Abstract
Objective: To evaluate the prevalence, sensitivity, and specificity of anti‐chromatin and anti‐C1q antibodies in systemic lupus erythematosus (SLE) and lupus nephritis compared to small vessel vasculitis and other connective tissue diseases. To provide long‐term follow‐up data for anti‐chromatin antibodies in lupus nephritis.Methods: We determined the significance of anti‐nuclear antibodies (ANA), anti‐ double‐stranded DNA (anti‐dsDNA), anti‐chromatin, and anti‐C1q antibodies, as well as complement factors C3 and C4, in relation to disease activity in SLE patients with (n = 47; long‐term follow‐up data for 33 patients) and without (n = 31) biopsy‐confirmed lupus nephritis, microscopic polyangiitis (n = 37), Wegener's granulomatosis (n = 66), primary Sjögren's syndrome (n = 17), limited scleroderma (CREST syndrome) (n = 6), and progressive systemic scleroderma (PSS) (n = 11).Results: Anti‐chromatin antibodies were more specific and sensitive than anti‐C1q antibodies in distinguishing SLE patients from those with other systemic autoimmune diseases [anti‐chromatin: sensitivity 64.1%, specificity 99.2%, odds ratio (OR) 219.6; anti‐C1q: sensitivity 50%, specificity 72.6%, OR 2.65]. Anti‐C1q antibodies were present in 75% of patients with Sjögren's syndrome and 35.1% of patients with microscopic polyangiitis. Anti‐chromatin antibodies could identify SLE in patients with positive ANA but negative anti‐dsDNA antibodies. Persisting anti‐chromatin antibodies indicated SLE disease activity, even if anti‐dsDNA antibodies had become negative. In long‐term follow‐up, those SLE patients with negative anti‐dsDNA antibodies but persisting ANA and anti‐chromatin antibodies relapsed if immunosuppression had been tapered. Anti‐chromatin antibodies correlated with the SLE disease activity index (SLEDAI) as a marker of disease activity.Conclusions: The measurement of anti‐chromatin, but not anti‐C1q, antibodies in patients with systemic autoimmune diseases increases diagnostic sensitivity and specificity for SLE and assists in treatment decisions in anti‐dsDNA‐negative patients.
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