title: Tumour necrosis factor-α inhibition can stabilize disease in progressive vitiligo.
abstract: Tumour necrosis factor (TNF)-α, a proinflammatory cytokine central to many autoimmune diseases, has been implicated in the depigmentation process in vitiligo. We review its role in vitiligo by exploring its pro- and anti-inflammatory properties and examine the effects of blocking its actions with TNF-α antagonist therapeutics in reports available in the literature. We found that TNF-α inhibition halts disease progression in patients with progressive vitiligo but that, paradoxically, treatment can be associated with de novo vitiligo development in some patients when used for other autoimmune conditions, particularly when using adalimumab and infliximab. These studies reinforce the importance of stating appropriate outcomes measures, as most pilot trials propose to measure repigmentation, whereas halting depigmentation is commonly overlooked as a measure of success. We conclude that TNF-α inhibition has proven useful for patients with progressive vitiligo, where TNF-α inhibition is able to quash cytotoxic T-cell-mediated melanocyte destruction. However, a lingering concern for initiating de novo disease will likely prevent more widespread application of TNF inhibitors to treat vitiligo.
authors.affiliation: Department of Dermatology, Loyola University Stritch School of Medicine, 2160 South First Ave, Maywood, IL, U.S.A.
authors.forename: K C
authors.initials: KC
authors.lastname: Webb
authors.affiliation: Department of Dermatology, Loyola University Stritch School of Medicine, 2160 South First Ave, Maywood, IL, U.S.A.
authors.forename: R
authors.initials: R
authors.lastname: Tung
authors.affiliation: Department of Dermatology, Loyola University Stritch School of Medicine, 2160 South First Ave, Maywood, IL, U.S.A.
authors.forename: L S
authors.initials: LS
authors.lastname: Winterfield
authors.affiliation: Department of Dermatology, Tufts University Medical Center, Boston, MA, U.S.A.
authors.forename: A B
authors.initials: AB
authors.lastname: Gottlieb
authors.affiliation: Oncology Research Institute, Loyola University Chicago, IL, U.S.A.
authors.forename: J M
authors.initials: JM
authors.lastname: Eby
authors.affiliation: Oncology Research Institute, Loyola University Chicago, IL, U.S.A.
authors.forename: S W
authors.initials: SW
authors.lastname: Henning
authors.affiliation: Departments of Pathology, Microbiology and Immunology, Loyola University Stritch School of Medicine, 2160 South First Ave, Maywood, IL, U.S.A.
authors.forename: I C
authors.initials: IC
authors.lastname: Le Poole
mesh_terms: D000328:Adult; D000368:Aged; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D002986:Clinical Trials as Topic; D003879:Dermatologic Agents / Q000627:therapeutic use*; D018450:Disease Progression; D005260:Female; D005544:Forecasting; D006801:Humans; D008297:Male; D008544:Melanocytes / Q000187:drug effects; D008875:Middle Aged; D013601:T-Lymphocytes / Q000187:drug effects; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*; D014820:Vitiligo / Q000188:drug therapy*
chemical_list: D000911:Antibodies, Monoclonal; D003879:Dermatologic Agents; D014409:Tumor Necrosis Factor-alpha