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Reducing Unmet Needs in Hidradenitis Suppurativa by Including the Hair Follicle Among an Arsenal of Targets
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DOI：10.1111/exd.70321.png)
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Abstract
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Hidradenitis suppurativa (HS) is a prevalent, debilitating disease affecting ~1% of the population, with limited therapeutic options and poor long-term remission rates. HS arises from inflammation and destruction of apocrine-bearing hair follicles, suggesting a multifactorial pathology involving immune dysregulation and follicular dysfunction. Emerging treatment strategies largely center on immune suppression, with three FDA-approved therapies targeting inflammatory pathways. However, most patients fail to achieve durable remission. Genetic evidence increasingly implicates the hair follicle as a key contributor to HS pathogenesis. For example, genes that cause ectodermal dysplasias (EDs) have been implicated by common risk variants identified in genome-wide association studies (GWAS) and by rare variants in sequencing studies of rare ED syndromes that co-present with HS. EDs are Mendelian (i.e., single-gene) disorders that disrupt the development of ectodermal derivatives, including hair follicles and sweat glands. The enrichment of ED-associated genes in HS genetic studies, together with HS phenotypes observed in ED patients, supports a critical role for aberrant follicular development in HS pathogenesis. We propose that HS represents a spectrum of related diseases entities spanning immune dysregulation and hair follicle pathology, underscoring the need for biomarkers and refined disease classification to tailor treatment strategies. This perspective argues for broadening drug-development programs and insurance coverage for therapeutic strategies beyond immunomodulation to include follicle-targeted approaches.
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