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Atopic eczema is predominantly a disease of childhood that gives rise to poorly demarcated chronic pruritic papular inflammation of the skin. Uncontrollable scratching is prominent. Most cases improve with age, although approximately 50% of children retain evidence of the condition into adult life. ‘Atopy’ defines those with an inherited tendency to develop asthma, allergic rhinitis, conjunctivitis or atopic eczema and is present in 15%–25% of the population. Atopics produce high levels of circulating immunoglobulin (Ig) E antibodies, commonly to inhalant allergens (e.g. house dust mite). Confusingly, not all those with the clinical pattern of ‘atopic eczema’ show raised IgE; therefore the diagnostic criteria do not include measurements of IgE.
Individuals with atopic eczema have an impaired skin barrier which allows excess water loss through the skin (drying effect) and an increased potential for exogenous irritants and allergens to penetrate (inducing inflammation). Discovery of a strong association between loss-of-function mutations in the gene encoding filaggrin, which is a skin barrier protein expressed in the outer layers of the epidermis, and individuals with atopic eczema has shown how critical epidermal function is to development of atopic eczema.
Individuals with atopic eczema make aberrant immune responses to environmental allergens which become skewed towards Th2 responses (p. 10), inducing allergen-specific IgE production. The basic cause of these immune defects is still unclear. However, the serum IgE is normal in 20% of atopic eczema subjects.
About 20%–30% of UK infants are affected. The condition usually starts within the first 6 months of life and, by 1 year, 60% of those likely to develop atopic eczema will have done so. Two-thirds have a family history of atopy. Remission occurs within 10–20 years in 40%–60%, although some relapse later.
The appearance of atopic eczema differs depending on the age of the patient.
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