This criteria set has been approved by the American College of Rheumatology (ACR) Board of Directors and the European League Against Rheumatism (EULAR) ExecutiveCommittee. This signifies that the criteria set has been quantitatively validated using patient data, and it has undergone validation based on an external data set. All presenting with undifferentiated inflammatory synovitis, factors that best discriminated between those who were and those who were not at high risk for persistent and/or erosive disease-this being the appropriate current paradigm underlying the disease construct "rheumatoid arthritis." Results. In the new criteria set, classification as "definite RA" is based on the confirmed presence of synovitis in at least 1 joint, absence of an alternative diagnosis that better explains the synovitis, and achievement of a total score of 6 or greater (of a possible 10) from the individual scores in 4 domains: number and site of involved joints (score range 0-5), serologic abnormality (score range 0-3), elevated acute-phase response (score range 0-1), and symptom duration (2 levels; range 0-1).Conclusion. This new classification system redefines the current paradigm of RA by focusing on features at earlier stages of disease that are associated with persistent and/or erosive disease, rather than defining the disease by its late-stage features. This will refocus attention on the important need for earlier diagnosis and institution of effective disease-suppressing therapy to prevent or minimize the occurrence of the undesirable sequelae that currently comprise the paradigm underlying the disease construct "rheumatoid arthritis."

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Objective. To estimate the prevalence, incidence, survival, and disease characteristics of systemic sclerosis (SSc) in the Detroit tricounty area.Methods. A census of SSc cases for the period 1989-1991 was conducted in the Detroit area, using multiple sources for case identification. Diagnoses were verified by medical record review. Capture-recapture analysis was used to estimate the total SSc population. Cases of localized scleroderma (morphea and linear disease) were excluded.Results. Based on 706 verified cases of SSc, prevalence was initially estimated to be 242.0 cases per million adults (95% confidence interval [95% CI] 213-274), with an annual incidence of 19.3 new cases per million adults per year (95% CI 12.4-30.2). Capturerecapture analysis, based on the degree of overlap of verified cases among multiple sources, resulted in a revised prevalence estimate of 276 cases per million adults (95% CI 245-310). Sex-and race-specific prevalence estimates were significantly higher for women than for men, and for blacks than for whites. The average age at diagnosis was significantly younger for blacks than for whites. Compared with white patients, black patients were almost twice as likely to have diffuse disease (prevalence proportion ratio 1.86, 95% CI 1.48-2.35). Median survival was ϳ11 years. Factors negatively affecting survival included male sex (hazard ratio 1.81, 95% CI 1.29-2.55) and older age at diagnosis (hazard ratio 1.04, 95% CI 1.03-1.05).Conclusion. This study establishes baseline estimates of SSc occurrence and characteristics in a large US cohort consisting primarily of black adults and white adults. These data should facilitate research regarding the role of geographic, ethnic, racial, and environmental factors for this disease in comparison populations.

Power Doppler sonography was used in eight symptomatic knees in seven patients with arthritis before and after joint aspiration and intraarticular administration of steroids. A qualitative decrease in synovial perfusion was observed in all eight knees, and symptoms improved in seven of the eight cases. These preliminary data suggest a role for power Doppler sonography in assessment of serial changes in synovial inflammation.

Current theories propose that systemic lupus erythematosus develops when genetically predisposed individuals are exposed to certain environmental agents, although how these agents trigger lupus is uncertain. Some of these agents, such as procainamide, hydralazine, and UV light inhibit T cell DNA methylation, increase lymphocyte function-associated antigen 1 (LFA-1) (CD11a/CD18) expression, and induce autoreactivity in vitro, and adoptive transfer of T cells that are made autoreactive by this mechanism causes a lupuslike disease. The mechanism by which these cells cause autoimmunity is unknown. In this report, we present evidence that LFA-1 overexpression is sufficient to induce autoimmunity. , hydralazine, and UV light can trigger human lupus (1, 2). These agents also inhibit T cell DNA methylation, and polyclonal as well as cloned human and murine CD4 ϩ T cells become autoreactive after treatment with these and other DNA hypomethylating agents (3-7). Adoptive transfer of T cells made autoreactive by this mechanism causes a lupuslike disease in unirradiated syngeneic recipients (6, 7), suggesting a mechanism by which these agents might induce lupus. However, how these agents modify T cells to make them pathogenic is unknown. LFA-1 overexpression was induced on cloned murineThe autoreactivity correlates with lymphocyte functionassociated antigen 1 (LFA-1) (CD11a/CD18) overexpression, and concentrations of anti-CD11a insufficient to affect antigen reactivity will completely inhibit the autoreactive response (8). This suggests that LFA-1 overexpression contributes to the autoreactivity, and inhibiting function of the additional molecules reverses it (8). Cloned human T cells transfected with a CD18 cDNA also overexpress CD11a/CD18 and become autoreactive (5), further supporting the relationship between LFA-1 overexpression and T cell autoreactivity. These observations raise the possibility that LFA-1 overexpression might also contribute to the development of autoimmunity induced by hypomethylated T cells. However, inhibiting T cell DNA methylation probably affects expression of multiple genes, and the ability of the hypomethylated cells to induce autoimmunity may require altered expression of more than one gene. In this report, we examined the role of LFA-1 overexpression in autoimmunity by stably transfecting a cloned murine T cell line with a CD18 cDNA construct. We then asked if the transfected cells become autoreactive and induce a disease similar to that caused by treating the same cells with Pca, a DNA methylation inhibitor. MethodsMice and peritoneal macrophage (Mø) isolation. Young (6-8 wk of age) female AKR (H-2, and SJL (H-2 s ) mice were obtained from The Jackson Laboratories (Bar Harbor, ME) and maintained in a specific pathogen-free environment. Peritoneal Mø were obtained by i.p. thioglycollate (Becton Dickinson and Co., Cockeysville, MA) injection and harvested 3 d later as previously described (6, 7).T cell culture. D10.G4.1 cells (9), obtained from the American Type Culture Collection (Rock...