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ID PMID Title PublicationDate abstract
12776222 Therapeutic strategies for rheumatoid arthritis. 2003 Jun Recent years have seen considerable advances in our understanding of both the clinical and basic-research aspects of rheumatoid arthritis. Clinical progress has come from a better recognition of the natural history of the disease, the development and validation of outcome measures for clinical trials and, consequently, innovative trial designs. In parallel, basic research has provided clues to the pathogenic events underlying rheumatoid arthritis, and advances in biotechnology have facilitated the development of new classes of therapeutics. Here, we summarize the fruits of these advances: innovative approaches to the use of existing, traditional disease-modifying antirheumatic drugs; novel agents approved very recently; and further avenues that are presently under investigation or which are of more distant promise.
15479868 What precedes development of rheumatoid arthritis? 2004 Nov Studies on aetiology of inflammatory diseases such as rheumatoid arthritis (RA) need to investigate the potential environmental triggers that are active before onset of disease, the genetic context in which these triggers act, and whether the presence of such triggers in an arthritis prone genetic context will give rise to the immune reactions associated with/preceding RA. Such knowledge would help not only to address much better the issue of causality of these potential triggers and the immune reactions, but also to carry out various interventions aimed at influencing the disease provoking immune events before development of clinical signs of disease. This short report summarises recent data demonstrating (a) the presence of anticitrullin antibodies or rheumatoid factors in between a third and half of patients with RA before development of clinical signs; (b) long term smoking is associated with a high risk of future development of seropositive but not seronegative RA; and (c) a strong gene-environment interaction between smoking and SE genes in the development of seropositive RA. We conclude that, in a certain genetic context, smoking is a potential trigger of RA, and a combination of the two factors is associated with the occurrence of immune reactions long before the onset of RA.
12922950 Normal intestinal microbiota in the aetiopathogenesis of rheumatoid arthritis. 2003 Sep A series of observations have led to the hypothesis that normal intestinal microbiota in patients with rheumatoid arthritis may harbour, for genetic reasons, bacteria with cell walls capable of inducing arthritis. Differences occur between bacterial species, and even between strains of a single species, because some cell walls induce experimental chronic arthritis, whereas some others induce only a transient acute arthritis or no arthritis at all. In susceptible subjects, with continuous seeding of bacterial products from the gut, the synovial inflammation is followed by erosion, exposition of cartilage antigens, and self perpetuating chronic arthritis.
15623977 Biological agents in rheumatoid arthritis. 2004 Oct Rheumatoid arthritis (RA) is the commonest inflammatory joint disease with considerable morbidity and mortality. Conventional disease-modifying antirheumatic drugs like methotrexate form the cornerstone of therapy. However, they have several limitations in terms of slow onset of action, adverse effects and modest remission and retention rates. Several cytokines are involved in the pathogenesis of RA. Biological agents that specifically inhibit the effects of tumour necrosis factor-a (TNF-a) or Interleukin-1 (IL-1) represent a major advancement in the treatment of RA. By targeting molecules that are directly involved in the pathogenesis of RA, these therapies are proving to be efficacious, highly specific and better tolerated than standard therapies. The use of these agents needs to be monitored carefully for possible side-effects, including the development of infections. Additional anti-cytokine agents for the treatment of RA are under further development.
12810193 Molecular genetics of rheumatoid arthritis. 2003 Jun Following the successful determination of the molecular genetics of single-gene disorders, attention has not surprisingly turned to complex genetic disorders. However, preliminary experience suggests that unravelling the genetic component of common inflammatory disorders, such as rheumatoid arthritis, multiple sclerosis and systemic lupus erythematosus, might be a harder nut to crack.
15224650 Risk factors for rheumatoid arthritis. 2004 Both genetic and environmental factors contribute to the development of rheumatoid arthritis (RA). A long-term latent process often precedes the onset of arthritis. Hence, the ultimate causes of RA cannot be clarified by studying only the inflamed joints. Longitudinal studies focusing on risk factors are crucial in approaching the true aetiology. At present, most information gained from epidemiological studies is contradictory or vague. For instance, there is no consensus concerning the long-term effects of pregnancy or the putative protective role of oral contraceptives. There is no doubt that diet plays a role, but no specific nutrient has proved to be either protective or deleterious. Smoking is the only environmental risk factor that has been firmly verified epidemiologically for RA. It can be reasonably regarded as a contributory cause of RA. Studying the immunological effects of exposure to cigarette smoke may offer an opportunity to combine information from basic and epidemiological research to clarify the causal chains leading to RA.
