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PubMed1999

Multiple rheumatoid papules characteristic of the early stage of rheumatoid vasculitis.

The rheumatoid papule has recently been described as the skin manifestation of rheumatoid arthritis (RA). The papules represent leukocytoclastic vasculitis and necrobiosis clinicopathologically. We report a 59-year-old Japanese woman with multiple recurrent rheumatoid papules located on the bilateral extensor forearms in correlation with the level of RA activity and as a cutaneous manifestation of rheumatoid vasculitis. These papules appeared prior to other cutaneous manifestations. It was suggested that rheumatoid papules represent the early stage of rheumatoid vasculitis and that they are a reliable early clinical marker of rheumatoid vasculitis.

Arthritis, Rheumatoid↗

PubMed1986

[Class II HLA antigens and rheumatoid factors in rheumatoid polyarthritis. Inverse influence of DR4 and DR7 antigens?].

A linkage disequilibrium was searched for between HLA-DR antigens and rheumatoid factor level both measured using latex agglutination and a solid phase immuno-enzymic assay (FR-PAP) among 251 sera from patients suffering from classical rheumatoid arthritis for at least 5 years, recorded in the Cooperative Swiss Study on Rheumatoid Arthritis. An association between the presence of HLA-DR7 and low levels of rheumatoid factor was found. This association was stronger when the DR4, 7 heterozygous subjects were excluded. The comparison of the DR7, not equal to 4 and DR not equal to 4, not equal to 7 subjects demonstrated that the DR7 effect was independent of DR4. Although the association between DR4 and high levels of rheumatoid factor was not statistically significant in this study, these data suggested an opposite influence of DR4 and DR7 on rheumatoid factor level among rheumatoid arthritis suffering patients. The influence of DR4 appeared to be dominant among heterozygous DR4, 7 patients.

Arthritis, Rheumatoid↗

PubMed1979

IgG-, IgM- and IgA-rheumatoid factors in healthy adults and rheumatoid patients determined by an indirect immunofluorescence method.

Sera from 173 healthy adults and 55 rheumatoid patients were studied for IgG-, IgM- and IgA-rheumatoid factors (RFs) by a modification of Este's indirect immunofluorescence method. Rabbit IgG bound to smeared sheep red cells was used as antigen. With each serum tested a smear on non-sensitized cells was used as control antigen. Anti-IgG of the sera studied, binding to the antigen, was demonstrated by fluorescein-conjugated antisera, monospecific for gamma, mu and alpha chains, and not containing antibodies to sheep erythrocytes or rabbit IgG. Positive reactions were obtained with IgG as antigen, but not with the F(ab')2 fragment. The sera tested were treated with dithiothreitol before they were assayed for IgG-RF, in order to abolish false-positive reactions due to IgM-RF activity. The detection limit for IgM-RF was 1 IU per ml. IgM-RF titres of 9 occurred in 7% of healthy adults and 73% of rheumatoid patients, titres greater than or equal to 18 in 3.5% and 67% respectively. IgG-RF titres of 9 occurred in 9% of healthy adults, 21% of seronegative and 24% of seropositive rheumatoid patients. Titres of 18 occurred in 3% of healthy adults and in 14% of seronegative rheumatoid patients. Titres of greater than or equal to 18 occurred in 22% of seropositive rheumatoid patients. IgG-RF was correlated with an involvement of more than 20 joints. IgA-RF was found in 83% of seropositive, 11% of seronegative rheumatoid patients and in none of the healthy adults (serum dilution 1:9).

Adult↗

PubMed1983

Administration of nonsteroidal anti-inflammatory agents in patients with rheumatoid arthritis. Effects on indexes of cellular immune status and serum rheumatoid factor levels.

