The Many Forms of Allergic GI Disorders

Pediatric Food Allergy

Understanding food allergies and avoiding misdiagnosis.

A. Wesley Burks, MD | Professor and Chief | Division of Pediatric Allergy and Immunology | Duke University Medical Center | Durham, NC

"I've been treating children in the field of allergy immunology for 15 years, and in recent years I've really seen the rates of food allergy skyrocket," says Dr. Jacqueline Pongracic, head of the allergy department at Children's Memorial Hospital in Chicago. "Where in the past it only represented a small proportion of my practice, now more than half of the children I care for have a food allergy."1

Estimates have been that from 6-8% of children under 4 years old have food allergies, but some experts believe the percentage is growing. A study published in the Journal of Allergy and Clinical Immunology in late 2003 reported that the prevalence of peanut allergies in children doubled between 1997 and 2002, increasing from 0.4 percent to 0.8 percent.2

Whether there are truly more children suffering from food allergies now than in years past is debatable, and the data to support either theory is sparse. "There are no studies in this country looking at whether the rate of food allergies has increased over long periods of time," says Dr. Scott Sicherer of Mt. Sinai School of Medicine in New York City.3 Children are sometimes misdiagnosed with food allergies, causing parents to avoid serving foods that children may tolerate just fine. "Without a definitive allergy diagnosis from a food challenge," says Robert Wood, M.D., a pediatric allergist at the Johns Hopkins Children's Center, "children with low IgE levels who may no longer be allergic, or who were misdiagnosed with a food allergy, may be unnecessarily avoiding foods like milk, eggs, and peanuts which have significant nutritional benefits."4

The presumptive diagnosis of food allergy based on a patient's history and prick skin tests or in vitro IgE results alone is no longer acceptable. It is vitally important that the medical care provider use history, physical exam, and appropriate diagnostic tools to make an unequivocal diagnosis of food allergy. The question is, is this truly a food allergy, or some other stomach ailment?

What is Food Allergy?
An adverse food reaction is a general term for any untoward response to the ingestion of a food, and can include food allergies, which are immunologically mediated, and all other reactions, which are non-immunologic. Adverse food reactions are common and often assumed by patients to be allergic in nature. Between 20-30 percent of people report food allergy in themselves or their children, although true food allergy is present in only 6-8 percent of children under the age of five, and in 3-4 percent of adults!5

True food allergies are adverse immune responses toward food proteins.6 (The terms allergy and hypersensitivity are used interchangeably in this article.) A common problem in the pediatric age range, to most physicians, "food allergy" is synonymous with reactions that involve the immunoglobulin E (IgE) mechanism, of which anaphylaxis is a classic example. While it is true IgE-mediated (Type I) hypersensitivity accounts for the majority of well-characterized food allergic reactions, non-IgE-mediated immune mechanisms are also responsible for a variety of hypersensitivity disorders, as well as entities that have both IgE- and non-IgE-mediated mechanisms. 

Non-immunologic adverse food reactions are far more common than food allergy and, as implied by the term, arise from non-immunologic reactions to food ingestion. Examples include lactose intolerance, gastroesophageal reflux, auriculotemporal syndrome (or Frey syndrome, a gustatory flushing appearing on the skin below the ear and along the jawline), and disorders resulting from anatomic and neurological abnormalities, enzymatic deficiencies, metabolic diseases, toxins, gastrointestinal infections, and a host of other processes.

IgE-mediated Food Allergy
IgE-mediated reactions occur rapidly after ingestion of the culprit food, i.e., within seconds to minutes.7 Rarely, reactions up to two hours and beyond can also occur. Symptoms are believed to be caused by mediator release from tissue mast cells and circulating basophils, and include a combination of nausea, vomiting, cramping, diarrhea, flushing, pruritus, urticaria, swelling of the lips, face, or throat, wheezing, lightheadedness, or syncope. A patient may present with only one or two of these symptoms, or virtually all of them. In children, a classic presentation is vomiting and urticaria. 

