667 Red blood cells, 613, 625, 652, 667, 671 Reductase, 55, 639, 643, 667, 674 Refer, 1, 536, 592, 599, 608, 617, 625, 638, 639, 644, 646, 648, 649, 667, 682 Reflective, 282, 667 Reflux, 667 Refraction, 667, 675 Refractory, 4, 31, 285, 610, 667 Regeneration, 49, 616, 666, 667 Regimen, 12, 15, 57, 213, 269, 273, 275, 544, 571, 598, 609, 657, 667, 669 Regression Analysis, 29, 208, 607, 667 Regurgitation, 624, 667 Rehabilitation Centers, 667 Rehabilitative, 56, 667 Relapse, 190, 497, 667 Relative risk, 28, 282, 667
706 Arthritis
Relaxant, 667 Relaxation Techniques, 264, 453, 489, 511, 538, 550, 667 Reliability, 42, 667 Remission, 27, 57, 481, 667 Renal amyloidosis, 667 Renal failure, 668 Renal tubular, 226, 661, 668 Renal tubular acidosis, 226, 668 Repressor, 650, 668 Reproduction Techniques, 660, 668 Research Design, 34, 39, 47, 668 Research Support, 537, 668 Resection, 554, 668 Resorption, 481, 651, 666, 668 Respiration, 593, 603, 644, 652, 668 Respiratory Burst, 193, 668 Response rate, 11, 668 Restoration, 18, 49, 656, 666, 668, 688 Retina, 29, 291, 590, 597, 601, 636, 650, 668, 670, 673, 688 Retinal, 607, 617, 650, 668, 669, 687 Retinal Vein, 668, 669 Retinal Vein Occlusion, 669 Retinoid, 614, 669 Retinol, 203, 668, 669 Retreatment, 669 Retrospective, 59, 196, 226, 669 Retrospective study, 196, 226, 669 Retroviral vector, 620, 669 Retrovirus, 669 Reverse Transcriptase Polymerase Chain Reaction, 51, 669 Reversion, 669, 684 Rheumatoid Nodule, 14, 669 Rhodopsin, 650, 668, 669 Rhusiopathiae, 613, 669 Ribose, 81, 580, 669 Ribosomal Proteins, 670 Ribosome, 670, 683 Rickets, 670, 688 Rigidity, 670 Rituximab, 497, 670 Rod, 588, 670, 673, 689 Rotator, 22, 670 Rotator Cuff, 22, 670 Rubella, 479, 482, 670 Ruminants, 622, 670 Rutin, 224, 665, 670 S Sacroiliac Joint, 482, 670 Saimiri, 632, 670 Salivary, 604, 607, 615, 670, 673, 678, 688 Salivary glands, 604, 607, 615, 670, 673 Salmonella, 4, 6, 76, 536, 619, 670 Salpingitis, 622, 671
Salvage Therapy, 671 Saponins, 671, 676 Sarcoma, 491, 616, 671 Scans, 272, 274, 278 Scatter, 655, 671 Schizoid, 671, 688 Schizophrenia, 671, 688 Schizotypal Personality Disorder, 671, 688 Sciatica, 671 Sclera, 597, 601, 613, 671 Scleritis, 29, 671 Scleroderma, 454, 536, 551, 615, 671 Scleroproteins, 634, 671 Sclerosis, 507, 587, 599, 645, 671 Screening, 271, 276, 278, 291, 598, 672, 685 Sebaceous, 606, 672, 688 Sebaceous gland, 606, 672, 688 Secretory, 49, 650, 672 Sedative, 672, 686 Sedentary, 52, 672 Sediment, 672, 685 Sedimentation, 6, 11, 19, 25, 29, 31, 290, 488, 659, 672 Segregation, 48, 589, 666, 672 Selenium, 197, 203, 227, 231, 672 Self Care, 535, 540, 579, 672 Self Tolerance, 672 Sella, 608, 657, 672 Sella Turcica, 608, 657, 672 Semen, 238, 240, 241, 609, 662, 672 Semisynthetic, 644, 672 Senile, 651, 672 Sensory loss, 665, 672 Sepsis, 5, 83, 504, 642, 672 Septicemia, 83, 86, 672 Sequela, 672 Sequencing, 32, 659, 672 Sequester, 49, 672 Serine, 71, 229, 611, 663, 673, 684 Serine Endopeptidases, 611, 673 Serologic, 287, 479, 628, 673 Serology, 673 Serositis, 485, 673 Serotonin, 507, 648, 666, 673, 684 Serous, 611, 658, 673 Serrata, 217, 245, 597, 673 Serrated, 673 Serum Globulins, 481, 673 Sex Characteristics, 580, 583, 673, 680 Sexually Transmitted Diseases, 673 Sharpness, 673, 687 Shedding, 606, 673 Shigella, 4, 6, 536, 673 Shock, 80, 583, 673, 683 Shoulder Impingement Syndrome, 26, 673 Shunt, 673