We have previously reported that nonsteroidal anti-inflammatory agents (NSAIAs) stimulate cellular immune responses and inhibit production of IgM rheumatoid factor in cultures of lymphocytes from patients with rheumatoid arthritis. We had 20 patients with rheumatoid arthritis stop taking NSAIAs for two weeks and then take piroxicam, a new NSAIA, for an additional ten weeks to assess the in vivo effects of NSAIAs on cellular immunity and rheumatoid factor levels. In each case, serum rheumatoid factor levels rose and phytohemagglutinin response fell when placebo was substituted for NSAIAs. Piroxicam administration was associated with a fall in rheumatoid factor levels to approximately 62% of the baseline level and with an increase in phytohemagglutinin response. The action of NSAIAs in rheumatoid arthritis may be mediated to a degree by partial correction of the disordered immunoregulation in this disease.

Adult↗

PubMed1997

Relations between absolute number of CD4 + CD29+ memory cells and levels of interleukin-6, rheumatoid factors, and acute phase proteins in rheumatoid synovial fluid.

Synovial fluid samples from 21 rheumatoid arthritis patients were analyzed for lymphocyte subsets using flow cytometry and antibodies to the lymphocyte surface antigens CD3, CD4, CD8, CD16, CD19, CD29, and CD45RA. Synovial fluid levels of interleukin-6, rheumatoid factors and acute phase proteins were also measured. Depletion of CD45RA+ cells and predominance of CD29+ cells were found. Interleukin-6 levels were markedly elevated (1155 pg/ml; range, 24-3875 pg/ml), as were levels of IgM, IgG and IgA rheumatoid factors and of acute phase proteins. CD4 + CD29+ counts were significantly correlated with interleukin-6 levels. Interleukin-6 levels were significantly correlated with levels of all three rheumatoid factor classes but not with levels of acute phase proteins. Significant correlations were also found between CD19+ B counts and levels of all three rheumatoid factor classes. These data suggest that synovial fluid CD4 + CD29+ cells may be involved in the immune dysregulation characteristic of rheumatoid arthritis. The correlation between CD4 + CD29+ counts and interleukin-6 levels is consistent with the recent hypothesis that, together with monocytes, CD4 + CD29+ cells are an important source of the elevated levels of interleukin-6 seen in rheumatoid synovial fluid.

Acute-Phase Proteins↗

PubMed1998

Pathogenic mechanisms in the rheumatoid nodule: comparison of proinflammatory cytokine production and cell adhesion molecule expression in rheumatoid nodules and synovial membranes from the same patient.

OBJECTIVE: To investigate the production of proinflammatory cytokines and expression of cell adhesion molecules in the rheumatoid nodule. METHODS: Cytokine content (tumor necrosis factor alpha [TNFalpha], interleukin-1beta [IL-1beta], and IL-1 receptor antagonist [IL-1Ra]), at the messenger RNA (mRNA) and protein levels, and cell adhesion molecule expression were studied in 16 rheumatoid nodules and 6 synovial membranes. RESULTS: Macrophages in the rheumatoid nodules contained TNFalpha, IL-1beta, and IL-1Ra mRNA and protein, particularly in perivascular cells of the stroma and in the palisading layer. All cell adhesion molecules studied were expressed in both the rheumatoid nodules and synovial membranes, with increased expression of E-selectin in the rheumatoid nodule compared with the synovial membrane, and with the absence of vascular cell adhesion molecule 1 expression on cells of the palisading layer in the rheumatoid nodule. CONCLUSION: The presence of similar proinflammatory cytokines and cell adhesion molecules in the rheumatoid nodule and synovial membrane suggests that similar pathogenic processes result in the chronic inflammation and tissue destruction in these lesions.

Adult↗

PubMed1988

Antigen induced rheumatoid factors: characteristics of monoclonal rheumatoid factors produced after protein and carbohydrate immunization.