IgE-mediated food allergy occurs most often in association with certain foods, although any food has the potential to cause allergy. In young American children, 90 percent of IgE-mediated allergies are caused by cow's milk, egg, soy, peanut, wheat, tree nuts, fish and shellfish.8 In adolescents and adults, the most common culprit foods are peanut, tree nut, shellfish, fish, and vegetables. Allergies to fresh fruits are common but usually less severe. Allergies to various seeds (sesame, poppy, canola) appear to be increasing.

Specific manifestations of IgE-mediated food hypersensitivity include the following:9

Urticaria and angioedema
Acute urticaria and angioedema are probably the most common cutaneous manifestations of food hypersensitivity reactions, generally appearing within minutes of ingestion of the food allergen. The exact incidence of such events is unclear, although food allergy may account for 20 percent of cases of acute urticaria.

By comparison, food allergies underlying chronic urticaria and angioedema (defined as greater than six weeks of regular outbreaks) appear to be uncommon. Food can also cause acute contact urticaria. In this condition, urticaria develops only on skin that was in direct contact with the food. 

Conjunctival and nasal symptoms are common components of systemic food allergic reactions. However, isolated allergic rhinoconjunctivitis in response to foods is rare. Similarly, only a small minority of patients with asthma has symptoms triggered by food allergy.

Gastrointestinal anaphylaxis
Gastrointestinal anaphylaxis refers to IgE-mediated gastrointestinal symptoms: nausea, abdominal pain, abdominal cramping, vomiting, and/or diarrhea.10 Symptoms in other target organs are often associated. The onset of upper gastrointestinal symptoms (nausea, vomiting, abdominal pain) is generally minutes to two hours after ingestion of the offending food, but lower gastrointestinal symptoms (which generally follow upper GI symptoms), such as diarrhea, can begin two to six hours after ingestion.

Generalized anaphylaxis
Food allergy has been estimated to account for up to one-half of all anaphylaxis in pediatric patients treated in emergency department settings.11 Peanuts, tree nuts, fish, and shellfish cause more anaphylactic reactions than other foods.12 Patients may develop symptoms and signs related to the cutaneous, respiratory, and cardiovascular system. This may culminate in hypotension, vascular collapse, cardiac dysrhythmias, or death. Anaphylaxis occasionally follows a biphasic course, with a recurrence of symptoms hours after the initial onset. Risk factors associated with fatal, food-induced anaphylaxis include co-existent asthma, delay in the administration of epinephrine, the adolescent/young adult age group and absence of skin symptoms.13

Oral allergy syndrome
The oral allergy syndrome, or pollen-food related syndrome, is considered a form of contact allergy that is seen in up to 50 percent of patients with allergic rhinitis to pollen.14 It is caused by the presence of heat-labile proteins within these foods that are cross reactive with allergenic pollen proteins. Symptoms are confined almost exclusively to the oropharynx, and include the immediate onset of pruritus, irritation, and mild swelling of the lips, tongue, palate, and throat upon ingestion of fresh, uncooked fruits and vegetables. As examples, a birch-allergic patient may develop itching of the lips or mouth upon eating apple, pear, cherry, carrot, celery, and potato, while a ragweed-allergic patient may react to melons and banana and a mugwort-allergic patient may react to celery or mustard. 

Symptoms usually subside within minutes after ingestion ceases. However, progression to systemic symptoms is thought to occur in approximately ten percent of patients, with anaphylaxis reported in one to two percent. Importantly, the symptoms are not elicited by cooked fruits and vegetables. Tree nuts and peanuts causing oral symptoms are best avoided, even in the roasted form, because of the frequency with which these foods cause more severe reactions.

Associated conditions
The two principal examples of atopic diseases that are affected by food allergy are atopic dermatitis and asthma. 

