Food Allergy
(See also Overview of Allergic and Atopic Disorders.)
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). 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.
Etiology
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.
Food allergies are more common among children whose parents have food allergies, allergic rhinitis, or allergic asthma.
In general, food allergy is mediated by IgE, T cells, or both:
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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.
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T-cell–mediated allergy (eg, dietary protein gastroenteropathies, celiac disease) manifests gradually and is chronic; it is most common among infants and children.
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Allergies mediated by both IgE and T cells (eg, atopic dermatitis, eosinophilic gastroenteropathy) tend to be delayed in onset or chronic.
Eosinophilic gastroenteropathy
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 may accompany eosinophilic gastroenteropathy or occur in isolation. Eosinophilic esophagitis is characterized by chronic inflammation of the esophagus and may cause dysphagia, nonacid-related dyspepsia, and dysmotility or, in children, feeding intolerance and abdominal pain. Eosinophilic esophagitis may cause strictures; diagnosis is by endoscopic biopsy.
Symptoms and Signs
Symptoms and signs of food allergies vary by allergen, mechanism, and patient age.
The most common manifestation in infants is atopic dermatitis alone or with gastrointestinal (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 years, 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 with a dominance of T-cell–mediated reactions, 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.
Diagnosis
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 other 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. Patients should keep a food diary, meticulously listing everything they consume and any adverse effects they have, to help guide decisions regarding elimination of suspect foods.
If a food reaction is suspected, the relationship of symptoms to foods is assessed by one of the following:
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 minutes, 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 (oral challenge testing). (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 one or both of the following:
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Eliminating foods the patient suspects of causing symptoms based on the patient's food diary
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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.
A discussion with the patient and observations from the patient's food diary can help with the choice of the initial elimination diet. If no improvement occurs after 1 week of the initial diet, another diet should be tried; however, T-cell–mediated reactions may take weeks to resolve. If symptoms are relieved and if patients have less severe symptoms, one new food is added and eaten in large amounts for > 24 hours or until symptoms recur. But if patients have particularly severe symptoms, 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
Treatment of food allergies 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. In a recent placebo-controlled phase III trial, ingesting a small amount of a peanut protein preparation enabled children and adolescents with peanut allergy to eat a larger amount of peanut protein (up to the equivalent of two peanuts). However, the effect of the preparation was not significant in study participants ≥ 18 years (1).
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.
Patients with severe food allergies should be advised to carry antihistamines to take immediately if a reaction starts and a prefilled, self-injecting syringe of epinephrine to use when needed for severe reactions.
Prevention
For many years, avoiding feeding young infants allergenic foods (eg, peanuts) has been recommended as a way to prevent food allergies. However, a recent study (2) showed that early introduction and regular consumption of food that contains peanuts can prevent peanut allergy in infants at high risk of developing this allergy (eg, infants with egg allergy or eczema).
Prevention references
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1. PALISADE Group of Clinical Investigators, Vickery BP, Vereda A, et al: AR101 oral immunotherapy for peanut allergy. N Engl J Med. 379 (21):1991–2001, 2018. doi: 10.1056/NEJMoa1812856.
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2. Du Toit G, Roberts G, Sayre PH, et al: Randomized trial of peanut consumption in infants at risk for peanut allergy. N Engl J Med 372 (9):803-813, 2015. doi: 10.1056/NEJMoa1414850.
Key Points
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Food allergy is commonly mediated by IgE (typically resulting in acute systemic allergic reactions) or T cells (typically resulting in chronic GI symptoms).
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Distinguish food allergy 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.
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If the diagnosis is not clinically obvious in adults or if children are being evaluated, do skin tests, an allergen-specific serum IgE test, or an elimination diet.
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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).
More Information
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National Institute of Allergy and Infectious Diseases (NIAID): Guidelines for the diagnosis and management of food allergy in the United States
