Abstract
A large body of evidence exists that strongly supports the role of IgE-mediated mechanisms in the pathogenesis of atopic dermatitis (AD). Clinical and laboratory evidence, as well as studies of allergen avoidance and immunotherapy, suggests that there is a population of patients with AD where the role of aeroallergens and foods can explain a significant component of their disease. The mechanisms that allow IgE mediated reactions to progress to lesions of AD are yet to be determined. Allergen may gain access to immunoreactive cells by direct penetration through barrier-defective skin or indirectly via inhalation or ingestion. Histologic evidence suggests that IgE-bearing dermal mast cells, once activated by allergen, may elaborate mediators to initiate pruritus. Additional mediators and chemoattractants, especially those for eosinophils, may perpetuate the reaction leading to a "late-phase" response. Allergen interaction with IgE-bearing T-lymphocyte-associated antigen-presenting cells (e.g., Langerhans cells) may activate a delayed cell-mediated response more classically felt representative of the lesions of AD. The double-blind, placebo-controlled food challenge has been established as a reliable method of identifying foods suspected as triggers of AD. The importance of immediate hypersensitivity prick testing and delayed patch testing in the identification of suspected aeroallergens in AD has yet to be developed adequately. We believe the patch test will become a useful tool in the identification of suspected aeroallergens in patients with AD.
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