Food Allergy Treatments

Pathophysiology

Allergic reactions to food are IgE-mediated or non–IgE-mediated. Immune responses mediated by specific IgE antibodies are the most widely recognized mechanism of food hypersensitivity. Patients with atopy produce IgE antibodies to specific epitopes of the food allergen. These antibodies bind to high-affinity IgE receptors on circulating basophils and tissue mast cells present in the skin, gastrointestinal tract, and respiratory tract. Subsequent allergen exposure binds two adjacent IgE antibodies, resulting in receptor cross-linking and intracellular signaling that initiates the release of numerous mediators, including histamine, prostaglandins, leukotrienes, chemotactic factors, and cytokines. The effects of these mediators on surrounding tissues result in vasodilatation, smooth muscle contraction, and mucus secretion, which, in turn, are responsible for the spectrum of clinical symptoms observed during allergic reactions to food.

Food allergens are typically water-soluble glycoproteins resistant to heating and proteolysis with molecular weights of 10-70 kd. These characteristics facilitate the absorption of these allergens across mucosal surfaces. Numerous food allergens are purified and well-characterized, such as peanut Ara h1, Ara h2, and Ara h3; chicken egg white Gal d1, Gal d2, and Gal d3; soybean-Gly m1; fish-Gad c1; and shrimp-Pen a1. Closely related foods frequently contain allergens that cross-react immunologically (ie, lead to the generation of specific IgE antibodies detectable by skin prick or in vitro testing) but less frequently cross-react clinically. Finally, cross-reactive allergens have been identified among certain foods and airborne pollens. Conserved homologous proteins shared by pollens and foods likely account for this cross-reactivity.

Frequency

United States

General surveys report that as many as 25-30% of households consider at least 1 family member to have a food allergy. This high rate is not supported by controlled studies in which food challenges are used to confirm patient histories. The actual prevalence of food allergies is estimated to be approximately 6% in infants and children and 3.7 % in adults. Several published prospective investigations have determined the prevalence of certain common food allergies in children (eg, cow milk, 2.5%; eggs, 1.3%; peanuts, 0.8%; wheat, 0.4%; soy, 0.4%).

International

Prospective studies from several different countries indicate that approximately 2.5% of newborn infants experience hypersensitivity reactions to cow milk in the first year of life. A hypersensitivity reaction to peanuts occurs in approximately 0.5% of children in the United Kingdom. Surveys from the United Kingdom indicate that 1.4-1.8% of adults experience adverse food reactions and 0.01-0.23% of adults are affected by adverse reactions to food additives. Studies from the Netherlands demonstrate that approximately 2% of the adult Dutch population is affected.

Mortality/Morbidity

• Severe anaphylactic reactions, including death, can occur following the ingestion of food. Typical symptoms observed in a food-induced anaphylactic reaction involve the skin, gastrointestinal tract, and respiratory tract. Frequently observed symptoms include oropharyngeal pruritus, angioedema (eg, laryngeal edema), stridor, dysphonia, cough, dyspnea, wheezing, nausea, vomiting, diarrhea, flushing, urticaria, and angioedema. Fatalities result from severe laryngeal edema, irreversible bronchospasm, refractory hypotension, or a combination thereof. Food allergy has been confirmed in approximately one third of the patients with anaphylaxis presenting to the emergency department at the Mayo Clinic.
  
  
• Peanuts, tree nuts, and shellfish are the foods most often implicated in severe food-induced anaphylactic reactions, although anaphylactic reactions have been reported to a wide variety of foods.
  
  
• Risk factors for fatal food-induced anaphylaxis include (1) the presence of asthma, especially in patients with poorly controlled disease; (2) previous episodes of anaphylaxis with the incriminated food; (3) a failure to recognize early symptoms of anaphylaxis; and (4) a delay or lack of immediate use of emergency medications (eg, epinephrine, antihistamines) to treat the allergic reaction.

Race

• No predilection is known.

Sex

• No predilection is known.

Age

• In infants and children younger than 3 years, the prevalence of food allergy is approximately 6%.
  
  
• The estimated prevalence in adults is approximately 3.7%.

Clinical

History

Physical

• The physical examination findings are most useful for assessing overall nutritional status, growth parameters, and signs of other allergic disease, such as atopic dermatitis, allergic rhinitis, or asthma.
  
  
• Findings from a comprehensive physical examination can help rule out other conditions that may mimic food allergy.

Causes

• Any food protein can trigger an allergic response, and allergic reactions to a large number of foods have been documented; however, only a small group of foods account for most of these reactions.
  
  
• Eggs, milk, peanuts, soy, fish, shellfish, tree nuts, and wheat are the foods most often implicated in allergic reactions that have been confirmed in well-controlled blinded food challenges.
  
  
• Investigations of near-fatal or fatal anaphylactic reactions following food ingestion reveal that most are caused by peanuts, tree nuts, and shellfish.

Differentials

Anorexia Nervosa
Bulimia
Celiac Sprue
Clostridium Difficile Colitis
Constipation
Diverticulitis
Dumping Syndrome
Esophageal Motility Disorders
Esophageal Spasm
Esophageal Stricture
Esophagitis
Factitious Disorder
Food Poisoning
Gastritis, Acute
Gastritis, Chronic
Gastroenteritis, Bacterial
Gastroenteritis, Viral
Gastroesophageal Reflux Disease
Giardiasis
Hiatal Hernia
Inflammatory Bowel Disease
Intestinal Motility Disorders
Irritable Bowel Syndrome
Lactose Intolerance
Trichosporon Infections
Urethral Diverticula
Urticaria
VIPomas
Vocal Cord Dysfunction
Wasp Stings
Whipple Disease

Workup

Lab Studies

• Serum testing for specific IgE antibodies to foods
  
  
  • Specific IgE antibodies to foods can be measured by in vitro laboratory methods (eg, IgE radioallergosorbent testing), which offers advantages when dermatographism, generalized dermatitis, or a clinical history of severe anaphylactic reactions to a given food limit skin testing.
    
