Professor and Chief
1Pediatric Allergy and Immunology; Duke University Medical Center
The author owns stock, stock options, and/or bonds in SEER, Inc.
Food hypersensitivity (allergy) and food intolerance constitute the category of adverse reactions to food.1,2 An adverse food reaction is a clinically abnormal response to an ingested food or food additive. Both food hypersensitivity and food intolerance have often been overdiagnosed, and both terms have been applied incorrectly to all adverse reactions to foods.
Food intolerance is a general term describing an abnormal physiologic response to an ingested food or food additive. Such reactions are apparently nonimmunologic in nature and have many possible causes, including toxic contaminants (e.g., histamine in scombroid fish poisoning or toxins secreted by Salmonella, Shigella, and Campylobacter), pharmacologic properties of the food (e.g., caffeine in coffee and tyramine in aged cheeses), characteristics of the host (e.g., metabolic traits such as lactase deficiency), and idiosyncratic responses.
Food hypersensitivity is an immunologic reaction resulting from the ingestion of a food or food additive. This reaction can develop after ingestion of a small amount of the substance, and it is unrelated to any physiologic effect of the food or food additive. To most physicians, the term is synonymous with reactions that involve the immunoglobulin E (IgE) mechanism, of which anaphylaxis is the classic example. Although IgE-mediated (type I) hypersensitivity accounts for the majority of well-characterized allergic reactions to food, non-IgE-mediated immune mechanisms are believed to be responsible for a variety of hypersensitivity disorders. This chapter examines adverse food reactions that are IgE mediated, those that are non-IgE mediated, and those that have characteristics of both.
The true incidence of adverse food reactions is still unknown. Up to 15% of the general population believes that they may be allergic to some food. The best available studies, however, suggest that the actual prevalence of food allergy is 3% to 4% of the adult population.3 The incidence of adverse food reactions in young children is estimated to be between 6% and 8%. Several well-controlled studies have shown that the vast majority of allergic reactions occur in the first year of life.3 The foods that commonly cause these reactions in children include eggs, milk, peanuts, and tree nuts. In adults, this list includes fish, shellfish, tree nuts, and peanuts.
A variety of hypersensitivity responses to an ingested food antigen may result from the lack of development of oral tolerance or a breakdown of oral tolerance in the gastrointestinal tract of a person who is genetically predisposed to such hypersensitivity. Either a failure to develop oral tolerance or a breakdown in oral tolerance results in excessive production of food-specific IgE antibodies. These food-specific antibodies bind high-affinity FcεI receptors on mast cells and basophils and low-affinity FcεII receptors on macrophages, monocytes, lymphocytes, eosinophils, and platelets.2 After antigen-presenting cells process the food allergen and present the antigen to specific antibodies on mast cells or basophils, the mast cells and basophils release mediators such as histamine, prostaglandins, and leukotrienes [see 6:X Allergic Response]. These mediators promote vasodilatation, smooth muscle contraction, and mucus secretion, resulting in the symptoms of immediate hypersensitivity. The activated mast cells may also release various cytokines that play a part in the IgE-mediated late-phase response. A rise in plasma histamine levels has been associated with IgE-mediated allergic symptoms after blinded food challenges.
Although a variety of non-IgE-mediated immune mechanisms for allergic reactions to food have been proposed, the scientific evidence supporting these mechanisms is limited. Type III (antigen-antibody complex-mediated) hypersensitivity reactions have been examined in several studies. Whereas food antigen-IgE complexes are seen more commonly in patients with food hypersensitivity, there is little evidence supporting disease mediated by other food antigen-immune complexes. Type IV (cell-mediated) hypersensitivity has been suggested as the mechanism for several disorders in which the clinical symptoms do not appear until several hours after the ingestion of the suspected food. This type of immune response may contribute to some adverse food reactions (e.g., enterocolitis), but except in gluten-sensitive enteropathy, significant supporting evidence of a specific cell-mediated hypersensitivity disorder is lacking.
