Henry Ford Hospital Medical Journal

Volume 36 Number 4 Article 9

12-1988

The Pediatrician's Guide to Food Allergy

John A. Anderson

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Recommended Citation Anderson, John A. (1988) "The Pediatrician's Guide to Food Allergy," Henry Ford Hospital Medical Journal : Vol. 36 : No. 4 , 198-203. Available at: https://scholarlycommons.henryford.com/hfhmedjournal/vol36/iss4/9

This Article is brought to you for free and open access by Henry Ford Health System Scholarly Commons. It has been accepted for inclusion in Henry Ford Hospital Medical Journal by an authorized editor of Henry Ford Health System Scholarly Commons. The Pediatrician's Guide to Food Allergy

John A. Anderson, MD*

Food allergy occurs in as many as 5% of infants less than 1 year old. Most food sensitivities disappear by age 3 to 4. Most immunologically mediated food allergy reactions are due to type I IgE mechanisms, with skin, gastrointestinal, and respiratory signs and symptoms the most common manifestations. U sing the double-blind, placebo-controlled food challenge (DBPCFC) technique and atopic dermatitis as a model, the most common foods to which children are allergic are cow's milk, eggs, peanuts, wheat, fish, and soy proteins. Anaphylactic sensitivity in older children often involves crustacean seafoods (eg, shrimp), nuts, peanuts, fish, and eggs. Such sensitivities may be lifelong. Infant colic is not due to allergy but may be improved with dietary manipulation. Food-induced diarrhea may be due to food intolerance or allergy. In severe milk-induced enterocolitis, casein- hydrolysate formula rather than soy formula is advised. Specific foods can exacerbate atopic dermatitis: their elimination from the diet will improve the condition. Gluten sensilivirv is both a food intolerance and food allergy. A few cases ofthe attention deficit disorder can be improved with a diet absent of food dyes, particularly yellow #5. Although migraine headaches can be triggered by a number of factors, food allergy is not included. Pulmonary infiltrates due to cow's milk hyperimmune reactions (the Heiner syndrome) is thought to be a rype III milk immune-complex reaction. In the infant, asthma and allergic rhinitis may be a manifestation of food allergy. The diagnosis of food allergy depends upon the history, an IgE-mediated skin prick test or radioallergosorbent test, followed by dietary elimination, open challenge, or DBPCFC. In food anaphylaxis management, however, no food challenge is advised because of the risk. Some tests of unproved validity have been promoted in the diagnosis of food allergy. The principal treatment, strict avoidance of a specific food, is sometimes difficult. Because anaphylaxis is a life-threatening risk, patients are advised always to have an aqueous epinephrine 1:1,000 self injector unit available. Manipulation of the diet of the pregnant woman, nursing mother, and infant helps reduce the risk of allergy in the infant. Medications are of limited use in food allergy prevention, but specific drugs such as epinephrine and cortisone are helpful in treating allergic reactions. (Henry Ford Hosp MedJ 1988;36:198-203)

The Definition child's adverse reaction. Studies of 473 unselected infants in eople often use the word "allergy" to describe the unpleas­ Sweden and 501 successively bom infants in the United States Pant and usually harmless effects resulting from exposure to revealed the suspicion of an adverse reaction to a food in 20% something, almost anything (1). A better term is "adverse reac­ and 28%, respectively (2,3). Most of the adverse reactions, such tion. " Medical professionals reserve the term allergy to refer to as a rash around the mouth or diarrhea, were caused by fruits. an adverse reaction caused by or affected by an immunologic The organic acids in the fmits most likely caused the rash, and event, especially a type I (Gell and Coombs') IgE-mediated one. the fruit sugar caused the diarrhea. These food intolerances are Thus, allergy to cow's milk refers to an IgE-mediated reaction to usually diagnosed by diet elimination and challenge one month a protein in the milk. All other adverse reactions to a food are later Reactions to other foods such as cow's milk and eggs, con­ called intolerances. The cause of these reactions may be known firmed by either open challenge (5%) or double-blind, placebo- as in the reaction to the lactose sugar in cow's milk which occurs controlled food challenge (DBPCFC) (3%) are most likely food in patients lacking the enzyme lactase in their bowel wall, or un­ allergies (3,4). known as is the case of infant colic apparentiy associated with the ingestion of cow's milk-base formula.