    
  • This form of testing provides information similar to prick skin tests, but it is more expensive and generally less specific.
    
    
  • The CAP System fluorescent-enzyme immunoassay (FEIA) (Pharmacia Diagnostics, Uppsala, Sweden) provides a more quantitative method of determining allergen-specific IgE to food allergens.
    
    
  • When compared with the outcome of well-controlled oral food challenges, results of the CAP system FEIA are generally similar to those of prick skin tests in predicting symptomatic food allergy.
    
    
  • Quantitating food-specific IgE antibodies with this automated system can help identify patients who are highly likely to have allergic reactions (>95% probability).
    
    
  • Published positive and negative predictive values using this system are available. These predictive values aid in making the diagnosis, thereby reducing the need for confirmatory food challenges in some patients.
    
    
  • Currently, the predictive values of CAP System FEIA results are limited to several major food allergens (ie, egg, milk, peanut, fish).
    
    

  • The predictive values developed using the CAP System FEIA are useful in predicting the likelihood of a reaction but do not predict the severity of a reaction  

• Peripheral serum measurements of eosinophils or total IgE concentrations: Results from these tests support but do not confirm the diagnosis of food allergy. Likewise, normal values do not exclude diagnosis.

• Basophil histamine-release assays: These tests are mainly limited to research settings and have not been shown conclusively to provide reproducible results useful for diagnostic testing in a clinical setting.

Other Tests

• Diet diary
  
  
  • This consists of keeping a chronological record of all foods eaten and any associated adverse symptoms. It is an inexpensive endeavor that documents the frequency of symptoms and their occurrence in relationship to food ingestion. In addition, it encourages patients to focus on their diet.
    
    
  • This record is occasionally helpful for identifying the food implicated in an adverse reaction; however, it is not usually diagnostic, especially when symptoms are delayed or infrequent.
    
    
  • Occasionally, review of the diet diary reveals that the patient is not experiencing a reaction even when eating, as an ingredient in other foods, a significant amount of a food to which they were thought to be allergic. 
     
• Elimination diet
  
  
  • This is used in determining the diagnosis as well as in the treatment and prevention of food allergy.
    
    
  • When used as a diagnostic tool, the elimination diet requires complete avoidance of suspected foods or groups of foods for a given time period (usually 7-14 d) while monitoring for an associated decrease in symptoms.
    
    
  • Success depends on identifying the correct food allergen and completely eliminating it in all forms from the diet. These diets are increasingly difficult to develop and follow as more foods or foods that commonly occur in the diet are eliminated.
    
    
  • Additional limitations of this method include potential effects of patient or physician biases, variable patient compliance, and the time-consuming nature of the endeavor.
    
    
  • When the elimination diet is used as treatment, identified food allergens are removed from the diet indefinitely unless evidence exists that the food allergy has been outgrown.
     
• Skin testing
  
  
  • Prick and puncture tests are the most common screening tests for food allergy and can even be performed on infants in the first few months of life. However, the reliability of the results depends on multiple factors, including use of the appropriate extracts and testing technique, accurate interpretation of the results, and avoidance of medications that might interfere with testing (eg, antihistamines).
    
    
  • When used in conjunction with a standard criterion of interpretation and appropriate controls (eg, histamine: positive, saline: negative), these tests provide useful and reproducible clinical information in a short period (ie, 15-20 min) with minimal expense and negligible risk to the patient.
    
    
  • This is a reliable method of excluding IgE-mediated food allergies. The negative predictive accuracy is greater than 95%; however, the positive predictive accuracy is generally less than 50%, which limits clinical interpretation of positive skin test results.
    
    
  • Positive skin test results, in addition to the suggestion of clinical reactivity based on the history, must often be confirmed by an oral food challenge unless the patient has a thoroughly convincing history of significant food allergy.
     
• Intradermal skin testing
  
  
  • The risk of inducing a systemic reaction with this type of testing is increased in comparison to the prick or puncture method; as a result, intradermal skin testing should be avoided.
    
    
  • In addition, the results obtained by using this method are less specific compared to those obtained by using prick or puncture testing.
     
• Tests with uncertain diagnostic value: The diagnostic value of performing the following tests is not currently supported by objective scientific evidence:
  
  
  • Results from food-specific immunoglobulin G (IgG) or IgG subclass antibody concentration testing have not been proven to be helpful with diagnosis.
    
    
  • Testing for food antigen-antibody complexes has no proven diagnostic value.
    
    
  • Performing leukocyte cytotoxic tests is not supported by objective scientific evidence.
    
    
  • Results from subcutaneous provocation and neutralization testing have not been proven to be helpful for diagnosis.
    
    
  • Kinesiology-based testing is not recommended because objective scientific evidence has indicated this type of testing does not aid in diagnosis.

Procedures

• Food challenge confirmation of food allergy
  
  
  • This includes properly conducted elimination of and subsequent oral challenge with foods suspected of causing allergic reactions based on the medical history, skin testing results, or in vitro testing results.
    
    
  • Of these procedures, the double-blind placebo-controlled food challenge (DBPCFC) is the most reliable method to help diagnose and confirm food allergy and other adverse food reactions because it eliminates both patient and observer bias. However, in a clinical setting where minimal bias is suspected, open food challenges may be preferable because blinding of the food is often not required.
    
