King Andrew D, Lam Lauren, Goh Carolyn
Division of Dermatology, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA.
Dermatol Online J. 2019 Jul 15;25(7):13030/qt8nw631wq.
The mechanism underlying frontal fibrosing alopecia (FFA) is unknown, but proposed mechanisms share commonality of T cell-mediated destruction of the hair follicle bulge. IL-12 and IL-23 are key cytokines involved in CD4 T cell differentiation towards Th1 and Th17 phenotypes. We present a 62-year-old woman who developed persistent FFA while on ustekinumab for treatment of preexisting psoriasis. This case presents evidence against Th1 and Th17 pathways as essential to pathogenesis in FFA. This case also suggests that IL-12 and IL-23 inhibition is ineffective for this form of scarring alopecia.
额部纤维性秃发（FFA）的潜在机制尚不清楚，但所提出的机制具有T细胞介导的毛囊隆突破坏这一共同特征。白细胞介素12（IL-12）和白细胞介素23（IL-23）是参与CD4 T细胞向Th1和Th17表型分化的关键细胞因子。我们报告了一名62岁女性，她在使用乌司奴单抗治疗已有的银屑病时出现了持续性FFA。该病例提供了证据，反驳了Th1和Th17途径是FFA发病机制所必需的这一观点。该病例还表明，抑制IL-12和IL-23对这种瘢痕性秃发形式无效。