The Condition Submined for publication: January 5. 1989. Accepted for publication: January 10. 1989, While food intolerances are more common, food allergy does *Department of Pediatrics, and Department of Inlemal Medicine. Division of Allergy. exist. Most tme food allergy problems occur in early infancy. Henry Ford Hospilal, Address cortespondence to Dr. Anderson. Depariment of Pediatrics. Henry Ford Hospi­ The exact incidence is unknown, but the mother perceives her tal. 2799 W Grand Blvd. Detroit. Ml 48202.

198 Henry Ford Hosp Med J—Vol 36. No 4, 1988 Guide to Food Allergy—Anderson The Foods Table Most children who are allergic to foods are allergic to one or Foods Commonly Causing Allergy in Infants and Children two foods at most, not multiple foods as is commonly assumed. Infants Children Usual Natural Usual Natural The best model to study the relationship of foods to allergy Foods History Foods History has been atopic dermatitis. Utilizing the DBPCFC method, Cow's milk 2-4 years Peanuts May be lifelong Sampson (5) not only proved specific food sensitivity in a group Eggs 2-4 years Fish May be lifelong of patients but also related it to possible in-vivo (immediate re­ Peanuts May be lifelong Seafood (shrimp. acting skin test) and in-vitro (radioallergosorbent test [RAST]) crab, lobster) May be lifelong Wheat 2-4 years Nuts (walnuts. evidence of IgE food allergen specific antibodies. These meth­ cashews, ods can predict 90% those foods to which children become Brazil nuts) May be lifelong allergic. They are, in decreasing order: cow's milk, eggs, pea­ Soy 2-4 years Melons and bananas nuts, wheat, fish, and soy protein. Although unlikely, a child (local anaphylaxis) May be lifelong with sufficient exposure can become allergic to any other single food protein. Foods that need to be considered in older individuals, includ­ ing adolescents, are those commonly associated with urticaria continue to produce clinical reaction after accidental reexposure and systemic anaphylaxis (Table). These include crustaceans or challenge were peanuts, tree nuts, and fish. These sen­ (shrimp, crab, lobster) and tree nuts (walnuts, cashews, Brazil sitivities may be lifelong. nuts), as well as eggs, peanuts, and fish (6). Other foods to be considered in older patients are those associated with local anaphylaxis (isolated swelling and itching of the mouth) which Clinical Reactions is caused by a cross-reaction between the food and inhaled pol­ Anaphylaxis len sensitivity. These foods, usually melons (watermelon, can­ Anaphylaxis may be mild (urticaria) or severe (systemic taloupe) and bananas, cross react with ragweed pollen which is anaphylaxis). Systemic symptoms include laryngeal edema, found only in North America (7). Less common in the United bronchial spasm (asthma-like symptoms), shock, and car­ States is local anaphylaxis with carrots, parsnips, apples, diovascular collapse. Urticaria, common in infants and chil­ potatoes, and hazelnuts (which is associated with birch pollen dren, is frequently associated with viral infection, medication, sensitivity) (8). and food ingestion. The condition is usually not serious, fre­ A new form of anaphylaxis is associated with exercise, partic­ quently self-limited, and easily managed. When associated with ularly jogging. In some cases the urticaria or shock occurs only systemic symptoms of anaphylaxis, however, urticaria is poten­ when the patient exercises after eating a particular food such as tially life-threatening. Any food may be associated with celery or shrimp (9). urticaria/systemic anaphylaxis. Cow's milk, cow's milk-base formula, and eggs are most likely causes for the problem in in­ fants, whereas peanuts, nuts, fish, and shrimp are more likely in The Natural History of Food Allergy older children. Most suspected and proved allergic reactions to food occur Most skin reactions in early infancy such as simple urticaria during the first year of life. In a prospective study of 501 chil­ and red rash around the mouth caused by fmits and juices are not dren. Bock (10) found that only two of 15 cases of proved allergy due to IgE-mediated reactions to those foods but to the organic (by DBPCFC) during the first year of life were still reactive at 13 acids in them (especially citms fmits and tomatoes (3). A rash to 24 months of age and that none of the 15 were reactive at 25 to immediately upon eating strawberries in older individuals is 36 months of age. The mean age of initial onset of symptoms usually due to nonimmunologic release of histamine—not was six months, and the mean time until the food could be safely to allergy. reintroduced was 14 months. The foods most likely to be elimi­ nated from the diet because of an untoward reaction were eggs, Colic cow's milk, and soy protein. Bock (11) also found that seven of Colic is a common problem which occurs in approximately nine children who had had life-threatening anaphylaxis to cow's 20% of all infants whether breast- or formula-fed (12). While the milk, eggs, or soy within the first two years of life later tolerated exact etiology of colic is unknown, many theories have been either normal amounts (four patients) or small amounts of proposed (13). Cow's milk food allergy has been postulated as a the food. cause of colic for over 25 years, but this has never been con­ For many of these foods, such as cow's milk and eggs, which clusively demonstrated. Although colic may disappear with no had caused a reaction in early infancy but which were tolerated diet change, controlled studies have demonstrated that some in­ by age 3 or 4, Foucard (2) found that IgE evidence of sensitivity fants are better when fed either a soy-base or a casein-hydroly- (skin-test positivity or in vitro IgE allergen specific antibody- sate formula (14). RAST positivity) could still be demonstrated. Bock (10) showed that children who developed their food allergy after their third Diarrhea birthday were less likely to become tolerant to the food one to The most common cause of loose stools in infants secondary seven years later in contrast to those who had experienced the to food ingestion is sugar overload from ingesting fmit or fmit reaction before their third birthday. The foods most likely to juice (2,3). Furthermore, some fruits contain sorbitol, a