Atopic dermatitis is a chronic skin disorder that generally begins in early infancy and is characterized by a typical distribution, extreme pruritus, and chronically relapsing course; it is associated with asthma and allergic rhinitis. There also appears to be a significant association between atopic dermatitis and food hypersensitivity, with approximately 40 percent of infants and young children with moderate to severe atopic dermatitis demonstrating food allergies.15

The mechanisms underlying food-related exacerbations of atopic dermatitis involve both IgE-mediated and non-IgE-mediated hypersensitivity. The relationship between atopic dermatitis and food is characterized by these features: the elimination of suspected food allergens frequently improves symptoms of atopic dermatitis, repeated exposure to suspect foods commonly exacerbates skin symptoms, and eliminating foods to which an infant has demonstrable allergy can partially prevent the development of atopic dermatitis.

Isolated asthma, without gastrointestinal or dermatologic symptoms, is uncommonly a manifestation of food allergy. More typically, however, asthma is seen as a component of more generalized, IgE-mediated reactions (i.e., anaphylaxis). Another relationship between food allergy and asthma is that food allergy is a risk factor for life-threatening asthma, as evidenced by a substantially higher rate of food allergy in children requiring intubation for asthma compared to a control group of asthmatic children.

Non-IgE-mediated Food Allergies 
Non-IgE-mediated food allergies usually involve isolated gastrointestinal symptoms, such as reflux, nausea, vomiting, cramping, and diarrhea. These types of food allergies should also be considered in infants in the first year of life with varying degrees of blood and mucous in the stool. 

Patients with these forms of food allergy usually appear well. An exception is seen in the infantile syndrome of dietary-protein induced enterocolitis, in which infants can present with dehydration or failure to thrive and also develop severe hypotension upon food exposure. 

Because the symptoms of non-IgE-mediated allergic disorders are non-specific, the history and physical alone are rarely sufficient to distinguish them from non-allergic disorders unless they present as one of several well-recognized syndromes. Gastroenterological tests, including blood tests, stool examinations, endoscopy, colonoscopy, and mucosal biopsy may be required for diagnosis.

Non-IgE-mediated reactions have more subacute and/or chronic symptoms that are more commonly isolated to the gastrointestinal tract and generally present hours to days after the food is ingested.16 Affected patients commonly present with a characteristic constellation of clinical and demographic features that are consistent with well described disorders. These disorders principally include the following:

Food protein-induced enterocolitis
Food protein-induced enterocolitis (FPIES) (or dietary protein-induced enterocolitis syndrome) is an allergic syndrome that is believed to be cell-mediated, rather than IgE-mediated.17 It is diagnosed most commonly in infants, and represents the severe end of the spectrum of allergy-related gastrointestinal diseases in this age group. Older children and adults are affected less frequently. 

FPIES most often develops in response to cow's milk or soy, although oat, rice, and poultry are other causative foods. It is typically seen in infants younger than nine months of age, with a higher incidence between one week and three months of age. These infants are usually receiving cow's milk- or soy-based formulas. 

Patients with FPIES who are regularly ingesting a causative food present with chronic gastrointestinal symptoms: vomiting, diarrhea, malabsorption, or melena. Symptoms of FPIES resolve upon elimination of the causative food, although this may take weeks. If the causative food is later reintroduced, there is a characteristic delayed onset (approximately two hours) of profuse vomiting, followed by return of the other symptoms. Children can require emergency treatment for hypotension, lethargy, or shock in this setting and laboratory studies may show acidosis, methemoglobinemia, and an increase in neutrophils. Most children with FPIES become tolerant of milk, soy, or other causative solid foods by the age of three years. However, persistent FPIES has been described.

Food protein-induced proctitis
Food protein-induced proctitis usually presents in the first months of life with microscopic or gross blood in the stool. The severe illness and failure to thrive that is typical of FPIES is not observed in this disorder. Stools can appear normal and blood loss is usually mild, although anemia can be seen. The condition may present in infants who are exclusively nursed, which is another characteristic of this condition that differs from FPIES.

Like FPIES, food protein-induced colitis is secondary to cell-mediated reactions to cow's milk and soybean protein, with unusual other causative foods. Symptoms usually improve in days upon elimination of the causative food. This disorder is believed to subside after a period of allergen avoidance ranging from six months to two years, although there are no large series for analysis. 