    
  • Conduct any food challenge in a clinic or hospital setting with the personnel and equipment necessary to treat a systemic allergic reaction available at all times. Patients undergoing a food challenge should not be on beta-blocker medications or any medication that might interfere with the treatment of anaphylaxis. Obtain intravenous access in patients with history findings that indicate the potential for a systemic reaction.
    
    
  • If the history of the patient suggests an anaphylactic reaction is possible following food ingestion, do not perform an oral food challenge. 
     
• Open food challenge
  
  
  • This test involves the patient ingesting the suspected food, prepared in its customary fashion (ie, the challenge food is not disguised in any way).
    
    
  • Both the patient and the observer (eg, physician, nurse) are aware of the food being ingested.
    
    
  • The open food challenge is best used in clinical practice when patient and physician bias is minimal.
    
    
  • This type of challenge is typically used when the skin test results for the suspect food are negative or if a specific food reaction is unlikely.
    
    
  • Whenever the results are equivocal, perform a blinded challenge.
    
    
  • Patients with histories of a previous reaction should never perform an open food challenge at home, even if the chance they will develop severe symptoms is remote.
     
• Single blinded food challenge
  
  
  • This challenge involves the patient ingesting the suspected food disguised in a challenge food so the patient is unaware of the contents.
    
    
  • This type of challenge, which is suitable for clinical practice and some research investigations, is designed to reduce patient bias during the procedure. However, subjective attitudes regarding the outcome of the challenge cannot be completely eliminated.
    
    
  • This test is also useful for screening patients for entry into studies in which the findings will be unequivocally confirmed by DBPCFC results.
     
• Double-blind placebo-controlled food challenge
  
  
  • DBPCFC involves ingestion of the suspected food disguised in another food so that both the patient and observer are unaware of the contents of the challenge.
    
    
  • This type of challenge is designed to reduce both patient and observer bias and subjective attitudes during the procedure.
    
    
  • Always perform this challenge in a clinic or hospital setting.
    
    
  • Consider this the criterion standard for diagnosing food allergy, especially in research investigations. Currently, it is the only completely objective method for determining the validity of the history of an adverse reaction to a food.
    
    
  • Do not perform a challenge if the patient has a clearly convincing history of a severe life-threatening anaphylactic reaction following the isolated ingestion of a specific food.

Treatment

Medical Care

Consultations

• Consultation with a nutritionist or nutrition service is invaluable in the overall management. The elimination diet can be reviewed and appropriate substitutions can be recommended. Dietary deficiencies can be anticipated and prevented.
  
  
• Consultation with a gastroenterologist is also useful in the evaluation of selected patients. For example, patients presenting with possible anatomic gastrointestinal abnormalities, eosinophilic esophagitis or gastroenteritis, failure to thrive, and malabsorption syndromes may benefit from consultation with both an allergist and a gastroenterologist.

Diet

• A properly managed well-balanced elimination diet (eg, allergen restriction) can lead to resolution of symptoms and help avoid nutritional deficiencies.
  
  
• Educate the patient and family about how to properly read food labels and identify common words used for indicating the presence of the food allergen of concern (eg, casein and whey for milk).
  
  
• With elimination diets, only exclude those foods confirmed to provoke allergic reactions.
  
  
• Review obvious and hidden sources of food allergens. Be aware of the potential for exposures by routes other than ingestion, such as skin contact, inhalation, or injection.
  
  
• Anticipate potential candidates for food allergen cross-reactivity, such as the following:
• • Eggs and chicken (<5%)
    
    
  • Cow milk and beef (10%)
    
    
  • Cow milk and goat milk (>90%)
    
    
  • Fish (>50%)
    
    
  • Peanuts and related legumes (<10%)
    
    
  • Soy and related legumes (<5%)
    
    
  • Wheat and other grains (25%)
    
    
  • Tree nuts and other nuts (>50%)
     
• Encourage avoidance of high-risk situations (eg, buffets, picnics), where accidental or inadvertent ingestion of food allergens can occur.

Medication

Despite following stringent avoidance measures for clinically relevant food allergens, accidental or inadvertent ingestions occur all too often. Therefore, a concise written plan for the treatment of allergic reactions resulting from accidental exposure to the food must be available to the patient. For patients with a history of a mild reaction, such as urticaria and pruritus following the ingestion of a food allergen, treatment may be limited to an oral antihistamine. However, the potential for a more severe reaction on subsequent exposures must be taken into consideration because of the possibility of the ingestion of a larger dose than previously ingested or an unexpected or unrecognized increase in the patient’s degree of sensitivity.

If the patient has significant systemic symptoms, the treatment of choice is epinephrine administered by intramuscular injection in the lateral thigh. Examples of systemic manifestations of food allergy include generalized urticaria, laryngeal edema, lower respiratory symptoms (eg, chest tightness, dyspnea, wheezing), and hypotension. Administer epinephrine to any patient with history of a severe allergic reaction as soon as ingestion of the food allergen is discovered and the first symptoms appear.

For the medical therapy of food allergen–induced allergic reactions, the use of antianaphylactic agents, antihistamines, bronchodilators, and corticosteroids in combination with the administration of intravenous fluids and oxygen (when indicated), is suggested.

Drug Category: Adrenergic agonists

Used in the emergency management of systemic allergic reactions or anaphylaxis (eg, urticaria, angioedema, bronchospasm, cardiovascular collapse). Effects are immediate and dramatic. Appropriate use of this class of medication can be lifesaving, especially in the emergency management of anaphylaxis.

