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Food Allergies

Overview

Practice Essentials

Food allergies are immunologically mediated adverse reactions to foods that are often but not exclusively IgE mediated. Any food protein, and sometimes carbohydrate moieties,^{[1, 2]} 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 the majority of these reactions. In children, 90% of food allergies can be attributed to cow's milk, chicken egg, soybean, wheat, peanut, tree nuts, fish, and shellfish.^{[3, 4]} In adults, shellfish, fish, peanuts, and tree nuts are the foods most often implicated. The most serious allergic reaction is anaphylaxis, but food-related allergic reactions can include other types of reactions such as limited IgE reactions (eg, urticaria, angioedema), oral allergy syndrome (OAS) also known as pollen food allergy syndrome (PFAS), food protein-induced enterocolitis (FPIES), milk protein-induced allergic proctocolitis, and eosinophilic esophagitis and eosinophilic gastroenteritis.

Signs and symptoms

IgE-mediated reactions

Signs and symptoms of IgE-mediated reactions, including anaphylaxis, which is a rapidly progressive, life-threatening reaction, include:

Oropharyngeal pruritus
Angioedema (eg, laryngeal edema)
Stridor
Dysphonia
Cough
Dyspnea^[5]
Wheezing
Nausea
Vomiting
Diarrhea
Abdominal pain
Flushing
Urticaria
Ocular injection, ocular pruritus, conjunctival edema, periocular swelling
Nasal congestion, nasal pruritus, rhinorrhea, and sneezing
Feeling of impending doom
Cardiovascular symptoms including hypotension, cardiac arrhythmias, and cardiac arrest can be associated with anaphylaxis^[6]

OAS/PFAS

Allergic rhinitis, conjunctivitis, and asthma symptoms with pollen exposure associated with oropharyngeal pruritis after exposure to raw fruits, vegetables, and sometimes nuts that cross react with sensitizing pollen^[7]

FPIES^{[8, 9]}

Weight loss
Vomiting
Diarrhea
Dehydration and hypovolemia

Milk protein-induced proctocolitis (infants)^{[8, 9, 10]}

Blood and mucous in stool
Diarrhea
Poor weight gain or weight loss

Esinophilic gut disease^[11]

Dependent on areas of gut where eosinophilic infiltration is present
Esophageal disease results in reflux, weight loss, failure to thrive, difficulty swallowing, and food impaction
Gastrointestinal disease results in nausea, vomiting, diarrhea, and weight loss

Diagnosis

Medical history

Complete list of all foods suspected of causing symptoms (including foods and food additives listed on prepared food labels)
Manner in which the food was prepared (cooked, raw, added ingredients)
Minimum quantity of food exposure required to cause the symptoms
Reproducibility of symptoms on exposure to the food
Exercise after ingestion but prior to reaction to elicit possible food-dependent, exercise-induced anaphylaxis^[12]
Personal or family history of other allergic disease
Factors that can potentiate a food-allergic reaction (eg, exercise,^[13] nonsteroidal anti-inflammatory drugs [NSAIDs], or alcohol)^[12]

In addition, obtain a thorough description of each reaction, including the following:

Route of exposure (ingestion, skin contact (especially in patients with atopic dermatitis)^{[14, 15, 16]} and inhalation) and dose
Timing of symptom onset in relation to food exposure (IgE reactions usually occur very soon after ingestion, other reactions slower onset)
All observed symptoms and each one’s severity
Duration of the reaction
Treatment provided and clinical response to treatment
Most recent reaction

Physical examination

Physical examination findings are most useful for the following:

Skin: urticaria and angioedema
Lungs: wheezing
Cardiovascular: assess for signs of vasodilation and shock (hypotension, tachycardia)
Assess for dehydration especially if there are GI symptoms (mucous membranes, capillary refill, skin turgor, weight if patient stable enough to obtain)
Assessing nutritional status, growth parameters, and signs of other allergic disease, especially in children

See Clinical Presentation for more detail.

Diagnosis

Specific laboratory tests for some hypersensitivities are not available; food protein-induced enterocoloitis and milk protein-induced proctocolitis cannot be identified by laboratory tests.

