SUMMARY This prospective study evaluates the usefulness of clinical features and measurements of circulating immune complexes and autoantibodies for identification of patients with rheumatoid arthritis with a poor life prognosis. One hundred and seven hospital clinic patients, 64 with extra-articular manifestations, were followed up for a mean period of eight years, during which 50 deaths occurred. Comparison with an age and sex matched control population showed an increased incidence of deaths from myocardial infarction, pneumonia, and complications of rheumatoid arthritis. Patients with cutaneous ulcers, vasculitic rash, neuropathy, and scleritis had a higher mortality than patients whose disease was confined to the joints. Positive serological tests for precipitating antibodies to soluble cellular antigens and cryoglobulinaemia also predicted a poor prognosis. Eleven out of 12 patients (92%) with antibodies to soluble cellular antigens died compared with 21 out of 64 patients (33%) without antibodies. The presence of cryoglobulinaemia was associated with almost a twofold higher mortality. The laboratory measurements may reflect immunopathogenic mechanisms which lead to the occurrence of extraarticular disease features and reduce life expectancy.
As a two-phase exercise in inter-district audit, with the emphasis on critical evaluation of routine clinical practice, three rheumatologists each examined the same 44 patients with shoulder pain, and recorded their diagnosis and the investigations and treatment they would carry out. In the first phase, 26 patients were seen by each rheumatologist separately; there was complete diagnostic agreement in only 46%, with wide variation in the frequency of requests for standard investigations, but all three rheumatologists recommended steroid injections for most patients. In the second phase, all three rheumatologists examined a further 18 patients together, discussed the symptoms and signs, and recorded their diagnoses separately. There was complete agreement in 78%. The presence of more than one lesion, and differences in the interpretation of certain physical signs, partly explain the lack of agreement in Phase 1. Treatment of specific shoulder lesions is highly concordant, with injection the major treatment modality, followed by physiotherapy. Perhaps the different diagnoses reached, and the fact that treatment might therefore be administered for the wrong diagnosis, may explain some treatment failures. Also, recruitment of patients for studies of the treatment of shoulder lesions requires care to avoid selection of a heterogeneous group.
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The disease specificity of antibodies to rheumatoid arthritis nuclear antigen (RANA) was examined by comparing anti-RANA titers in sera from 100 patients with rheumatoid arthritis (RA) with sera from 93 healthy controls. Anti-RANA antibodies were found in 86% of the RA sera and 56% of the controls. The higher titers in the RA sera were unrelated to clinical features or to measurements of circulating immune complexes or rheumatoid factors. To study the relationship of these antibodies to previous Epstein-Barr virus (EBV) infection, antibodies to the EB virus capsid antigen (VCA) were examined and found in 94% of the RA sera and 97% of the adult controls. Four of the six RA sera without anti-VCA antibodies had detectable anti-RANA antibodies, so that we might suggest anti-RANA can arise in the absence of EBV infection. From absorption experiments with non-EBV transformed extracts, we inferred that high anti-RANA titers could be due to reactions with non-Epstein-Barr virus related nuclear antigens. These data cast doubt on current speculation about a possible pathogenic role for Epstein-Barr virus in this disease. Rheumatoid arthritis is characterized by a number of immunologic abnormalities that may represent an abnormal response to an infective agent such as a virus (1). Studies (2) of antibodies in children to conventional and well-characterized viral antigens have failed to demonstrate a specific immune response in rheumatoid arthritis (RA) to any particular virus, including Epstein-Barr virus (EBV). Speculation about a possible etiologic role for EBV in RA has been stimulated by the observations of Alspaugh et a1 (3,4) who demonstrated a precipitating antibody system that was found in 6681% of RA sera and 6 4 % of controls. The reacting antigen RANA, demonstrated by immunofluorescence and immunodiffusion, was detectable only in B cell lines containing the EBV genome or normal human lymphocytes infected with EBV in vitro (5). The claim that anti-RANA antibodies are characteristic of RA has been challenged by their detection with more sensitive techniques in up to 75% of normal sera (6), though the same study has provided stronger evidence of a link with EBV infection by showing that anti-RANA occurred only in normal subjects in whom previous EBV infection could be demonstrated by the presence of antibodies to EB virus capsid antigen (VCA). This finding is at variance with reports (7,8) of RA sera in which anti-RANA antibodies have been described in the absence of previous EBV infection.The purpose of this study was to reexamine the original claim that anti-RANA antibodies are characteristic of RA by using a quantitative immunodiffusion assay to compare titers of anti-RANA antibodies in RA and normal sera, and to examine factors that influence the level of the titers. To investigate the role of EBV infection, the prevalence of antibodies to the
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