15098368 [Early rheumatoid arthritis]. 2003 The diagnosis and treatment of early rheumatoid arthritis are presented.
14770102 Employment and work disability in rheumatoid arthritis. 2004 Mar PURPOSE OF REVIEW: The cost of work disability due to rheumatoid arthritis is substantial to both individuals and society. Approximately one third of people with rheumatoid arthritis will leave employment prematurely. Several studies over the past two decades have identified risk factors for work disability, and recent literature suggests increasing interest in ways to assess work limitations and offer interventions to prevent work loss. RECENT FINDINGS: Work disability results from a complex interaction of characteristics of individuals, the nature of their work, and their environment, including the physical workplace, policies related to work accommodation, and interpersonal relationships. Practitioners need tools to help identify patients experiencing limitations in the workplace and at risk for permanent work disability. Two new tools show promise in this area. Although there is general agreement that vocational assessment and intervention should occur early in the course of rheumatoid arthritis, evidence for vocational rehabilitation is sadly lacking. A recent systematic review identified only six studies, all uncontrolled, but suggestive of beneficial effects. SUMMARY: Assessment of possible work limitations and potential for vocational rehabilitation should be considered in the evaluation of employed patients and those wishing to work. Further development and evaluation of work retention and return-to-work programs for people with rheumatoid arthritis is required.
12039453 The molecular pathogenesis of collagen-induced arthritis in mice--a model for rheumatoid a 2002 Feb The most widely used model for rheumatoid arthritis is the collagen-induced arthritis (CIA) in mice. This model has gained acceptance since it is reproducible, well defined and has proven useful for development of new therapies for rheumatoid arthritis, as exemplified by the most recent advancement using TNFalpha neutralization treatment. The collagen-induced arthritis model, however, represents only certain pathways leading to arthritis and there is no consensus on how they operate. Nevertheless, we are beginning to understand the immune recognition structures, such as MHC molecules, lymphocyte receptors and type II collagen epitopes, which are of crucial importance for the development of this disease. These provide useful tools for further investigations of the pathogenesis of CIA as well as for understanding the pathogenesis of rheumatoid arthritis.
12491122 [Pharmacotherapy of rheumatoid arthritis]. 2002 The therapeutic goals in rheumatoid arthritis have been so far pain reduction, improvement of function and inhibition of disease progression. Nowadays therapeutic strategies must aim at the induction of remission. Long-term results clearly improve with an early start of DMARD therapy. Additional corticosteroid therapy can further reduce joint destruction. After an early start with DMARD therapy (methotrexate in most cases) corticosteroids should be additionally given in moderate and severe cases. Reconsideration of the therapeutic regime should be performed no later than three months after start of therapy. In the case of remission corticosteroids should be reduced. If there is no remission the DMARD therapy should be intensified, if necessary together with a combination therapy. After another three months a step-down concept can be applied if remission occurs. Otherwise therapy should again be intensified, if necessesary with the use of biologicals.
12455813 Hematological manifestations of rheumatoid arthritis. 2002 OBJECTIVE: To inform clinical rheumatologists about the common and rarer hematological manifestations of rheumatoid arthritis with an emphasis on diagnosis and therapy and a particular reference to Felty's syndrome. METHODS: Literature review. RESULTS: The hematological manifestations can be conveniently categorized into the broad areas of; anemia, particularly NSAID induced iron deficiency anemia and the anemia of chronic disease, neutropenia, particularly Felty's syndrome and the large granular lymphocyte syndrome and drug induced neutropenia; thrombocytopenia, particularly autoimmune and drug induced thrombocytopenia; and hematological malignancy. Rarer conditions, their diagnosis and therapy are also described in this review. CONCLUSION: Hematological manifestations of rheumatoid arthritis are very common. A logical approach using easily available tests should allow straightforward decisions about diagnosis and therapy to be made, even in patients with some of the rarer manifestations.