Index 707
Sicca, 673 Signal Transduction, 35, 53, 674 Signs and Symptoms, 10, 15, 45, 209, 281, 283, 453, 561, 667, 674 Silicosis, 674 Simvastatin, 674 Sindbis Virus, 581, 674 Skeletal, 482, 556, 583, 603, 645, 674, 675, 679, 684 Skeleton, 579, 616, 634, 661, 674, 681 Skull, 603, 650, 674, 680 Small intestine, 481, 597, 609, 620, 626, 633, 674, 684 Smallpox, 674, 685, 686 Smooth muscle, 583, 588, 601, 626, 645, 648, 674, 675, 678 Sneezing, 673 Soaps, 617 Social Environment, 665, 674 Social Perception, 674 Social Security, 543, 666 Social Support, 45, 58 Socialization, 509 Sodium, 201, 203, 569, 570, 607, 613, 622, 644, 646, 666, 682 Soft tissue, 513, 514, 591, 615, 616, 674 Solid tumor, 584, 611, 674 Solvent, 614, 674 Soma, 675 Somatic, 84, 580, 598, 626, 641, 650, 655, 675 Sound wave, 606, 667, 675 Soybean Oil, 659, 675 Spasm, 18, 675 Spatial disorientation, 608, 675 Specialist, 24, 564, 607, 675 Spectroscopic, 675 Spectrum, 665, 675, 689 Sperm, 583, 597, 675 Spermatozoa, 672, 675, 680 Spinal cord, 52, 591, 592, 595, 596, 609, 611, 619, 641, 642, 647, 648, 652, 655, 665, 675 Spinal Cord Injuries, 665, 675 Spinal Nerve Roots, 665, 671, 675 Spirochete, 67, 675, 679 Spleen, 12, 583, 604, 639, 675 Splint, 26, 675 Spondylarthritis, 676 Spontaneous Abortion, 660, 676 Sporotrichosis, 479, 483, 676 Sports Medicine, 676 Sprains and Strains, 639, 676 Stabilization, 16, 18, 676 Staging, 676 Standard therapy, 272, 676
Staphylococcus, 66, 69, 75, 83, 513, 619, 644, 676 Stasis, 676 Statistically significant, 11, 676 Stem cell transplantation, 62, 213, 624, 676 Stem Cells, 624, 676 Stenosis, 676 Sterile, 5, 587, 653, 676 Steroid, 194, 288, 503, 512, 603, 660, 671, 674, 676 Steroid therapy, 194, 676 Stillbirth, 660, 677 Stimulant, 626, 634, 677, 686 Stimulus, 608, 609, 614, 632, 635, 636, 677, 680 Stoma, 677 Stomachic, 677 Stomatitis, 677 Stomatognathic System, 677 Stool, 599, 630, 636, 677 Strand, 659, 677 Streptococcal, 50, 82, 83, 84, 226, 228, 483, 677 Streptococcus, 4, 66, 76, 615, 677 Stroke, 53, 292, 455, 463, 520, 594, 677 Stroma, 633, 677 Stromal, 85, 591, 677 Stromal Cells, 85, 591, 677 Stupor, 646, 677 Subacute, 18, 227, 504, 630, 677 Subarachnoid, 623, 656, 677 Subcapsular, 512, 677 Subclinical, 630, 677 Subcutaneous, 6, 268, 270, 273, 285, 595, 609, 653, 669, 676, 677, 682 Submaxillary, 612, 678 Subspecies, 675, 678, 686 Substance P, 613, 642, 666, 672, 678 Substrate, 48, 594, 612, 678 Substrate Specificity, 678 Sulfinpyrazone, 553, 571, 678 Sulfur, 203, 214, 615, 678 Superantigens, 678 Superoxide, 668, 678 Superoxide Dismutase, 678 Supplementation, 25, 218, 219, 220, 227, 678 Support group, 535, 678 Suppressive, 228, 678 Suppurative, 482, 595, 622, 678 Survival Rate, 274, 678 Sweat, 606 Sweat Glands, 606 Sympathomimetic, 613, 649, 678 Symphysis, 662, 678 Symptomatic, 11, 19, 27, 52, 221, 227, 479, 678
