Search for: rheumatoid arthritis methotrexate autoimmune disease biomarker gene expression GWAS HLA genes non-HLA genes
| ID | PMID | Title | PublicationDate | abstract |
|---|---|---|---|---|
| 1844376 | [Methotrexate in rheumatoid arthritis]. | 1991 Jun | Methotrexate may be effective in patients with rheumatoid arthritis refractory to other treatments (gold salts, d-penicillamine and antimalarial drugs). Success rates from 39 to 88% have been reported. The mechanism of action is unknown, but is supposedly related to anti-inflammatory and immunosuppressive effects. Frequent side effects are observed on prolonged treatment. Most of these are mild and disappear with dose reduction. An exception is pneumonitis, a hypersensitivity reaction that may appear early and at low doses. Hepatotoxic effects are milder than those observed in patients with psoriasis. Intraarticular administration is not effective. No carcinogenic effects have been observed in humans. The drug should be administered with caution in fertile males and females due to possible teratogenic effects. New studies involving larger number of patients may help establish a significant role for methotrexate in the treatment of rheumatoid arthritis. | |
| 2643493 | Rheumatoid arthritis in the cervical spine. | 1989 Feb | Rheumatoid arthritis causes synovitis in the cervical spine and injures skeletal structures at any level. Subluxations occur with pain and spinal cord dysfunction. Subluxations are common; neurological problems are less so, but death from subluxations is not common. However, once myelopathy is established, the natural history is poor. Advances in radiologic imaging through computed tomography and magnetic resonance imaging greatly assist anatomic assessment. Neurologic deterioration and pain are indications for surgery. Preoperative skeletal traction is often required to align the spine, and fusion techniques are used for stabilization. | |
| 2286222 | Epidemiology of rheumatoid arthritis: update. | 1990 | We have highlighted advances and new developments in the epidemiology of rheumatoid arthritis in four major areas. Further research, as suggested by us and others (48) should focus on understanding the mechanisms which underlie the association of etiologic and protective factors with rheumatoid arthritis, and on identifying and modifying prognostic factors associated with long-term morbidity and mortality among patients with rheumatoid arthritis. Major increases in funding provided by the National Institute of Arthritis and Musculoskeletal and Skin Diseases and the Arthritis Foundation will be needed to realize such efforts in the United States. | |
| 3512928 | Rheumatoid arthritis: clinical features and pathogenetic mechanisms. | 1986 Mar | Rheumatoid arthritis is a disorder characterized by chronic inflammation affecting predominantly articular tissues, leading in some instances to disruption of the normal structure and function of the joint. In some patients extra-articular manifestations are also present. In the joints, the pathologic lesion consists of synovial cell proliferation with infiltration by inflammatory cells. The complex interaction among these cells is likely responsible for the connective tissue abnormalities that characterize the rheumatoid lesion. The factors responsible for inducing the inflammatory process are unknown. | |
| 3317806 | Diagnostic criteria in rheumatoid arthritis. | 1987 | For rheumatoid arthritis (RA), criteria have been developed for classification of groups of patients in population surveys, selection for therapeutic trials, inter-institutional comparison of patients, evaluation of diagnostic trials, diagnosis of RA in individual patients, estimation of disease frequency, and assistance in determining prognosis. The American Rheumatism Association (ARA) "Criteria for the Classification of Rheumatoid Arthritis-Diagnostic Criteria for Rheumatoid Arthritis" were published in 1958 and have become a standard. These criteria are empiric and attempt to incorporate reasonable combinations of sensitivity and specificity. Despite the recognition that these criteria should be expected to change with improved knowledge, no further modification has been published. Other criteria such as the ARA "Proposed Criteria for Rheumatoid Arthritis" represent an important effort to encourage uniformity in definitions and use of the term remission. Yet it is well to remember that they have never been tested in prospective studies and are considered preliminary. The Co-operative Systematic Studies in Rheumatic Diseases, when studying slow-acting anti-rheumatic drugs, have chosen to use clinical endpoints such as 50% improvement in joint tenderness and swelling counts (or scores) rather than combined variables which include morning stiffness and changes in laboratory variables. This approach permits the true assessment of drug effects. In summary, current criteria have served us well. Nonetheless, we should not become complacent and should always question their sensitivity, specificity and application. | |