Food-induced, IgE-mediated GI allergy may manifest itself as a variety of syndromes, including the oral allergy syndrome, immediate GI hypersensitivity, and a small subgroup of cases of allergic eosinophilic gastroenteritis.4
Pollen-associated food allergy syndrome
The pollen-associated food allergy syndrome is considered a form of contact urticaria that is confined almost exclusively to the oropharynx and rarely involves other target organs [see Table 1]. The symptoms include rapid onset of pruritus and angioedema of the lips, tongue, palate, and throat. The symptoms generally resolve quite rapidly. This syndrome is most commonly associated with the ingestion of fresh fruits and vegetables. Interestingly, patients with allergic rhinitis associated with certain airborne pollens (especially ragweed and birch pollens) are frequently afflicted with this syndrome. Patients with ragweed allergy may experience these symptoms after contact with certain melons (e.g., watermelons, cantaloupe, and honeydew) and bananas. Patients with birch sensitivity often have symptoms after the ingestion of raw potatoes, carrots, celery, apples, and hazelnuts. The diagnosis of this syndrome is based on a suggestive history and positive prick skin tests with the implicated fresh fruits and vegetables, although the sensitivity of these tests may be limited in this disorder [see Prick Skin Tests, below].5
Table 1 Pollen-Associated Food Allergy Syndrome27
Immediate GI hypersensitivity
Immediate GI hypersensitivity may accompany allergic manifestations in other target organs [see Table 2].6,7 The GI symptoms vary but may include nausea, abdominal pain, abdominal cramping, vomiting, and diarrhea. In children with atopic dermatitis and food allergy, the frequent ingestion of a food allergen appears to induce partial desensitization of GI mast cells, resulting in less pronounced symptoms.
Table 2 Immediate Gastrointestinal Hypersensitivity27
The diagnosis of immediate GI hypersensitivity is based on a suggestive clinical history, positive prick skin tests, resolution of symptoms after complete elimination of the suspected food allergen for up to 2 weeks, and positive results on oral food challenges. After patients have avoided a particular food for 10 to 14 days, it is not unusual for them to experience vomiting during a challenge, even though they were previously able to eat the food without vomiting.
Respiratory and Skin Reactions
Respiratory and ocular symptoms are common manifestations of IgE-mediated reactions to foods.2,7 Symptoms may include periocular erythema, periocular pruritus, tearing, nasal congestion, nasal pruritus, sneezing, rhinorrhea, coughing, voice changes, and wheezing. Isolated naso-ocular symptoms are an uncommon manifestation of food hypersensitivity reactions.
The skin is a frequent target organ in IgE-mediated food hypersensitivity reactions. The ingestion of food allergens can either trigger immediate cutaneous symptoms or aggravate chronic cutaneous symptoms. Acute urticaria and angioedema are probably the most common cutaneous manifestations of food hypersensitivity, generally appearing within minutes after ingestion of the food allergen. Atopic dermatitis is a chronic skin disorder that generally begins in early infancy and is characterized by typical distribution, extreme pruritus, and a chronically relapsing course; it is associated with asthma and allergic rhinitis [see 2:IV Eczematous Disorders, Atopic Dermatitis, and Ichthyoses].8 Approximately one third of young children with atopic dermatitis have one or more food allergies. The immediate allergic reaction to foods in these patients is IgE mediated. However, their skin disease may be worsened by a mixed IgE-mediated and non-IgE-mediated reaction. Most young children with atopic dermatitis who have food allergy have reactions to milk, eggs, or peanuts.
Systemic Anaphylactic Reactions
Systemic anaphylactic reactions to foods are not uncommon. Systemic symptoms can involve the skin, gastrointestinal tract, and respiratory tract (see above). The foods that most commonly cause anaphylaxis include peanuts, tree nuts, shellfish, and fish, but any food may cause anaphylaxis. Fatal food-induced anaphylaxis occurs most often in adolescents and young adults. Risk factors include asthma and a history of previous severe reactions to food.