We generated a panel of monoclonal rheumatoid factors (MRF) from BALB/c mice immunized with ovalbumin, dextran or group-A-carbohydrate. Individual MRF were analyzed in terms of their binding to the four isotypes of murine IgG, isotypes of human IgG, and rabbit IgG, the idiotypes they express, and the VH gene families they employ. We found that antigen induced rheumatoid factors could be divided into three different families based on their isotypic specificity for murine IgG: an IgG1 binding family, and IgG3 binding family, and a family of MRF that bound all four murine isotypes. Rheumatoid factors belonging to all three families were isolated from mice immunized with carbohydrate antigens. The rheumatoid factors isolated from protein immunized mice all belonged to the IgG1 binding family. We were able to define two cross-reactive idiotypes among MRF, one expressed by a subgroup of the IgG1 binding family, and a second cross-reactive idiotype expressed by some members of the pan-binding family. We determined VH gene use in five of six MRF belonging to the IgG1 binding family and four of four members of the pan-binding family. Four of the IgG1 binding rheumatoid factors and three of the pan-binding rheumatoid factors utilize the J558 VH gene family. Rheumatoid factors produced after carbohydrate antigen immunization, as compared with those generated by protein immunization, are diverse in their isotypic specificity, and show a greater ability to bind heterologous IgG.

Animals↗

PubMed2007

Pulmonary rheumatoid nodules demonstrating features usually associated with rheumatoid synovial membrane.

OBJECTIVES: To describe the unusual immunohistological characteristics of two pulmonary rheumatoid nodules showing ectopic lymphoid follicles and the features normally associated with rheumatoid synovial membrane, and to discuss the implications of this novel observation. METHODS: Two formalin-fixed wax-embedded pulmonary rheumatoid nodules were processed for immunohistology. RESULTS: The central structure of the pulmonary nodules was typical of that uniformly expected in a rheumatoid nodule with central necrosis surrounded by a palisade of macrophages. However, a feature not previously observed in nodules was the presence of lymphoid aggregates containing B lymphocytes and, in some cases, showing characteristic features of lymphoid follicles. CONCLUSIONS: The presence of B lymphocytes and the development of ectopic lymphoid follicles in rheumatoid nodules have not been described previously. It is similar to synovial membrane, and contrasts with the expected structure of subcutaneous nodules where B cells and lymphoid follicles are normally absent. These observations establish that the morphology of rheumatoid nodules can vary in different tissues. They further suggest that the inflammatory process in the nodule and synovial membrane are likely to be similar, and that the characteristics of different tissues may be an important determinant of apparent differences between inflammatory lesions in synovial membrane and extra-articular nodules in rheumatoid arthritis.

B-Lymphocytes↗

PubMed1981

Rheumatoid arthritis and pseudo-rheumatoid arthritis in calcium pyrophosphate dihydrate crystal deposition disease.

Calcium pyrophosphate dihydrate (CPPD) crystal deposition disease can lead to many clinical syndromes. One syndrome simulates rheumatoid arthritis and is thus called "pseudo-rheumatoid arthritis." Since some patients have true rheumatoid arthritis with CPPD crystal deposition disease, the clinician may have difficulty differentiating those patients from others who have the pseudo-rheumatoid syndrome. Such a diagnostic problem can be solved radiographically. Eleven patients with CPPD crystal deposition disease were studied; five had true rheumatoid arthritis and six had pseudo-rheumatoid arthritis. Because osseous erosions were not apparent in the arthropathy of uncomplicated CPPD crystal deposition disease, the detection of skeletal erosive changes indicated a true rheumatoid arthritis process.

Aged↗

PubMed2004

A case of rheumatoid arthritis exhibiting accelerating rheumatoid pleurisy during low-dose weekly methotrexate therapy.

A 75-year-old Japanese man suffering from rheumatoid arthritis (RA) had received methotrexate (MTX) treatment for 9 years and developed bilateral pleural thickening with exudative pleural effusions despite remission of the polyarthritis. A diagnosis of rheumatoid pleurisy, made by exclusion, was supported by the elevated rheumatoid factor level of the pleural fluid. The pleurisy developed concomitantly with MTX-induced leukocytopenia, and discontinuation of the MTX treatment partially improved the CRP level. These findings indicate a causal relation between the rheumatoid pleurisy and MTX and suggest that MTX therapy may be ineffective in the treatment of rheumatoid pleurisy. Treatment with 10 mg of prednisolone and 100 mg of cyclosporine A daily resulted in rapid resolution of the pleurisy. Although MTX-induced rheumatoid pleurisy is a rare condition, MTX therapy should be considered carefully in RA patients with concomitant rheumatoid pleurisy.

