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Editorial
November 30, 2016

Effect of Counting Genetic Variants on Precision Treatment for Pediatric Atopic DermatitisDo Count Your Chickens Before They Hatch

Author Affiliations
  • 1Division of Dermatology, Department of Internal Medicine, Washington University School of Medicine, St Louis, Missouri
  • 2Center for Pharmacogenomics, Washington University School of Medicine, St Louis, Missouri
  • 3Center for the Study of Itch, Washington University School of Medicine, St Louis, Missouri
  • 4Department of Pediatrics, Washington University School of Medicine, St Louis, Missouri
JAMA Dermatol. Published online November 30, 2016. doi:10.1001/jamadermatol.2016.4468

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.

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