Laboratory studies that may be helpful in identifying IgE-induced food hypersensitivity include the following:

Specific IgE serum antibody testing: Positive results primarily denote sensitization and may not confirm clinical allergy and can be done by serum testing or by skin prick testing.^[17]
IgE testing (skin testing or laboratory testing) is a better negative predictor that positive predictor. A positive test is meaningful only when coupled with a probable reaction to the food.
Component testing more specifically defines the protein involved in food allergies and can, in some cases, add prognostic value to food allergy testing, especially for peanut, milk, and egg.^{[18, 19]}
Basophil histamine-release assays (BATs) have historically been limited to research settings, but may be emerging as clinical tests for severe allergic reactions. BAT measures immediate histamine release from basophils. It may be a useful tool in evaluating IgE reactions from low-molecular-weight substances.^{[17, 20]}
Specific IgG is of no proven efficacy in identifying food allergens
When anaphylaxis has occurred, tryptase determination within first few hours of reaction can verify allergic etiology. Tryptase is released from mast cells during IgE-mediated allegic reactions. Tryptase peaks within 1–2 hours of reaction and returns to baseline in about 6 hours. It correlates with mast cell degranulation and is also elevated in mast cell disorders. Handling of specimen (on ice to laboratory, and serum separation with expediency) is critical.^[17]

Skin testing

Skin prick testing: This is the most common screening test for IgE-mediated food allergy; negative predictive accuracy exceeds positive predictive accuracy (> 90% vs < 50%).^[17]
If IgE skin prick testing is negative shortly after anaphylaxis repeat in 4–6 weeks to avoid erroneously negative results. Specific IgE may be depleted by severe allergic reactions giving a false negative result. This waiting period for testing is standard practice for drug allergy, especially interoperative drugs, but may also be of benefit in food allergy testing.^[21]
Intradermal testing: Generally avoided for food allergy testing because of the risk of inducing a systemic reaction, and increased risk of false positivity.
Patch testing is sometimes utilized to detect delayed, nonIgE-mediated food sensitivity but is not standardized.

Biopsy

When eosinophilic gut disease is suspected, biopsy of the gut for evaluation of eosinophilic infiltrates is warranted.

≥ 15 eosinophils per high-power field (40x magnification) is major criteria for diagnosis of eosinophilic esophagitits^[11]

Diet-related diagnostic measures

These may be helpful as follows for most forms of food allergy:

The double-blind, placebo-controlled food challenge remains the gold standard for identification of food allergy, but in the case of severe reactions (eg, anaphylaxis) it may be unsafe. It can also be laborious and difficult to perform in office
Diet diary
Elimination diet (may be used for diagnostic as well as therapeutic purposes)
Food challenge confirmation of food allergy (may be open; single-blind; or double-blind, placebo-controlled)
For FPIES and milk protein-induced enterocolitis, elimination of the suspected food is the only diagnostic and treatment tool currently available

See Workup for more detail.

Management

There are currently no curative therapies for food allergy. The only proven treatment is strict dietary elimination of the offending food allergen. A properly managed, well-balanced elimination diet includes the following elements:

Education of patients and families regarding how to read food labels properly and identify common words used for indicating the presence of the food allergen of concern
Avoidance of cross-contact (eg, through shared utensils or fryers) of allergens with otherwise safe foods during meal preparation
Elimination of only those foods that are confirmed as provoking allergic reactions; both obvious and hidden sources of food allergens (eg, medications and cosmetics) must be considered
Consideration of potential exposures by route other than ingestion (eg, skin contact in atopic dermatitis patients who are more susceptible or inhalation of aerosolized allergens such as fish while being cooked)
Anticipation of potential candidates for food allergen cross-reactivity (eg, peanut and peas or legules or cow milk with goat milk)^[22]
Avoidance of high-risk situations where accidental or inadvertent ingestion of food allergens can occur (eg, buffets or picnics)
School emergency plan for avoidance of allergen and treatment if necessary with specific attention to avoiding bullying
Education on vaccines that cross-react with food and those that do not: The measles and influenza vaccines have been shown to be safe in egg-allergic children. However, the yellow fever vaccine, which includes egg concentrations ranging from 2·43 μg/mL to 4·42 μg/mL according to the vaccine batch, is contraindicated in patients with egg allergies^{[23, 24, 25, 26, 27]}

Adherence to avoidance measures notwithstanding, accidental or inadvertent ingestions may occur and lead to a reaction. Strategies for dealing with such a reaction include the following:

