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PubMed2005

Human Lyme arthritis and the immunoglobulin G antibody response to the 37-kilodalton arthritis-related protein of Borrelia burgdorferi.

In Borrelia burgdorferi-infected C3H-scid mice, antiserum to a differentially expressed, 37-kDa spirochetal outer-surface protein, termed arthritis-related protein (Arp), has been shown to prevent or reduce the severity of arthritis. In this study, we determined the immunoglobulin G (IgG) antibody responses to this spirochetal protein in single serum samples from 124 antibiotic-treated human patients with early or late manifestations of Lyme disease and in serial serum samples from 20 historic, untreated patients who were followed longitudinally from early infection through the period of arthritis. These 20 patients were representative of the spectrum of the severity and duration of Lyme arthritis. Among the 124 antibiotic-treated patients, 53% with culture-proven erythema migrans (EM) had IgG responses to recombinant glutathione S-transferase (GST)-Arp, as did 59% of the patients with facial palsy and 68% of those with Lyme arthritis. In addition, 75 to 80% of the 20 past, untreated patients had reactivity with this protein when EM was present, during initial episodes of joint pain, or during the maximal period of arthritis. There was no association at any of these three time points between GST-Arp antibody levels and the severity of the maximal attack of arthritis or the total duration of arthritis. Thus, after the first several weeks of infection, 60 to 80% of patients had IgG antibody responses to GST-Arp, but this response did not correlate with the severity or duration of Lyme arthritis.

Anti-Bacterial Agents↗

PubMed2000

Interventions for psoriatic arthritis.

OBJECTIVES: To assess the effects of salazopyrin, auranofin, etretinate, fumaric acid, IMI gold, azathioprine, and methotrexate, in psoriatic arthritis. SEARCH STRATEGY: We searched Medline up to 1995, and Excerpta Medica (June 1974-95). Search terms were psoriasis, arthritis, therapy and/or controlled trial. This was supplemented by manually searching bibliographies of previously published reviews, conference proceedings and contacting drug companies. All languages were included in the initial search. SELECTION CRITERIA: All randomized trials comparing salazopyrin, auranofin, etretinate, fumaric acid, IMI gold, azathioprine, and methotrexate, in psoriatic arthritis. The main outcome measures included individual component variables derived from Outcome Measures in Rheumatology Clinical Trials (OMERACT). These include Acute Phase Reactants, Disability, Pain, Patient Global Assessment, Physician Global Assessment, Swollen joint count, Tender joint count and radiographic changes of joints in any trial of 1 year or longer [Tugwell 1993], and the change in pooled disease index. Only English trials were included in the review. DATA COLLECTION AND ANALYSIS: Data were independently extracted from the published reports by two of the reviewers. An independent blinded quality assessment was also performed. MAIN RESULTS: Nineteen randomized trials were identified of which eleven were included in the quantitative analysis with data from 777 subjects. Although all agents were better than placebo, parenteral high dose methotrexate (not included), salazopyrin, azathioprine and etretinate were the agents that achieved statistical significance in a global index of disease activity (although it should be noted that only one component variable was available for azathioprine and only one trial was available for etretinate suggesting some caution is necessary in interpreting these results). Analysis of response in individual disease activity markers was more variable with considerable differences between different medications and responses. In all trials the placebo group improved over baseline (pooled improvement 0.43 DI units, 95% CI 0. 28-0.59). There was insufficient data to examine toxicity. REVIEWER'S CONCLUSIONS: Parenteral high dose methotrexate and salazopyrin are the only two agents with well demonstrated published efficacy in psoriatic arthritis. The magnitude of the effect seen with azathioprine, etretinate, oral low dose methotrexate and perhaps colchicine suggests that they may be effective but that further multicentre clinical trials are required to establish their efficacy. Furthermore, the magnitude of the improvement observed in the placebo group strongly suggests that uncontrolled trials should not be used to guide management decisions in this condition.

Antirheumatic Agents↗

PubMed2000

Balneotherapy for rheumatoid arthritis and osteoarthritis.