Journal Article↗

PubMed2003

Rheumatoid nodulosis: is it a different subset of rheumatoid arthritis?

Rheumatoid nodulosis is an entity that describes a particular variant of polyarthritis associated with early manifestations of palindromic rheumatism, radiologic subchondral bone cysts, and subcutaneous rheumatoid nodules. This study describes the clinical, radiologic, histologic, crystallographic, and laboratory findings, as well as the outcome in a group of 16 patients with rheumatoid nodulosis that were followed for a period of 1-12 years. Six of these patients had an aggressive course and developed classic erosive polyarticular rheumatoid arthritis, while the others continued having episodic arthritis without erosive disease. Seven patients had cholesterol crystals in olecranon bursae containing nodules. Second-line drugs used to control the articular manifestations did not improve the nodulosis, erosive, or cystic subchondral bone changes. Rheumatoid nodulosis mimics several other rheumatic diseases, and in about 40%, classic erosive rheumatoid arthritis develops. The presence of cholesterol crystals in rheumatoid nodules or affected bursae can increase the confusion with other crystal-induced arthritis, in particular, tophaceous monosodium urate gout or xanthomatosis.

Journal Article↗

PubMed2000

Cyclophosphamide for rheumatoid arthritis.

OBJECTIVES: To estimate the short-term effects of cyclophosphamide for the treatment of rheumatoid arthritis. SEARCH STRATEGY: We searched the Cochrane Musculoskeletal Group's Register, the Cochrane Controlled Trials Register, Medline and Embase up to and including July 1997. We also carried out a handsearch of the reference lists of the trials retrieved from the electronic search. SELECTION CRITERIA: All randomized controlled trials (RCTs) and controlled clinical trials (CCTs) comparing oral cyclophosphamide against placebo (or an active drug at a dosage considered to be ineffective) in patients with rheumatoid arthritis. DATA COLLECTION AND ANALYSIS: Data abstraction was carried out independently by two reviewers. The same two reviewers using Jadad's scale (Jadad 1995) assessed the methodological quality of the RCTs and CCTs. Rheumatoid arthritis outcome measures were extracted from the publications for baseline and end-of-study. The pooled analysis was performed using standardized mean differences (SMDs) for joint counts. Weighted mean differences (WMDs) were used for erythrocyte sedimentation rate (ESR). Toxicity was evaluated with pooled odds ratios for withdrawals. A chi-square test was used to assess heterogeneity among trials. Fixed effects models were used throughout. MAIN RESULTS: A total of 70 patients were included in the pooled analysis of two trials, 31 receiving cyclophosphamide. A statistically significant benefit was observed for cyclophosphamide when compared to placebo for tender and swollen joint scores: SMDs were -0.57 and -0.59 respectively. The difference in ESR also favoured the active drug but did not reach statistical significance (-12 mm, 95%CI: -26 to 2.5). One trial reported the number of patients developing new or worse erosions: the OR for cyclophosphamide compared to placebo was 0.17 (95% CI: 0.05 to 0.57). Patients receiving placebo were six times more likely to discontinue treatment because of lack of efficacy than patients receiving cyclophosphamide. Withdrawals from adverse reactions were higher in the cyclophosphamide group (Odds ratio=2.9), although this difference was not statistically significant. Side effects from cyclophosphamide included hemorrhagic cystitis, nausea, vomiting, leucopenia, thrombocytopenia, alopecia, amenorrhea and herpes zoster infections. REVIEWER'S CONCLUSIONS: Cyclophosphamide appears to have a clinically and statistically significant benefit on the disease activity of patients with RA, similar to some disease modifying antirheumatic drugs (DMARDs) such as antimalarials or sulfasalazine, but lower than methotrexate. Toxicity however is severe, limiting its use given the low benefit-risk ratio compared to other antirheumatic agents.

