Atopic dermatitis (AD; atopic eczema, eczema) is an inflammatory, chronically relapsing, and intensely pruritic skin disease occurring often in families with atopic diseases (atopic dermatitis, bronchial asthma, and/or allergic rhino-conjunctivitis). AD is a noncontagious inflammation of the epidermis and dermis with characteristic clinical (itch, erythema, papule, seropapule, vesicle, squames, crusts, lichenification, in synchronous, or metachronous polymorphy) and dermatopathological (spongiosis, acanthosis, hyper- and parakeratosis, lymphocytic infiltrates, and exocytosis, eosinophils) signs. With a prevalence of 2% to 5% (in children and young adults around 15%), AD is one of the most common skin diseases. The varying etiologic concepts of this disease are mirrored by the different names that are or have been used: “neurodermatitis,” “neurodermitis,” and “endogenous eczema” are just a few examples of current terms. Atopy is a strikingly common finding in these patients (Hanifin and Rajka 1980). It can be defined as familial hypersensitivity of the skin and the mucosa to environmental substances, associated with increased production of immunoglobulin E (IgE) and/or altered pharmacologic reactivity (Ring et al. 2006; Ring 2004). More recently, a new definition for atopy, restricted to IgE production, has been proposed: “a personal or familial tendency to produce IgE antibodies in response to low doses of allergens, usually proteins, and to develop typical symptoms such as asthma, rhinoconjunctivitis, or eczema/dermatitis” (Johansson et al. 2004, pp. 832–836).
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