To evaluate the predictive power of changes in levels of antibodies to double-stranded DNA (antidsDNA) as a predictor of disease exacerbations in systemic lupus erythematosus (SLE), we performed a prospective study on 72 unselected patients with SLE (mean duration of study 18.5 months, range 6-35 months). Patients were seen at least once every 3 months, and disease activity was scored according to a specific protocol. Plasma samples were obtained at least once every month and were assessed for anti-dsDNA antibody (by the Crifhidiu luciliue assay, an enzymelinked immunosorbent assay [ELISA], and the Farr assay) and for complement components C3 and C4. Twenty-seven of 33 disease exacerbations observed during the study period were accompanied by a positive test result for anti-dsDNA antibody (27 by the Farr assay, 19 by the C luciliae assay, and 23 by the ELISA). Twentyfour of these exacerbations were preceded by a significant increase in anti-dsDNA antibody levels (23 by the Farr assay, 12 by the C luciliae assay, and 17 by the ELISA). The first observance of a significant increase in anti-dsDNA antibody levels preceded the exacerbation by 8-10 weeks. Significant increases in anti-dsDNA antibody levels not followed by an exacerbation were observed in 5 cases by the Farr assay, in 7 cases by the C luciliue assay, and in 3 cases by the ELISA; however, in 3 cases, 2 cases, and 1 case, respectively, these increases were followed by an increase in disease activity that did not fulfill the criteria for an exacerbation. Serial measurement of anti-dsDNA antibody levels was more sensitive for predicting exacerbations than was measurement of C3 andor C4 levels (P < 0.03). Serial assessment of anti-dsDNA antibody levels, especially by the Farr assay, is a sensitive and reasonably specific method for predicting disease exacerbations in SLE.Systemic lupus erythematosus (SLE) is characterized by protean clinical manifestations and the occurrence of a variety of autoantibodies. Among these, anti-double-stranded DNA (anti-dsDNA) antibodies are highly specific for SLE and are detected at a high frequency (75-

Objective-This study investigated the predictive value of rises in IgM class antibodies against double stranded DNA (anti-dsDNA) for ensuing relapses in systemic lupus erythematosus (SLE) in comparison with rises in IgG class antibodies. In addition, it was analysed whether rises in IgM class anti-dsDNA were associated with specific clinical manifestations of SLE. Methods-Thirty

We determined the discriminative value of the Farr assay in comparison to ELISA and Crithidia luciliae immunofluorescence assay (IFT) for detecting anti-dsDNA antibodies as a diagnostic tool for systemic lupus erythematosus (SLE). Special attention was paid to the diagnostic significance of IgM-class anti-dsDNA. Sera were analyzed from 74 patients with SLE, 257 patients with other auto-immune diseases, and 50 healthy controls. All sera were tested for anti-dsDNA using the IFT (anti-total immunoglobulin conjugate), ELISA (anti-IgG and anti-IgM conjugates), and the 125I Farr assay. Specificity and sensitivity for a diagnosis of SLE appeared to be highest for the Farr. All SLE sera with IgM-class anti-dsDNA without IgG-class anti-dsDNA as detected by ELISA, were positive when tested by the Farr assay. In contrast, most of the sera with IgM-class anti-dsDNA as detected by ELISA from patients with diseases other than SLE were negative when tested by Farr assay.

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In the systemic vasculitides, serial measurement of titres of anti-neutrophil cytoplasmic autoantibodies (ANCA) is useful for follow-up of disease activity and prediction of relapses. ANCA have been detected in patients with inflammatory bowel disease, but their relation to disease activity in these diseases is unclear. We analysed the relation between disease activity and ANCA titres as determined by indirect immunofluorescence in paired samples obtained during active disease and at remission from individual patients with ulcerative colitis (n=60) and Crohn's disease (n=101). In addition, patients were followed prospectively, to study the fluctuations of ANCA with time in relation to disease activity. We did not detect a correlation between disease activity and ANCA titres, either in paired samples from active disease and remission, or in serial samples, either in ulcerative colitis or in Crohn's disease. In contrast to the ANCA-associated systemic vasculitides, serial measurement of ANCA titres is not useful in the monitoring of disease activity in patients with inflammatory bowel disease.