Creation of a concise written emergency management plan (see www.foodallergy.org), copies of which should be available in appropriate places (eg, daycare, schools, work locations, and college dormitory advisors)
Epinephrine autoinjector for every food allergic patient who may have anaphylaxis to be carried with patient/parent/guardian
Use of medical identification jewelry indicating food allergies
Ensuring that the patient has an emergency contact number available
Provision of anticipatory guidance measures (eg, educating the patient about potential sources of accidental exposure)
Treatment for anxiety and depression that may accompany food allergy with particular attention to avoiding bullying in school-aged children

Emergency medications include the following:

Injectable epinephrine: This is the drug of choice for initial management of a food-induced anaphylactic reaction; the patient/parents/school should have self-injectable epinephrine readily available at all times and should be properly trained in its use
Antihistamines may be used for the treatment of mild symptoms but never sole therapy for anaphylaxis
Bronchodilators may be used but should not be depended upon for anaphylaxis; epinephrine should be given
Histamine-2 blockers as adjunctive therapy
Corticosteroids as adjunctive therapy
Intravenous fluids for hypotension
Glucagon for refractory anaphylaxis

In severe anaphylaxis, ventilatory and circulatory support may be needed.

Preventive therapies include the following:

Omalizumab was initially approved only for peanut-allergic patients now shown to be effective in increasing the reaction threshold for patients 1 year or older with multiple food allergies.^[28]
Oral or sublingual immunotherapy appears to be a promising therapeutic option to increase the reaction threshold.^{[29, 30]} The first immunotherapy for peanut allergy was approved by the FDA in 2020. This therapy does carry the risk of allergic reaction/anaphylaxis from the therapy itself.^{[31, 32, 33, 34]}

See Treatment and Medication for more detail.

Next: Background

Background

Food allergies are immunologically mediated adverse reactions to foods that are often but not exclusively immunoglobulin E (IgE) mediated. Any food protein, and sometimes carbohydrate moieties, 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 the majority of these reactions. In children, 90% of food allergies can be attributed to cow's milk, chicken egg, soybean, wheat, peanut, tree nuts, fish, and shellfish.^{[3, 4]} In adults, shellfish, fish, peanuts, and tree nuts are the foods most often implicated. Symptoms observed in a food-induced anaphylactic reaction most frequently involve the skin, gastrointestinal tract, and respiratory tract.^[1]

The most serious allergic reaction is anaphylaxis, but food-related allergic reactions can include other types of reactions such as limited IgE reactions (eg, urticaria, angioedema), oral allergy syndrome (OAS) also known as pollen food allergy syndrome (PFAS), food protein-induced enterocolitis (FPIES), milk protein-induced allergic proctocolitis, and eosinophilic gut disease. While IgE-mediated reactions are immediate, some food allergies result in chronic disorders (eg, FPIES, eosinophilic esophagitis). Investigations of near-fatal or fatal anaphylactic reactions following food ingestion reveal that most are caused by peanuts, tree nuts, and shellfish, although milk has been increasingly reported.^[35] (See Workup.)

Adverse reactions to food that are not immune mediated are not considered to be food allergies. An example is lactose intolerance, which is caused by a deficiency of lactase. Adverse reactions to foods can also occur from toxic (eg, bacterial food poisoning) or pharmacologic (eg, caffeine) effects.

Next: Background

Pathophysiology

IgE-mediated reactions

IgE antibody–mediated responses are the most widely recognized form of food allergy and account for most reactions. IgE-mediated reactions are generally acute, and most reactions occur within minutes of ingesting the offending food.

Patients with atopy produce IgE antibodies to specific epitopes (areas of the protein or carbohydrate moieties) of one or more food allergens. These antibodies bind to high-affinity IgE receptors on circulating basophils and tissue mast cells present throughout the body, including in the skin, gastrointestinal tract, and respiratory tract.^[4]

Subsequent allergen exposure binds and cross links IgE antibodies on the cell surface, resulting in receptor activation and intracellular signaling that initiates the release of inflammatory mediators (eg, histamine) and synthesis of additional factors (eg, chemotactic factors, cytokines) that promote allergic inflammation. The effects of these mediators on surrounding tissues result in vasodilation, smooth muscle contraction, and mucus secretion, which, in turn, are responsible for the spectrum of clinical symptoms observed during acute allergic reactions to food.