Celiac disease
Celiac disease is an extensive enteropathy leading to malabsorption.18 Total villous atrophy and an extensive cellular infiltrate are associated with sensitivity to gliadin, the alcohol-soluble portion of gluten found in wheat, oat, rye, and barley. The general incidence is thought to be 1:4000 but has been reported as high as 1:500 in Ireland. Patients have an apparent genetic predisposition to this disease because approximately 90% of patients are HLA-B8 positive and nearly 80% have the HLA-DW3 antigen. Patients often have presenting symptoms of diarrhea or frank steatorrhea, abdominal distention and flatulence, weight loss, and occasionally nausea and vomiting. Other extra-intestinal symptoms and oral ulcers secondary to malabsorption are not common.

Eosinophilic Gastrointestinal Disorders
The eosinophilic gastrointestinal disorders are characterized by symptoms of postprandial gastrointestinal dysfunction accompanied by eosinophilic infiltration of various segments of the intestinal tract on biopsy.19

The pathophysiology of the eosinophilic gastrointestinal disorders in poorly understood. Many patients have evidence of allergic sensitivities to food and/or environmental allergens, but the causal role of these sensitivities is unclear.

Eosinophilic esophagitis
Eosinophilic esophagitis (EE) should be suspected in patients of any age presenting with esophageal symptoms. Very young children may present with feeding disorders, whereas older children and adults present with dysphasia, vomiting, and abdominal pain. A history of food impaction is common. Failure to respond to antacids and antireflux therapies is an important aspect of the history.

Many patients with EE have other atopic diseases. The most commonly implicated foods in EE are cow's milk, egg, soy, corn, wheat, and beef, and most patients with evidence of food sensitivity tested positive for multiple foods. Elimination of these foods or the use of elemental diets results in clinical and histologic improvement in most. However, the pathophysiological relationship between this disorder and food and aeroallergens remains unclear. 

Eosinophilic gastroenteritis
Eosinophilic gastroenteritis can present at any age with abdominal pain, nausea, diarrhea, malabsorption, and weight loss. In infants, it may present as outlet obstruction with post-prandial projectile vomiting. In adolescents, it can mimic irritable bowel syndrome. Symptoms vary depending on the portion of the gastrointestinal tract that is involved. 

Approximately one-half of patients have allergic disease, such as defined food sensitivities, asthma, eczema, or rhinitis. However, in contrast to eosinophilic esophagitis, avoidance of implicated foods in those with an allergic food history has limited or no clinical benefit.

Evaluation for Possible Food Allergy
The evaluation of a patient with possible food allergy is a clinical exercise that includes some combination of the following diagnostic tools, although not all of these elements are necessary in every patient: history and physical examination, prick/puncture skin testing, in vitro testing, gastroenterologic tests, elimination diets, and food challenge.

Every evaluation begins with a detailed history and physical examination. The physical examination should focus on physical findings of allergic reactions if the patient is evaluated acutely or stigmata of allergic disease if the patient presents with chronic symptoms. The clinical history is critical in the diagnosis of food allergy, as it is used to determine subsequent testing and interpretation of results. Supported by the physical exam, history can be used to distinguish food allergy from a host of other adverse food reactions, distinguish among different types of food allergy, and identify a possible culprit food.

The history is also used to determine what type of testing should be performed and how that testing is interpreted, particularly for IgE-mediated food allergy. The information obtained from the clinical history is used to assess the patient's pretest probability of having food allergy. Testing for specific allergic conditions can then be performed and interpreted in the context of this assessment. 

A positive result on skin testing or in vitro testing is meaningful only if there is a clinical history of symptoms upon exposure; a test result alone is not typically adequate to make the diagnosis of allergy. 

Role of Allergy Tests in Diagnosis
The diagnosis of food allergy remains a clinical exercise that utilizes a careful history, selective prick skin tests or in vitro IgEs (if an IgE-mediated disorder is suspected), appropriate exclusion diet, and blinded provocation. Other diagnostic tests that don't appear to be of significant value include food-specific IgG or IgG4 antibody levels, food antigen-antibody complexes, evidence of lymphocyte activation (3H uptake, IL-2 production, leukocyte inhibitory factor, etc.), and low-dose sublingual or intracutaneous provocation. Blinded challenges may not be necessary in suspected gastrointestinal disorders where pre- and post-challenge laboratory values and biopsies are often used.