Mixed IgE-Mediated and Non-IgE-Mediated Hypersensitivity
Allergic Eosinophilic Gastroenteropathy
Allergic eosinophilic gastroenteropathy is a disorder characterized by infiltration of the gastric or intestinal walls with eosinophils; absence of vasculitis; and, frequently, peripheral blood eosinophilia [see Table 3].4,9 Patients with this syndrome frequently have postprandial nausea and vomiting, abdominal pain, diarrhea, and, occasionally, steatorrhea; young infants experience failure to thrive, and adults have weight loss. There appears to be a subset of patients with allergic eosinophilic gastroenteritis who have symptoms secondary to food. These patients generally have the mucosal form of this disease, which is characterized by IgE-staining cells in jejunal tissue, elevated IgE levels in duodenal fluids, atopic disease, elevated serum IgE concentrations, positive prick skin tests to a variety of foods and inhalants, peripheral blood eosinophilia, iron deficiency anemia, and hypoalbuminemia.
Table 3 Allergic Eosinophilic Gastroenterocolitis27
The diagnosis of allergic eosinophilic gastroenteropathy is based on an appropriate history and a GI biopsy demonstrating a characteristic eosinophilic infiltration. Biopsies may need to be performed in multiple sites (up to eight) to effectively exclude eosinophilic gastroenteritis, because the eosinophilic infiltrates may be quite patchy. Patients with the mucosal form of the disease may have atopic symptoms, including food allergy, elevated serum IgE concentrations, and peripheral eosinophilia; they may also have positive skin tests or positive in vitro IgE results. Other laboratory results consistent with this disease include findings of Charcot-Leyden crystals in the stool; anemia; and hypoalbuminemia. Such patients may also have abnormal results on D-xylose testing. An elimination diet for up to 12 weeks may be necessary before complete resolution of symptoms and normalization of intestinal histology.
Some investigators are using the atopy patch test in the diagnosis of allergic eosinophilic gastroenteropathy. Although this practice is interesting from a research standpoint, these studies are not currently proved to be diagnostic.
Enterocolitis from dietary protein (also known as protein intolerance and food protein-induced enterocolitis) occurs most commonly in young infants between 1 week and 3 months of age [see Table 4]. The typical symptoms are isolated to the GI tract and consist of recurrent vomiting, diarrhea, or both. The symptoms can be severe enough to cause dehydration. Cow's milk and soy protein (particularly in infant formulas) are most often responsible for this syndrome, although egg sensitivity has been reported in older patients. The stools in affected children will often contain occult blood, polymorphonuclear neutrophils (PMNs), and eosinophils and are frequently positive for reducing substances (indicating malabsorbed sugars). Prick skin tests for the putative food protein are characteristically negative. Jejunal biopsies classically reveal flattened villi, edema, and increased numbers of lymphocytes, eosinophils, and mast cells. A food challenge with the responsible protein generally results in vomiting, diarrhea, or both within minutes to several hours; occasionally, patients experience shock.4,10 It is not uncommon to find children who are sensitive to both cow's milk and soy protein. This sensitivity also tends to be lost by 18 to 24 months of age. Elimination of the offending allergen generally will result in improvement or resolution of the symptoms within 72 hours, although secondary disaccharidase deficiency may persist longer. Oral food challenges, which should be done in a medical setting because they can induce severe vomiting, diarrhea, dehydration, or hypotension, consist of administering 0.3 to 0.6 g/kg body weight of the suspected food allergen.
Table 4 Dietary Protein Enterocolitis27
Patients with dietary-protein proctitis generally present in the first few months of life. This disorder is often secondary to cow's milk or soy protein hypersensitivity,11 but in general, more than 50% of infants with dietary-protein proctitis are exclusively breast-fed at the time that symptoms are observed. Most infants with this disorder do not appear ill and have normally formed stools; they generally come to medical attention because of blood (gross or occult) in their stools. GI lesions are confined to the small bowel. Grossly, the lesions range from patchy mucosal injection to severe friability with small aphthoid ulcerations and bleeding. Microscopically, they are characterized by mucosal edema with eosinophils in the epithelium and lamina propria. If lesions are severe, with crypt destruction, PMNs are also prominent.12 It is believed that colitis induced by cow's milk or soy protein resolves by 6 months to 2 years after allergen avoidance; however, this belief is not strongly supported by well-controlled studies. Elimination of the offending food allergen leads to resolution of hematochezia within 72 hours, but the mucosal lesions may take up to 1 month to disappear.
