A child with atopy produces IgE antibodies after exposure to commonenvironmental allergens. Both genetic and environmental factors determine thedevelopment of atopic disease. The presence of specific IgE antibodies toenvironmental allergens is determined with skin prick or radioallergosorbenttesting in children with atopy. Test results should be interpreted in the contextof the clinical history and further investigations (eg. allergen avoidance orchallenge test).Preventing atopic disease in high-risk infants and hindering progressionof disease in children with established disease are the areas of active research.Although atopic disease is commonly exacerbated by non-allergen triggers(e.g. viral infection in asthma, skin irritants in eczema), identification andavoidance of potential allergens may significantly improve the disease.Management of atopic disease is frequently symptomatic, but it isimportant to avoid identified allergen triggers. Immunotherapy may beconsidered in selected school-age children with severe rhinoconjunctivitis.The medications used are either anti-inflammatory and/or designed toblock the effects of mediators released during the allergic or atopic response.The anti-inflammatory action of topical, inhaled, and sometimes oral steroids isa mainstay of treatment. The recent development of leukotriene antagonists foruse in mild persistent asthma, topical calcineurin inhibitors for eczema(Tacrolimus and Pimecrolimus), and monoclonal anti- IgE antibodies forasthma provide non-steroidal anti-inflammatory alternatives.The hygiene hypothesis of atopic disease suggests that environmentalchanges in the industrialized world have lead to reduced microbial contact at anearly age and thus resulted in the growing epidemic of atopic eczema, allergicrhinoconjunctivitis and asthma.