There is currently a concerted effort among researchers in the field of allergy to define the sensitivity and specificity of tests for individual foods (and other allergens), as discussed herein. However, these values have not been determined or validated for the majority to foods. Thus, the pre-test probability is essential for effective use of available testing modalities. 

Skin Testing
Prick/puncture skin testing
Prick/puncture (or epicutaneous) skin testing ($3-5/test) is best used to investigate the possibility of an IgE-mediated reaction to a specific food in a patient with a suggestive clinical history (i.e., a high pre-test probability) of allergy. It is also highly effective for excluding IgE-mediated allergy, particularly in a patient with a low pre-test probability. Because of the low specificity of skin testing, it should not be used to screen patients for allergy by testing with broad panels of food allergens without regard for clinical history, as this is likely to yield false positive results. 

Prick/puncture skin tests are highly reproducible and less costly to perform than in vitro testing. Skin testing causes minimal patient discomfort and yields results within 15 minutes. This type of testing can be safely performed in patients of any age. 

It has been observed that the skin of infants may be less reactive, yielding more false negative results, although this difference has not been formally studied. Nevertheless, positive results are commonly obtained. Unfortunately, very young children may also have more systemic reactions to skin testing. Thus, skin testing can be performed in children of all ages, with appropriate precautions. 

The larger the wheal of the skin test the greater the likelihood of clinical allergy. In contrast, the negative predictive accuracy for skin prick testing to foods is uniformly high. A negative skin test confirms the absence of an IgE-mediated reaction with 90 to 95 percent accuracy. Therefore, skin testing is highly useful for excluding IgE-mediated food allergy.

Intradermal skin testing
Intradermal skin testing should not be performed in the evaluation of food allergy, as it does not add to the diagnosis and carries a greater risk of inducing a systemic reaction than does prick skin testing. Fatalities have been reported with intradermal testing to foods.

Atopy patch testing
Atopy patch testing involves the topical application of a food-containing solution to the skin for 48 hours, and has shown possible utility in the diagnosis of non-IgE-mediated food allergy. However, there are currently no standardized reagents, application methods, or guidelines for interpretation, and this type of testing cannot be recommended outside of research settings for clinical use.

In Vitro IgE Testing
Radioallergosorbent tests (RASTs) and fluorescent enzyme immunoassay (FEIA) tests (ranging from $15-50/test) are in vitro assays used to identify food-specific IgE antibodies in the serum. The commercially available tests currently in use do not employ radioactivity, although the term RAST is still in common use. In vitro IgE would be the preferable term.

Immunoassays are considered less sensitive than skin prick tests, although the two modalities may be equivalent for certain foods. Immunoassays are also significantly more costly than skin testing, and the results are not immediately available. However, immunoassays for food-specific IgE have several features that make them useful—they are widely available, unaffected by the presence of antihistamines or other medications, useful in patients with severe anaphylaxis in whom skin testing may carry an unacceptable degree of risk, and useful in patients with dermatologic conditions that may preclude skin testing, such as severe atopic dermatitis and dermatographism.

Based primarily upon studies performed in the United States, the 95 percent predictive levels for egg, milk, peanut, tree nuts, and fish are as follows:20

  • Egg, 7 kUA/L. The value for infants less than two years of age is 2 kUA/L.
  • Milk, 15 kUA/L. The value for infants less than two years of age is 5 kUA/L.
  • Peanut, 14 kUA/L.
  • Tree nuts, approximately 15 kUA/L.
  • Fish, 20 kUA/L.


Thus, a child over the age of two with a convincing history of egg allergy has a greater than 95 percent likelihood of experiencing an allergic reaction to egg upon challenge if their egg-specific IgE exceeds 7 kUA/L. Therefore, challenge is unnecessary in such children. Equivalent predictive positive levels for soy and wheat have not yet been established. In addition, these data were developed in children, and there are currently no recommendations regarding their interpretation in adults with food allergy.

