Alopecia areata (AA) is characterized by nonscarring patchy hair loss on the scalp that can progress to involve the entire scalp (AA totalis) and eventually the entire body (AA universalis). Increasing evidence indicates that multiple cytokines—such as tumor necrosis factor (TNF) α, interleukin-1α, and interferon-γ—might be relevant to the autoimmune pathogenesis of AA because peribulbar inflammation is believed to inhibit hair growth by the actions of inflammatory cytokines.1 Novel biologic therapies that block TNF-α–mediated processes are used in the treatment of autoimmune diseases, including AA.2 Adalimumab, a human monoclonal TNF-α antibody, is administered by subcutaneous injection for the treatment of rheumatoid arthritis. Owing to the suspected involvement of TNF-α in the pathogenesis of AA, one might expect adalimumab therapy to be beneficial for patients with AA. We describe a patient who developed rapidly progressive AA universalis during treatment with adalimumab for rheumatoid arthritis.
Natalie Garcia Bartels, Hae-Huyk Lee, Margitta Worm, Gerd-Rüdiger Burmester, Wolfram Sterry, Ulrike Blume-Peytavi. Development of Alopecia Areata Universalis in a Patient Receiving Adalimumab. Arch Dermatol. 2006;142(12):1650–1666. doi:10.1001/archderm.142.12.1654