Cell-mediated responses

T-cell–mediated responses to food allergens may also mediate allergic responses, particularly in disorders with delayed or chronic symptoms. For example, food protein–induced enterocolitis syndrome (FPIES), a gastrointestinal food allergy, appears to be mediated by T-cell production of the cytokine tumor necrosis factor (TNF)-alpha.^[36] Persons with atopic dermatitis that flares with ingestion of milk have been noted to have T cells that, in vitro, express the homing receptor cutaneous lymphocyte antigen, which is thought to home the cell to the skin and mediate the response.^[37]Celiac disease is the result of an immune response to gluten proteins in grains.

Eosinophilic esophagitis and gastrointestinal disease are eosinophilic mediated. Eosinophil granules release substances toxic to multiple tissues. These substances include major basic protein 1 and 2, eosinophilic cationic protein, eosinophilic-derived neurotoxin, and eosinophil peroxidase. Triggering of eosinophils leads to the generation of proinflammatory cytokines including Il-1, Il-3, Il-4, Il-5, and Il-13, and granulocyte-macrophage colony-stimulating factor.^[11] Eosinophil degranulation is responsible for tissue damage in eosinophilic gut disease.

Characteristics of food allergens

Food allergens that cause IgE-mediated reactions have been studied extensively. They 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.^[22] Delayed allergic reactions to meat proteins have been attributed to reactions to carbohydrate moieties.^[2]

Next: Background

Etiology

Food allergies are primarily the result of immune responses to food proteins (allergic reactions to non-protein food additives are uncommon but do occur).^[38] Normally, noninflammatory immune responses develop to ingested foods in a process called oral tolerance.^{[39, 40]}For reasons that remain unclear, but likely include environmental and genetic factors, tolerance may be abrogated, leading to adverse immune responses.

While sensitization (eg, development of an immunoglobulin E [IgE] immune response) to an allergen has been primarily assumed to occur from ingestion, this may not always be the case. For example, oral allergy syndrome (pollen-food allergy syndrome) describes an allergic response to specific raw fruits or vegetables that share homologous proteins with pollens; the initial route of sensitization is respiratory exposure to pollen proteins rather than oral exposure to food proteins. The skin may be another potential route of sensitization, especially in patients with atopic dermatitis.^[41]

Controversy surrounds the role of food allergy in the pathogenesis of atopic dermatitis.^[14] Studies show that among patients with moderate chronic atopic dermatitis, 35–40% have IgE-mediated food allergy.^{[42, 43]} Food-specific IgE-mediated and cellular mechanisms may be partially responsible for chronic eczematous inflammation.

Removal of a specific food allergen may lead to reduction or resolution of clinical symptoms in affected patients; reintroduction of the food may then exacerbate the atopic dermatitis if it is food-responsive.^{[44, 45]}Reintroduction of a suspected food allergen should be performed under medical supervision because, in some instances, initial reintroduction of the food after a period of dietary elimination has resulted in more significant symptoms than were observed when the food was regularly ingested. ^[46]

Because it is often difficult to isolate which food/foods are responsible for atopic dermatitis exacerbations, consideration must be given to false positive–specific IgE in the face of elevated total IgE. Nutritional concerns (especially for children) and practicality of multiple food elimination diets for atopic dermatitis must also be considered.

Risk factors

Risk factors or associations 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 epinephrine to treat the allergic reaction.^{[47, 35]}Teenagers and young adults appear to be overrepresented in registries of food allergy fatalities and present a special risk group.

Risk of atopy is more common in children of atopic parents.

Next: Background

Epidemiology

General surveys report that as many as 25–30% of households consider at least 1 family member to have a food allergy.^{[48, 49]}However, this high rate is not supported by controlled studies in which oral food challenges are used to confirm patient histories.

Comprehensive studies that include oral food challenges are few in number. Considering allergy to milk, egg, peanut, and seafood in a meta-analysis of 6 international studies using oral food challenges, estimated rates of 1–10.8% were obtained.^[50]

In a meta-analysis including allergy to fruits and vegetables (excluding peanut), only 6 international studies included oral food challenges, and estimates of allergy varied widely from 0.1–4.3% for fruits and tree nuts to 0.1–1.4% for vegetables to under 1% for wheat, soy, and sesame.^[51]

Sex- and age-related demographics

Among children, males appear to be more affected; among adults, females are more frequently affected.^[52]The prevalence of food allergies has been estimated to be up to 8% in infants and children and 3.7 % in adults.^{[53, 54]}

However, variations in prevalence have been reported according to method used (self-report, testing, physician evaluation), geographic region, and foods included in the assessment.^[55]

