title: Infliximab treatment-induced formation of autoantibodies is common in Behçet's disease.
abstract: OBJECTIVE
  To study autoantibody formation in patients with Behçet's disease (BD) who received long-term treatment with the anti-TNF monoclonal antibody infliximab.
  
  
  METHODS
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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-Beta<inf>2</inf>GPI antibodies. A possible clinical significance of these findings needs to be documented in further studies, including more patients and longer follow-up periods.
authors.affiliation: Department of Internal Medicine, Laikon Hospital, Athens University Medical School, Athens, Greece.
authors.forename: A
authors.initials: A
authors.lastname: Elezoglou
authors.forename: N
authors.initials: N
authors.lastname: Kafasi
authors.forename: P H
authors.initials: PH
authors.lastname: Kaklamanis
authors.forename: P G
authors.initials: PG
authors.lastname: Theodossiadis
authors.forename: V
authors.initials: V
authors.lastname: Kapsimali
authors.forename: E
authors.initials: E
authors.lastname: Choremi
authors.forename: G
authors.initials: G
authors.lastname: Vaiopoulos
authors.forename: P P
authors.initials: PP
authors.lastname: Sfikakis
mesh_terms: D000328:Adult; D000911:Antibodies, Monoclonal / Q000009:adverse effects*; D001323:Autoantibodies / Q000276:immunology* / Q000378:metabolism; D001528:Behcet Syndrome / Q000188:drug therapy*; D016022:Case-Control Studies; D005260:Female; D006801:Humans; D007155:Immunologic Factors / Q000009:adverse effects*; D000069285:Infliximab; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
chemical_list: D000911:Antibodies, Monoclonal; D001323:Autoantibodies; D007155:Immunologic Factors; D014409:Tumor Necrosis Factor-alpha; D000069285:Infliximab