Paradoxical Alopecia Areata Induced by IL‐17 and IL‐23 Inhibitors: A Systematic Review

ABSTRACT Background Alopecia areata (AA) is an autoimmune disorder characterized by non‐scarring hair loss driven by dysregulated immune responses at the hair follicle. While targeted biologic therapies have transformed the management of inflammatory skin disease, paradoxical induction of autoimmune conditions has been increasingly reported. Although interleukin (IL)‐17 and IL‐23 inhibitors have been explored as potential therapies for AA, reports of paradoxical AA associated with these agents remain poorly synthesized. Objectives Systematically review all published cases of biopsy‐confirmed AA in patients treated with IL‐17 or IL‐23 inhibitors. Synthesize available clinical evidence to improve recognition of this rare adverse event. Methods A systematic review was conducted in accordance with PRISMA guidelines using PubMed, EMBASE, and Scopus. Eligible studies included case reports, case series, or clinical studies describing histopathologically confirmed AA in patients treated with IL‐17 or IL‐23 inhibitors. Study quality was assessed using the Joanna Briggs Institute checklist, and causality was evaluated using the World Health Organization‐Uppsala Monitoring Center system. Results Twelve studies comprising 15 patients met inclusion criteria. Most cases occurred in patients treated for psoriasis and developed within the first year of biologic therapy. Secukinumab ( n = 5) and ustekinumab ( n = 3) were the most frequently implicated agents, with additional cases reported with ixekizumab, guselkumab, tildrakizumab, risankizumab, and bimekizumab. Clinical presentations ranged from patchy AA to alopecia universalis. Management strategies included biologic discontinuation, therapeutic switching, corticosteroids, or JAK inhibitors, with variable outcomes. Most cases were assessed as possible or probable/likely associations, and overall study quality was moderate to high. Conclusions These cases highlight the context‐dependent effects of cytokine blockade and suggest that immune redirection, rather than uniform immune suppression, may underlie paradoxical AA. Greater clinical awareness, mechanistic investigation, and prospective surveillance are needed to support personalized biologic therapy and optimize patient safety.