title: Autoantibodies in psoriatic patients treated with anti-TNF-α therapy.
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.
  
  
  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.
authors.affiliation: Divisione di Dermatologia, Dipartimento di Medicina Specialistica, Diagnostica e Sperimentale Ospedale S. Orsola-Malpighi, Università di Bologna, Bologna, Italy.
authors.forename: Federico
authors.initials: F
authors.lastname: Bardazzi
authors.forename: Giulia
authors.initials: G
authors.lastname: Odorici
authors.forename: Annalucia
authors.initials: A
authors.lastname: Virdi
authors.forename: Valentina Angela
authors.initials: VA
authors.lastname: Antonucci
authors.forename: Vera
authors.initials: V
authors.lastname: Tengattini
authors.forename: Annalisa
authors.initials: A
authors.lastname: Patrizi
authors.forename: Riccardo
authors.initials: R
authors.lastname: Balestri
mesh_terms: D000068879:Adalimumab; D000328:Adult; D000974:Antibodies, Antinuclear / Q000097:blood; D000911:Antibodies, Monoclonal / Q000009:adverse effects* / Q000627:therapeutic use*; D061067:Antibodies, Monoclonal, Humanized / Q000009:adverse effects* / Q000627:therapeutic use*; D015535:Arthritis, Psoriatic / Q000188:drug therapy* / Q000276:immunology*; D001323:Autoantibodies / Q000097:blood*; D001327:Autoimmune Diseases / Q000139:chemically induced* / Q000276:immunology; D004247:DNA / Q000276:immunology; D000068800:Etanercept; D005260:Female; D006801:Humans; D007074:Immunoglobulin G / Q000009:adverse effects* / Q000627:therapeutic use*; D000069285:Infliximab; D008180:Lupus Erythematosus, Systemic / Q000139:chemically induced / Q000276:immunology; D008297:Male; D008875:Middle Aged; D011565:Psoriasis / Q000188:drug therapy* / Q000276:immunology*; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use*; D012189:Retrospective Studies; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
chemical_list: D000974:Antibodies, Antinuclear; D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D001323:Autoantibodies; D007074:Immunoglobulin G; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; C033055:anti-extractable nuclear antigen antibodies; D004247:DNA; D000069285:Infliximab; D000068879:Adalimumab; D000068800:Etanercept