Drug Category: Antihistamines (histamine-1 blockers)

Inhibit many responses to histamine. Histamine, via H1 receptors, causes smooth muscle contraction, increased capillary permeability, and formation of edema. During hypersensitivity reactions, histamine is one of the major potent mediators released. Blocking effects of this mediator with specific antihistamines is useful in emergency management of allergy symptoms.

Drug Category: Antihistamines (histamine-2 blockers)

Drug Category: Bronchodilators

Patients experiencing significant adverse respiratory symptoms as part of their food-induced allergic reaction must be managed aggressively with nebulized bronchodilators. Nebulized adrenergic agonists or bronchodilators are usually administered for treatment of bronchospasm. Supplemental oxygen can also be administered with nebulizations. In selected cases, parenteral agents may be employed to achieve sufficient bronchodilation.

Drug Category: Corticosteroids

Ameliorate delayed effects of anaphylactoid reactions and may limit biphasic anaphylaxis. In severe cases of serum sickness, parenteral steroids may be beneficial to reduce inflammatory effects of this immune complex–mediated disease.

Follow-Up

Deterrence/Prevention

• Emergency plan
  
  
  • Provide a written emergency treatment plan for the patient. Have copies of this plan available in appropriate places (eg, daycare, schools, work locations, college dormitory advisors).
    
    
  • Patients with food allergies should be advised to obtain and wear Medic Alert tags or bracelets indicating their specific food allergies.
    
    
  • Ensure that the patient has an emergency contact number available (eg, 911, their physician's office phone number, or a local emergency department) that can be used in the event of a major food-induced allergic reaction.
    
    
  • Anticipatory guidance measures cannot be overemphasized; for example, educate the patient about potential sources of accidental or inadvertent exposure to relevant food allergens (eg, daycare, school, travel, picnics, dining out).
     
• Emergency medications
  
  
  • Ensure that the patient has self-injectable epinephrine readily available at all times. Also ensure that the patient receives proper training regarding when and how to use the device. An antihistamine (syrup or chewable tablet) should also be available. Patients with food allergies and asthma should always have access to a rapid-acting bronchodilator.
    
    
  • Self-injectable epinephrine is typically available by prescription (ie, Epi-Pen, Epi-Pen Jr, Twinject). These devices should be stored properly (avoiding extremes of temperature) and replaced before the expiration date.
    
    
  • Injectable epinephrine is the drug of choice for the initial management of a food-induced anaphylactic reaction.

Prognosis

• Developing intolerance
  
  
  • In general, most infants and young children outgrow or become clinically tolerant of their food hypersensitivities.
    
    
  • Well-controlled prospective investigations of food allergy in infants and children demonstrate that by following proper elimination diets, 85% of confirmed symptoms resolve by 3 years of age.
    
    
  • Adults with food allergy can also lose their clinical allergic reactions to foods after implementation of appropriate food elimination diets.
    
    
  • Approximately one third of all children and adults lose their clinical reactivity to specific food allergens after 1-2 years of appropriate food allergen elimination therapy. Patients with allergies to peanuts, tree nuts, fish, and shellfish rarely lose their clinical reactivity.
     
• Avoidance of allergen
  
  
  • How strictly the patient complies with the allergen avoidance diet appears to be directly associated with the ultimate clinical outcome (ie, development of oral tolerance).
    
    
  • Patients with allergic reactions to peanuts, tree nuts, shellfish, and fish rarely lose their clinical reactivity.
     
• Breastfeeding
  
  
  • While exclusive breastfeeding is frequently promoted as a means of preventing food allergy and atopic disease in general, considerable controversy remains regarding the effectiveness of this practice.
    
    
  • Some investigations suggest that lactating mothers should eliminate highly allergenic foods (eg, peanuts, tree nuts, shellfish) that may induce life-long allergic sensitivity in their infants.
    
    
  • Further studies are needed to clarify the role of early elimination diets and breastfeeding in the prevention of food allergy.

Patient Education

Miscellaneous

Medical/Legal Pitfalls

• When performing oral food challenges, be prepared to recognize and treat adverse clinical symptoms immediately. Appropriately trained personnel and the necessary equipment for the treatment of anaphylactic shock must be available prior to and throughout the entire oral food challenge and observation period because of the risk of triggering an allergic reaction.
  
  
• Do not perform an oral food challenge if the patient has a clear and convincing history of a severe life-threatening anaphylactic reaction following the isolated ingestion of a specific food. This is an absolute contraindication.
  
  
• Patients should never perform an open food challenge at home if even a remote chance exists that the patient will develop severe symptoms.
  
  
• Confirm negative results from a DBPCFC using an open feeding (open food challenge) of the food in question before giving final advice on dietary restrictions.
  
  
• If the patient has a history of severe allergic reactions following the ingestion of food allergens, give specific advice in the form of a written emergency treatment plan. In addition, educate the patient on how to administer emergency medications (eg, injectable epinephrine, antihistamines) in the event of a severe life-threatening allergic reaction. Encourage the patient (when appropriate) or a caretaker to carry these medications with them at all times in case they are needed to manage symptoms.

Special Concerns

• Diagnosis
  
  
  • Because specific laboratory tests for some food hypersensitivities are not available, diagnosing non–IgE-mediated food allergies (eg, cow milk–induced and soy-induced enterocolitis syndromes, allergic eosinophilic gastroenteritis) is more difficult than diagnosing IgE-mediated food allergies.
    
    
  • In cases of allergic eosinophilic gastroenteritis, a biopsy may need to be performed. Elimination diets with gradual reintroduction of foods and supervised oral food challenges are often needed to help identify the causative foods.
    
