BACKGROUND: TNF-α inhibitors have been associated with induction of autoantibodies and autoimmune diseases. We retrospectively evaluated the incidence of autoantibodies ANA, ENA, anti-dsDNA, the occurrence of clinical symptoms and possibly related treatment failure. PATIENTS AND METHODS: The titers of ANA, ENA and anti-dsDNA were evaluated from blood samples every six months in 128 patients receiving a TNF-α inhibitor (adalimumab, etanercept, infliximab). RESULTS: Overall 37% of 128 patients treated with anti-TNF-α drug developed autoantibodies, mostly induced by infliximab; 48.48 % of patients who received infliximab presented autoantibodies. One patient developed a drug-induced lupus erythematosus. Forty-five patients were switched to one or more additional TNF-α inhibitors and 25 developed autoantibodies. CONCLUSIONS: An increased autoantibody titer is not predictive of treatment failure; particular attention to all phenomena suggestive for autoimmunity is needed in patients with a positive autoantibody titer. Further studies are needed to clarify the role of autoantibodies during anti-TNF- α therapy.
Bardazzi F, Odorici G, Virdi A, Antonucci VA, Tengattini V, Patrizi A, et al. (2014). Autoantibodies in psoriatic patients treated with anti-TNF-α therapy. JOURNAL DER DEUTSCHEN DERMATOLOGISCHEN GESELLSCHAFT, 12(5), 401-406 [10.1111/ddg.12339].
Autoantibodies in psoriatic patients treated with anti-TNF-α therapy.
BARDAZZI, FEDERICO;TENGATTINI, VERA;PATRIZI, ANNALISA;
2014
Abstract
BACKGROUND: TNF-α inhibitors have been associated with induction of autoantibodies and autoimmune diseases. We retrospectively evaluated the incidence of autoantibodies ANA, ENA, anti-dsDNA, the occurrence of clinical symptoms and possibly related treatment failure. PATIENTS AND METHODS: The titers of ANA, ENA and anti-dsDNA were evaluated from blood samples every six months in 128 patients receiving a TNF-α inhibitor (adalimumab, etanercept, infliximab). RESULTS: Overall 37% of 128 patients treated with anti-TNF-α drug developed autoantibodies, mostly induced by infliximab; 48.48 % of patients who received infliximab presented autoantibodies. One patient developed a drug-induced lupus erythematosus. Forty-five patients were switched to one or more additional TNF-α inhibitors and 25 developed autoantibodies. CONCLUSIONS: An increased autoantibody titer is not predictive of treatment failure; particular attention to all phenomena suggestive for autoimmunity is needed in patients with a positive autoantibody titer. Further studies are needed to clarify the role of autoantibodies during anti-TNF- α therapy.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