BACKGROUND: Balneotherapy (hydrotherapy or spa therapy) for patients with arthritis is one of the oldest forms of therapy. One of the aims of balneotherapy is to soothe the pain and as a consequence to relieve patients' suffering and make them feel well. OBJECTIVES: To perform a systematic review to assess the effects of balneotherapy for rheumatoid arthritis and osteoarthritis. SEARCH STRATEGY: Using the Cochrane search strategy, studies were found by screening: 1) The Medline CD-ROM database from 1966 to June 1999 and 2) the database from the Cochrane Field 'Rehabilitation and Related Therapies', which contains also studies published in journals not covered by Medline. Also, 3) reference checking and 4) personal communications with authors was carried out to retrieve eligible studies. To perform an adequate assessment of the methodological quality the languages of the publications had to be: Dutch, English, French or German. Date of the most recent literature search: June, 1999 SELECTION CRITERIA: Studies were eligible if they were randomized controlled trials (RCT) comparing balneotherapy with any intervention or with no intervention. Patients included had rheumatoid arthritis (RA), osteoarthritis (OA) or some other form of arthritis. Trials incorporating patients with definite or classical rheumatoid arthritis (RA) as defined by the American Rheumatism Association Criteria (ARA) (Ropes 1958) (these criteria have changed over time) or by the criteria of Steinbrocker (1949) were regarded as a separate group. At least one of the WHO/ILAR core set of endpoints for RA clinical trials had to be the main outcome measures. DATA COLLECTION AND ANALYSIS: A criteria list used to assess the methodological quality was the one developed at the Department of Epidemiology at the Maastricht University, called "the Maastricht list". The quality scores and data abstraction of the studies were carried out independently by two reviewers (HdV, RdB). Disagreements were solved by consensus. MAIN RESULTS: Ten trials with 607 patients were included in this review. Most trials reported positive findings, but were methodologically flawed to some extent. A 'quality of life' outcome was reported by two trials. Just one of the randomized trials mentioned an intention-to-treat analysis and only three performed a comparison of effects between groups. Pooling of the data was not performed, because of heterogeneity of the studies, multiple outcome measurements, and, apart from two studies, the overall data presentation was too scarce to enable pooling of the data. REVIEWER'S CONCLUSIONS: One cannot ignore the positive findings reported in most trials. However the scientific evidence is weak because of the poor methodological quality, the absence of an adequate statistical analysis, and the absence, for the patient, of most essential outcome measures (pain, quality of life), Therefore, the noted "positive findings" should be viewed with caution. Because of the methodological flaws an answer about the efficacy of balneotherapy cannot be provided at this time. Flaws found in the reviewed studies could be avoided in future trials.

Arthritis, Rheumatoid↗

PubMed2000

Penicillamine for rheumatoid arthritis.

OBJECTIVES: To estimate the short-term effects of D-penicillamine for the treatment of rheumatoid arthritis (RA). SEARCH STRATEGY: We searched the Cochrane Musculoskeletal Group's trials register, the Cochrane Controlled Trials Register, Medline up to and including December 1998 and Embase from 1988-1998. We also carried out a handsearch of the reference lists of the trials retrieved from the electronic search. SELECTION CRITERIA: All randomized controlled trials and controlled clinical trials comparing D-penicillamine against placebo in patients with rheumatoid arthritis. DATA COLLECTION AND ANALYSIS: The methodological quality of the trials was assessed independently by two reviewers (CS, EB) and checked by a third (MS) using a validated quality assessment tool. Rheumatoid arthritis outcome measures were extracted from the publications for the six-month endpoint and stratified according to D-penicillamine dosages: low (<500mg/day), moderate (500 to <1000mg/day) and high (1000 mg/day or greater). Data was abstracted by one reviewer and checked by a second (CS, MS). The pooled analysis was performed using the standardized mean difference for joint counts, pain and global assessments. The weighted mean difference was used for erythrocyte sedimentation rate (ESR). Toxicity was evaluated with pooled odds ratios for withdrawals and adverse reactions. A chi-square test was used to assess heterogeneity among trials. Fixed effects models were used throughout, since no statistical heterogeneity was found. MAIN RESULTS: Six trials were identified, with 425 patients randomized to D-penacillamine and 258 to placebo. A statistically significant benefit was observed for D-penicillamine when compared to placebo for all three-dose ranges and for most outcome measures including: tender joint counts, pain, physician's global assessments and ESR. The standardized weighted mean differences between treatment and placebo in moderate doses were -0. 51 [95% CI -0.88, -0.14] for tender joint counts, -0.56 (95% CI -0. 87, -0.26) for pain and -0.97 (95% CI -1.25, -0.70) for global assessment. The difference for ESR was -10.6 mm/hr. Similar results were observed for the higher dose group. Total withdrawals were significantly higher in the moderate and high dosage D-penicillamine groups (OR=1.63 and 2.13 respectively), mostly due to increased adverse reactions (OR = 2.60 and 4.95 respectively), including renal and hematological abnormalities. REVIEWER'S CONCLUSIONS: D-penicillamine appears to have a clinically and statistically significant benefit on the disease activity of patients with rheumatoid arthritis. Its efficacy appears to be similar to that of other disease modifying anti-rheumatic drugs (DMARDs), but with a significantly higher toxicity. Its effects on long-term functional status and radiological progression are not clear from this review.