    
  • For food protein–induced enterocolitis syndrome, perform a food challenge with 0.15–0.30 grams of protein per kilogram of body weight of the implicated protein and observe the patient for several hours. Positive reactions (eg, profuse vomiting and diarrhea) are typically accompanied by a rise in the absolute neutrophil count of more than 3500 cells/mm³. Because of the potential for shock, these challenges are best performed in the hospital setting.
    
    
  • When the history of an allergic reaction to a food suggests that the onset of symptoms is delayed by hours or days following ingestion, adjust the timing and monitoring of the challenge to correspond to these characteristics.
    
    
  • The successful administration of oral food challenges to young children requires a great deal of preparation, patience, and creativity. Young children may refuse to ingest the challenged food. Prior planning with the family is important to choose proper vehicles (eg, juice, cereal, solid food) for disguising the challenged substance.
     
• Vaccines
  
  
  • Recent scientific data support the routine 1-dose administration of the measles-mumps-rubella vaccine to all patients with egg allergy, even those with severe anaphylactic reactions following egg ingestion.  In the child with a history of a previous reaction to the measles-mumps-rubella vaccine, consider the possibility of allergy to gelatin or neomycin. 
    
    
  • If the patient has a clinical history of egg allergy and has experienced systemic reactions (eg, anaphylaxis) following the ingestion of egg, the administration of the influenza vaccine requires special diagnostic consideration. Test the patient's skin with diluted preparations of the influenza vaccine (ie, puncture skin testing and, if needed, intradermal skin testing). If skin test results with the vaccine are positive, the vaccine can be safely given in a graded, multidose scheme. If results are negative, the vaccine may be administered in the routine 1-dose manner.

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• Lever R, MacDonald C, Waugh P, Aitchison T. Randomised controlled trial of advice on an egg exclusion diet in young children with atopic eczema and sensitivity to eggs. Pediatr Allergy Immunol. Feb 1998;9(1):13-9. [Medline].
• Ma S, Sicherer SH, Nowak-Wegrzyn A. A survey on the management of pollen-food allergy syndrome in allergy practices. J Allergy Clin Immunol. Oct 2003;112(4):784-8. [Medline].
• Nelson HS, Lahr J, Rule R, et al. Treatment of anaphylactic sensitivity to peanuts by immunotherapy with injections of aqueous peanut extract. J Allergy Clin Immunol. Jun 1997;99(6 Pt 1):744-51. [Medline].
• Odze RD, Wershil BK, Leichtner AM, Antonioli DA. Allergic colitis in infants. J Pediatr. Feb 1995;126(2):163-70. [Medline].
• Ortolani C, Ispano M, Pastorello E, et al. The oral allergy syndrome. Ann Allergy. Dec 1988;61(6 Pt 2):47-52. [Medline].
• Ortolani C, Ispano M, Pastorello EA, et al. Comparison of results of skin prick tests (with fresh foods and commercial food extracts) and RAST in 100 patients with oral allergy syndrome. J Allergy Clin Immunol. Mar 1989;83(3):683-90. [Medline].
• Pastorello EA, Stocchi L, Pravettoni V, et al. Role of the elimination diet in adults with food allergy. J Allergy Clin Immunol. Oct 1989;84(4 Pt 1):475-83. [Medline].
• Powell GK. Food protein-induced enterocolitis of infancy: differential diagnosis and management. Compr Ther. Feb 1986;12(2):28-37. [Medline].
• Powell GK. Milk- and soy-induced enterocolitis of infancy. Clinical features and standardization of challenge. J Pediatr. Oct 1978;93(4):553-60. [Medline].
• Pumphrey RS, Stanworth SJ. The clinical spectrum of anaphylaxis in north-west England. Clin Exp Allergy. Dec 1996;26(12):1364-70. [Medline].
• Roberts G, Patel N, Levi-Schaffer F, et al. Food allergy as a risk factor for life-threatening asthma in childhood: a case-controlled study. J Allergy Clin Immunol. Jul 2003;112(1):168-74. [Medline].