708 Arthritis
Symptomatology, 192, 209, 678 Synaptic, 648, 674, 678 Syncope, 679, 687 Synergistic, 35, 661, 679 Syphilis, 22, 679 Systemic disease, 5, 672, 679 Systolic, 40, 627, 679 Systolic blood pressure, 40, 679 T Tachycardia, 588, 679 Tachypnea, 588, 679 Tacrolimus, 282, 679 Talus, 679, 681 Tarsal Bones, 592, 679 Taurine, 679 Telophase, 643, 679 Temporal, 6, 37, 45, 54, 624, 659, 679, 680, 687 Temporal Lobe, 680, 687 Tendinitis, 205, 463, 465, 536, 680 Tendon, 18, 26, 484, 539, 558, 592, 619, 680 Tendonitis, 680 Tenosynovitis, 454, 556, 680 Teratogenic, 581, 614, 680 Teratogenicity, 680 Terminator, 598, 680 Testicle, 273, 622, 680 Testicular, 680 Testis, 680 Testosterone, 34, 667, 680 Tetracycline, 608, 644, 680 Thalamus, 680, 687 Theophylline, 664, 680 Therapeutics, 44, 192, 194, 197, 232, 572, 680 Thermal, 18, 230, 591, 608, 648, 659, 680 Thigh, 616, 680 Thoracic, 606, 639, 641, 658, 680, 688 Thorax, 639, 680 Threonine, 663, 673, 680 Threshold, 627, 680 Thrombocytopenia, 657, 680 Thrombocytosis, 681 Thromboembolism, 681 Thrombolytic, 657, 681 Thrombomodulin, 662, 681 Thrombophlebitis, 37, 681 Thrombopoietin, 681 Thrombosis, 589, 662, 677, 681 Thromboxanes, 586, 681 Thrombus, 602, 630, 658, 681 Thrush, 491, 593, 681 Thymus, 628, 639, 681 Thyroid, 592, 627, 633, 653, 681, 684 Thyroid Gland, 627, 653, 681 Thyroiditis, 681 Tibia, 584, 616, 681
Ticks, 681 Tin, 594, 653, 655, 681 Tinea Pedis, 606, 681 Tissue Distribution, 51, 68, 592, 681 Tissue Extracts, 32, 681 Tolerance, 13, 43, 62, 80, 85, 282, 285, 290, 580, 621, 672, 682 Tome, 226, 246, 256, 682 Tomography, 286, 682 Tone, 650, 682 Tonicity, 625, 634, 682 Tooth Preparation, 682 Tophus, 682 Topical, 11, 17, 20, 22, 208, 252, 478, 504, 535, 536, 568, 614, 656, 682 Torsion, 630, 682 Tourniquet, 682 Toxic, v, 18, 55, 515, 561, 581, 603, 604, 605, 611, 623, 628, 629, 648, 672, 682 Toxicodendron, 243, 682 Toxicology, 33, 522, 682 Toxin, 66, 612, 682 Toxoplasmosis, 491, 588, 682 Trace element, 591, 681, 682 Trachea, 592, 656, 681, 682 Traction, 18, 682 Transcriptase, 71, 80, 82, 669, 683 Transcription Factors, 54, 683 Transcutaneous, 231, 511, 522, 537, 683 Transdermal, 34, 683 Transduction, 48, 53, 674, 683 Transfection, 590, 620, 683 Transfer Factor, 628, 683 Transforming Growth Factor beta, 683 Transgenes, 36, 683 Translation, 582, 613, 647, 683 Translational, 53, 683 Translocation, 56, 76, 613, 683 Transmitter, 579, 641, 649, 683, 687 Transplantation, 62, 491, 585, 610, 628, 635, 639, 640, 683 Trauma, 5, 477, 478, 513, 554, 647, 683 Trees, 582, 682, 683 Triage, 683 Trichomoniasis, 643, 683 Tricuspid Atresia, 602, 683 Tricyclic, 507, 684 Triglyceride, 627, 684 Tropomyosin, 684 Troponin, 684 Trypsin, 476, 612, 684, 689 Trypsin Inhibitors, 476, 684 Tryptophan, 599, 673, 684 Tuberculosis, 22, 479, 497, 504, 601, 639, 646, 684 Tumor marker, 590, 684
