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Alopecia areata is an autoimmune nonscarring hair loss characterized by peribulbar infiltrates of activated T cells and by degenerative changes in the hair follicle matrix that eventually result in alopecia. The cause of immune dysregulation, including the role of cytokines in this disease, is under active investigation. The immune system is likely an integral part of normal hair growth and hair growth cycle1 since epidermal keratinocytes, including those of the hair follicle, synthesize a number of cytokines including interleukins, granulocyte colony-stimulating factor, and tumor necrosis factor α (TNF-α).2 These cytokines, however, may also act as mediators of immunity and inflammation and have been implicated in a number of hair diseases including alopecia areata.
In vitro studies looking at the effects of various cytokines demonstrated significant inhibition of hair growth by TNF-α, interleukin (IL)-1α, and IL-1β. The changes induced by these cytokines included distortion of the dermal papilla, vacuolization, and abnormal keratinization of the matrix, and disruption of melanocytes.3 Because TNF-α significantly inhibited hair growth in vitro, it was hypothesized that in association with other cytokines (specifically IL-1α and IL-1β), it may be an important mediator of the pathological changes in hair follicle morphology seen in alopecia areata.4
A 51-year-old white woman with rheumatoid arthritis and Sjögren syndrome undergoing intravenous infliximab therapy for 11 months developed nonscarring hair loss consistent with alopecia areata. The hair loss affected 75% of her scalp as well as her eyebrows and eyelashes and eventually evolved to 100% scalp involvement despite discontinuation of infliximab treatment. The patient had no history of hair loss or atopy. A biopsy specimen of the scalp showed a peribulbar lymphocytic infiltrate with a reduced number of diminutive hairs most consistent with alopecia areata.
Infliximab is a chimeric monoclonal antibody to TNF-α, which acts by binding to the molecule and inactivating it via lysis of cells. The observation that our patient developed alopecia areata with progression to alopecia totalis in the setting of TNF-α depletion may provide insight into the complex immune signaling involved in this disease. It is likely that the immune signals responsible for the onset of hair loss in alopecia areata are not dependent on or do not involve TNF-α. We propose that TNF-α is not a necessary component for the inflammation seen in alopecia areata. It is, however, possible that TNF-α blockade can cause a dysregulation of cytokines leading to triggering of inflammation and hair loss.
The authors have no relevant financial interest in this letter.
Correspondence: Dr Ettefagh, Department of Dermatology, Case Western Reserve University, 11100 Euclid Ave, Cleveland, OH 44106 (leilaettefagh@yahoo.com).
Country-Specific Mortality and Growth Failure in Infancy and Yound Children and Association With Material Stature
Use interactive graphics and maps to view and sort country-specific infant and early dhildhood mortality and growth failure data and their association with maternal
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