Antirheumatic Agents↗

PubMed2002

Evaluation of quantitative trait loci regulating severity of mycobacterial adjuvant-induced arthritis in monocongenic and polycongenic rats: identification of a new regulatory locus on rat chromosome 10 and evidence of overlap with rheumatoid arthritis susceptibility loci.

OBJECTIVE: To evaluate the regulatory potential of genetic loci controlling Mycobacterium butyricum adjuvant-induced arthritis (Mbt-AIA) using mono- and polycongenic rats. METHODS: Of 4 quantitative trait loci (QTLs) that regulate Mbt-AIA, F344 alleles at 3 of these loci, Aia1, Aia2, and Aia3, are associated with lower arthritis severity, whereas F344 alleles at Aia4 are associated with greater arthritis severity. In this study, we constructed congenic lines by transferring 1 or more of the F344 genomic segments containing Aia1, Aia2, and Aia3 onto the DA genome. We comparatively evaluated their responses to Mbt-AIA with the responses of parental DA and F344 rats. RESULTS: Aia1, encompassing the rat major histocompatibility complex, reduced arthritis severity in monocongenic rats of both sexes. The arthritis-lowering effects of Aia2 and Aia3 were sex-influenced and were therefore observed in only males and only females, respectively. Polycongenic rats containing F344 genomic regions at Aia1, Aia2, and Aia3 developed Mbt-AIA of relatively greater severity than did F344 rats, implying that in DA and F344 rats, there could be other Mbt-AIA loci in addition to Aia1, Aia2, Aia3, and Aia4. To test the possibility that some of these Mbt-AIA-regulatory loci may colocalize with other arthritis QTLs, we evaluated Mbt-AIA in DA.F344 monocongenic rats containing collagen-induced arthritis QTLs. Cia5 (the QTL region on chromosome 10), but not Cia5a, Cia4, or Cia6, also regulated Mbt-AIA, and was named Aia5. CONCLUSION: F344 genomic regions at Aia1, Aia2, and Aia3 and the newly identified Aia5 contain genes that reduce Mbt-AIA severity in DA rats. These Mbt-AIA-regulatory loci overlap rheumatoid arthritis-susceptibility loci in humans.

Alleles↗

PubMed1997

Inhibition of cartilage degradation in rat collagen-induced arthritis but not adjuvant arthritis by the neutrophil elastase inhibitor MDL 101,146.