| 2487699 | An introduction to rheumatoid arthritis. | 1989 Sep | To understand the many forms of treatment available for patients with rheumatoid arthritis and the variable responses to these therapies, one must appreciate the complexity of this disease, the role played by immune mechanisms in its initiation and perpetuation, and its natural history, including factors that may predict a good or bad outcome. This introduction to rheumatoid arthritis will focus briefly on each of these areas. | |
| 3275843 | Rheumatoid arthritis: can the long-term outcome be altered? | 1988 Jan | Although several agents (for example, intramuscularly administered gold, auranofin, D-penicillamine, hydroxychloroquine, and methotrexate) are of clinical benefit in the management of rheumatoid arthritis (RA), their effect on the long-term outcome of the disease is controversial. Assessment of the influence of therapeutic interventions in RA is difficult because the natural history of the disease remains poorly defined and unpredictable, and neither the traditional clinical and laboratory measurements of inflammation nor radiographic analyses of progression of joint destruction provide an accurate estimate of the long-term outcome of RA. Furthermore, there is little evidence that second-line agents yield benefits beyond 3 years. Therefore, adequately tested comprehensive measures should be used in large, long-term, multicenter controlled clinical trials to determine whether the long-term outcome of RA can be altered. | |
| 3281174 | Cervical spine management in patients with rheumatoid arthritis. Review of the literature. | 1988 Apr | Rheumatoid arthritis of the cervical spine is a well-recognized source of neck pain. Discussion of the potential effects of various treatment interventions on the tissues of patients with rheumatoid arthritis of the cervical spine, however, has been scarce in the physical therapy literature. Physical therapists should understand the implications of this type of inflammatory arthritis when treating patients with rheumatoid arthritis. The end-stage results of the inflammatory process and the mechanical forces on the cervical spine can cause atlantoaxial subluxation, atlantoaxial impaction, and subaxial subluxation. The purpose of this article is to review the literature on several aspects of rheumatoid arthritis of the cervical spine: 1) pathological anatomy, 2) clinical findings, 3) surgical management, 4) management with cervical orthoses, and 5) physical therapy management. | |
| 2042057 | Osteoporosis associated with rheumatoid arthritis: pathogenesis and management. | 1991 Feb | Rheumatoid arthritis is associated with both localized and generalized osteoporosis. Localized osteoporosis can be considered to be caused by local disease mechanisms, including the generation of factors from activation of the cytokine pathway. The etiology of generalized osteoporosis has been difficult to elucidate, particularly because of the lack of sensitive techniques to measure bone mineral density. The introduction of single- and dual-photon absorptiometry and quantitative computed tomography has allowed more accurate assessment of bone mineral density. In general, bone mineral density loss at appendicular sites does not correlate well with axial bone density loss. Corticosteroid treatment exaggerates the development of osteoporosis in up to 40% of patients with rheumatoid arthritis. Sex hormone status, physical activity, disease duration, and functional class are all significant predictors for the development of osteoporosis. Current therapy for prevention and treatment is based largely on theoretical considerations. Physical activity should be encouraged once acute joint inflammation has settled. Postmenopausal women and amenorrheic premenopausal women will benefit from cyclical estrogen replacement. Patients with low serum 1,25-dihydroxy vitamin D3 levels, and males with low serum testosterone levels, are candidates for replacement therapy with the appropriate hormones. In patients who are receiving corticosteroids the dose should be limited, and oral calcium supplements are of benefit. The use of the newer corticosteroid deflazacort, and disease-modifying immunosuppressive drugs, are discussed. Other therapeutic options which should be considered, although published trials are scarce, are calcitonin and the diphosphonates. Further studies are awaited concerning the optimum prevention and treatment of osteoporosis associated with rheumatoid arthritis.(ABSTRACT TRUNCATED AT 250 WORDS) | |
| 1764845 | Sex hormones, HLA and rheumatoid arthritis. | 1991 Nov | Recent evidence indicates that the HLA system might, in some way, regulate androgen concentrations. Male patients affected by rheumatoid arthritis have been shown to possess low serum testosterone levels associated with a particular HLA haplotype. Furthermore, androgen receptors have been recently described in macrophage-like synoviocytes that are HLA-DR positive. Since androgens generally are immunosuppressive, the possible mechanisms of their action in rheumatoid arthritis are here reviewed and discussed. It has now become evident that the well known relationship between sex hormones and the immune system is more complex than was previously suspected. | |
