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Food allergy is an exaggerated immune response to dietary components, usually proteins. Manifestations vary widely and can include atopic dermatitis, GI or respiratory symptoms, and anaphylaxis. Diagnosis is by history and sometimes allergen-specific serum IgE testing, skin testing, and/or elimination diets. Treatment is with elimination of the food that triggers the reaction and sometimes oral cromolyn.
Food allergy should be distinguished from nonimmune reactions to food (eg, lactose intolerance, irritable bowel syndrome, infectious gastroenteritis) and reactions to additives (eg, monosodium glutamate, metabisulfite, tartrazine) or food contaminants (eg, latex dust in food handled by workers wearing latex gloves), which cause most food reactions. Prevalence of true food allergy ranges from < 1 to 3% and varies by geography and method of ascertainment; patients tend to confuse intolerance with allergy.
Almost any food or food additive can cause an allergic reaction, but the most common triggers include
Cross-reactivity between food and nonfood allergens exists, and sensitization may occur nonenterally. For example, patients with oral allergies (typically, pruritus, erythema, and edema of the mouth when fruits and vegetables are eaten) may have been sensitized by exposure to pollens that are antigenically similar to food antigens; children with peanut allergy may have been sensitized by topical creams containing peanut oil used to treat rashes. Many patients who are allergic to latex are also allergic to bananas, kiwis, avocados, or a combination.
In general, food allergy is mediated by IgE, T cells, or both. IgE-mediated allergy (eg, urticaria, asthma, anaphylaxis) is acute in onset, usually develops during infancy, and occurs most often in people with a strong family history of atopy. T-cell–mediated allergy (eg, dietary protein gastroenteropathies, celiac disease) manifests gradually and is chronic; it is most common among infants and children. Allergies mediated by both IgE and T cells (eg, atopic dermatitis, eosinophilic gastroenteropathy) tend to be delayed in onset or chronic.
This unusual disorder causes pain, cramps, and diarrhea with blood eosinophilia, eosinophilic infiltrates in the gut, and protein-losing enteropathy; patients have a history of atopic disorders. Eosinophilic esophagitis sometimes accompanies eosinophilic gastroenteropathy and may cause dysphagia, nonacid-related dyspepsia, and dysmotility or, in children, feeding intolerance and abdominal pain.
Symptoms and signs vary by allergen, mechanism, and patient age. The most common manifestation in infants is atopic dermatitis alone or with GI symptoms (eg, nausea, vomiting, diarrhea). Children usually outgrow these manifestations and react increasingly to inhaled allergens, with symptoms of asthma and rhinitis; this progression is called atopic march. By age 10 yr, patients rarely have respiratory symptoms after the allergenic food is eaten, even though skin tests remain positive. If atopic dermatitis persists or appears in older children or adults, its activity seems largely independent of IgE-mediated allergy, even though atopic patients with extensive dermatitis have much higher serum IgE levels than atopic patients who are free of dermatitis.
When food allergy persists in older children and adults, the reactions tend to be more severe (eg, explosive urticaria, angioedema, even anaphylaxis). In a few patients, food (especially wheat and shrimp) triggers anaphylaxis only if they exercise soon afterward; mechanism is unknown. Food may also trigger nonspecific symptoms (eg, light-headedness, syncope). Occasionally, cheilitis, aphthous ulcers, pylorospasm, spastic constipation, pruritus ani, and perianal eczema are attributed to food allergy.
T-cell–mediated reactions tend to involve the GI tract, causing symptoms such as subacute or chronic abdominal pain, nausea, cramping, and diarrhea.
Severe food allergy is usually obvious in adults. When it is not or when it occurs in children (the most commonly affected age group), diagnosis may be difficult, and the disorder must be differentiated from functional GI problems. For diagnosis of celiac disease, see Celiac Disease : Diagnosis. Testing (eg, allergen-specific serum IgE testing, skin testing) and elimination diets are most useful in diagnosing IgE-mediated reactions.
If a food reaction is suspected, the relationship of symptoms to foods is assessed by an allergen-specific serum IgE test (see Allergic, Autoimmune, and Other Hypersensitivity Disorders:Specific tests) or by skin testing (see Specific tests). In either case, a positive test does not confirm a clinically relevant allergy. Both tests can have false-positive or false-negative results. Skin testing is generally more sensitive than the allergen-specific serum IgE test but is more likely to have to false-positive results. The skin test provides a result within 15 to 20 min, much more quickly than the allergen-specific serum IgE test. If either test is positive, the tested food is eliminated from the diet; if eliminating the food relieves symptoms, the patient is reexposed to the food (preferably in a double-blind test) to see whether symptoms recur. (See also the National Institute of Allergy and Infectious Diseases (NIAID) medical position statement: Guidelines for the diagnosis and management of food allergy in the United States .)
Alternatives to skin testing include eliminating foods the patient suspects of causing symptoms and/or prescribing a diet that consists of relatively nonallergenic foods and that eliminates common food allergens (see Table: Allowable Foods in Elimination Diets*). For the latter diet, no foods or fluids may be consumed other than those specified. Pure products must always be used. Many commercially prepared products and meals contain an undesired food in large amounts (eg, commercial rye bread contains wheat flour) or in traces as flavoring or thickeners, and determining whether an undesired food is present may be difficult.
If no improvement occurs after 1 wk, another diet should be tried; however, T-cell–mediated reactions may take weeks to resolve. If symptoms are relieved, one new food is added and eaten in large amounts for >24 h or until symptoms recur. Alternatively, small amounts of the food to be tested are eaten in the clinician’s presence, and the patient’s reactions observed. Aggravation or recrudescence of symptoms after addition of a new food is the best evidence of allergy.
Allowable Foods in Elimination Diets*
Treatment consists of eliminating the food that triggers the allergic reaction. Thus, diagnosis and treatment overlap. When assessing an elimination diet’s effect, clinicians must consider that food sensitivities may disappear spontaneously.
Oral desensitization (by first eliminating the allergenic food for a time, then giving small amounts and increasing them daily) and immunotherapy using sublingual drops of food extracts are under study.
Oral cromolyn has been used to decrease the allergic reaction with apparent success. Antihistamines are of little value except in acute general reactions with urticaria and angioedema. Prolonged corticosteroid treatment is helpful for symptomatic eosinophilic enteropathy.
Food allergy is commonly mediated by IgE (typically resulting in acute systemic allergic reactions) or T cells (typically resulting in chronic GI symptoms).
Food allergy should be distinguished from nonimmune reactions to food (eg, lactose intolerance, irritable bowel syndrome, infectious gastroenteritis) and reactions to additives (eg, monosodium glutamate, metabisulfite, tartrazine) or food contaminants.
If the diagnosis is not clinically obvious in adults or if children are being evaluated, skin tests, an allergen-specific serum IgE test, or an elimination diet may be used.
Make sure patients understand that in an elimination diet, they can eat only foods on the list and only pure foods (which excludes many commercially prepared foods).
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