PRURITUS IN VULVAR LICHEN SCLEROSUS: NEUROIMMUNE MECHANISMS AND THERAPEUTIC IMPLICATIONS

Abstract

Vulvar lichen sclerosus is a chronic inflammatory and fibrosing dermatosis of the anogenital region, in which pruritus is one of the most frequent, burdensome, and clinically relevant symptoms. Although itch in vulvar lichen sclerosus is often interpreted as a direct consequence of local inflammation and epithelial fragility, emerging evidence suggests a more complex neuroimmune phenotype involving barrier disruption, keratinocyte-derived inflammatory signaling, immune-cell infiltration, altered innervation, perineural inflammation, neurogenic inflammation, and possible peripheral or central sensitization. Pruritus is clinically important not only as a symptom of active disease, but also as a driver of scratching, fissuring, sleep disruption, sexual avoidance, anxiety, and impaired quality of life. Topical potent or ultrapotent corticosteroids remain the cornerstone of treatment and are effective for many patients; however, persistent pruritus, pain, burning, or vulvodynia may continue despite adequate control of visible inflammation. In such cases, clinicians should reassess diagnosis, adherence, irritant exposure, infection, genitourinary syndrome of menopause, contact dermatitis, architectural change, and neuropathic pain. Recent studies highlighting perineural inflammation, altered nerve-fiber distribution, quality-of-life impairment, steroid hesitancy, and preliminary responses to neuromodulatory or biologic therapies support a more multidimensional approach to symptom control. This review summarizes current evidence on pruritus in vulvar lichen sclerosus, focusing on neuroimmune mechanisms, patient-reported burden, clinical assessment, and therapeutic implications.