title: Infliximab treatment does not induce organ-specific or nonorgan-specific autoantibodies other than antinuclear and anti-double-stranded DNA autoantibodies in Crohn's disease.
abstract: BACKGROUND
  Treatment of Crohn's disease (CD) by infliximab has been associated with the induction of antinuclear (ANA) and anti-double stranded DNA (dsDNA) autoantibodies. As yet, little is known about the effect of the humoral response induced by infliximab on the production of other organ-specific or nonorgan-specific autoantibodies.
  
  
  METHODS
  Thirty-five patients with CD treated with repeated infusions of infliximab were prospectively studied. Thirty-two patients with CD who had never received infliximab served as controls. A large panel of autoantibodies directed against phospholipid, beta2-glycoprotein I, mitochondria, smooth muscle, liver--kidney microsomes, filaggrin, thyroid, adrenals, and rheumatoid factor was tested along with ANA and anti-dsDNA autoantibodies during 1 year of intermittent treatment with infliximab. Autoantibodies were detected using the appropriate methods (i.e., indirect immunofluorescence, a radioimmunological technique, and ELISA assays).
  
  
  RESULTS
  Induction of ANA and anti-dsDNA autoantibodies was observed in 53% and 35% of infliximab-treated patients with CD, respectively. Overall, no other organ-specific or nonorgan-specific autoantibodies were detected during follow-up. A single patient who developed ANA and anti-dsDNA autoantibodies showed clinical features consistent with drug-induced lupus, which quickly resolved after discontinuation of infliximab. The other patients with CD receiving infliximab did not develop any clinical symptoms of autoimmunity.
  
  
  CONCLUSIONS
  The humoral response induced by infliximab was restricted to ANA and anti-dsDNA autoantibodies, which persist for up to 1 year of follow-up. We confirmed the significant prevalence of such autoantibodies induced by infliximab in CD, but they are not generally associated with clinical signs of autoimmunity.
authors.affiliation: Department of Gastroenterology, Lyon-Sud Hospital, Hospices Civils de Lyon, Pierre Bénite, France.
authors.forename: Stéphane
authors.initials: S
authors.lastname: Nancey
authors.forename: Elodie
authors.initials: E
authors.lastname: Blanvillain
authors.forename: Béatrice
authors.initials: B
authors.lastname: Parmentier
authors.forename: Bernard
authors.initials: B
authors.lastname: Flourié
authors.forename: Corinne
authors.initials: C
authors.lastname: Bayet
authors.forename: Jacques
authors.initials: J
authors.lastname: Bienvenu
authors.forename: Nicole
authors.initials: N
authors.lastname: Fabien
mesh_terms: D000328:Adult; D000368:Aged; D000911:Antibodies, Monoclonal / Q000276:immunology* / Q000494:pharmacology*; D000917:Antibody Formation / Q000187:drug effects; D001323:Autoantibodies / Q000187:drug effects*; D003424:Crohn Disease / Q000188:drug therapy* / Q000276:immunology; D004247:DNA / Q000276:immunology; D005260:Female; D000091344:Filaggrin Proteins; D005765:Gastrointestinal Agents / Q000276:immunology* / Q000494:pharmacology*; D006801:Humans; D000069285:Infliximab; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies
chemical_list: D000911:Antibodies, Monoclonal; D001323:Autoantibodies; C000717249:FLG protein, human; D000091344:Filaggrin Proteins; D005765:Gastrointestinal Agents; D004247:DNA; D000069285:Infliximab