12794377 [Vilnius rheumatoid arthritis registry]. 2003 OBJECTIVE: To analyze the disease characteristics, health status, working ability, treatment specificities of rheumatoid arthritis (RA) patients referred to Vilnius rheumatoid arthritis register and to compare the data with those reported from other countries rheumatoid arthritis registers. MATERIALS AND METHODS: Rheumatoid arthritis patients' characteristics were analysed using the data of the Vilnius Rheumatoid arthritis register established in the end of 1998 and comprising 1018 rheumatoid arthritis patients from 486506 adult Vilnius citizens. The data were compared to those reported from Oslo Rheumatoid arthritis register, Norfolk Arthritis Register and German rheumatological database. RESULTS: Of all patients, 83.7% were women on the average 60.4 years old. The average disease duration was 12.2 years. Of the whole group of patients, 24% were working people, as many as 58.2% were disabled and most often had the second-third functional class. Non-steroidal anti-inflammatory drugs were taken practically by all rheumatoid arthritis patients (98.3%); 74.3% of the patients were taking corticosteroids. The corticosteroid injections into the joints, mostly into the knee-joints, had been performed to 53.5% of the patients in the past. The treatment with disease-modifying antirheumatic drugs (DMARDs), most commonly sulfasalazine, was applied to 85.6% of rheumatoid arthritis patients. Surgery of joints was applied to 13.4% of the patients: synovectomy to 8.7%, prosthesis operations to 4.7%. Prosthesis operations were performed on the average after 16 years from the beginning of the disease. CONCLUSION: The majority of rheumatoid arthritis patients were elder women. As a rule, the treatment with DMARDs, most commonly sulfasalazine, was prescribed to the patients who had been ill for a short period of time. The rheumatoid arthritis patients in Vilnius were more often unemployed, disabled, with worse physical function. The demografical data of responders and non-responders were similar.
15288002 Epstein-Barr virus and rheumatoid arthritis. 2004 Jul The cause of rheumatoid arthritis (RA) is still unknown. Both genetic and environmental factors may help its development. For 25 years, the Epstein-Barr Virus (EBV) has been suspected to contribute to RA pathogenesis. RA patients have higher levels of anti-EBV antibodies than healthy controls. EBV-specific suppressor T cell function is defective in RA. HLA-DRB1*0404, an RA predisposing allele, is associated with low frequencies of T cells specific for EBV gp110, a replicative phase glycoprotein critical for the control of EBV infection. Patients with RA have higher EBV load in peripheral blood lymphocytes (median 8.84 copies per 500 ng DNA) than healthy controls (median 0.6 copies/500 ng DNA). EBV, a widespread virus, highly recognized by antibodies but never eliminated, is an ideal candidate to trigger chronic immune complex disease. Anti-EBV antibody responses should be considered as one of the chronic autoantibody responses that are most relevant to the development of RA.
15338251 [Cervical myelopathy as a complication of rheumatoid arthritis]. 2004 Aug Arthritis of the cervical spine with instability of the atlantodental joint is a typical and frequent complicaiton in rheumatoid arthritis. Subsequent cervical myelopathy is rare but usually a severe complication. There is no stringent correlation between arthritis of cervical spine an occurrence of cervical myelopathy. Cervical myelopathy is often difficult to discern from parallel multilating peripheral joint damage, which makes the diagnosis difficult. The decision between conservative and operative therapeutic intervention has to be based on subtle clinical, neurophysiological and radiological assessment and-in particular-requires exact analysis of the course of the underlying rheumatoid arthritis and myelopathy. In this diagnostic process close collaboration of rheumatologist, surgeon and neurologist is essential.
15353290 Synovial activation in rheumatoid arthritis. 2004 Sep 1 Rheumatoid arthritis (RA) is a chronic inflammatory disease with progressive articular damage. Activated cells of the synovium produce pro-inflammatory and matrix-degrading effector molecules, which maintain the inflammation and lead to the destruction of the involved joints. In addition to macrophages and T- and B-cells, fibroblast-like synoviocytes must be considered key cells in driving the pathological processes. They can be distinguished by their transformed-appearing phenotype and their invasion into adjacent cartilage and bone. Synovial activation is driven by pro-inflammatory cytokines as well as cytokine independent pathways including endogenous retroviral elements and Toll-like receptors (TLR). These pathways are connected by a complex network of autocrine and paracrine acting factors. Another feature of RA synovium is hyperplasia of the lining layer, which results from increased proliferation and decreased apoptosis of synovial fibroblasts. Thanks to new techniques in basic research, novel insights into the cellular and molecular mechanisms of the pathogenesis of RA were gained and led to the development of new, specific therapeutic strategies.