In a population-based survey study of 40,443 US adults, an estimated 10.8% were food allergic at the time of the survey, whereas nearly 19% of adults believed that they were food allergic. Nearly half of food-allergic adults had at least 1 adult-onset food allergy, and 38% reported at least 1 food allergy–related ED visit in their lifetime.^[56]

Studies in the United States and the United Kingdom indicate a rise in peanut allergy among young children in the past decade.^{[52, 57, 54]} One study showed an increase of peanut allergy in children from 0.4% in 1997 to 0.8% in 2002.^[52]Studies from Canada and the United Kingdom indicate allergy rates to peanut of over 1% in children.^{[58, 59]}

A report from the US Centers for Disease Control and Prevention (CDC) indicated that 5.8% of children nationwide had a food allergy in 2021. The percentage of children with a food allergy increased with age, from 4.4% in children 0–5 years old to 5.8% in children 6–11 years old, and 7.1% in children 12–17 years old.^[60]

Based on available studies, estimations of the rate of food allergies in children have been summarized as follows for common food allergens:^[53]

Cow milk - 2.5%
Eggs - 1.3%
Peanuts - 0.8%
Wheat - 0.4%
Soy - 0.4%

Racial and ethnic disparities

Research indicates that racial and socioeconomic disparities play a crucial role in shaping the landscape of food allergy prevalence, access to care, and health outcomes.

According to a 2023 study, in the United States, Hispanic, Black, and Asian individuals experience higher rates of allergies across all age groups. Prevalence rate was 10.6% in Hispanic and Black individuals, 10.5% in Asian individuals, and 9.5% in White individuals. The study also found that prevalence of food allergies was lowest among households in the highest income bracket (> $150,000 annually).^[61]

Another study found that people of color are less likely to have an allergy diagnosis but have higher rates of food-induced anaphylaxis.^[62]

Next: Background

Non-IgE-Mediated Food Allergies

Eosinophilic esophagitis and gastroenteritis

Symptoms vary according to location of the eosinophilia. Typical symptoms include postprandial nausea, abdominal pain, and a sensation of early satiety. Eosinophilic esophagitis may manifest as reflux symptoms and dysphagia; food impaction can occur as well. Children may experience weight loss or failure to thrive.^{[63, 11]}

A complete blood count (CBC) and differential findings may show eosinophilia in approximately 50% of patients; however, this is not diagnostic. Typically, endoscopy and biopsy must be performed in order to establish the presence of eosinophils in the affected segment of the gut. While a dense eosinophil infiltrate may be seen anywhere from the lower esophagus through the large bowel, involvement is patchy and variable.

Eosinophilic esophagitis is characterized by symptoms related to esophageal dysfunction, such as dysphagia and pain, and histologically by eosinophil-predominant inflammation.

Pathologically, one or more biopsy specimens must show a peak of 15 or more eosinophils per high-power field. Alternative explanations (eg, reflux) for symptoms/histopathologic abnormalities should be excluded.

An elemental (no potential allergens) or oligoantigenic diet (a diet that removes common allergenic foods) and trials of food elimination may be required to determine the role of foods in a patient's condition, and may also be the treatment.

In addition to diet therapy (or in place of diet therapy), anti-inflammatory medications (eg, corticosteroids) may be needed. Eosinophilic esophagitis appears to be a chronic disease, and fibrosis and stricture formation can occur. Updated diagnostic and treatment approaches have been proposed.^[64]

Food protein–induced enterocolitis

Food protein–induced enterocolitis syndrome (FPIES) typically manifests in the first few months of life with severe projectile vomiting, diarrhea, and failure to thrive.^[8] Cow milk and soy protein formulas are usually responsible for these reactions. However, solid foods may also trigger these reactions, especially rice and oats.^[9]

When the allergen is removed from the diet, symptoms resolve. Re-exposure prior to resolution results in a delayed (about 2 hours) onset of vomiting, lethargy, increase in the peripheral blood polymorphonuclear leukocyte count, and, later, diarrhea. Hypotension and methemoglobinemia may occur.

Infants with FPIES who are chronically ingesting the allergen typically appear lethargic, wasted, and dehydrated. The presentation may mimic sepsis. An oral food challenge may establish the diagnosis but is not always needed if the history is clear. No other definitive diagnostic tests are available.