| 2218554 | Renal disorders in rheumatoid arthritis. | 1990 Aug | Renal disorders are a frequent cause of death in patients with rheumatoid arthritis (RA), but are less apparent in living RA patients. In part, this may be because of insensitive screening methods. In this review, some of the relations among renal pathology, renal function, and antirheumatic therapy are clarified. A classification of renal disorders according to etiology is proposed. Two categories of disorders are distinguished: those related to RA and its complications, and those related to drug therapy. The disorders belonging to these categories are reviewed. Finally, a case is made for the existence of a third category, "RA nephropathy." It is hypothesized that this mild and nonspecific nephropathy is the result of cumulative minor insults caused by the disease and its therapy. The presence of such a "subclinical" nephropathy would explain the greater sensitivity of RA patients to other renal insults, and the high prevalence of renal failure at death. | |
| 2218551 | Therapeutic exercise for rheumatoid arthritis and osteoarthritis. | 1990 Aug | Therapeutic exercise in rheumatoid arthritis and osteoarthritis may be useful in improving aerobic capacity, strengthening muscles, improving endurance and increasing flexibility. This article reviews the major studies of exercise in these conditions and summarizes the authors recommendations regarding the use of therapeutic exercise in the treatment of rheumatoid arthritis osteoarthritis. | |
| 1862245 | Fasting, intestinal permeability, and rheumatoid arthritis. | 1991 May | Otherwise healthy and well-nourished patients with rheumatoid arthritis show significant clinical improvement from practising prolonged fasting for 7 to 10 days. The improvement is reversible and lost when eating is taken up again. Although of little therapeutic value, the anti-inflammatory effect of short-term fasting is of significant interest and better understanding of the mechanisms is desirable. | |
| 2009675 | Do infectious agents cause rheumatoid arthritis? | 1991 Apr | Although rheumatoid arthritis (RA) has been widely suspected to have an infectious etiology, this hypothesis has remained difficult to prove. Epstein-Barr virus, parvoviruses, and retroviruses are considered by some investigators to be the primary candidates. An increasing body of data, on the other hand, appears to implicate bacteria or their products in the syndrome. Important evidence has surfaced in support of this view. Lyme arthritis, a disease caused by a bacterium, can mimic RA. Bacteria and their products have been conclusively linked to many forms of inflammatory "reactive" arthropathies. RA-like diseases can be induced in certain inbred strains of rats with bacterial cell-wall fragments, e.g., streptococcal and other bacterial peptidoglycans. Immunologic relationships between host and bacterial peptidoglycans, relevant to RA, have been well documented, e.g., heat shock proteins, bacterial IgG Fc binding proteins, and rheumatoid factors. These data not only support the hypothesis that bacteria may play an important role in RA but also indicate that current concepts of infection and autoimmune disease are broadening and overlapping. | |
| 2200936 | [Rheumatoid arthritis and Sjögren's syndrome. Special reference to the course time of rhe | 1990 May 5 | The frequency of Sjögren's syndrome (SS) was evaluated in 45 patients with rheumatoid arthritis (RA). Subsequently, the clinical, biological and evolutive profiles of RA associated or not with SS were compared. The prevalence of definitive SS was 55%, while in 24% isolated data of gland involvement were found. The variables related with the development of SS in patients with RA were: sex, functional respiratory parameters, and, basically, the duration of RA. The latter relationship had a uniform association model, i.e., the prevalence of SS increased in a constant fashion following the duration increments of RA. The change of patients from negative to definite SS was uniform throughout the evolution of RA. | |
| 3522022 | A scientific basis for surgery in rheumatoid arthritis. | 1986 Jul | Understanding a disease process provides the scientific basis for specific treatment. In rheumatoid arthritis (RA), disease(s) of unknown cause, the lack of knowledge about the intrinsic involvement of the articular collagenous tissues (ACT) as a site for the deposition and persistence of immune complexes may have led to poor long-term results of surgery, especially synovectomy. Because we may now presume that immune complexes in ACT provide inflammatory, immune foci for chronic synovitis, ablative surgery of the damaged cartilaginous tissues is a specific remedy. Such knowledge may be used judiciously with techniques of fusion, resection, and arthroplasty to improve and maintain the long-term function of patients with the crippling seropositive form of the disease. | |