Index 709
Tumor suppressor gene, 84, 684 Tumour, 20, 66, 619, 684 Typhimurium, 684 Tyrosine, 226, 684 U Ulcer, 19, 595, 609, 644, 654, 684, 686 Ulceration, 194, 221, 636, 684 Ulcerative colitis, 485, 486, 630, 684 Ulna, 684 Ultrasonography, 684 Unconscious, 584, 605, 628, 685 Uncontrolled study, 511, 685 Unsaturated Fats, 617, 685 Urea, 586, 635, 685 Uremia, 635, 668, 685 Ureters, 635, 685, 687 Urethra, 662, 685 Urethritis, 480, 557, 622, 685 Uric, 21, 30, 553, 581, 622, 627, 664, 685 Uricosuric, 20, 660, 678, 685 Uricosuric Agents, 20, 685 Urinalysis, 536, 685 Urinary, 16, 36, 87, 576, 588, 593, 620, 630, 649, 685, 688 Urinary Retention, 16, 685 Urinary tract, 588, 685 Urinary tract infection, 589, 685 Urinate, 685, 688 Urogenital, 4, 536, 558, 620, 622 Urokinase, 87, 685 Urticaria, 583, 685 Uterus, 596, 602, 611, 617, 619, 642, 652, 661, 685, 686 V Vaccination, 26, 685 Vaccine, 479, 482, 580, 685, 686 Vaccinia, 483, 685 Vaccinia Virus, 483, 685 Vagina, 593, 596, 642, 686 Vaginal, 639, 686 Vaginitis, 37, 593, 686 Valerian, 17, 686 Valine, 654, 686 Varicella, 479, 483, 686 Varicose, 636, 686 Varicose Ulcer, 636, 686 Variola, 483, 685, 686 Vascular endothelial growth factor, 686 Vasculitis, 454, 486, 686 Vasoconstriction, 613, 686 Vasodilation, 628, 686 Vasodilator, 592, 626, 686 Vasomotor, 614, 686 VE, 190, 192, 686 Vector, 72, 653, 683, 686
Vein, 272, 277, 278, 286, 633, 649, 653, 668, 669, 681, 686 Venereal, 480, 679, 686 Venom, 70, 195, 229, 686 Venous, 589, 592, 595, 636, 648, 662, 683, 686 Ventricle, 587, 602, 628, 664, 679, 680, 683, 686 Ventricular, 602, 683, 686 Venules, 591, 593, 611, 687 Vertebrae, 633, 675, 676, 687 Vertebral, 485, 487, 589, 657, 687 Vertebrobasilar Insufficiency, 687 Vertigo, 687 Vesicoureteral, 687 Vesicular, 625, 674, 686, 687 Veterinary Medicine, 521, 687 Video Recording, 489, 687 Videodisc Recording, 687 Viral vector, 228, 687 Virulence, 66, 682, 687 Virulent, 501, 687 Viscera, 675, 687 Visceral, 481, 655, 687 Visual Acuity, 290, 671, 687 Visual field, 590, 687 Vitamin A, 56, 203, 455, 547, 669, 687 Vitamin D, 191, 200, 211, 272, 571, 670, 688 Vitamin K, 283, 651, 688 Vitreous, 290, 636, 668, 688 Vitreous Body, 668, 688 Vitro, 32, 34, 43, 44, 48, 51, 54, 56, 62, 63, 76, 476, 481, 610, 620, 625, 630, 659, 673, 679, 688 Vivo, 32, 36, 41, 44, 48, 51, 56, 62, 76, 211, 265, 481, 620, 625, 630, 639, 679, 681, 688 Vocational Education, 546, 688 Void, 688 Volition, 633, 688 Vulgaris, 244, 688 W Warts, 463, 634 Weight Gain, 503, 511 Windpipe, 656, 681, 688 Withdrawal, 688 Wound Healing, 616, 641, 688 X Xanthine, 581, 688 Xanthine Oxidase, 581, 688 Xenograft, 584, 688 Xerostomia, 30, 634, 688 X-ray therapy, 634, 688 Y Yeasts, 593, 656, 688 Yersinia, 4, 6, 70, 76, 536, 689 Yttrium, 689
710 Arthritis
Z Zoster, 483, 689
Zymogen, 662, 689
Index 711
712 Arthritis
Index 713
714 Arthritis