Milk protein–induced proctocolitis

This allergic proctocolitis does not typically lead to anemia and is not associated with vomiting or poor growth. Maternal exclusion of the allergen resolves the bleeding if the infant is breastfed, and elimination of the cow's milk formula will resolve symptoms in bottle-fed infants. The majority of infants will tolerate cow's milk protein by the first year of life. Eosinophilic inflammation of the rectum is noted if a biopsy is performed.^[10] Additional causes of bleeding (eg, infection, fissures) should be considered.

Food-induced pulmonary hemosiderosis (Heiner syndrome)

This is a rare disorder characterized by recurrent episodes of pneumonia associated with pulmonary infiltrates, hemosiderosis, gastrointestinal blood loss, iron deficiency anemia, and failure to thrive in infants.

While the precise immunologic mechanism is unknown, it is thought to be secondary to a non-IgE hypersensitivity process.

Next: Background

Cross-Reactivity Food Allergy Syndromes

Pollen-food allergy syndrome (oral allergy syndrome)

Patients with this syndrome are sensitized to pollen (allergic rhinitis and/or asthma) that cross-reacts with particular foods, most commonly raw fruits or vegetables. They develop itching or tingling of the lips, tongue, palate, and throat following the ingestion of certain foods. In addition, edema of the lips, tongue, and uvula and a sensation of tightness in the throat may be observed. In fewer than 3% of cases, symptoms progress to more systemic reactions, such as laryngeal edema or hypotension.^[7]

This syndrome is caused by cross-reactivity between certain pollen and food allergens. For example, individuals with ragweed allergy may experience oropharyngeal symptoms following the ingestion of bananas or melons, and patients with birch pollen allergy may experience these symptoms following the ingestion of apple, raw carrots, celery, potato, peach or hazelnut.

Latex food syndrome

This is a cross-reactivity syndrome in persons sensitized (IgE) to natural rubber. Of those patients sensitized to latex, 30%–50% also have reactions to avocado, banana, chestnut, kiwi, peach, tomato, potato, and bell pepper.^{[65, 4]}

Alpha-gal syndrome

This is an IgE-mediated response to the glycan galactose-alpha-1,3-galactose (alpha-gal) primarily associated with hard-bodied tick bites with cross-reactivity to mammalian meats.^[2]

Next: Background

Food-dependent Exercise-induced Anaphylaxis

This syndrome is IgE mediated, but anaphylaxis occurs only when the offending food ingestion is coupled with exercise. Symptoms are primarily angioedema and urticaria, wheezing and shortness of breath, abdominal pain, diarrhea, and vomiting. Symptoms generally occur within the first 30 min of exercise.

It can be a challenge to differentiate this syndrome from exercise induced anaphylaxis not associated with food allergy.

It is treated as any other anaphylaxis is treated, but precautions should include not exercising alone. Epinephrine injector should always be carried during exercise, and a medical alert bracelet is advised.

Although wheat was one of the first food allergens associated with this syndrome multiple foods and alcohol have been associated with this syndrome.^[66]

Next: Background

Prognosis

Many infants and young children outgrow or become clinically tolerant of their early IgE food hypersensitivities, specifically allergies to milk, egg, soy, and wheat. However, allergies to peanut, tree nuts, fish, and shellfish are more persistent.^[67]

Component testing for certain allergens such as peanut and egg can allow prediction of whether or not the IgE allergy to these foods will be permanent and severe or transitory and less severe.^{[18, 19]}

Population-based studies generally show that 85% of young children outgrow their allergy to milk or egg by age 3–5 years.^[67]However, studies reported from a referral center showed more persistence of egg, milk, and soy allergies, with only about 50% of patients resolving these allergies by age 8–12 years.^{[68, 69, 70]}Children continued to lose their allergy into adolescent years.

About 20% of infants and young children experience resolution of their peanut allergy by the time they reach school age.

Children with non-IgE–mediated food allergies, such as proctocolitis and enterocolitis, typically resolve their food allergy in the first years of life.^[71]Eosinophilic esophagitis and eosinophilic gastroenteritis are persistent disorders.^[72]

Morbidity and mortality

Severe anaphylactic reactions from food can result in death.^{[47, 35]}Fatalities result from severe laryngeal edema, irreversible bronchospasm, refractory hypotension, or a combination thereof.