OBJECTIVE AND DESIGN: The neutrophil elastase inhibitor MDL 101,146 was examined for its anti arthritic effect and to determine the role of neutrophil elastase in collagen-induced arthritis and adjuvant arthritis. MATERIAL: The collagen-induced arthritis model was performed in female DA rats immunized on day 0 an 1.7 with chick type II collagen in Freund's incomplete adjuvant. Adjuvant arthritis was induced in female Lewis rats by an intradermal injection of heat-killed Mycobacterium tuberculosis H37RA. METHODS: The clinical signs of arthritis were assessed, joint swelling was measured using calipers and bone degradation, new bone proliferation, pannus formation and cartilage degradation were evaluated histologically. RESULTS: MDL 101,146 administered orally inhibited the severity of collagen-induced arthritis as measured by a reduction in clinical score and joint swelling. Histological evaluation demonstrated a bone and cartilage sparing effect of MDL 101,146 in the tibio-tarsal joint of animals with collagen-induced arthritis. CONCLUSIONS: These results suggest that destruction of the joint in collagen-induced arthritis is at least partially due to neutrophil elastase.

Animals↗

PubMed1998

1,25-Dihydroxycholecalciferol inhibits the progression of arthritis in murine models of human arthritis.

1,25-Dihydroxycholecalciferol [1,25-(OH)2D3] has been shown to inhibit the progression of experimental autoimmune encephalomyelitis (EAE). Here we tested the possibility that 1, 25-dihydroxycholecalciferol might be therapeutic for another autoimmune disease, arthritis. Two different animal models of arthritis were tested, namely, murine Lyme arthritis and collagen-induced arthritis. Infection of mice with Borrelia burgdorferi (the causative agent of human Lyme arthritis) produced acute arthritic lesions including footpad and ankle swelling. Supplementation with 1,25-dihydroxycholecalciferol of an adequate diet fed to mice infected with B. burgdorferi minimized or prevented these symptoms. Mice immunized with type II collagen also developed arthritis. The symptoms of this disease were also prevented by dietary supplementation with 1,25-dihydroxycholecalciferol. 1, 25-Dihydroxycholecalciferol given to mice with early symptoms of collagen-induced arthritis prevented the progression to severe arthritis compared with untreated controls. These results suggest that 1,25-dihydroxycholecalciferol and/or its analogs may be a valuable treatment approach to this disease.

Animals↗

PubMed1992

Aetiological role of bacteria associated with reactive arthritis in pauciarticular juvenile chronic arthritis.

BACKGROUND: The cause of juvenile chronic arthritis (JCA) is unknown. Pauciarticular JCA is the most common subtype and can be subdivided into early (type I) and late onset (type II) forms, the latter clinically resembling reactive arthritis. METHODS: The cellular immune responses to bacteria associated with reactive arthritis in blood and synovial fluid from 39 children with pauciarticular JCA, three children with classical reactive arthritis, and two children with psoriatic arthritis were examined. Specific titres of antibodies to bacteria in serum samples were measured in all patients. RESULTS: A bacteria specific synovial cellular immune response was found in two of three (67%) patients with reactive arthritis and 14 of 28 (50%) patients with pauciarticular JCA type II but only in one of 11 (9%) patients with pauciarticular JCA type I and none in patients with psoriatic arthritis. Six patients responded specifically to Chlamydia trachomatis and 11 to Yersinia enterocolitica. Antigen specific lymphocyte proliferation correlated poorly with the specific antibody response. CONCLUSIONS: These findings suggest that bacteria with associated reactive arthritis may have a causative role in pauciarticular JCA type II but not in JCA type I.

Adolescent↗

PubMed1992

Craniomandibular disorders in rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis. A clinical study.

Sixty-one subjects with rheumatoid arthritis, 61 with psoriatic arthritis, 61 with ankylosing spondylitis, and 61 healthy controls were examined with regard to subjective symptoms and clinical signs of craniomandibular disorders (CMD). The frequencies of most subjective and clinical variables were higher in all three disease groups than in the control group. Subjects with rheumatoid arthritis and psoriatic arthritis showed more frequent and severe signs and symptoms than subjects with ankylosing spondylitis. It is concluded that subjective symptoms and clinical signs of CMD are common in rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis and are mainly caused by the respective general joint disease. None of the signs and symptoms is pathognomonic for rheumatoid arthritis, psoriatic arthritis, or ankylosing spondylitis.

Adult↗

PubMed2001

The human endoplasmic reticulum molecular chaperone BiP is an autoantigen for rheumatoid arthritis and prevents the induction of experimental arthritis.

