Precision medicine in atopic dermatitis: Present and future.

Atopic dermatitis (AD) is a chronic, multifactorial inflammatory skin disease characterized by barrier dysfunction, immune dysregulation, genetic predisposition, and environmental factors, including microbiome and allergens. As more is learned about its pathophysiology, treatment evolves using precision medicine-leveraging phenotype, endotype, biomarkers, disease severity, and response predictors, molecular profiling, and omics. Oral and topical corticosteroids may be effective and most accessible, but their use has been associated with various adverse effects. Cyclosporine also has proven efficacy for moderate to severe AD but is an immunosuppressive and is typically reserved for short-term therapy because of its prominent adverse effects. The advent of systemic and topical biologics and small molecule therapies targeting key cytokines involved in the pathogenesis of AD-namely, cytokines interleukin (IL)-4 (dupilumab), IL-13 (tralokinumab and lebrikizumab), and IL-31 (nemolizumab), and Janus kinase inhibitors has revolutionized treatment of moderate to severe AD. Although biomarkers defining distinct molecular endotypes are now available to use for precision targeting, such tools are not yet widely accessible or sufficiently validated for routine clinical use. Thus, in current practice, treatment decisions can use a combination of biomarkers, if possible, phenotype-based patterns, and observable constellations of age, disease distribution, morphology, barrier integrity, pruritus predominance, and associated comorbidities.