IgE-mediated food allergies affect about 1–4% of American and European adults and are slightly more frequent in children (around 5%). About 25% of food allergy in children is due to peanuts, and peanut allergy is increasing in incidence. Figure 14.15 lists risk factors for developing IgE-mediated food allergy. IgE-mediated food allergy can manifest itself in a variety of ways, ranging from a swelling of the lips and oral tissue on contact with the allergen, to gastrointestinal cramping, diarrhea, or vomiting. Local gastrointestinal symptoms are due to activation of mucosal mast cells, leading to transepithelial fluid loss and smooth muscle contractions. Food allergens that subsequently reach the bloodstream can lead to urticaria, asthma, and, in the most severe cases, systemic anaphylaxis that can lead to cardiovascular collapse (see Section 14-10). Certain foods, most importantly peanuts, tree nuts, and shellfish, are particularly associated with severe anaphylaxis. Around 150 deaths occur each year in the United States as a result of a severe allergic reaction to food, with peanut and tree nut allergies accounting for most of the deaths. Peanut allergy is a significant public health problem, especially in schools, where children may be unwittingly exposed to peanuts, which are present in many foods. Recent studies offer hope for reducing the incidence of severe food allergy. In one study, infants with severe eczema who were at high risk for developing peanut allergy were randomly assigned either to be fed peanuts regularly, starting between ages 4 and 11 months, or to be on a peanut-avoidance diet for 5 years. At the age of 5, the children who had consumed peanuts showed more than a threefold reduction in the frequency of peanut allergy; the reduction was associated with decreased production of peanut-specific IgE. This suggests that deliberate introduction into the diet of allergen at the appropriate time to at-risk individuals may suppress the development of food allergy.
Of interest is that one of the characteristic features of food allergens is a high degree of resistance to digestion by pepsin in the stomach. This allows them to reach the mucosal surface of the small intestine as intact allergens. Cases of IgE-mediated food allergies arising in small numbers of previously unaffected adults who were taking antacids or proton-pump inhibitors for ulcers or acid reflux have been proposed to be due to impaired digestion of potential allergens in the less acidic stomach conditions produced by these medications.
14-13 IgE-mediated allergic disease can be treated by inhibiting the effector pathways that lead to symptoms or by desensitization techniques that aim at restoring biological tolerance to the allergen.
Most of the current drugs that are used to treat allergic disease either treat only the symptoms—examples of such drugs are antihistamines and β-agonists—or are general anti-inflammatory or immunosuppressive drugs such as the corticosteroids (Fig. 14.16). Treatment is largely palliative, rather than curative, and the drugs often need to be taken throughout life. Anaphylactic reactions are treated with epinephrine, which stimulates the re-formation of endothelial
Fig. 14.16 Approaches to the treatment of allergic disease. Examples of treatments in current clinical use for allergic reactions are listed in the top half of the table, with approaches under investigation listed below.