Food allergy as seen by an allergist

The clinical expression of allergic disease is the consequence of a series of complex gene-environment interactions that occur at the materno-fetal interface and throughout infancy, leading to persistence of the Th2 immune response. It has been proposed that atopic eczema is the cutaneous manifestation of a systemic disorder that also gives rise to asthma, food allergy, and allergic rhinitis. The recent emergence of genes regulating epidermal barrier function has raised the question of whether the skin barrier in atopic eczema is defective from the outset, rendering the epidermis "leaky," thereby increasing the risk of allergen penetration and the succeeding inflammatory reaction that contributes to atopic eczema. Food allergic sensitisation and eczema frequently coexist during the first 2 years of life, and food allergy is more prevalent in infants and children with moderate to severe eczematous inflammation. The majority of food allergic reactions are caused by 8 foods, with milk, egg, and peanut occurring with greatest frequency. The acquisition of food-specific tolerance occurs predominantly with foods in which the epitopes are grouped together in a conformational structure (milk, egg, wheat, soy), whilst it rarely occurs in patients allergic to foods in which the epitopes are arranged in a linear fashion (nuts, seeds, fish). Better tests and novel therapies, such as immunotherapy and oral tolerance induction, are required for the management of food allergy.