Atopic dermatitis (AD) is a common inflammatory skin disorder, and its prevalence in the pediatric population has tripled in the past several decades alone.1 Atopic dermatitis is characterized by xerotic or scaly patches of skin with intense pruritus, resulting in eczematous lesions.2 Loss-of-function (LOF) mutations for the skin gene filaggrin (FLG [OMIM 135940]) are the most significant and widely replicated risk factors for AD.3 Immunologically, AD is characterized by type 2 inflammation through type 2 interleukin 4 (IL-4), IL-5, and IL-13 cytokine production. Together, the evidence supports a prevailing paradigm of AD pathogenesis originating with a skin barrier deficiency that results in downstream immune dysregulation and triggers a chronic and relapsing inflammatory cascade.
Mathyer ME, Coughlin CC, de Guzman Strong C. Effect of Counting Genetic Variants on Precision Treatment for Pediatric Atopic Dermatitis: Do Count Your Chickens Before They Hatch. JAMA Dermatol. 2017;153(3):269–270. doi:10.1001/jamadermatol.2016.4468
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