The evaluation and management of food allergy in atopic dermatitis

Abstract

Atopic dermatitis (AD) is a form of eczema that generally begins in early infancy and is characterized by extreme pruritus, chronically relapsing course, and distinctive morphology and distribution. AD is typically the first clinical manifestation of a child prone to develop atopic disease, with 50% of all AD developing in the first year of life and 80% by 5 years of age. Approximately 80% of children with AD develop asthma or allergic rhinitis; many lose their AD with the onset of respiratory allergy. The acute rash of AD is typically an erythematous, papulovesicular eruption, occasionally with weeping and crusting that is more commonly seen in early life. It typically progresses to a subacute form marked by erythema and scaling papules, and, especially in older patients, to a chronic form characterized by thickened, lichenified skin and fibrous papules. The distribution of the rash varies with age, involving the cheeks and extensor surfaces of the arms and legs in infancy, the flexor surfaces in the young child, and flexor surfaces, hands, and feet in the teenage patient and young adult. Atopic dermatitis is identified by a constellation of symptoms. Standard diagnostic criteria exist and are an accepted standard for diagnosing atopic dermatitis, and the SCORAD Index adapted by the European Task Force on Atopic Dermatitis provides a standardized method for gauging severity. The pathogenic role of allergy in atopic dermatitis has been debated since Besnier first described the eczematous rash that has become known as AD. However, recent studies delineating the immunopathogenic role of immunoglobulin (Ig)E-bearing antigen-presenting cells (eg, Langerhans cells and other dendritic cells) in establishing the initial Th2 lymphocytic response and of the IgE-mediated late-phase response in provoking cutaneous inflammation, numerous clinical studies demonstrating the provocation and resolution of skin symptoms in a subset of AD patients with the introduction and elimination of allergen, and the development of a murine model of a food-induced eczematous rash leave little doubt about the pathogenic role of allergy in some AD patients.