Rheumatoid arthritis (RA) is the most common, crippling human autoimmune disease. Using Western blotting and tandem mass spectroscopy, we have identified the endoplasmic reticulum chaperone BiP, a 78-kDa glucose-regulated protein, as a possible autoantigen. It preferentially stimulated increased proliferation of synovial T cells from patients with RA but not from patients with other arthritides. Mice with established collagen- or pristane-induced arthritis developed IgG Abs to BiP. Although BiP injected in CFA failed to induce arthritis in several strains of rats and mice, including HLA-DR4(+/-)- and HLA-DR1(+/+)-transgenic animals, it completely inhibited the development of arthritis when given i.v. 1 wk before the injection of type II collagen arthritis. Preimmunization with BiP suppressed the development of adjuvant arthritis in Lewis rats in a similar manner. This is the first report of a mammalian chaperone that is an autoantigen in human RA and in experimental arthritis and that can also prevent the induction of experimental arthritis. These findings may stimulate the development of new immunotherapies for the treatment of RA.

Adult↗

PubMed1995

The arthritis knowledge questionnaire. A test for measuring patient knowledge of arthritis and its self-management.

OBJECTIVE: To develop a questionnaire for measuring patients' knowledge about arthritis and its self-management. METHODS: An initial item pool of 175 multiple-choice questions was developed, based on the Stanford Arthritis Self-Management Program and on basic medical knowledge about arthritis and its management. A rheumatologist, psychologist, physiotherapist, and several lay individuals assessed the questions for content validity, breadth of coverage, and face validity. Patients assessed the questions for comprehensibility. Four subject groups with varying knowledge levels were recruited to answer the entire set of questions. Item analysis was undertaken to develop parallel forms of subtests so that repeated assessments could be undertaken. RESULTS: The final instrument, the Arthritis Knowledge Questionnaire, consists of 2 tests, each comprising 3 subtests: self-management (15 items), arthritis in general (15 items), and rheumatoid arthritis (11 items). CONCLUSION: We present psychometric evidence that these parallel forms provide highly reliable and valid estimates of knowledge concerning arthritis and arthritis self-management.

Arthritis↗

PubMed2006

Reexamining the arthritis-employment interface: perceptions of arthritis-work spillover among employed adults.

OBJECTIVE: To examine employed individuals' perceptions of arthritis-work spillover (AWS), the reciprocal influence of arthritis on work and work on arthritis, and the demographic, illness, and work context factors associated with AWS. METHODS: The study group comprised 492 employed individuals with osteoarthritis or inflammatory arthritis. Participants completed an interview-administered, structured questionnaire assessing AWS, demographic (e.g., age, sex), illness (e.g., disease type, pain, activity limitations), and work context (e.g., workplace control, hours of work) variables. Principal components analysis, reliability analysis, and multiple linear regression were used to analyze the data. RESULTS: A single factor solution emerged for AWS. The scale had an internal reliability of 0.88. Respondents were more likely to report that work interfered with caring for their arthritis than they were to report that their disease affected their work performance. Younger respondents, those with more fatigue and workplace activity limitations, and those working in trades and transportation reported more AWS. Individuals with more control over their work schedules reported less AWS. CONCLUSION: The results of this study extend research on arthritis by reexamining the interface between arthritis and employment. This study introduces a new measure of AWS that enhances the range of tools available to researchers and clinicians examining the impact of arthritis in individuals' lives.

Arthritis↗

PubMed1997

Altered (oxidized) C1q induces a rheumatoid arthritis-like destructive and chronic inflammation in joint structures in arthritis-susceptible rats.

