INTRODUCTION
Atopic dermatitis (AD) is a chronic relapsing-remitting condition that affects approximately 25% of children and 7% to 10% of adults globally.1 Pruritus (itch) is the most bothersome symptom for patients with AD, substantially impacting sleep and health-related quality of life (QoL).2,3
Pruritus is stimulated by the activation of pruriceptive sensory neurons and can be experienced anywhere on the skin or mucosa.4 Cytokines involved in AD pathogenesis, including interleukin (IL)-4, IL-13, and IL-31, are also implicated as pruritus mediators.5-8 IL-4, IL-13, and IL-31 may directly or indirectly influence pruritus through activation of sensory neurons.5,7,8 Semaphorin 3A is a nerve repulsion factor that inhibits sensory nerve growth; increased epidermal nerve density and decreased semaphorin 3A levels are associated with pruritus in patients with AD.9,10
Important goals of AD treatment include the rapid relief of core symptoms including pruritus, with sustained efficacy, and rapid healing of skin lesions.11 Topical corticosteroids (TCSs) are a mainstay of treatment and are generally efficacious when used as directed, but are associated with adverse events (AEs) that can limit their use.12,13,14,15 TCS effectiveness may also be limited by the potential for tachyphylaxis (loss of response).16,17 Furthermore, TCSs have restrictions relating to patient age, duration, and extent of use, and use in specific anatomic locations.16,18 Consequently, TCS use is often restricted,
Pruritus is stimulated by the activation of pruriceptive sensory neurons and can be experienced anywhere on the skin or mucosa.4 Cytokines involved in AD pathogenesis, including interleukin (IL)-4, IL-13, and IL-31, are also implicated as pruritus mediators.5-8 IL-4, IL-13, and IL-31 may directly or indirectly influence pruritus through activation of sensory neurons.5,7,8 Semaphorin 3A is a nerve repulsion factor that inhibits sensory nerve growth; increased epidermal nerve density and decreased semaphorin 3A levels are associated with pruritus in patients with AD.9,10
Important goals of AD treatment include the rapid relief of core symptoms including pruritus, with sustained efficacy, and rapid healing of skin lesions.11 Topical corticosteroids (TCSs) are a mainstay of treatment and are generally efficacious when used as directed, but are associated with adverse events (AEs) that can limit their use.12,13,14,15 TCS effectiveness may also be limited by the potential for tachyphylaxis (loss of response).16,17 Furthermore, TCSs have restrictions relating to patient age, duration, and extent of use, and use in specific anatomic locations.16,18 Consequently, TCS use is often restricted,
