Food Allergy and Intolerance
Food allergy is reproducible symptoms occurring after ingestion of a specific food and for which an immunologic basis (IgE antibodies to the food) is proved. Food intolerance involves clinical GI reactions in which the mechanism is not immunologic or is not known.
Many common (probably psychophysiologic) adverse food reactions are attributed to food allergy when no convincing cause-and-effect evidence exists, at least of the type of allergy that can be evaluated by skin tests and is associated with specific IgE antibodies to foods. Certain claims are controversial and almost surely untrue; eg, that intolerance (or allergy) to food or food additives can be responsible for hyperactive children, the tension-fatigue syndrome, and enuresis. Unsubstantiated claims blame food allergy for arthritis, obesity, suboptimal athletic performance, and depression, among other conditions.
Occasionally, cheilitis, aphthae, pylorospasm, spastic constipation, pruritus ani, and perianal eczema have been attributed to food allergy or intolerance, but the association is difficult to prove. Recently, food intolerance was found to be responsible for symptoms of some patients with the irritable bowel syndrome, confirmed by double-blind food challenge. An increase in rectal prostaglandin levels was noted when a reaction occurred. Preliminary information suggests that the same phenomenon may take place occasionally in patients with chronic ulcerative colitis.
Eosinophilic enteropathy, which may be related to specific food allergy, is an unusual illness involving pain, cramps, and diarrhea associated with blood eosinophilia, eosinophilic infiltrates in the gut, protein-losing enteropathy, and a history of atopic disease. Rarely, dysphagia occurs, indicating esophageal involvement.
True IgE-mediated food allergy usually develops in infancy, most often in those with a strong family history of atopy.
Symptoms and Signs
The first manifestation may be eczema (atopic dermatitis) alone or in association with GI symptoms. By the end of the first year, dermatitis usually has lessened and allergic respiratory symptoms may develop. Asthma and allergic rhinitis can be aggravated by allergy to foods that can be identified by skin testing. However, as the child grows, foods become less important, and he reacts increasingly to inhaled allergens. By the time the child with asthma and hay fever is 10 yr old, it is rare for a food to provoke respiratory symptoms, even though positive skin tests persist. If atopic dermatitis persists or appears in the older child or adult, its activity seems to be largely independent of IgE-mediated allergy, even though atopic patients with extensive dermatitis have much higher IgE levels in the serum than those who are free of dermatitis.
Most young food-allergic patients are sensitive to potent allergens (eg, allergens in eggs, milk, peanuts, and soy). Older people may react violently to ingesting even a trace of such foods and other foods (especially shellfish), experiencing explosive urticaria, angioedema, and even anaphylaxis. Anaphylaxis may occur in patients with a lower level of sensitivity only if they exercise after eating the offending food.
Milk intolerance is sometimes caused by an intestinal disaccharidase deficiency and is expressed by GI symptoms (see also Carbohydrate Intolerance in Ch. 30). In other patients, milk causes GI and even respiratory symptoms for no known reason. Food additives can produce systemic symptoms (monosodium glutamate); asthma (metabisulfite, tartrazine--a yellow dye); and possibly urticaria (tartrazine). These reactions are not caused by IgE antibodies. A few patients suffer from food-induced or aggravated migraine, confirmed by blinded oral challenge.
Digestion effectively prevents food allergy symptoms in most adults. This is illustrated by allergic patients who react on inhalation or contact but not on ingestion of an allergen (eg, in baker's asthma, the affected workers wheeze on exposure to flour dust and have positive skin tests to wheat and/or other grains, yet have no problem eating grain products).
Diagnosis
Severe food allergy is usually obvious in adults. When it is not, or in most children, diagnosis may be difficult and the condition must be differentiated from functional GI problems.
In persons suspected of having reactions to foods after eating, the relationship of symptoms to foods is first tested by appropriate skin tests. A positive test does not prove clinically relevant allergy, but a negative test rules it out. With a positive skin test, clinically relevant sensitivity can be determined by an elimination diet and, if symptoms improve, by reexposure to the food to determine if it can induce symptoms. All positive challenges should be followed by a double-blind challenge to be considered definitive. The basic diet is determined by eliminating foods suspected by the patient of causing symptoms or by prescribing a diet composed of relatively nonallergenic foods (see Table 148-3).
Foods that commonly cause allergy are milk, eggs, shellfish, nuts, wheat, peanuts, soybeans, and all products containing one or more of these ingredients. Most common allergens and all suspected foods must be eliminated from the starting diet. No foods or fluids may be consumed other than those specified in the starting diet. Eating in restaurants is not advisable, since the patient (and physician) must know the exact composition of all meals. Pure products must always be used; eg, ordinary rye bread contains some wheat flour.
If no improvement occurs after 1 wk, another diet should be tried. If symptoms are relieved, one new food is added and more than the usual amount is eaten for > 24 h or until symptoms recur. Alternatively, small amounts of the food to be tested are eaten in the physician's presence, and the patient's reactions observed. Aggravation or recrudescence of symptoms after the addition of a new food is the best evidence of allergy. Such evidence should be verified by noting the effect of removing that food from the diet for several days, then restoring it.
Treatment
The only treatment is eliminating the offending food. Elimination diets can be used for both diagnosis and treatment. When only a few foods are involved, abstinence is preferred. Sensitivity to one or more foods may disappear spontaneously. Oral desensitization (by first eliminating the offending food for a time and then giving small, daily increased amounts) has not been proved effective nor has the use of sublingual drops of food extracts. Antihistamines are of little value except in acute general reactions with urticaria and angioedema. Oral cromolyn has been used with apparent success in other countries, but the oral form is approved for use in the USA only for mastocytosis (see below). Prolonged glucocorticoid treatment is not indicated except in symptomatic eosinophilic enteropathy.
For treatment of the severe, potentially fatal acute attack, see Anaphylaxis, below.
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