Celiac disease is an extensive enteropathy leading to malabsorption. Total villous atrophy and an extensive cellular infiltrate are associated with sensitivity to gliadin, the alcohol-soluble portion of gluten found in wheat, oats, rye, and barley. The overall incidence of celiac disease is thought to be one in 4,000 population, but there is wide regional variation; for example, the incidence in Ireland has been reported to be as high as one in 500 population. There is apparently a genetic predisposition to this disease, given that approximately 90% of patients are HLA-B8 positive and nearly 80% have the HLA-DW3 antigen. Patients often present with diarrhea or frank steatorrhea, abdominal distention and flatulence, and weight loss; occasionally, they have nausea and vomiting. Other extraintestinal symptoms and oral ulcers secondary to malabsorption are not common. Laboratory studies for patients with suspected celiac disease include measurement of serum transglutaminase and IgA antiendomysial and antigliadin antibodies.
History and Physical Examination
As with virtually all medical disorders, the diagnostic approach to a patient with a suspected adverse food reaction begins with the history and physical examination. Depending on the information derived from these initial steps, various laboratory studies may be helpful [seeTable 5].13,14,15
Table 5 Methods Used in the Evaluation of Allergic Reactions to Food
In cases of suspected adverse food reactions, the value of the history depends largely on the patient's recollection of symptoms and on the examiner's ability to differentiate disorders provoked by food hypersensitivity from disorders with other etiologies. The history may be directly useful in diagnosing food allergy involving acute events (e.g., anaphylaxis after eating fish) but is not always reliable: in many series, less than 50% of reported allergic reactions to food could be substantiated by a double-blind, placebo-controlled food challenge (DBPCFC).3,7 In chronic disorders such as atopic dermatitis, the history is often an unreliable indicator of the offending allergen.
Several items of information are important in establishing that an allergic reaction to food occurred: (1) the type of food suspected of having provoked the reaction (i.e., typical foods for that age); (2) the quantity of the food ingested; (3) the length of time between ingestion and onset of symptoms; (4) the specific symptoms provoked (e.g., skin, respiratory tract, or gastrointestinal tract); (5) whether similar symptoms developed on other occasions when the same food was eaten; (6) whether other factors (e.g., exercise) were involved in the episode; and (7) the length of time since the last reaction.
Although any food may cause an allergic reaction, only a few foods account for 90% of such reactions. In children, these foods are eggs, milk, peanuts, soy, wheat, and, in Scandinavian countries, fish.
A diet diary is often a useful adjunct to the medical history. Patients are asked to keep a chronological record of all foods ingested over a specified period of time and to record any symptoms they experience during this period. The diary can be reviewed at a subsequent visit to determine whether there is a relationship between the foods ingested and the symptoms experienced. Uncommonly, this method will reveal an unrecognized association between a food and a patient's symptoms.
Elimination diets are often used both in diagnosis and in management of adverse food reactions. If a certain food or foods are suspected of provoking the reaction, they are completely eliminated from the diet. The success of an elimination diet depends on several factors, including the correct identification of the allergen or allergens involved, the ability of the patient to maintain a diet completely free of all forms of the possible offending allergen, and the assumption that other factors will not provoke similar symptoms during the study period. The likelihood of all of these conditions being met is often slim. For example, in a young infant who is reacting to cow's milk formula, resolution of symptoms after substitution of soy formula or casein hydrolysate (e.g., Alimentum, Nutramigen) is highly suggestive of cow's milk allergy but also could reflect lactose intolerance. Avoidance of suspected food allergens before a blinded challenge is recommended so that reactions may be heightened. Elimination diets are rarely diagnostic of food allergy, particularly in chronic disorders such as atopic dermatitis or asthma.
