BH25 Frontal fibrosing alopecia arising on a background of vitiligo: a case presentation and review of the literature

Abstract

Frontal fibrosing alopecia (FFA) is an autoimmune condition causing scarring hair loss. It is characterized by progressive frontotemporal hairline recession. Vitiligo is an autoimmune depigmenting disorder marked by melanocyte destruction and well-­demarcated hypopigmented or depigmented patches. The coexistence of FFA and vitiligo is rare, and the pathophysiological interplay between these conditions remains poorly understood. We present the case of a 61-year-old woman with long-standing vitiligo who developed FFA evidenced by receding hairline, well-demarcated depigmented patches on both temples and dermoscopic findings of lonely hair, loss of follicular ostia, and perifollicular erythema on a background of depigmented patches on the temples. On microscopy, the 4-mm punch biopsy showed advanced loss of hair follicles, with only three terminal anagen follicles remaining and six stelae. There were some intraepithelial lymphocytes with mild perifollicular fibrosis. The features represented a long-standing scarring alopecia. Masson–Fontana stain confirmed the lack of basal epidermal melanin. SOX-10 showed near total loss of junctional melanocytes, confirming the diagnosis of coincidental vitiligo. FFA is a T-cell-mediated autoimmune reaction involving hair follicle stem cells, predominantly via CD8+ lymphocytes, interferon (IFN)-γ and the Janus kinase (JAK)–signal transducer and activator of transcription pathway. Vitiligo similarly involves autoimmune destruction of melanocytes via CD8+ T cells, IFN-γ and chemokines that recruit cytotoxic T cells to the epidermis. We hypothesize that the chronic inflammation of vitiligo might have contributed to antigen expression resulting in cytokine pathway activation and development of FFA, as both conditions share similar cytokine pathways. We suggest that ruxolitinib, which is a licensed successful treatment for vitiligo, may have a role in treating FFA. This case highlights the coexistence of FFA and vitiligo and the IFN-γ-driven autoimmune pathways underpinning the pathophysiological connection, suggesting a common immunological mechanism. JAK inhibitors like ruxolitinib may have a role in treating FFA and further studies are needed to establish the efficacy of this de novo therapeutic option.