Peanuts, tree nuts, fish, and shellfish are the foods most often implicated in severe food-induced anaphylactic reactions, although anaphylactic reactions to a wide variety of foods have been reported. Fatalities caused by reactions to milk have increasingly been noted.^[35]

Next: Background

Patient Education

Preparation

Patients should always carry a self-injectable epinephrine device that has been properly stored and is current (ie, not expired). Ensure that the patient receives proper training regarding when and how to use the injection device. Patients should also have an H1-blocker medication (again, properly stored and not expired and preferably in a syrup or chewable tablet form) available. In addition, patients should be instructed to obtain immediate medical assistance (eg, call 911) in the event of anaphylaxis.

Caregivers of children should be instructed on identification and treatment of allergic and anaphylactic reactions.

School treatment plans and allergen avoidance plans should be provided to parents of school-age children.^{[27, 73, 74]}

Avoidance of allergens

Complete avoidance of the offending food allergen is the best strategic approach and the only proven therapy once the diagnosis of food hypersensitivity is established. Therefore, patients with food allergies should be taught to recognize relevant food allergens that must be eliminated from their diet.

Instruct the patient about the proper reading of food labels and the need to inquire about food ingredients when dining out. If the patient is in doubt about a food or food ingredient, suggest avoidance of the food in question. Educate patients about the potential for food allergens to be present in medications and cosmetics.

Support groups

Inform patients with food allergies how to identify and use support groups. One such organization is the Food Allergy Research and Education group.

Early detection and treatment

Educate patients regarding recognition of the early signs and symptoms of a food-induced allergic reaction, and provide them with a written management plan for successfully dealing with these reactions.

Write a specific list of clinical signs and symptoms to look for if a reaction may be occurring, and include a clear management plan. An excellent example of such a plan is available on the Food Allergy Research and Education Web site.

Demonstrate to the patient and family how to actually administer medications, especially injectable epinephrine, in the event of an allergic reaction. To accomplish this, use demonstration trainer devices in the clinic setting. Reinforce that if injectable epinephrine is administered, the patient must be immediately evaluated in a medical setting.

Clinical Presentation

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Author

Elizabeth A Secord, MD Professor (Clinical), Division Chief of Allergy and Immunology, Medical Director of Horizons Project for Pediatric and Adolescent HIV Treatment and Prevention, Director, Primary Immune Deficiency Clinic, Department of Pediatrics, Wayne State University School of Medicine; Physician, Division of Allergy, Immunology and Rheumatology, Children's Hospital of Michigan (Detroit Medical Center)

Elizabeth A Secord, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American Academy of Pediatrics, American College of Allergy, Asthma and Immunology, American Medical Association, Clinical Immunology Society, Michigan Allergy and Asthma Society

Disclosure: Received research grant from: Novavax; pfizer; gilead.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Michael A Kaliner, MD Clinical Professor of Medicine, George Washington University School of Medicine; Medical Director, Institute for Asthma and Allergy

Michael A Kaliner, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American Association of Immunologists, American College of Allergy, Asthma and Immunology, American Society for Clinical Investigation, American Thoracic Society, Association of American Physicians

Disclosure: Nothing to disclose.

Additional Contributors

Scott H Sicherer, MD Professor of Pediatrics, Jaffe Food Allergy Institute, Mount Sinai School of Medicine of New York University

Scott H Sicherer, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American Academy of Pediatrics

Disclosure: Nothing to disclose.

Acknowledgements

Dan Atkins, MD Assistant Professor, Department of Pediatrics, University of Colorado Health Sciences Center; Head, Division of Ambulatory Pediatrics, Department of Pediatrics, Director, Pediatric Day Program, National Jewish Medical and Research Center

Dan Atkins, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology and American Thoracic Society

Disclosure: Nothing to disclose.

Stephen C Dreskin, MD, PhD Professor of Medicine, Departments of Internal Medicine, Director of Allergy, Asthma, and Immunology Practice, University of Colorado Health Sciences Center

Stephen C Dreskin, MD, PhD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American Association for the Advancement of Science, American Association of Immunologists, American College of Allergy, Asthma and Immunology, Clinical Immunology Society, and Joint Council of Allergy, Asthma and Immunology

Disclosure: Genentech Consulting fee Consulting; American Health Insurance Plans Consulting fee Consulting; Johns Hopkins School of Public Health Consulting fee Consulting; Array BioPharma Consulting fee Consulting

John M James, MD Consulting Staff, Department of Pediatrics, Department of Allergy and Immunology, Colorado Allergy and Asthma Centers, PC

John M James, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Allergy Asthma and Immunology, American Academy of Pediatrics, American College of Allergy, Asthma and Immunology, American Medical Association, Colorado Medical Society, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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