Atopic dermatitis (AD), characterized by intense pruritus, eczematous lesions, and a relapsing disease course, is a chronic inflammatory skin disease that affects both children and adults. AD often begins in infancy and is associated with atopic diseases in the personal or family history.1
Environmental factors may trigger AD by affecting the skin barrier and by triggering inflammation. The elicitation of T-helper type 2 cytokines further impairs the epidermal barrier and leads to the penetration of irritants and allergens into the epidermis and thereby perpetuating inflammation.
The presence of AD and its severity has been shown to positively correlate with risk of developing food allergy (FA). Children with AD are estimated to be six times more likely to develop FA compared with their healthy peers. It has been reported that nearly 40% of children with moderate-to-severe
AD have immunoglobulin E (IgE) mediated FA compared with only 6% in the general population. Although analysis of experimental data has linked skin inflammation in AD to FA, with food challenges reproducing symptoms and avoidance diets improving AD, elimination diets are not known to cure AD
and may have unfavorable consequences, such as loss of tolerance, which leads to immediate-type allergy, including anaphylaxis, nutritional deficiencies, growth failure, and reduction of quality of life for the patient and family. Exacerbation of AD can be inaccurately attributed to foods.
Individuals with AD are often sensitized to foods with positive testing results, however, able to tolerate the food. In light of widespread ordering and commercial availability of serum specific IgE for FA, testing for FA is recommended only if, from a detailed clinical history, immediate-type
allergic symptoms occur with ingestion of food, or in infants with AD who do not improve with optimal skin care.
Persistent eczema leads to both impaired growth and food allergy: JECS birth cohort