| 3052055 | Role of disease-modifying antirheumatic drugs versus cytotoxic agents in the therapy of rh | 1988 Oct 14 | Disease-modifying antirheumatic drugs are used to modify or alter the rheumatoid arthritis disease process. Disease-modifying antirheumatic drugs do not demonstrate the characteristic analgesic, antipyretic, and anti-inflammatory actions of the nonsteroidal anti-inflammatory drugs, since weeks or months of treatment are required before clinical benefit is observed. Although they have not been proved to delay, prevent, or reverse articular damage, therapy with disease-modifying antirheumatic drugs, when successful, is associated with decreased pain and joint swelling and improved function. Disease-modifying antirheumatic drugs and cytotoxic agents should not be considered as routine treatment for patients with rheumatoid arthritis. Before disease-modifying antirheumatic drug therapy is implemented, an optimal basic program of physical therapy, rest, and nonsteroidal anti-inflammatory drugs should be implemented, and it must be documented that the patient still has sufficient disease to justify the costs, risks, and benefits of these treatments. Drugs that are approved by the Food and Drug Administration (FDA) are preferred over nonapproved drugs. Hydroxychloroquine, parenteral gold salts, oral gold, D-penicillamine, and the cytotoxic drug azathioprine are the FDA-approved disease-modifying antirheumatic drugs for use in rheumatoid arthritis. Many, not all, rheumatologists would employ hydroxychloroquine as the first-choice disease-modifying antirheumatic drug in patients who have early, mild, and nonerosive disease; treatment should be continued for six months before being abandoned for lack of efficacy, and appropriate ophthalmologic examination every four to six months is indicated. An alternative would be auranofin, whose efficacy approaches that of parenteral gold, yet may be safer. For patients who have severe active rheumatoid arthritis, especially with erosive changes, parenteral gold salts are usually a first choice. D-penicillamine is also effective in controlling the signs and symptoms of rheumatoid arthritis, but serious toxicity may occur. Azathioprine might be considered a competitor to D-penicillamine, although the FDA approval restricts its use to patients who have failed gold therapy. Two cytotoxic drugs that are not FDA approved are methotrexate and cyclophosphamide. Methotrexate can be very effective, but its side effects, particularly pulmonary and hepatic, must be carefully monitored. Cyclophosphamide is generally considered too toxic for use in patients with rheumatoid arthritis, although it may be helpful in patients with systemic rheumatoid vasculitis or patients who have failed all other therapies.(ABSTRACT TRUNCATED AT 400 WORDS) | |
| 1749947 | Pathogenesis of rheumatoid arthritis: basis for future therapies. | 1991 Oct | Despite an increase in the number of rheumatologists in clinical practice over the past 15 years, the outcome for patients with rheumatoid arthritis (RA) remains relatively poor. The poor prognosis for patients with this disease is due to a lack of effective therapies. Better therapies will be developed only after the cause and pathogenesis of RA are better understood. Although the precise cause is unknown, a variety of evidence indicates that RA results from the presentation of a relevant antigen to an immunogenetically susceptible host. This report reviews recognized potential antigens and known genetic variables affecting the immune response, as well as the various cellular and humoral immune responses that result from the antigen-host interaction. More successful therapy for RA will most certainly result from a better understanding of the pathobiology of the disease. | |
| 1805356 | Negative association between schizophrenia and rheumatoid arthritis. | 1991 | Persuasive evidence has accumulated demonstrating a strong negative association between rheumatoid arthritis and schizophrenia at the population level. Explanations for this phenomenon have taken into consideration immunological, biochemical, and genetic factors. In this article, we examine these and other factors in closer detail. We then propose hypotheses at the molecular level that might account for the negative association between the two diseases. These hypotheses may provide clues for our colleagues in molecular biology as they search for candidate genes, "anti-genes," and molecular mechanisms relevant to schizophrenia. | |
| 1749948 | Prognostic staging for therapy of rheumatoid arthritis. | 1991 Oct | An attempt should be made to predict the most likely course of individual disease when a patient is first diagnosed as having rheumatoid arthritis (RA). Such a prediction can be called prognostic staging for therapy. While no specific marker will accomplish this accurately, the summation of demographic, genetic, historical, physical, laboratory, radiologic, and scanning data may be used to make a reasonable estimation of outcome. The use of immunogenetic typing is the newest technique that can help identify patients likely to develop more serious disease. Once patients are identified as having probable aggressive disease, that is, beyond stage I, combination therapy should be initiated. Goals of therapy should include the prevention and/or interference of progression of radiologic erosions, as well as functional improvement as measured by life-style and productivity. |