Infliximab treatment-induced formation of autoantibodies is common in Behçet's disease

To study autoantibody formation in patients with Behçet's disease (BD) who received long-term treatment with the anti-TNF monoclonal antibody infliximab.

Serial sera from infliximab-treated patients (5 mg/kg at weeks 0, 4, 8, and every 6-8 weeks thereafter) were tested for various autoantibodies, using commercially available methods, at baseline and at 6 months (n = 20), at 12 months (n = 16), and at 18 months post-baseline (n = 12). Thirty-five age- and sex-matched BD patients, not treated with infliximab, served as controls.

Autoantibodies were rarely seen in controls, as well as in infliximab treated patients at baseline. Formation of antinuclear antibodies (ANA) at low titers was evident in 13/20 (65%) patients at 6 months post-baseline; one additional patient developed anti-beta2 glycoprotein-I IgM antibodies (anti-beta(2)GPI). Of the 13 ANA-positive sera, low titers-IgM of anti-dsDNA or anti-beta(2)GPI were detected in 7 (35%) and 6 (30%) patients, respectively. Additional measurements at 12 and 18 months showed that the persistence and/or increasing titers of these autoantibodies depended on continuation of treatment. Antibodies to extractable nuclear antigens (anti-RNP, anti-SS-A/Ro, anti-SS-B/La, anti-Sm), rheumatoid factors, anti-cyclic citrullinated peptide antibodies and antineutrophil cytoplasmic antibodies, were never detected. No antibody-related symptoms, lupus-like disease, or thrombosis were observed in any patient up to 18 months of follow-up.

Early induction of ANA and specific autoantibodies is common in BD patients treated with infliximab, including low titers of non-pathogenic anti-dsDNA and anti-Beta2GPI antibodies. A possible clinical significance of these findings needs to be documented in further studies, including more patients and longer follow-up periods.