Henry Ford Hosp Mod J—Vol 36. No 4,1988 Guide lo Food Allergy—Anderson 199 crystalline alcohol formed from sugar, which is a laxative. Prob­ would cure or improve this condition at least 50% of the time. ably the second most common cause is lactose intolerance sec­ The Feingold hypothesis was tested in several well designed ondary to viral or bacterial enteritis. With the temporary loss of clinical studies. In evaluating this theory, a National Institutes of the capacity to digest lactose found in cow's milk, the child de­ Health Consensus Development Conference found that: I) the velops diarrhea when given milk-based formula. Milk allergy is Feingold diet may be helpful in a small number of younger chil­ more common in the first year of life, and diarrhea is a common dren (preschool age) with the ADD, but not 50% as Feingold manifestation of allergy to this food protein (2,3). Diarrhea last­ stated; and 2) the adverse effect on children with ADD was due ing over one month can be caused by either food allergy or food to a drug-like action from food colors, particularly yellow #5, intolerance. Enterocolitis, the most serious food-induced diar­ not allergy. rhea, is usually manifested by bloody diarrhea (15). This condi­ ADD is frequentiy misdiagnosed. Basing a diagnosis simply tion usually results from allergy to cow's milk. Severely allergic on the activity level of the child is risky since many children infants and children may develop allergy to soy protein when without this condition are very active at home and at school. Be­ they are fed a soy-base formula to treat the diarrhea induced by cause allergy occurs in 20% of children and overactivity is also cow's milk. For this reason, the Nutrition Committee of the common, it is not unusual to find both conditions in the same American Academy of Pediatrics advises against the use of soy child even though they are not directly related. formula for children with milk allergy (16). Instead they recom­ mend use of a casein-hydrolysate-base formula, such as Pro- gestimil™ or Nutramigen™ (Mead Johnson Co, Evansville, IN), for children with gastrointestinal complaints. Migraine Commercial soy formula, containing sucrose instead of lac­ Headaches are common among people from a variety of so­ tose, is helpful for primary or secondary lactose intolerance cioeconomic, cultural, geographic, and ethnic backgrounds (17). Some cases of prolonged diarrhea may be relieved by a spe­ (23) . Migraine or "vascular" headaches were described over 25 cial formula of soy protein and lactose (18). In children with in­ centuries ago by Hypocrates. The migraine syndrome is a ge­ termittent loose stools separated by long intervals of normal netic disorder inherited as an autosomal dominant trait with bowel movements, allergy is highly unlikely. greater penetrance in females, or is polygenic. The family his­ tory is positive in 65% to 90% of patients. The prevalence of Eczema migraine is 15% in adult men and 25% in adult women. By age Eczema or atopic dermatitis occurs in 1% to 4.5% of Ameri­ 7, 1.5% of children have migraine headaches, and by age 15 the can children (19). Food allergy is involved in the pathogenesis of incidence increases to 5%. this condition in some cases (5,19). Using the DBPCFC tech­ Migraine attacks may be initiated by diverse factors including nique, specific foods have been shown to cause a flare-upi n the anxiety, stress, fatigue, excessive sleep, minor head trauma, ex­ rash, associated with the release of mediators such as histamine ercise, travel, menses, illness, diet, hunger, odors, light, and and accumulation of eosinophils in the skin. Positive IgE im­ medications. It has been suspected but not proved that naturally mediate reacting .skin test reaction to the specific food or the occurring or added chemical agents in foods, such as tyrosine presence of IgE food allergen antibodies (RAST) to DBPCFC (cheese and chocolate), histamine (red wine), and caffeine (cof­ correlated closely with the presenting clinical history of fee, cola), may trigger the migraine headaches (24). food sensitivity. A possible relationship between migraine and food allergy was proposed as early as 1913 but has remained unproved (25). This theory was recently examined in two separate studies by the Gluten sensitivity DBPCFC technique (24,25). In an English study, Egger et al Gluten sensitivity enteropathy or celiac disease is a well- (24) evaluated 40 of 88 children with migraine in whom diet re­ known reaction to gluten and is usually associated with wheat sulted in a decrease in headaches. Over 55 different dietary sub­ ingestion. The malabsorption which is the primary manifesta­ stances were identified as triggers. These included not only food tion of the disease varies in degree depending on the extent of "allergens" but also nonprotein foods and food additives such as intestinal involvement. In classic celiac disease the damage is tatarazine (yellow dye #5), benzoic acid (preservatives), and caused by the toxic effect of undigested gliadin on the epithelial sugar Of the 88 patients, 52% were shown to be allergic by hav­ cells of the small bowel. The reaction is probably a food intol­ ing one or more positive immediate reacting allergy skin tests to erance which is influenced by immunologic events, probably common allergens. However, there was no difference between cell-mediated sensitivity (Gell and Coombs'-type IV) (1,20). the allergic and nonallergic groups in response to the diet, and specific food allergy tests correlated with food challenge in only Hyperactivity three of the 40 children (24). The attenrion deficit disorder (ADD), first described by In studying 43 adult migraine patients, Mansfield et al (25) Kaufman in 1845, is a term used to describe a child who is diffi­ found that food allergy skin tests identified significant numbers cult to discipline or who receives poor grades in school (21). of patients who improved with food elimination (11 of 16 in the This condition can occur with or without hyperactivity and has positive skin test group versus two of 27 in the negative skin test been estimated to involve between 5% and 10% of American group). In seven patients the specific migraine-provoking food school children. In 1973 Feingold (22) claimed that a diet free of was confirmed by DBPCFC. In two of these cases, a rise in the food additives (especially food dyes) and natural salicylates plasma histamine correlated with the headache. This finding has

