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Role of allergy in atopic dermatitis (eczema)

Jonathan M Spergel, MD, PhD, FAAAAI
Section Editor
Scott H Sicherer, MD, FAAAAI
Deputy Editor
Elizabeth TePas, MD, MS


There is some controversy with regard to the role of allergy in atopic dermatitis (AD; eczema). Some clinicians believe that allergic responses to aeroallergens are a rare cause of exacerbations of AD and that food allergy is generally not a factor. Other clinicians believe that allergy plays a strong role in exacerbating AD in some patients [1]. They believe that food allergies trigger symptoms primarily in young children and environmental allergens play a greater role in older children and adults.

Despite its name, AD itself is not a type I allergy, nor is it necessarily associated with allergic sensitization. However, overall, the data indicate that allergy plays a role in selected patients with AD.

The epidemiology, clinical manifestations, diagnosis, and treatment of AD, as well as the role of delayed-type hypersensitivity to chemicals in topical medications and skin care products in exacerbating AD, are discussed separately. (See "Atopic dermatitis (eczema): Pathogenesis, clinical manifestations, and diagnosis" and "Treatment of atopic dermatitis (eczema)".)


Patients with AD have higher rates of allergic diseases than the general population. Up to 80 percent of children with AD develop asthma and/or allergic rhinitis later in childhood [2]. This progression from AD in infancy to allergic rhinitis and asthma in childhood and young adulthood is referred to as the "allergic march" or "atopic march" [3-6].

The converse is true as well. A higher rate of AD is seen in teenagers with asthma than those without asthma (risk ratio [RR] 4.5, 95% CI 3.1-6.5) [7]. Ten to 20 percent of patients with AD have food-induced urticaria/anaphylaxis [8,9] compared with 1 to 3 percent of the general population [10,11]. In infants with eczema, the prevalence of immunoglobulin E (IgE)-mediated food allergy confirmed by double-blind, placebo-controlled food challenge (DBPCFC), except in patients with a history of anaphylaxis and positive specific IgE, ranges from 33 to 63 percent [8,12-16]. Earlier onset (<3 months of age) and more severe AD is associated with high egg, milk, and/or peanut-specific IgE [17]. Patients with AD and concomitant egg, peanut, or dust mite allergy are more likely to have AD that persists beyond five years of age [18].

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Literature review current through: Nov 2017. | This topic last updated: Feb 09, 2017.
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