Allergy Skin Tests
Prick skin tests
Prick skin tests are highly reproducible16 and are often utilized to screen patients with suspected IgE-mediated food allergies. The glycerinated food extracts (1:10 or 1:20 dilution)7 and appropriate positive (histamine) and negative (saline) controls are applied by either the prick or puncture technique. A test that elicits a wheal (not including erythema) at least 3 mm greater than the negative control is considered positive; any smaller result is considered negative. Appropriate and good-quality food extracts must be utilized for results to be reliable.
A negative skin test confirms the absence of an IgE-mediated reaction (overall negative predictive accuracy is greater than 95%). However, skin testing with commercial reagents often fails to detect IgE-mediated sensitivity to certain fruits and vegetables (e.g., apples, oranges, bananas, pears, melons, potatoes, carrots, and celery), presumably because of the labile nature of the responsible allergens in these foods. In such cases, it may be necessary to use the so-called prick-by-prick method, in which the device used for introducing the allergen into the skin is first pricked into the food. In addition, false negative results are particularly common in very young children, possibly because of lower skin reactivity: children younger than 1 year may have IgE-mediated food allergy without a positive skin test.
A positive skin test to a food is not definitive; it merely indicates the possibility that the patient has symptomatic reactivity to that specific food (overall, the positive predictive accuracy is less than 50%). However, a positive skin test to a food that provokes a severe anaphylactic reaction when eaten by itself may be considered diagnostic. Atopy patch tests for food allergy have been developed, but there is as yet insufficient evidence to support their adoption in clinical practice.
Intradermal skin tests
An intradermal skin test is more sensitive than a prick skin test but is much less specific than a DBPCFC.17 In one study, no patient who had a negative prick skin test but a positive intradermal skin test to a specific food had a positive DBPCFC to that food.17 In addition, intradermal skin testing is more likely to induce a systemic reaction than is prick skin testing. For those reasons, intradermal skin tests have no role in the diagnosis of food allergy.
In Vitro Assays
Radioallergosorbent tests (RASTs) and similar in vitro assays (including enzyme-linked immunosorbent assays [ELISAs]) are often used to screen for IgE-mediated food allergies. Although RASTs are generally considered slightly less sensitive than skin tests, one study comparing skin tests and Phadebas RAST (a first-generation test for specific IgE) with DBPCFCs found prick skin tests and Phadebas RAST to have similar sensitivity and specificity when a Phadebas score of 3 or greater was considered positive.18 In this study, lowering the cutoff point for a positive result to a score of 2 brought a slight improvement in sensitivity at the expense of a significant decrease in specificity. In general, in vitro measurements of serum food-specific IgE performed in high-quality laboratories provide information similar to that of prick skin tests. The newest generation of in vitro studies for specific IgE includes the capsulated hydrolic carrier polymer-fluoroenzyme immunoassay (CAP-FEIA). For patients with suspected food allergy, there are now accepted levels of food-specific IgE concentrations on CAP-FEIA testing that can predict a patient's being allergic to that food with greater than 95% certainty.15 CAP-FEIA is best used for patients with allergic reactions to milk, eggs, peanuts, and, possibly, wheat, soy, and fish [see Table 6].
Table 6 Diagnostic Levels of Food-Specific IgE in CAP-FEIA Studies
Certain foods are able to sensitize and elicit reactions after oral exposure and could trigger responses that generalize to related foods (e.g., peanut sensitivity can generalize to legumes). Other foods (e.g., apple) with labile proteins are not strong oral sensitizers. In this latter group of foods, however, sensitization to homologous proteins encountered through respiratory exposure (e.g., birch pollen) may mediate reactions to cross-reacting proteins in the food, with generally mild clinical manifestations. For many of the cross-reactive proteins, lability of proteins in commercial extracts is an issue. Prick skin tests using the prick-prick method with fresh fruits and vegetables may increase sensitivity when evaluating these labile allergens. In general, the cross-reactivity of the major foods is less than 10% for peanuts and other legumes, about 25% for wheat and other grains, about 35% for peanuts and tree nuts, and greater than 50% for tree nuts and other nuts.