Antirheumatic Agents↗

PubMed2000

Azathioprine for rheumatoid arthritis.

OBJECTIVES: To assess the short-term effects of azathioprine 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 July 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 azathioprine against placebo in patients with rheumatoid arthritis. DATA COLLECTION AND ANALYSIS: Data was extracted independently by two reviewers (CS, EB); disagreements were resolved by discussion or third party adjudication (MS). The same reviewers (CS, EB) assessed the methodological quality of the trials using a validated quality assessment tool. Rheumatoid arthritis outcome measures were extracted from the publications for the six-month endpoint. The pooled analysis was performed using standardized mean differences for joint counts, pain and functional status assessments. Weighted mean differences were used for erythrocyte sedimentation rate (ESR). Toxicity was evaluated with pooled odds ratios for withdrawals and for adverse reactions. The 95% confidence intervals (95% CI) are presented. 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: Three trials with a total of 81 patients were included in the analysis. Forty patients were randomized to azathioprine and forty-one to placebo. A pooled estimate was calculated for two outcomes. A statistically significant benefit was observed for azathioprine when compared to placebo for tender joint scores. The standardized weighted mean difference between treatment and placebo was -0.98 (95% CI -1.45, -0.50). Withdrawals from adverse reactions were significantly higher in the azathioprine group OR=4.56 (95% CI 1.16, 17.85). REVIEWER'S CONCLUSIONS: Azathioprine appears to have a statistically significant benefit on the disease activity in joints of patients with RA. This evidence however is based on a small number of patients, included in older trials. Its effects on long-term functional status and radiological progression were not assessed due to lack of data. Toxicity is shown to be higher and more serious than that observed with other disease-modifying anti-rheumatic drugs (DMARDs). Given this high risk to benefit ratio, there is no evidence to recommend the use of azathioprine over other DMARDs.

Antirheumatic Agents↗

PubMedDate not supplied

Cathepsin D agglutinators and neutral protease agglutinators in rheumatoid arthritis. II. Production of CDA and NPA by rheumatoid synovium and phagocytosis of CDA by synovial phagocytic cells.

Tissue culture methods demonstrated the production of agglutinators against the cathepsin D site in IgG (CDA) and a neutral protease site in IgG (NPA) by rheumatoid synovial tissue. Seven of 11 specimens from seropositive and 2 of 7 specimens from seronegative RA patients were positive for CDA, whereas 2 of 11 specimens from seropositive and 1 of 7 specimens from seronegative patients were positive for NPA. None of the 6 control specimens was positive for both types of agglutinators. Chromatography of two synovial tissue incubates showed that the CDA were of the IgG type. By the immunofluorescence technique, plasma cells containing CDA were demonstrated in rheumatoid synovial tissue and draining lymph nodes of rheumatoid joints. The staining for CDA in the synovium was different from the staining for pepsin agglutinators in adjacent sections. Phagolysosomes containing CDA were found in synovial exudate cells from rheumatoid patients as well as in phagocytosing lining cells and macrophages of the sublining layer of rheumatoid synovial tissue. These findings suggest that antibodies directed at hidden antigenic sites in IgG revealed by endogenous proteolysis take part in the immune reaction and in the inflammation of rheumatoid joints.

Agglutinins↗

PubMed1979

IgG rheumatoid factor. Relationship to seropositive rheumatoid arthritis and absence in seronegative disorders.

IgG rheumatoid factor was detected in the sera of the majority of patients with seropositive rheumatoid arthritis. Values suggestive of IgG rheumatoid factor were noted in one-quarter of patients with seronegative inflammatory arthropathies. These determinations were always low and correlated with elevated IgG concentrations, suggesting nonspecific adherence of IgG rather than a true antigen-antibody reaction. In support of this conclusion, nonrheumatoid factor IgG was capable of concentration-dependent nonspecific adsorption to the solid phase. IgG, but not IgM, rheumatoid factor corresponded with disease activity in patients with seropositive rheumatoid arthritis, suggesting that IgG rheumatoid factor may be important in the pathogenesis.