200 Henry Ford Hosp Med J—Vol 36. No 4. 1988 Guide to Food Allergy—Anderson not been confirmed by other investigators and is the only con­ and migraine headache are included in this category. The history vincing evidence relating atopy to migraine. of a relationship between a specific food reaction and the allergic signs and symptoms is usually reliable in cases of acute ur­ ticaria, systemic anaphylaxis, and respiratory allergic reactions. Pulmonary infiltrates due to cow's milk Usually the manifestation of allergy occurs within minutes to Heiner and coworkers (25) described seven children, aged six hours of exposure. Foods such as eggs and cow's milk in infants weeks to 15 months, with chronic pulmonary infiltrates in whom or peanuts, fish, shrimp, and nuts in older children are most semm precipitating antibodies to cow's milk protein were dem­ often implicated. With atopic dermatitis or gastrointestinal com­ onstrated. This syndrome was also associated with chronic plaints, however, the history of specific food sensitivity is often rhinitis, gastrointestinal blood loss, iron-deficiency anemia, unreliable (5,19). persistent eosinophilia, and possibly with hemosiderosis. Sampson and Albergo (29) found that the most reliable pre­ Additional findings included cor pulmonale due to upper airway dictors of specific food sensitivity in atopic dermatitis were the obstruction and in some cases a lupus erythematosus phe­ immediate-reacting IgE prick skin test (ST) or the in vitro food nomenon with antinuclear antibodies. IgE antibodies to cow's allergen specific RAST. In most cases, using the atopic der­ milk did not seem to be a factor in this syndrome, but IgG anti­ matitis model and the DBPCFC endpoint, five foods were in­ bodies and complexes were. The pathogenesis of the syndrome volved—cow's milk, eggs, peanuts, wheat, and soy beans. If may relate to the aspiration of cow's milk in early life, followed the ST was 2 -I- or greater with these foods, the likelihood of the subsequently by an exaggerated hyperimmune response to milk DBPCFC being positive was about 50%. If the RAST to any of protein with the formation of IgM and IgG antibodies, immune these foods was positive, the likelihood of a positive challenge complexes with cow's milk protein, and subsequent tissue was between 40% and 50%. With other foods the likelihood of a damage of the Gell and Combs' type III immune response positive DBPCFC was less. These studies show that an indi­ (1,27). Type IV cell-mediated immune reactions to milk may vidual child can have IgE antibodies to a food but be able to tol­ also occur. The syndrome resolves by eliminating cow's milk erate the food in the diet. from the diet but can reoccur with challenge. When foods have been identified to which the patient may be allergic, specific challenge is necessary to confirm a specific sensitivity (30). Except in the case of anaphylaxis, such a chal­ Respiratory allergies lenge can be open or the DBPCFC method can be utilized (30). Rhinitis and asthma secondary to food allergy are usually a In the case of systemic anaphylaxis, there is usually enough problem only in children (6). In Bock's (3) survey of 501 un­ circulating food-specific IgE available to produce a positive in selected infants over the first year of life, nasal