Trial Elimination Diets
The term elimination diet can be confusing, as it can also be applied to the avoidance that is prescribed once a food allergy is diagnosed. In this topic review, the term is used to refer to a diet that is prescribed by a clinician as part of an evaluation for food allergy. An exclusion diet eliminating all foods suspected by history and/or prick skin testing (or in vitro IgE for IgE-mediated disorders) should be conducted for at least 1-2 weeks. 

Some gastrointestinal disorders may need to have the exclusion diet extended for up to 12 weeks following appropriate biopsies. If no improvement is noted following the diet, it is unlikely that food allergy is involved. In the case of some chronic diseases, such as atopic dermatitis or chronic asthma, other precipitating factors may make it difficult to discriminate the effects of the food allergen from other provocative factors.

Food Diaries
Food diaries are written records of everything that is ingested by a patient, including all foodstuffs, beverages, condiments, and candies. Although rarely diagnostic on their own, food diaries sometimes may be helpful in identifying a food that was overlooked by the patient, a food containing hidden ingredients, or patterns of reactions.

Food Challenges
Oral food challenges are structured protocols in which the patient ingests a suspect food under clinician supervision. Food challenges should only be performed by allergy specialists familiar with food-allergic reactions and in settings equipped with the necessary medications, equipment, and staff to treat anaphylaxis. 

There are several clinical circumstances in which oral food challenges are needed for diagnosis or management. "Open" challenges are those in which the patient simply eats the suspect food. Open challenges are prone to bias because patients know when they are ingesting the food and may be fearful about doing so. Anxiety can give rise to mild symptoms that may mimic an early allergic reaction, such as perioral tingling or numbness. 

In single blind challenges, the patient cannot discern which doses contain the challenge food, although the person administering them knows. Single-blind challenges in a clinic setting may be helpful to screen suspected food allergens. The presumptive diagnosis of food allergy based on a patient's history and prick skin tests or in vitro IgE results is no longer acceptable. There are exceptions to this, such as the patients with severe anaphylaxis following the isolated ingestion of a specific food. In double-blind challenges, the doses are prepared by a third party and neither the patient nor the person administering the challenge knows what the doses contain. 

In placebo-controlled challenges, placebo doses of either a different masked food to which the patient is not sensitive, the vehicle food alone, or an inert sugar, such as dextrose are also given. The challenge food and placebos are administered in random order.

Double-blind placebo-controlled food challenge 
The double-blind placebo-controlled food challenge (DBPCFC) is considered the "gold standard" for the diagnosis of food allergies. Foods are selected for testing based upon the history and the results of skin and/or in vitro testing. 

For DBPCFC, the specific food is usually dried and masked in a vehicle food. These challenges are graded, and there should be an equivalent number of placebo and food steps, administered in random order. If a significant amount of the dried food is tolerated without a reaction, then the challenge is followed by an open feeding. If this is tolerated, then food allergy has been excluded with as much precision as possible.

Unvalidated Methods
Patients may present after having other types of food allergy tests performed.22 These can include food-specific IgG and IgG4 tests, which typically yield multiple positive results and may represent a normal immune response to food. They do not predict true food hypersensitivity and should not be used. Other types of testing for food allergy that are not supported by scientifically-valid concepts include sublingual or intradermal provocation tests, tests of lymphocyte activation, kinesiology, cytotoxic tests, and electrodermal testing. 

It's important that the medical care provider make an unequivocal diagnosis of food allergy. If the present practice continues, over one-quarter of the population will continue to alter their eating habits based on misconception of food allergy, which may cause people to change basic eating habits based on false information. 

Parents are more likely to think their infant is allergic to certain foods than is actually the case, according to a new study from England. Dr. Taraneh Dean of the University of Portsmouth and her colleagues found that 54% of a group of one-year-olds were avoiding some foods because their parents perceived them to have had reactions to ingredients such as cow's milk, wheat, eggs or additives. Overall, however, only 2-6% of the infants had clinically confirmed food hypersensitivity.23 These findings emphasize the need for accurate diagnosis to prevent infants being on unnecessarily restricted diets, which may be associated with inadequate nutrition.