Previous studies have identified an altered C1q molecule in synovial fluids from the joints of rheumatoid arthritis patients. We therefore immunized arthritis-susceptible Lewis 1A.AVN rats with either native C1q (C1q nat), altered (oxidized) C1q (C1q ox), or type II collagen (CII, induces arthritis in these animals), in order to induce arthritis. Unlike C1q nat, both CII and C1q ox were able to induce swelling and erythema of joints consistent with an arthritis-like inflammatory reaction. Histopathological evaluation of individual joint sections revealed synovitis, bursitis and tendovaginitis, massive joint destruction, and severe pannus formation. In a time-course study, no differences in onset of arthritis or pathology were observed between C1q ox-induced arthritis and that induced by CII. High titers of antibodies recognizing CII, but not C1q (native or oxidized), were detected in rats immunized with CII. In contrast C1q ox, but not C1q nat, induced antibodies reactive with both C1q and CII. Antibodies from C1q ox-immunized animals contained an antibody subset that reacted with C1q but not CII and a subset that reacted with CII but not C1q, implying that induction of an immune response to CII does not require CII. These data support the hypothesis that C1q may provide one of the early antigens involved in induction of arthritis, before CII becomes available as antigen.

Animals↗

PubMed1991

Serum aminoterminal propeptide of type III procollagen in psoriasis and psoriatic arthritis: relation to liver fibrosis and arthritis.

Levels of serum aminoterminal propeptide of type III procollagen were measured in 170 patients with psoriasis (49% with coexistent psoriatic arthritis) who had liver biopsies performed during or before treatment with methotrexate or, in some cases, with retinoids. Psoriasis patients with fibrosis or cirrhosis in their liver biopsy specimens had a significantly higher mean serum aminoterminal propeptide of type III procollagen than did patients without fibrosis and without arthritis. Only 4% of patients without cirrhosis or fibrosis and no arthritis had an elevated serum aminoterminal propeptide of type III procollagen. In contrast, 38% of patients with psoriatic arthritis had an increased aminoterminal propeptide of type III procollagen in the absence of detectable liver fibrosis. It is concluded that the number of liver biopsies performed on methotrexate-treated psoriasis patients with or without arthritis may be reduced to a minimum as long as serum aminoterminal propeptide of type III procollagen is normal. Increased serum aminoterminal propeptide of type III procollagen in the absence of arthritis is a strong indicator of liver fibrogenesis and suggests the need for liver biopsy to monitor possible methotrexate-induced toxicity. In patients with psoriatic arthritis an increased aminoterminal propeptide of type III procollagen may be related to the joint disease. Patients with psoriatic arthritis and increased levels of aminoterminal propeptide of type III procollagen should therefore follow the established guidelines for the use of methotrexate in psoriasis.

Alkaline Phosphatase↗

PubMed2000

Understanding the adoption of arthritis self-management: stages of change profiles among arthritis patients.

Clinical observations and recent studies suggest that arthritis patients vary considerably in their involvement in self-management efforts. In the literature on health promotion, there is growing recognition that patients may be at different stages of change with respect to the adoption of self-management strategies. The major goal of the present study was to examine whether cluster analysis could be used to identify homogeneous subgroups of patients having persistent arthritis pain based on their responses to a stages of change questionnaire. Participants in this study (103 patients having rheumatoid arthritis and 74 patients having osteoarthritis) completed a stages-of-change measure specific to adoption of a self-management approach to their arthritis. A cluster analysis identified five distinct subgroups of arthritis patients: (1) precontemplation - 44% of the sample; (2) contemplation - 11% of the sample; (3) preparation - 22% of the sample; (4) unprepared action - 6% of the sample; and (5) prepared maintenance - 17% of the sample. These subgroups are generally consistent with what might be expected based on the transtheoretical model of stages of change by Prochaska and DiClemente (Prochaska JO, DiClemente CC. Towards a comprehensive, transtheoretical model of change: states of change and addictive behaviors. In: Miller WR, Heather N, editors. Applied clinical psychology, 2nd ed. Treating addictive behaviors, New York: Plenum Press, 1998. pp. 3-24.), and may have important clinical implications. For example, it is possible that the arthritis subgroups identified may predict arthritis patients' participation in and responsiveness to pain-coping skills training, exercise interventions, or other formal self-management training programs. Also, one may be able enhance the outcomes of self-management interventions for arthritis by tailoring treatment to the patient's particular stage.

Adaptation, Psychological↗

PubMed2001

Arthritis induced in rats with nonimmunogenic adjuvants as models for rheumatoid arthritis.