congestion, rhi- vitro RAST, especially if the investigation is done within a rela­ norrhea, coughing, and wheezing due to food ingestion ranked tively short time of the reaction. Therefore, skin testing may be third to gastrointestinal and cutaneous signs and symptoms. avoided. If a positive food RAST is found, a presumptive diag­ DBPCFC confirmed one ca.se of allergic nasal congestion. This nosis of food anaphylaxis is made and no challenge is advised. technique has also confirmed asthma as a manifestation of food Ifthe history is suggestive of a food allergy, skin tests to foods allergy in older children (28). When Sampson and Albergo (29) are positive, and systemic anaphylaxis is not involved, the pa­ used DBPCFC in 132 cases presenting chiefly with atopic der­ tient is given a diet containing nonallergic foods for two weeks matitis, 85% of the positive challenges were associated with a (31). This is followed by open challenge over three to five days skin rash flare. However, only 28% of these patients manifested with specific foods. Those foods that are tolerated are added to a skin rash as the only symptom of the food allergy reaction. Of the basic diet, and the child is challenged with additional foods. the total group who reacted, 57% developed gastrointestinal One may not assume that children who are allergic cannot tol­ complaints (nausea, abdominal pain, vomiting, and diarrhea), erate a given food simply because of a history or a positive and 36% of the positive challenge cases developed respiratory skin test. Allergy diets are not intended to be therapeutic but symptoms with or without rash or gastrointestinal symptoms. rather diagnostic. Respiratory symptoms that occurred with challenge included A negative food allergy ST or RAST in a suspected food- nasal congestion, rhinorrhea, sneezing, stridor, and wheezing. allergic patient is perhaps of greater value, for when these are negative the DBPCFC will almost always be negative also (29). Other immunologic tests, such as cow's milk semm precipitans, The Diagnosis are occasionally helpful. However, some food allergy tests of Most tme food allergy reactions in children resemble allergic unproved validity have been promoted. These include the reactions from other substances, eg, dmgs, pollens, cats. Sys­ cytotoxic food test, the provocation and food neutralization test, temic anaphylaxis, urticaria, and atopic dermatitis as well as and in vitro assays for IgG food antibodies (32). The latter test both upper and lower respiratory allergic symptoms are easily deserves special mention, since it is gaining in popularity. All identifiable. More difficult to associate with food allergy are normal individuals make IgG antibodies to the food they ingest. gastrointestinal complaints in which food intolerances (such as Patients with IgA deficiency and with the Heiner syndrome lactose) must be considered along with nondiet-related condi­ (cow's milk antibodies) make more than the usual amount of tions. Those complaints that do not resemble the signs and IgM and IgG food antibodies. Except in these cases, there is symptoms of allergic reaction are usually not caused by food al­ no correlation between the level of IgG food antibodies and lergy. Problems such as hyperkinesis, behavioral abnormalities. clinical allergy.