Educating parents on the various potential causes of stomach ailments can help the family understand that the majority of children complaining of upset stomach do not have any type of food allergy. The diagnosis of food allergy remains a clinical exercise that utilizes a careful history, selective prick skin tests or in vitro IgEs (if an IgE-mediated disorder is suspected), appropriate exclusion diet, and food challenges if necessary. Avoiding incorrect diagnoses can save many children and their families from unnecessary diet restrictions, panic, and the use of medications that could have potentially adverse effects.

A. Wesley Burks, M.D., is Professor and Chief of the Division of Pediatric Allergy and Immunology at Duke University Medical Center in Durham, North Carolina. Dr. Burks' research interests are in the area of nutrition and immunology, primarily related to adverse reactions to foods. Dr. Burks and his collaborators are currently producing recombinant food proteins for use in mechanistic studies related to the immune system. Additionally, they are working on immunotherapy and vaccines for treatment of food allergy, primarily peanut allergy.


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  2. Sicherer SH, Munoz-Furlong A, Sampson HA. Prevalence of peanut and tree nut allergy in the United States determined by means of a random digit dial telephone survey: a 5-year follow-up study. J Allergy Clin Immunol 2003; 112(6):1203-7.
  3. Charles Sheehan. Scientists see spike in kids' food allergies. Chicago Tribune, 9 June 2006. Accessed at:
  4. Guidelines for food allergy testing. July 8, 2004. Accessed at:
  5. Sampson HA. Food allergy—accurately identifying clinical reactivity. Allergy 2005; 60 Suppl 79:19-24.
  6. Sampson HA. Update on food allergy. J Allergy Clin Immunol 2004; 113(5):805-19.
  7. Sampson HA. 9. Food allergy. J Allergy Clin Immunol 2003; 111(2 Suppl):S540-S547.
  8. Burks W. Food allergens. Clin Allergy Immunol 2004; 18:319-37.
  9. Sicherer SH. Manifestations of food allergy: evaluation and management. Am Fam Physician 1999; 59(2):415-30.
  10. Sampson HA. Food allergy. Part 1: immunopathogenesis and clinical disorders. J Allergy Clin Immunol 1999; 103(5 Pt 1):717-28.
  11. Sampson HA. Food-induced anaphylaxis. Novartis Found Symp 2004; 257:161-71.
  12. Bock SA, Munoz-Furlong A, Sampson HA. Fatalities due to anaphylactic reactions to foods. J Allergy Clin Immunol 2001; 107(1):191-3.
  13. Sampson HA. Food-induced anaphylaxis. Novartis Found Symp 2004; 257:161-71.
  14. Sicherer SH, Sampson HA. 9. Food allergy. J Allergy Clin Immunol 2006; 117 (2 Suppl Mini-Primer):S470-S475.
  15. Burks AW, James JM, Hiegel A, Wilson G, Wheeler JG, Jones SM et al. Atopic dermatitis and food hypersensitivity reactions. J Pediatr 1998; 132(1):132-6.
  16. Sicherer SH. Clinical aspects of gastrointestinal food allergy in childhood. Pediatrics 2003; 111(6 Pt 3):1609-16.
  17. Ibid.
  18. Sampson HA. Food allergy. Part 1: immunopathogenesis and clinical disorders. J Allergy Clin Immunol 1999; 103(5 Pt 1):717-28.
  19. Rothenberg ME. Eosinophilic gastrointestinal disorders (EGID). J Allergy Clin Immunol 2004; 113(1):11-28.
  20. Sampson HA. Utility of food-specific IgE concentrations in predicting symptomatic food allergy. J Allergy Clin Immunol 2001; 107(5):891-6.
  21. Ibid.
  22. Sampson HA. Food allergy. Part 2: diagnosis and management. J Allergy Clin Immunol 1999; 103(6):981-9.
  23. Infants' food allergies rarer than parents believe. Reuters Health. June 08, 2006. From J Allergy Clin Immunol, May 2006. Accessed at:
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