Abstract

Systemic contact dermatitis (SCD) is poorly understood, and its very existence has even been questioned. Allergic contact dermatitis (ACD) is an immune-mediated, delayed-type hypersensitivity (type-IV) reaction, usually manifesting itself as a visible and symptomatic inflammation of the skin. The majority of patients diagnosed with ACD improve clinically with allergen avoidance. The mainstay of avoidance for most allergens is the prevention of skin contact through discontinuation of products that contain the allergen(s), the selection of alternatives from “safe lists,” and counseling patients on environmental sources of allergens. While ACD affects a large percentage of the population, relatively few patients have been documented as having had a significant contribution to their allergic state by allergen exposure through sources other than by cutaneous contact. SCD is defined as provocation or exacerbation of dermatitis by non-cutaneous exposure to an allergen in a patient who is already cutaneously sensitized. Exposure routes in SCD are varied, with the most common and frequently documented being oral exposure. Diet may be an important source of exposure to contact allergens in some patients with ACD, and low-allergen diets have been developed for some common allergens, such as nickel, cobalt, and Balsam of Peru (Myroxylon pereirae). When contact avoidance and dietary restriction of allergen fail, escalation from topical treatments to systemic immune-suppressants may be necessary. Emerging therapies such as nickel oral hypo-sensitization may be beneficial in the future.

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