Atopic eczema is associated with IgE food allergy in around 30 – 50% of infants, and with non IgE food allergy (non-atopic eczema) in 40 – 50% of infants. This association decreases with age. For infants with severe and widespread eczema the association with IgE is strongest, with multiple food allergy to egg, cow’s milk, peanut and soya being common. It is thought that two-thirds of atopic eczema in children is due to egg allergy alone. In older children these common foods (egg, cow’s milk, peanut and soya) are implicated but also wheat, tree nuts, fish and shellfish. There is a strong family link, with 60% of children with one affected parent affected and 80% of children with both affected parents, develop eczema. This inherited factor is more strongly associated with atopy (including atopic asthma) than with eczema itself. It is now believed that the damaged skin is the source of sensitisation to food allergens via poor barrier function. The skin under normal circumstances is an effective barrier to organisms in our environment. Atopic eczema is not only affected by ingested foods via the gut but also by presence of inhaled food antigens via the respiratory tract, as well as via the a damaged skin barrier.
Untreated atopic eczema in infancy risks sensitisation to further food allergens, and is the first step in the so-called Allergic March. The diagram below shows the overlap between atopic conditions and food allergy and supports the view that food allergy is a multi-system condition.