12403341 Genetic influences on rheumatoid arthritis in African Americans. 2002 Rheumatoid arthritis is a common autoimmune disease characterized by inflammation of the synovial membrane of diarthrodial joints, which often leads to joint damage and disability. There are known associations between major histocompatibility complex class II alleles and susceptibility to rheumatoid arthritis and its severity in Caucasians. African Americans, an admixed population in the United States, has been underrepresented in genetic studies of the susceptibility and severity of rheumatoid arthritis. With the advent of biologic agents, which target specific molecules of the immune system (e.g., tumor necrosis factor, interleukin-1), biologic markers of treatment response in Caucasians and in African Americans would be clinically useful.
12804484 Patient education for adults with rheumatoid arthritis. 2003 BACKGROUND: Because of the unpredictability people with arthritis face on a daily basis, patient education programmes have become an effective complement to traditional medical treatment giving people with arthritis the strategies and the tools necessary to make daily decisions to cope with the disease. OBJECTIVES: To assess the effectiveness of patient education interventions on health status in patients with rheumatoid arthritis. SEARCH STRATEGY: We searched MEDLINE, EMBASE and PsycINFO and the Cochrane Controlled Trials Register. A selection of review articles (see references) were examined to identify further relevant publications. There was no language restriction. SELECTION CRITERIA: Randomised controlled trials (RCT's) evaluating patient education interventions that included an instructional component and a non-intervention control group; pre- and post-test results available separately for RA, either in the publication or from the studies' authors; and study results presented in full, end-of-study report. MAIN RESULTS: Thirty-one studies with relevant data were included. We found significant effects of patient education at first follow-up for scores on disability, joint counts, patient global assessment, psychological status, and depression. A trend favouring patient education was found for scores on pain. Physician global assessment was not assessed in any of the included studies. The dimensions of anxiety and disease activity showed no significant effects. At final follow up no significant effects of patient education were found, although there was a trend favouring patient education for scores on disability. REVIEWER'S CONCLUSIONS: Patient education as provided in the studies reviewed here had small short-term effects on disability, joint counts, patient global assessment, psychological status and depression. There was no evidence of long-term benefits in adults with rheumatoid arthritis.
12110150 Autoantibodies in rheumatoid arthritis and their clinical significance. 2002 Autoantibodies are proven useful diagnostic tools for a variety of rheumatic and non-rheumatic autoimmune disorders. However, a highly specific marker autoantibody for rheumatoid arthritis (RA) has not yet been determined. The presence of rheumatoid factors is currently used as a marker for RA. However, rheumatoid factors have modest specificity (~70%) for the disease. In recent years, several newly characterized autoantibodies have become promising candidates as diagnostic indicators for RA. Antikeratin, anticitrullinated peptides, anti-RA33, anti-Sa, and anti-p68 autoantibodies have been shown to have >90% specificity for RA. These autoantibodies are reviewed and the potential role of the autoantibodies in the pathogenesis of RA is briefly discussed.
12542739 Genetic epidemiology of rheumatoid arthritis. 2002 Dec Building on the spectacular success of molecular genetics in defining the biological basis of many rare single gene disorders over the past decade, epidemiologists have turned their attention to unravelling the complex genetic mysteries of common disorders, such as rheumatoid arthritis (RA). As a prelude to any such endeavour it is obviously important to establish that there is a significant genetic component to the disease. The classical approaches of twin and other family recurrence risk studies, coupled with prevalence studies in different ethnic and migrant populations, have been used to estimate the environmental and genetic contributions to RA. However, developing a consensus on these estimates has proved difficult, thereby providing an early warning to the unwary investigator that the road to gene discovery in RA is likely to be a rough ride.
12951849 [Pregnancy in women with rheumatoid arthritis]. 2003 Aug 4 As rheumatoid arthritis (RA) also affects women in the child-bearing years questions about interaction between the disease and a possible pregnancy are bound to arise. The article reviews the present knowledge of the influence of RA on fertility, inheritance, cause of pregnancy and its outcome, possible effect on the foetus and the disease post-partum and finally the treatment options before, during and after the pregnancy.