Open, Single-Blind and Double-Blind Placebo-Controlled Food Challenges
Open and single-blind food challenges are often the most practical method of diagnosing food allergy. Nevertheless, the DBPCFC has been considered the gold standard for the diagnosis of food allergy.4 This test has been used successfully by many investigators in both children and adults for the past several years to examine a wide variety of food-related complaints. The selection of foods to be tested in the oral challenge is based on the history or prick skin test (RAST) results.
A DBPCFC is the best means of controlling for the variability of chronic disorders (e.g., chronic urticaria and atopic dermatitis), any potential temporal effects, and acute exacerbations secondary to reducing or discontinuing medications. In particular, psychogenic factors and observer bias are eliminated. Rarely, a false negative DBPCFC occurs when the challenge material a patient receives is not of sufficient quantity to provoke the reaction or when the lyophilization of the food antigen has altered the relevant allergenic epitopes (as may occur with fish antigen). Nevertheless, at present, the DBPCFC has proved to be the most accurate means of diagnosing food allergy.
Practical Approach to Diagnosing Food Allergy
The diagnosis of food allergy remains a clinical exercise that utilizes a careful history, selective prick skin tests or in vitro IgE results (if an IgE-mediated disorder is suspected), appropriate exclusion diet, and blinded provocation. Other diagnostic tests that do not appear to be of significant value include assessment of food-specific IgG or IgG4 antibody levels, assessment of food antigen-antibody complexes, measures of lymphocyte activation (e.g., 3H uptake, interleukin-2 production, and presence of leukocyte inhibitory factor), and sublingual or intracutaneous provocation. Blinded challenges may not be necessary in suspected GI disorders, which often can be diagnosed on the basis of prechallenge and postchallenge laboratory values and biopsy results.
An exclusion diet that eliminates all foods suspected by history or prick skin testing (or, in IgE-mediated disorders, in vitro IgE results) should be conducted for at least 1 to 2 weeks. Some patients with GI disorders may need to have the exclusion diet extended for up to 12 weeks after appropriate biopsies. If no improvement is noted after institution of the diet, food allergy is unlikely. In patients with some chronic diseases, such as atopic dermatitis and chronic asthma, it may be difficult to discriminate the effects of the food allergen from the effects of those diseases (e.g., skin or respiratory tract manifestations).
Open or single-blind challenges in a clinic setting may be helpful to test for allergy to specific foods. Such challenges are less cumbersome and time consuming than DBPCFCs. It is important that the clinician make an unequivocal diagnosis of food allergy; a presumptive diagnosis of food allergy based on a patient's history and prick skin tests or RAST results is no longer acceptable. There are exceptions to this, however, such as the patient who experiences severe anaphylaxis after the isolated ingestion of a specific food. Because of reliance on presumptive diagnoses, over 25% of the United States population have altered their eating habits on the basis of misconceptions about food allergy.
The only proven therapy for food allergy is the strict elimination of that food from the patient's diet. In infants, breast-feeding avoids contact with potentially allergenic foods if the mother avoids those foods. In infants with a family history of atopy, moreover, exclusive breast-feeding for at least the first 4 months of life appears to lessen the likelihood of atopic dermatitis.19 Elimination diets should be supervised because they may lead to malnutrition or eating disorders, especially if they involve the elimination of a large number of foods or are utilized for extended periods of time. Studies have shown that symptomatic food sensitivity generally is lost over time, except for sensitivity to peanuts, tree nuts, and seafood.
Symptomatic food sensitivity is usually very specific; patients rarely react to more than one member of a botanical family or animal species. Consequently, clinicians should confirm that patients are not unnecessarily limiting their diet for fear of allergic reactions. Risk factors for more severe anaphylactic reactions include the following: (1) a history of a previous anaphylactic reaction; (2) a history of asthma, especially if poorly controlled; (3) allergy to peanuts, nuts, fish, or shellfish; (4) current treatment with beta blockers or angiotensin-converting enzyme inhibitors; and, possibly (5) female sex.
