Introduction

Atopic dermatitis (AD) is a chronic, relapsing inflammatory skin disease characterized by pruritus and eczematous lesions, often significantly impacting quality of life [1]. In recent years, biologic therapies have revolutionized the treatment of moderate-to-severe AD, with dupilumab emerging as the first monoclonal antibody targeting IL-4 and IL-13 pathways [2]. Since its approval, dupilumab has demonstrated remarkable efficacy in clinical trials and real-world settings, offering significant relief for patients with treatment-resistant disease.

Despite its favorable profile, emerging evidence points to rare but notable immune-mediated adverse events, including the onset or exacerbation of vitiligo, an acquired depigmenting disorder resulting from melanocyte loss [3-6]. To date, only a small number of cases of dupilumab-associated vitiligo have been reported in the literature, largely as isolated case reports and small case series. However, a recent scoping review by Mehta et al. found a mean latency of approximately three months between dupilumab initiation and vitiligo onset across the reported cases, suggesting a potential temporal signal despite the limited overall number of cases [7]. The pathogenesis of vitiligo in the context of biologic therapy remains incompletely understood but is hypothesized to involve immune dysregulation and cytokine imbalance, particularly a proposed shift from Th2-predominant signaling toward Th1 and Th17 responses following IL-4/IL-13 blockade, which may promote melanocyte destruction [3]. As more patients with AD are treated with targeted biologics, recognizing and managing such complications becomes increasingly important, and continued case-level reporting remains an important tool for characterizing this uncommon but clinically significant adverse effect.

The present case report describes a woman with longstanding AD who developed new-onset vitiligo following dupilumab therapy, with subsequent improvement after switching to nemolizumab, an IL-31 receptor antagonist, and topical tacrolimus and ruxolitinib use. This case contributes to the growing literature on biologic-induced pigmentary disorders and provides novel insights into potential therapeutic alternatives for affected patients, while highlighting important limitations that should inform interpretation of these observations.