Sensitisation of IgE mediated to a particular food can be induced by contact with skin that does not effectively fulfil the barrier role, secondary to gene mutation of that protein in the skin. Barrier defects allow skin penetration by various allergens, including by food proteins, promoting sensitisation induction and IgE synthesis, which may contribute to skin inflammation characteristic of atopic dermatitis.
It is estimated that 40% of children with moderate forms, and probably much more of those with severe AD, have associate food allergies. An even greater proportion of children with atopic dermatitis often have elevated levels of specific IgE, sometimes even in the absence of a genuine allergy. This explains why the role of allergies in the pathogenesis and severity of AD is intensely debated.
Skin manifestations of food allergies (IgE-mediated) consist of acute urticaria, angioedema, and contact reactions. If AD is aggravated by exposure to a food product, such reactions are not IgE-mediated hypersensitivity reactions, but rather delayed and usually develop 2 to 6 hours after exposure.
Milk, egg white, wheat flour, soy, fish and peanuts are among the foods most often involved in worsening AD symptoms.