@article{290a49233b994983b0cb6ea2e029ca2b,
title = "Comorbidity in Atopic Dermatitis",
abstract = "The negative impact of atopic dermatitis (AD) often extends beyond the skin. Children with AD experience increased rates of infectious, mental health, and allergic diseases compared to their non-atopic peers. The mechanisms underlying these associations remain elusive. New insights from genetic and epidermal research pinpoint the skin barrier as a primary initiator of AD. Epicutaneous sensitization represents an intriguing new model that links a disrupted skin barrier to the later development of IgE-mediated diseases in patients with AD. Recent epidemiologic studies have identified new comorbidities linked to AD as well, including several mental health disorders and obesity. This article reviews the recent literature regarding both classic and newly described AD comorbidities.",
keywords = "Asthma, Atopic dermatitis, Attention-deficit-hyperactivity-disorder, Autism, Cancer, Comorbidity, Depression, Eczema, Epicutaneous sensitization, Food allergy, Skin barrier",
author = "Simpson, {Eric L.}",
note = "Funding Information: Eczema herpeticum (EH), although rare, is another important example of an exaggerated clinical viral infection in patients with AD. One study found a history of EH to occur in less than 3% of tertiary referral patients with AD []. Classic EH presents with diffuse vesicles spreading beyond the initial site of infection and accompanied by fever and lymphadenopathy. EH may be complicated by herpetic keratitis, or even viral dissemination and death [, ]. Atypical presentations of EH are common, with pustules or crusts mimicking S. aureus infection []. The Atopic Dermatitis Vaccinia Network (ADVN) is a network of researchers funded by the National Institutes of Health, whose objective is to investigate the mechanisms underlying viral infection susceptibility in AD []. This group discovered patients with EH have more severe underlying AD, more IgE-mediated diseases, and a higher susceptibility to other types of cutaneous infections []. Mechanisms underlying the susceptibility to EH discovered by this group include altered interferon-γ responses and genetic defects in filaggrin, the tight junction protein claudin-1, and TSLP [•, , , •]. Funding Information: I would like to thank my mentor, Jon Hanifin, MD for his critical review of the manuscript, and Renato Goreshi, MD and Christine E. Carocci for their editorial assistance. This project was supported by grant number 5K23AR057486-02 from the National Institutes of Health. Funding Information: E.L. Simpson has received a grant (payable to his institution) from the National Institutes of Health.",
year = "2012",
month = mar,
doi = "10.1007/s13671-011-0003-5",
language = "English (US)",
volume = "1",
pages = "29--38",
journal = "Current Dermatology Reports",
issn = "2162-4933",
publisher = "Springer US",
number = "1",
}