• Roesler TA, Barry PC, Bock SA. Factitious food allergy and failure to thrive. Arch Pediatr Adolesc Med. Nov 1994;148(11):1150-5. [Medline].
• Romano A, Di Fonso M, Giuffreda F, et al. Diagnostic work-up for food-dependent, exercise-induced anaphylaxis. Allergy. Oct 1995;50(10):817-24. [Medline].
• Sampson HA. Differential diagnosis in adverse reactions to foods. J Allergy Clin Immunol. Jul 1986;78(1 Pt 2):212-9. [Medline].
• Sampson HA. Fatal food-induced anaphylaxis. Allergy. 1998;53(46 Suppl):125-30. [Medline].
• Sampson HA. Food allergy. JAMA. Dec 10 1997;278(22):1888-94. [Medline].
• Sampson HA. Food allergy. Part 1: immunopathogenesis and clinical disorders. J Allergy Clin Immunol. May 1999;103(5 Pt 1):717-28. [Medline].
• Sampson HA. Food allergy. Part 2: diagnosis and management. J Allergy Clin Immunol. Jun 1999;103(6):981-9. [Medline].
• Sampson HA. Food-induced anaphylaxis. Novartis Found Symp. 2004;257:161-71; discussion 171-6, 207-10, 276-85. 
• Sampson HA, Ho DG. Relationship between food-specific IgE concentrations and the risk of positive food challenges in children and adolescents. J Allergy Clin Immunol. Oct 1997;100(4):444-51. [Medline].
• Sampson HA, McCaskill CC. Food hypersensitivity and atopic dermatitis: evaluation of 113 patients. J Pediatr. Nov 1985;107(5):669-75. [Medline].
• Sampson HA, Mendelson L, Rosen JP. Fatal and near-fatal anaphylactic reactions to food in children and adolescents. N Engl J Med. Aug 6 1992;327(6):380-4. [Medline].
• Sampson HA, Scanlon SM. Natural history of food hypersensitivity in children with atopic dermatitis. J Pediatr. Jul 1989;115(1):23-7. [Medline].
• Sicherer SH, Burks AW, Sampson HA. Clinical features of acute allergic reactions to peanut and tree nuts in children. Pediatrics. Jul 1998;102(1):e6. [Medline].
• Sicherer SH, Eigenmann PA, Sampson HA. Clinical features of food protein-induced enterocolitis syndrome. J Pediatr. Aug 1998;133(2):214-9.                .
• Sicherer SH, Sampson HA. 9. Food allergy. J Allergy Clin Immunol. Feb 2006;117(2 Suppl Mini-Primer):S470-5.[Medline].        
• Sicherer SH, Sampson HA. The role of food allergy in childhood asthma. Immunol Clin North Am. 1998;18:49-60.
• Sigurs N, Hattevig G, Kjellman B. Maternal avoidance of eggs, cow's milk, and fish during lactation: effect on allergic manifestations, skin-prick tests, and specific IgE antibodies in children at age 4 years. Pediatrics. Apr 1992;89(4 Pt 2):735-9. [Medline].
• Simons FE. First-aid treatment of anaphylaxis to food: focus on epinephrine. J Allergy Clin Immunol. May 2004;113(5):837-44. [Medline].
• Simons FE. First-aid treatment of anaphylaxis to food: focus on epinephrine. J Allergy Clin Immunol. May 2004;113(5):837-44. [Medline].
• Sloan AE, Powers ME. A perspective on popular perceptions of adverse reactions to foods. J Allergy Clin Immunol. Jul 1986;78(1 Pt 2):127-33. [Medline].
• Spector SL, Nicklas RA. Practice Parameters for the Diagnosis and Treatment of Asthma. 1996:707.
• Steinman HA. "Hidden" allergens in foods. J Allergy Clin Immunol. Aug 1996;98(2):241-50. [Medline].
• Weber RW. Food additives and allergy. Ann Allergy. Mar 1993;70(3):183-90. [Medline].
• Yocum MW, Butterfield JH, Klein JS, et al. Epidemiology of anaphylaxis in Olmsted County: A population-based study. J Allergy Clin Immunol. Aug 1999;104(2 Pt 1):452-6. [Medline].
• Young E, Stoneham MD, Petruckevitch A, et al. A population study of food intolerance. Lancet. May 7 1994;343(8906):1127-30. [Medline].
• Yunginger JW, Sweeney KG, Sturner WQ, et al. Fatal food-induced anaphylaxis. JAMA. Sep 9 1988;260(10):1450-2. [Medline].
• Zeiger RS, Heller S. The development and prediction of atopy in high-risk children: follow- up at age seven years in a prospective randomized study of combined maternal and infant food allergen avoidance. J Allergy Clin Immunol. Jun 1995;95(6):1179-90. [Medline].