Arthritis, Juvenile↗

PubMed1991

Molecular analysis of V kappa III variable regions of polyclonal rheumatoid factors during rheumatoid arthritis.

We report the first molecular characterization of V kappa regions of the main human autoantibodies occurring during rheumatoid arthritis, the polyclonal rheumatoid factors. Using two sets of polymerase chain reactions in order to amplify the cDNA derived from both peripheral blood and synovial fluid rheumatoid factor-secreting cells, nucleotide analysis of the V kappa III family usage shows the following: (a) at least three different V kappa III genes are used to encode polyclonal rheumatoid factors in a single patient, (b) each one of these genes seems more or less somatically mutated (from 1 to 14 mutations), (c) the mutation process preferentially affects the complementarity determining regions suggesting a selective pressure of antigen and (d) there is no clear difference between the mutation rates affecting the synovial fluid and peripheral blood rheumatoid factor-secreting cells. These results are able to explain some of the known idiotypic differences between monoclonal and polyclonal rheumatoid factors in humans. They also provide evidence that polyclonal autoantibodies arising during an autoimmune disease can be the products of multiple somatically mutated genes and suggest that this process is antigen driven, whether this antigen is the Fc piece of IgG or another unknown antigen.

Amino Acid Sequence↗

PubMed1982

In vitro synthesis of immunoglobulins and IgM-rheumatoid factor by blood mononuclear cells of patients with rheumatoid arthritis.

In vitro synthesis of IgG, IgM and IgM-rheumatoid factor (IgM-RF) was investigated in unstimulated and pokeweed mitogen (PWM)-stimulated 7-day cultures of blood mononuclear cells (BMC) from 28 seropositive patients with active rheumatoid arthritis (RA), in a second group of 13-day cultures from 94 unselected rheumatoid patients, and in 21 healthy controls. Both normal and rheumatoid BMC cultures synthesized IgM-RF in response to PWM stimulation. Mitogen-induced stimulation was shown to be dependent on the presence of T-lymphocytes. PWM-induced IgM and IgM-RF synthesis were reduced in BMC from rheumatoid patients in comparison with healthy controls. However, the fraction of IgM-RF in the total IgM synthesized was significantly higher in the RA supernatants than in the controls, suggesting the presence of a larger precursor B-cell population committed to IgM-RF synthesis in those cultures. BMC from 44 of the 94 patients demonstrated spontaneous synthesis of IgM-RF, and this was positively correlated with disease activity and rheumatoid factor titer. Spontaneous production was shown to reside in the T-lymphocyte depleted, adherent cell-depleted, B-cell subpopulation. It is concluded that in active RA there is a specific activation and expansion of the circulating B-cell subpopulation committed to IgM-RF synthesis, possibly due to abnormal immunoregulatory mechanisms modulating synthesis of this antibody.

Adult↗

PubMed1989

Rheumatoid factor has increased reactivity with IgG from synovial fluids of patients with rheumatoid arthritis and osteoarthritis.

Synovial fluid IgG may be altered in rheumatoid arthritis (RA) and promote the formation of immune complexes with rheumatoid factor. To investigate this possibility, monomeric IgG was prepared from synovial fluids from a range of arthritides for use as the antigen in a rheumatoid factor microplate radioimmunoassay. In comparisons with normal serum IgG antigen, increased rheumatoid factor binding was shown to IgG antigens prepared from synovial fluids from patients with RA and osteoarthritis (OA). Increased binding was also shown to RA sera IgG, but not to OA sera IgG. This increased binding was not due to increased IgG antigen binding to the plate or to IgG rheumatoid factor in the antigen preparations. It was considered that cause was a structural alteration of the IgG as a result of inflammation within the rheumatoid and OA joint.

Antigens↗