ECZEMA AND FOOD HYPERSENSITIVITY

Prior to Columbus' voyage to the New World, an Italian physician, Paolo Bagellardo, wrote the first known scientific discussion of eczema in a pediatric textbook, Libellus de Aegretudinibus Infantium. The chapter on skin outlined recommendations for lubricating the skin and preventing scratching in children with this skin disorder. In the early 1600s, Helmont noted the association between a pruritic skin rash and asthma, and about 250 years later von Hebra described the flexural distribution of a chronic itchy skin disease. 34 However, it was the French physician, Besnier, who provided the first comprehensive description of atopic dermatitis in the late 1800s. 6 He emphasized the hereditary nature of the disorder, its chronic course, and its association with hay fever and asthma. Wise and Sulzberger 92 coined the term atopic dermatitis, further emphasizing the relationship between atopic eczema, asthma, and hayfever. The incidence of atopic dermatitis has been increasing over the past 40 years and now is estimated to affect between 12% and 15% of the pediatric population. 35 Atopic dermatitis [AD] is one form of eczema, which generally begins in early infancy and is characterized by extreme pruritus, chronically relapsing course, and distinctive distribution. AD is typically the first 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, with many losing their AD with the onset of respiratory allergy. The acute rash of AD is typically an erythematous, papulovesicular eruption, frequently 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. 9 The distribution of the rash varies with age, 38 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. AD is identified by a constellation of symptoms. The diagnostic criteria proposed by Hanifin and Rajka 36 are an accepted standard for diagnosing AD, and the SCORAD Index, 24 adapted by the European Task Force on Atopic Dermatitis provides a standardized method for gauging severity. The pathogenic role of allergy in AD has been debated since Besnier's original description; however, recent studies delineating the immunopathogenic role of IgE-bearing antigen-presenting cells [APCs; e.g., Langerhans' cells and other dendritic cells] in establishing the Th2 lymphocytic response and of the IgE-mediated late-phase response in provoking cutaneous inflammation are compelling. Acute skin lesions of AD are described as spongiotic, with epidermal hyperplasia and ballooning of the keratinocytes secondary to intracellular edema. Mast cell and basophil numbers are normal, and eosinophils are rare. 83 In chronic skin lesions, the epidermis has moderate to marked hyperplasia, with elongation of the rete ridges and prominent hyperkeratosis. Spongiosis is variable and the number of mast cells and Langerhans' cells are significantly increased. Eosinophils are sparse. Demyelination and fibrosis of cutaneous nerves are observed at all levels of the dermis, and capillary numbers are often increased.