Henry Ford Hosp Med J—Vol .36. No 4. 1988 Guide lo Fotxl Allergy—Anderson 201 Management of Food Allergies Evaluation of conflicting results indicates that breast-feeding for When food allergy is diagnosed, specific food avoidance is six months with delayed introduction of solid foods reduces the the only preventive treatment advised. The natural history of risk of atopic dermatitis and food allergy in infants from allergic food sensitivity must be considered in infants. Allergies to families (36). However, alteration in both the child's and the cow's milk and eggs are usually self-limited, and these foods are mother's diet is difficult to achieve. tolerated when the child is a few years of age. Bock (30) recom­ The use of medications to treat food allergy is limited to epi­ mends open challenge at six-month intervals. For an infant be­ nephrine for acute anaphylaxis, bronchial dilators to treat low age 1, food rechallenge should be postponed until the child asthma, HI antihistamines to treat urticaria and rhino-con­ is 2 or 3 years old. Some indication of decreasing immune sen­ junctivitis, and corticosteroids to treat severe gastroenteritis and sitivity may be obtained by serial IgE food RAST assays. life-threatening anaphylaxis (35,37). Sodium chromoglycate A special problem exists for the patient who is egg allergic which prevents local mast cell degranulation has been proposed and who requires the measles, mumps, and rubella (MMR) vac­ as a preventive oral agent for gastrointestinal food allergy. Al­ cination at 15 months of age. Herman et al (33) found that the though several European and United States investigators re­ vaccine contained enough egg protein to stimulate an allergic re­ ported encouraging results with this dmg, only one group used action in a few infants. These infants can be safely skin tested to the DBPCFC method to define a study population of food-sen­ the MMR vaccine, and if positive, can be quickly "desensi­ sitive patients. In this study of children allergic to eggs, oral tized" and safely immunized. chromoglycate was not effective in preventing food allergy signs When cow's milk or cow's milk base-formula induces severe and symptoms. enterocolitis, avoidance of soy protein as well as milk protein is H2 antihistamines have been advocated to treat chronic advised because of the risk of sensitization to soy (15,16). A urticaria and when combined with HI antihistamines suggested casein-hydrolysate formula is preferred. In prolonged infant di­ as preventive agents before exposure to foods known to produce arrhea, the specific sugar in the formula is also important symptoms. Ketotifin, a drug not yet released in the United (17,18). In the Heiner syndrome, cow's milk protein avoidance is States, has also been shown to be a preventive medication for essential for the affected infant (26). For unknown reasons this patients with either food allergy or food intolerance. condition usually disappears in time (24). A diagnosis of potentially life-threatening food anaphylaxis usually requires specific food avoidance for an indefinite period. This course is also essential in cases of other proven IgE anaphy­ lactic sensitivity, eg, penicillin or hymenoptera. Although the incidence of allergic anaphylactic reaction decreases with age, References the sensitivity may be lifelong in some patients. 1. Anderson JA. The establishment of common language conceming adverse reactions to foods and food additives. J Allergy Clin Immunol 1986; Fish sensitivity is of worldwide concem. The risk of reaction 78:140-4. exists not only with ingestion or skin contact but even when the 2. Foucard T. Developmental aspects of food sensiUvity in childhood. Nutr patient is simply near the fish. Fish protein is aerosolized, and Rev 1984:42:98-104. the odor of a fish market and the steam from cooking fishcon ­ 3. Bock SA. Prospective appraisal of complaints of adverse reactions to foods stitute a significant risk to these patients (34). Potent food al­ in children during the first 3 years of life. Pediatrics 1987;79:683-8. lergens such as cow's milk and eggs can initiate an anaphylactic 4. Bock SA, Sampson HA, Atkins FM, et al. Double-blind, placebo-con­ trolled food challenge (DBPCFC) as an office procedure: A manual. J Allergy reaction in previously sensitized nursing infants if the mother Clin Immunol 1988:82:986-97. ingests the food and transmits the allergen via breast milk. 5. Sampson HA. Food hypersensitivity as a pathogenic factor in atopic der­ In the United States, peanut anaphylaxis is a concern. The matitis. 