Rat models are useful for studies of the pathogenesis of rheumatoid arthritis (RA) since rats are extraordinarily sensitive to induction of arthritis with adjuvants. Injection of not only the classical complete Freund's adjuvant but also mineral oil without mycobacteria and pure adjuvants such as pristane and squalene, induce severe arthritis in many rat strains. Models like pristane-induced arthritis in rats are optimal models for RA since they fulfill the RA criteria including a chronic relapsing disease course. Arthritogenic adjuvants like pristane, avridine, squalene and mineral oil are not immunogenic since they do not contain major histocompatibility complex (MHC) binding peptides. Nevertheless, the diseases are MHC-associated and dependent on the activation of alphabetaTCR (T-cell receptor)-expressing T cells. However, it has not been possible to link the immune response to joint antigens or other endogenous components although immunization with various cartilage proteins induce arthritis but with different pathogeneses. To unravel the mechanisms behind adjuvant-induced arthritis, a disease-oriented genetic approach is optimal. Several loci that control onset of arthritis, severity and chronicity of the disease have been identified in genetic crosses and most of these have been confirmed in congenic strains. In addition, many of these loci are found in other autoimmune models in the rat as well as associated with arthritis in mice and humans.

Adjuvants, Immunologic↗

PubMed1996

Interleukin-10 suppresses the development of collagen type II-induced arthritis and ameliorates sustained arthritis in rats.

The collagen-induced arthritis model in DA rats induced with homologous rat type II collagen was chosen to determine the therapeutic capacity and effects on autoimmunity by IL-10. Systemic IL-10 treatment (100 or 10 micrograms/day) with mini-osmotic pumps during the periods of arthritis onset (days 12-20 after immunization) decreased the frequency of arthritis and delayed the onset and reduced the severity of arthritis in the few rats that eventually developed arthritis. Concomitantly, levels of autoantibodies to CII were reduced. To test the activity on established arthritis, IL-10 was administered subcutaneously in the paws. This treatment reduced the swelling but did not block the arthritis process. The effective treatment required 100 micrograms of IL-10 every 12th hour while 50 micrograms of IL-10 had little effect, although a tendency of reduced paw swelling was observed. Surprisingly, therapeutic IL-10 treatment led to higher serum levels of autoantibodies to CII. The highest doses of IL-10 (100 micrograms) did not show any apparent toxic effects when given locally or systematically. Taken together, this study suggests that IL-10 is a candidate for treatment of rheumatoid arthritis.

Animals↗

PubMed2004

Epstein-Barr virus, arthritis, and the development of lymphoma in arthritis patients.

PURPOSE OF REVIEW: Rheumatoid arthritis is a complex multisystem disorder. The manifestations of joint disease are usually clinically apparent, but the effects of the concomitant abnormalities of immune function are more subtle. It has been suggested that patients with rheumatoid arthritis have an impaired capacity to control infection with Epstein-Barr virus. Epstein-Barr virus has oncogenic potential and is implicated in the development of some lymphomas. This review analyses the relation between Epstein-Barr virus, rheumatoid arthritis, and the risk of lymphoma and considers the effect of immunosuppression on this triad. RECENT FINDINGS: Recent publications provide evidence for an altered Epstein-Barr virus-host balance in patients with rheumatoid arthritis, who have a relatively high Epstein-Barr virus load. Large epidemiologic studies confirm that lymphoma is more likely to develop in patients with rheumatoid arthritis than in the general population. The overall risk of development of lymphoma has not risen with the increased use of methotrexate or biologic agents. Histologic analysis reveals that most lymphomas in rheumatoid arthritis patients are diffuse large B cell lymphomas, a form of non-Hodgkin lymphoma. Epstein-Barr virus is detected in a proportion of these. SUMMARY: Overall, patients with rheumatoid arthritis have approximately a twofold increased risk of experiencing lymphoma. Some, but not all, of this increased risk reflects an increase in Epstein-virus-associated lymphomas. This in turn may be influenced by the elevated Epstein-Barr virus load found in rheumatoid arthritis patients and may reflect subtle impairment of antiviral immunity in this group of patients.

Arthritis, Rheumatoid↗