title: Treatment of generalized vitiligo with anti-TNF-α Agents.
abstract: BACKGROUND
  Although the exact pathogenesis of vitiligo is not fully understood, it appears to be an autoimmune disease. It is hypothesized that tumor necrosis factor alpha (TNF-?) plays an important role in vitiligo. TNF-? can destroy melanocytes through the induction of various apoptotic pathways. In addition, TNF-? can inhibit melanocyte stem cell differentiation.
  
  
  OBJECTIVE
  To evaluate the efficacy and safety of treating vitiligo patients with anti-TNF-? agents.
  
  
  METHODS
  A total of 6 patients were recruited. All patients had widespread non-segmental vitiligo. Biologics, including infliximab, etanercept, and adalimumab, were given according to treatment regimens used for psoriasis. Photographs were taken at the initial visit, every two months during the therapy and then six months after therapy completion.
  
  
  RESULTS
  All patients completed the treatment; two patients were treated with infliximab, two with etanercept, and two with adalimumab. All of the biologics were well tolerated throughout the treatment period, and none of the patients reported any significant adverse events. Digital images were compared before, during and after treatment. Repigmentation of the vitiliginous areas was not observed in any of the patients. Vitiligo worsened in one patient who was treated with infliximab and developed a psoriasiform rash. However, the remaining patients did not develop any new depigmented patches during treatment or at the six-month follow-up; vitiligo was considered stable in these five patients.
  
  
  CONCLUSIONS
  Although the anti-TNF-? agents were well tolerated in all six vitiligo patients, efficacy was not observed. Further evaluation with larger studies may be required.
authors.affiliation: Dermatology Department, Vitiligo Research Chair,College of Medicine, King Saud UniversityRiyadh, Saudi Arabia. kmgderm@yahoo.com
authors.forename: Khalid M
authors.initials: KM
authors.lastname: Alghamdi
authors.forename: Huma
authors.initials: H
authors.lastname: Khurrum
authors.forename: Alain
authors.initials: A
authors.lastname: Taieb
authors.forename: Khaled
authors.initials: K
authors.lastname: Ezzedine
mesh_terms: D000068879:Adalimumab; D000293:Adolescent; D000328:Adult; D000911:Antibodies, Monoclonal / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use; D003879:Dermatologic Agents / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use*; D000068800:Etanercept; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D007074:Immunoglobulin G / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use; D007155:Immunologic Factors / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use; D000069285:Infliximab; D008297:Male; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*; D014820:Vitiligo / Q000188:drug therapy* / Q000473:pathology; D055815:Young Adult
chemical_list: D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D003879:Dermatologic Agents; D007074:Immunoglobulin G; D007155:Immunologic Factors; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D000069285:Infliximab; D000068879:Adalimumab; D000068800:Etanercept