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Food-dependent exercise- posure. The most convenient device available is a self-injecting induced anaphylaxis. J Allergy Clin Immunol 1983:71:407-11. unit, Epi Pen® (0.03 mL) or Epi Pen Jr® (0.15 mL) (Center Lab­ 10. Bock SA. The natural history of adverse reactions to foods. New Engl Reg oratory, Port Washington, NY). One ofthese self-injector units Allergy Proc 1986:7:504-10. should be kept in the house, one in the car, and one on the per­ 11. Bock SA. Natural history of severe reactions to foods in young children. J son. If anaphylaxis occurs, the self-injector device can be Pediatr 1985;107:676-80. 12. Thomas DW, McGilligan K, Eisenberg LD. Lieberman HM. Rissman jammed into the thigh and the spring-loaded needle will pene­ EM. Infantile colic and type of milk feeding. Am J Dis Child 1987;141:451-3. trate clothing. A dose of 1:1,000 aqueous epinephrine is in­ 13. Hewson P, Oberklaid F, Menahem S. 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202 Henry Ford Hosp Med J—Vol 36. No 4. 1988 Guide to Food Allergy—Anderson 16. American Academy of Pediatrics Committee on Nutrition. Soy protein 27. Anderson JA. Weiss L, Rebuck JW, Cabal LA, Sweet LC. Hyperreac­ formulas: Recommendations for use in infant feeding. Pediatrics 1983; tivity to cow's milk in an infant with LE and tart cell phenomenon. J Pediatr 72:359-63. 1974;84:59-67. 17. Leake RD. Schroeder KC, Benton DA, Oh W. Soy-based formula in the 28. May CD. Objective clinical and laboratory studies of immediate hyper­ treatment of infantile diarrhea. Am J Dis Child 1974;127:374-6. sensitivity reactions to foods in asthmatic children. J Allergy Clin Immunol 18. Donovan GK, Torres-Pinedo R. Chronic diarrhea and soy fonnulas: Inhi­ 1976;58:.5(X)-15. bition of diarrhea by lactose. Am J Dis Child 1987; 141:1069-71. 29. Sampson HA, Albergo R. Comparison of results of skin tests. RAST. and 19. Broadbent JB. Sampson HA. Food hypersensitivity and atopic dermatitis. double-blind, placebo-controlled food challenges in children with atopic der­ Pediatr Clin North Am 1988:35:1115-30. matitis. J Allergy Clin Immunol 1984;74:26-33. 20. Ashkenazi A, Idar D, Barzilai N, Levin S, Or A, Handzel ZT. Effect of 30. Bock SA. Evaluation of patients with adverse reactions to foods. In: Bier- gluten-free diet on an immunological assay for coeliac disease. Lancet man CW. Peariman DS. eds. Allergic di.sease from infancy to adulthood. 2nd 1981:1:914-6. ed. Philadelphia: W.B. Saunders Co, 1988:359-66. 21. National Institutes of Health Consensus Development Panel Report. De­ 31. Mahan LK. Furukawa CT. General nutritional considerations and diet for fined diets in childhood hyperactivity. Bethesda. MD: Office for Medical Ap­ adverse food reactions. In: Biennan CW. Peariman DS. eds. Allergic disease plications of Research. 1982. from infancy to adulthood. 2nd ed. Philadelphia: W.B. Saunders Co. 22. Feingold BF. Food additives and child development (Editorial). Hosp !98H:.367-76. Pract [Off] 1973:8:11-21. 32. Shaperio GG, Anderson JA. Controversial techniques in allergy. Pedi­ 23. Rothner AD. The migraine syndrome in children and adolescents. Pediatr atrics 1988:82:935-7. Neurol 1986;2:121-6. 33. Herman JJ. Radin R. Schneiderman R. Allergic reactions to measles 24. Egger J, Wilson J, Carter CM, Tumer MW. Soothill JF Is migraine food (rubeola) vaccine in patients hypersensitive to egg protein. J Pediatrics allergy? A double-blind controlled trial of oligoantigenic diet treatment. Lancet 1983:102:196-9. 1983;2:865-8. 34. Aas K. Antigens in food. Nutr Rev 1984;42:85-91. 25. Mansfield LE, Vaughan TR. Waller SR HaveHy RW, Ting S. Food al­ 35. Squillace DL, Sweeney KG, Jones RT, Yunginger JW, Helm RM. Fatal lergy and aduh migraine: Double-blind and mediator confirmation ofan allergic food-induced anaphylaxis. J Allergy Clin Immunol 1988:81:239. etiology Ann Allergy 1985;55:126-9. 36. ZeigerRS. Heller S. Mellon M, O'Connor R, Hamburger RN. Effective­ 26. Heiner DC. Sears JW. Knicker WT. Multiple precipitins to cow's milk in ness of dietary manipulation in the prevention of food allergy in infants. J Al­ chronic respiratory disea.se: A syndrome including poor growth, gastrointestinal lergy Clin Immunol 1986:78:224-38. symptoms, evidence of allergy, iron deficiency anemia and pulmonary hemo­ 37. Sogn D. Medications and their use in the treatment of adverse reactions to siderosis. Am J Dis Child 1962:103:634-54. foods. J Allergy Clin Immunol 1986;78:238-43.

Henry Ford Hosp Med J—Vol 36. No 4. 1988 Guide to Fotxl Allergy—Anderson 203