Inflammatory bowel diseases · 2005
Infliximab treatment does not induce organ-specific or nonorgan-specific autoantibodies other than antinuclear and anti-double-stranded DNA autoantibodies in Crohn's disease.
Клиническое исследованиеСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Nancey Stéphane, Blanvillain Elodie, Parmentier Béatrice, Flourié Bernard, Bayet Corinne, Bienvenu Jacques, Fabien Nicole
Аннотация
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.
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.