title: [Alopecia areata during anti-TNF alpha therapy: Nine cases].
abstract: BACKGROUND
  In recent years, a growing number of biological agents have been introduced for the treatment of various diseases, and their principal adverse events are known. We present nine cases of alopecia areata (AA) developed in patients treated with TNF-α blocking agents.
  
  
  METHODS
  Nine cases are described: five men and four women of mean age 39.2 years (range: 29-54 years). Two patients had a past history of alopecia areata. The anti-TNF given was adalimumab (Humira(®)) in eight cases and etanercept (Enbrel(®)) in one case. The time lapse to development of AA following introduction of the anti-TNF alpha agent was between six weeks and eight months (mean: 4.2 months). There were five cases of patchy AA and four of AA universalis. Anti-TNF alpha treatment was stopped in all patients. Complete regrowth was seen in five patients. Two patients showed no improvement. In two patients, partial hair regrowth (<50%) was seen after systemic corticosteroid therapy and methotrexate.
  
  
  CONCLUSIONS
  Our nine cases of alopecia areata developed in patients treated with TNF-α blockers constitute the largest series reported to our knowledge. 17 cases of AA during anti-TNF-alpha therapy have previously been described in the literature. AA may be a side effect of anti-TNF-alpha drugs. In our patients, no conclusive triggers could be associated with the development of AA, except a context of stress in four patients. Complete regrowth in three patients after discontinuation of the anti-TNF-alpha (without other therapy) is an additional argument in favour of the implication of biotherapies. However, a random coincidence of AA with anti-TNF-alpha cannot be completely ruled out. The role of anti-TNF-alpha therapy in the pathogenesis of AA is poorly understood. Activation of self-reactive T cells by anti-TNF-alpha could lead to the development of AA.
authors.affiliation: Service de dermatologie, hôpital Porte-Madeleine, CHR d'Orléans, France. emmanuelle_lb@yahoo.fr
authors.forename: E
authors.initials: E
authors.lastname: Le Bidre
authors.forename: G
authors.initials: G
authors.lastname: Chaby
authors.forename: L
authors.initials: L
authors.lastname: Martin
authors.forename: M
authors.initials: M
authors.lastname: Perrussel
authors.forename: B
authors.initials: B
authors.lastname: Sassolas
authors.forename: M-L
authors.initials: ML
authors.lastname: Sigal
authors.forename: C
authors.initials: C
authors.lastname: Kaassis
authors.forename: E
authors.initials: E
authors.lastname: Lespessailles
authors.forename: A
authors.initials: A
authors.lastname: Nseir
authors.forename: E
authors.initials: E
authors.lastname: Estève
mesh_terms: D000068879:Adalimumab; D000328:Adult; D000505:Alopecia / Q000139:chemically induced; D000506:Alopecia Areata / Q000139:chemically induced*; D000893:Anti-Inflammatory Agents / Q000009:adverse effects* / Q000627:therapeutic use; D000911:Antibodies, Monoclonal / Q000009:adverse effects* / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized; D000068800:Etanercept; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D007074:Immunoglobulin G / Q000009:adverse effects* / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use; D012307:Risk Factors; D013315:Stress, Psychological / Q000150:complications; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
chemical_list: D000893:Anti-Inflammatory Agents; D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D007074:Immunoglobulin G; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D000068879:Adalimumab; D000068800:Etanercept