Food Allergies excerpt

• Altman DR, Chiaramonte LT. Public perception of food allergy. J Allergy Clin Immunol. Jun 1996;97(6):1247-51. [Medline].
• American Academy of Allergy and Immunology. Personnel and equipment to treat systemic reactions caused by immunotherapy with allergenic extracts. American Academy of Allergy and Immunology. J Allergy Clin Immunol. Feb 1986;77(2):271-3. [Medline].
• Bacharier LB. Are the results of oral food challenges predictable?. Ann Allergy Asthma Immunol. Feb 2004;92(2):195-7. [Medline].
• Barnes-Koerner C, Sampson HA. Diets and nutrition in food allergy. In: Metcalfe DD, Sampson HA, Simon RA, eds. Food Allergy: Adverse Reactions to Foods and Food Additives. 461-84.
• Bernhisel-Broadbent J. Allergenic cross-reactivity of foods and characterization of food allergens and extracts. Ann Allergy Asthma Immunol. Oct 1995;75(4):295-303; quiz 304-7. [Medline].
• Bernhisel-Broadbent J, Scanlon SM, Sampson HA. Fish hypersensitivity. I. In vitro and oral challenge results in fish- allergic patients. J Allergy Clin Immunol. Mar 1992;89(3):730-7. [Medline].
• Bernhisel-Broadbent J, Taylor S, Sampson HA. Cross-allergenicity in the legume botanical family in children with food hypersensitivity. II. Laboratory correlates. J Allergy Clin Immunol. Nov 1989;84(5 Pt 1):701-9. [Medline].
• Bock SA. Prospective appraisal of complaints of adverse reactions to foods in children during the first 3 years of life. Pediatrics. May 1987;79(5):683-8. [Medline].
• Bock SA. Respiratory reactions induced by food challenges in children with pulmonary disease. 3. 1992:82.
• Bock SA. The natural history of food sensitivity. J Allergy Clin Immunol. Feb 1982;69(2):173-7. [Medline].
• Bock SA, Atkins FM. Patterns of food hypersensitivity during sixteen years of double-blind, placebo-controlled food challenges. J Pediatr. Oct 1990;117(4):561-7. [Medline].
• Bock SA, Lee WY, Remigio L, et al. Appraisal of skin tests with food extracts for diagnosis of food hypersensitivity. Clin Allergy. Nov 1978;8(6):559-64. [Medline].
• Bock SA, Sampson HA, Atkins FM, et al. Double-blind, placebo-controlled food challenge (DBPCFC) as an office procedure: a manual. J Allergy Clin Immunol. Dec 1988;82(6):986-97. [Medline].
• Burks AW, James JM, Hiegel A, et al. Atopic dermatitis and food hypersensitivity reactions. J Pediatr. Jan 1998;132(1):132-6. [Medline].
• Condemni JJ. Unproved diagnostic and therapeutic techniques. In: Metcalfe DD, Sampson HA, Simon RA, eds. Food Allergy: Adverse Reactions to Foods and Food Additives. 541.
• David TJ, Waddington E, Stanton RH. Nutritional hazards of elimination diets in children with atopic eczema. Arch Dis Child. Apr 1984;59(4):323-5. [Medline].
• Eigenmann PA, Sampson HA. Interpreting skin prick tests in the evaluation of food allergy in children. Pediatr Allergy Immunol. Nov 1998;9(4):186-91. [Medline].
• Hawrylowicz CM, Jarman ER, Guida L, et al. T-cell receptor peptides that inhibit the T-cell response to allergen induce transforming growth factor-beta 1 production. J Allergy Clin Immunol. Feb 1996;97(2):707-9. [Medline].
• Hide DW, Guyer BM. Cows milk intolerance in Isle of Wight infants. Br J Clin Pract. Sep 1983;37(9):285-7. [Medline].
• Hide DW, Matthews S, Matthews L, et al. Effect of allergen avoidance in infancy on allergic manifestations at age two years. J Allergy Clin Immunol. May 1994;93(5):842-6. [Medline].
• Horan RF, Sheffer AL. Food-dependent exercise-induced anaphylaxis. 1991:757.
• Host A, Halken S. A prospective study of cow milk allergy in Danish infants during the first 3 years of life. Clinical course in relation to clinical and immunological type of hypersensitivity reaction. Allergy. Nov 1990;45(8):587-96. [Medline].
• Hourihane JO, Roberts SA, Warner JO. Resolution of peanut allergy: case-control study [see comments]. BMJ. Apr 25 1998;316(7140):1271-5. [Medline].
• James JM. Adverse reactions to foods. In: Ziegler EE, Filer LJ, eds. Present Knowledge in Nutrition. 604-11.
• James JM, Bernhisel-Broadbent J, Sampson HA. Respiratory reactions provoked by double-blind food challenges in children. Am J Respir Crit Care Med. Jan 1994;149(1):59-64. [Medline].
• James JM, Burks AW. Food-associated gastrointestinal disease. Curr Opin Pediatr. Oct 1996;8(5):471-5. [Medline].
• James JM, Burks AW. Foods. 15. 1995:477.
• James JM, Burks AW, Roberson PK, Sampson HA. Safe administration of the measles vaccine to children allergic to eggs. N Engl J Med. May 11 1995;332(19):1262-6. [Medline].
• James JM, Eigenmann PA, Eggleston PA, Sampson HA. Airway reactivity changes in asthmatic patients undergoing blinded food challenges. Am J Respir Crit Care Med. Feb 1996;153(2):597-603. [Medline].
• James JM, Sampson HA. An overview of food hypersensitivity. 3. 1992:67.
• James JM, Zeiger RS, Lester MR, et al. Safe administration of influenza vaccine to patients with egg allergy. J Pediatr. Nov 1998;133(5):624-8. [Medline].
• Jansen JJ, Kardinaal AF, Huijbers G, et al. Prevalence of food allergy and intolerance in the adult Dutch population. J Allergy Clin Immunol. Feb 1994;93(2):446-56. [Medline].
• Jones SM, Magnolfi CF, Cooke SK, Sampson HA. Immunologic cross-reactivity among cereal grains and grasses in children with food hypersensitivity. J Allergy Clin Immunol. Sep 1995;96(3):341-51. [Medline].
• Kelly KJ, Lazenby AJ, Rowe PC, et al. Eosinophilic esophagitis attributed to gastroesophageal reflux: improvement with an amino acid-based formula. Gastroenterology. Nov 1995;109(5):1503-12. [Medline].
• Lee CM, Changchien CS, Chen PC, et al. Eosinophilic gastroenteritis: 10 years experience. Am J Gastroenterol. Jan 1993;88(1):70-4. [Medline].