It is important to develop a specific, written action plan for patients with food allergy. This plan should include foods to be eliminated; symptoms to watch for; a listing of when and how to use medications, including antihistamines and epinephrine; and when and how to contact emergency medical personnel.
Several medications have been used in an attempt to protect patients with food hypersensitivity, including oral cromolyn sodium, H1 and H2antihistamines, ketotifen, corticosteroids, and prostaglandin synthetase inhibitors. Some of these medications may modify food allergy symptoms, but overall, they have minimal efficacy or unacceptable side effects.
The importance of prompt administration of epinephrine when symptoms of systemic reactions to foods develop cannot be overemphasized [see 6:XIII Urticaria, Angioedema, and Anaphylaxis]. Patients with a history of anaphylaxis should always carry an epinephrine autoinjector (Epi-Pen [0.3 mg], Epi-Pen, Jr. [0.15 mg], or Twinject [0.3 mg]). For anaphylaxis, epinephrine is given in a dose of 0.01 mg/kg (generally up to a maximum of 0.3 mg). The route of administration can be intramuscular or subcutaneous, but studies suggest that intramuscular administration is better. If necessary, the dose can be repeated in 15 minutes.
Blinded, placebo-controlled studies of rush immunotherapy for the treatment of peanut hypersensitivity have demonstrated efficacy in a small number of patients.20 The adverse-reaction rates have been significant, however, and such reactions preclude general clinical application of rush immunotherapy at this time. Except for patients who are at risk of life-threatening reactions to minuscule amounts of peanut, there is no use for immunotherapy in patients with food allergies. Newer types of immunotherapy for prevention of food-induced anaphylaxis are being developed, such as the following: (1) humanized anti-IgE monoclonal antibody therapy, (2) plasmid-DNA immunotherapy, (3) peptide fragments (so-called overlapping peptides), (4) cytokine-modulated immunotherapy, (5) immunostimulatory sequence-modulated immunotherapy, (6) bacterial-encapsulated allergen immunotherapy, and (7) recombinant protein immunotherapy.21 A 2003 study of anti-IgE in peanut-allergic patients22 demonstrated that this medication may eventually be helpful for preventive treatment of food-induced anaphylaxis.
Patient education and support are essential aspects of treatment for patients with food allergy. In particular, adults and older children who are prone to anaphylaxis, as well as parents of pediatric patients, must be informed in a direct but sympathetic way that these reactions are potentially fatal.
When eating away from home, food-sensitive persons should feel comfortable requesting information about the contents of prepared foods. For school-aged children, the American Academy of Pediatrics Committee of School Health has recommended that schools be equipped to treat anaphylaxis in allergic students. Children older than 7 years can usually be taught to inject themselves with epinephrine. The physician must be willing to explain these issues to school personnel and, with the parents, help instruct these personnel in how to deal with them. In the home, the family should eliminate the incriminated allergen or, if this is not practical, place warning stickers on foods with the offending antigens. A variety of groups can help provide patients with support, advocacy, and education about food allergy [see Table 7]. The Food Allergy and Anaphylaxis Network (FAAN) is an excellent resource for patients, families, and other health care professionals.
Table 7 Resources for Patients with Food Allergy
Children younger than 3 years who are diagnosed with anaphylaxis to foods such as milk, eggs, wheat, or soybeans often outgrow this clinical sensitivity after several years.9,23,24 Children who develop food sensitivity after 3 years of age are less likely to lose their food reactions over a period of several years. Patients who have very mild reactions (i.e., skin symptoms only) to peanuts during the first 12 to 24 months of life may outgrow their symptoms.25,26 Allergies to foods such as tree nuts, fish, and seafood are generally not outgrown regardless of the age at which they develop. These persons appear likely to retain their allergic sensitivity for a lifetime. Consequently, new strategies are being evaluated to desensitize patients to these foods.
Editors: Dale, David C.; Federman, Daniel D.