Atopic dermatitis (AD) is an immune-mediated inflammation of the skin arising from an interaction between genetic and environmental factors. The genetic factors involve both epidermal barrier function as well as the immune system. Pruritus is the primary symptom; skin lesions range from mild erythema to severe lichenification. Diagnosis is by history and examination. Treatment is moisturizers, avoidance of allergic and irritant triggers, and often topical corticosteroids or immune modulators. Childhood atopic dermatitis frequently resolves or lessens significantly by adulthood.
Pathophysiology
AD has been historically divided into 2 forms: extrinsic or IgE-mediated (70 to 80% of cases) and intrinsic or non‒IgE-mediated (the remainder). However, both forms are now often thought to be different phases of the same disorder.
Many patients with AD have a mutation in the gene encoding for the filaggrin protein, which is a component of the cornified cell envelope produced by differentiating keratinocytes. Also, skin affected by AD is deficient in ceramides, which increases transepidermal water loss. One hypothesis is that the non-IgE form is the initial phase resulting from poor barrier function of the epidermis; subsequently, in most patients, IgE-mediated sensitization occurs to a variety of environmental allergens. Also, some autosensitization may result from IgE autoantibodies produced to autoantigens released from damaged skin cells.
http://www.merckmanuals.com/professional/dermatologic_disorders/dermatitis/atopic_dermatitis.html
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