• Lever R, MacDonald C, Waugh P, Aitchison T. Randomised controlled trial of advice on an egg exclusion diet in young children with atopic eczema and sensitivity to eggs. Pediatr Allergy Immunol. Feb 1998;9(1):13-9. [Medline].
• Ma S, Sicherer SH, Nowak-Wegrzyn A. A survey on the management of pollen-food allergy syndrome in allergy practices. J Allergy Clin Immunol. Oct 2003;112(4):784-8. [Medline].
• Nelson HS, Lahr J, Rule R, et al. Treatment of anaphylactic sensitivity to peanuts by immunotherapy with injections of aqueous peanut extract. J Allergy Clin Immunol. Jun 1997;99(6 Pt 1):744-51. [Medline].
• Odze RD, Wershil BK, Leichtner AM, Antonioli DA. Allergic colitis in infants. J Pediatr. Feb 1995;126(2):163-70. [Medline].
• Ortolani C, Ispano M, Pastorello E, et al. The oral allergy syndrome. Ann Allergy. Dec 1988;61(6 Pt 2):47-52. [Medline].
• Ortolani C, Ispano M, Pastorello EA, et al. Comparison of results of skin prick tests (with fresh foods and commercial food extracts) and RAST in 100 patients with oral allergy syndrome. J Allergy Clin Immunol. Mar 1989;83(3):683-90. [Medline].
• Pastorello EA, Stocchi L, Pravettoni V, et al. Role of the elimination diet in adults with food allergy. J Allergy Clin Immunol. Oct 1989;84(4 Pt 1):475-83. [Medline].
• Powell GK. Food protein-induced enterocolitis of infancy: differential diagnosis and management. Compr Ther. Feb 1986;12(2):28-37. [Medline].
• Powell GK. Milk- and soy-induced enterocolitis of infancy. Clinical features and standardization of challenge. J Pediatr. Oct 1978;93(4):553-60. [Medline].
• Pumphrey RS, Stanworth SJ. The clinical spectrum of anaphylaxis in north-west England. Clin Exp Allergy. Dec 1996;26(12):1364-70. [Medline].
• Roberts G, Patel N, Levi-Schaffer F, et al. Food allergy as a risk factor for life-threatening asthma in childhood: a case-controlled study. J Allergy Clin Immunol. Jul 2003;112(1):168-74. [Medline].
• Roesler TA, Barry PC, Bock SA. Factitious food allergy and failure to thrive. Arch Pediatr Adolesc Med. Nov 1994;148(11):1150-5. [Medline].
• Romano A, Di Fonso M, Giuffreda F, et al. Diagnostic work-up for food-dependent, exercise-induced anaphylaxis. Allergy. Oct 1995;50(10):817-24. [Medline].
• Sampson HA. Differential diagnosis in adverse reactions to foods. J Allergy Clin Immunol. Jul 1986;78(1 Pt 2):212-9. [Medline].
• Sampson HA. Fatal food-induced anaphylaxis. Allergy. 1998;53(46 Suppl):125-30. [Medline].
• Sampson HA. Food allergy. JAMA. Dec 10 1997;278(22):1888-94. [Medline].
• Sampson HA. Food allergy. Part 1: immunopathogenesis and clinical disorders. J Allergy Clin Immunol. May 1999;103(5 Pt 1):717-28. [Medline].
• Sampson HA. Food allergy. Part 2: diagnosis and management. J Allergy Clin Immunol. Jun 1999;103(6):981-9. [Medline].
• Sampson HA. Food-induced anaphylaxis. Novartis Found Symp. 2004;257:161-71; discussion 171-6, 207-10, 276-85. [Medline].
• Sampson HA, Ho DG. Relationship between food-specific IgE concentrations and the risk of positive food challenges in children and adolescents. J Allergy Clin Immunol. Oct 1997;100(4):444-51. [Medline].
• Sampson HA, McCaskill CC. Food hypersensitivity and atopic dermatitis: evaluation of 113 patients. J Pediatr. Nov 1985;107(5):669-75. [Medline].
• Sampson HA, Mendelson L, Rosen JP. Fatal and near-fatal anaphylactic reactions to food in children and adolescents. N Engl J Med. Aug 6 1992;327(6):380-4. [Medline].
• Sampson HA, Scanlon SM. Natural history of food hypersensitivity in children with atopic dermatitis. J Pediatr. Jul 1989;115(1):23-7. [Medline].
• Sicherer SH, Burks AW, Sampson HA. Clinical features of acute allergic reactions to peanut and tree nuts in children. Pediatrics. Jul 1998;102(1):e6. [Medline].
• Sicherer SH, Eigenmann PA, Sampson HA. Clinical features of food protein-induced enterocolitis syndrome. J Pediatr. Aug 1998;133(2):214-9. [Medline].
• Sicherer SH, Sampson HA. 9. Food allergy. J Allergy Clin Immunol. Feb 2006;117(2 Suppl Mini-Primer):S470-5. [Medline].
• Sicherer SH, Sampson HA. The role of food allergy in childhood asthma. Immunol Clin North Am. 1998;18:49-60.
• Sigurs N, Hattevig G, Kjellman B. Maternal avoidance of eggs, cow's milk, and fish during lactation: effect on allergic manifestations, skin-prick tests, and specific IgE antibodies in children at age 4 years. Pediatrics. Apr 1992;89(4 Pt 2):735-9. [Medline].
• Simons FE. First-aid treatment of anaphylaxis to food: focus on epinephrine. J Allergy Clin Immunol. May 2004;113(5):837-44. [Medline].
• Simons FE. First-aid treatment of anaphylaxis to food: focus on epinephrine. J Allergy Clin Immunol. May 2004;113(5):837-44. [Medline].
• Sloan AE, Powers ME. A perspective on popular perceptions of adverse reactions to foods. J Allergy Clin Immunol. Jul 1986;78(1 Pt 2):127-33. [Medline].
• Spector SL, Nicklas RA. Practice Parameters for the Diagnosis and Treatment of Asthma. 1996:707.
• Steinman HA. "Hidden" allergens in foods. J Allergy Clin Immunol. Aug 1996;98(2):241-50. [Medline].
• Weber RW. Food additives and allergy. Ann Allergy. Mar 1993;70(3):183-90. [Medline].
• Yocum MW, Butterfield JH, Klein JS, et al. Epidemiology of anaphylaxis in Olmsted County: A population-based study. J Allergy Clin Immunol. Aug 1999;104(2 Pt 1):452-6. [Medline].
• Young E, Stoneham MD, Petruckevitch A, et al. A population study of food intolerance. Lancet. May 7 1994;343(8906):1127-30. [Medline].
• Yunginger JW, Sweeney KG, Sturner WQ, et al. Fatal food-induced anaphylaxis. JAMA. Sep 9 1988;260(10):1450-2. [Medline].
• Zeiger RS, Heller S. The development and prediction of atopy in high-risk children: follow- up at age seven years in a prospective randomized study of combined maternal and infant food allergen avoidance. J Allergy Clin Immunol. Jun 1995;95(6):1179-90. [Medline].

From http://www.webmd.com/allergies/guide/food-allergy-