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## Complete Summary

#### GUIDELINE TITLE

Food allergy: a practice parameter.

#### BIBLIOGRAPHIC SOURCE(S)

American College of Allergy, Asthma, & Immunology. Food allergy: a
practice parameter. Ann Allergy Asthma Immunol 2006 Mar;96(3 Suppl
2):S1-68. \[682 references\]
[PubMed](http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16597066)

#### GUIDELINE STATUS

This is the current release of the guideline.

### COMPLETE SUMMARY CONTENT

 SCOPE\
 METHODOLOGY - including Rating Scheme and Cost Analysis\
 RECOMMENDATIONS\
 EVIDENCE SUPPORTING THE RECOMMENDATIONS\
 BENEFITS/HARMS OF IMPLEMENTING THE GUIDELINE RECOMMENDATIONS\
 QUALIFYING STATEMENTS\
 IMPLEMENTATION OF THE GUIDELINE\
 INSTITUTE OF MEDICINE (IOM) NATIONAL HEALTHCARE QUALITY REPORT
CATEGORIES\
 IDENTIFYING INFORMATION AND AVAILABILITY\
 DISCLAIMER

### SCOPE

#### DISEASE/CONDITION(S)

Food allergy, defined as a condition caused by an immunoglobulin E
(IgE)-mediated reaction to a food substance

#### GUIDELINE CATEGORY

Diagnosis\
Evaluation\
Management\
Prevention\
Risk Assessment\
Treatment

#### CLINICAL SPECIALTY

Allergy and Immunology\
Emergency Medicine\
Family Practice\
Internal Medicine\
Pediatrics\
Preventive Medicine

#### INTENDED USERS

Health Care Providers\
Physicians

#### GUIDELINE OBJECTIVE(S)

To improve the care of patients by providing the practicing physician
with an evidence-based approach to the diagnosis and management of
immunoglobulin E (IgE)-mediated (allergic) food reactions

#### TARGET POPULATION

Patients with food allergy or suspected of having food allergy

#### INTERVENTIONS AND PRACTICES CONSIDERED

**Diagnosis**

1.  Patient history (including diet records)

2.  Physical examination

3.  Skin prick or puncture tests

4.  Serum tests for food specific immunoglobulin E (IgE) antibody

5.  Oral challenge testing

6.  Trial elimination diet

7.  Periodic reassessment of food allergy

8.  Tests for differential diagnosis of non-IgE mediated adverse
    reactions to food

**Management/Treatment**

1.  Food avoidance

2.  Education of patients and caregivers in dietary management

3.  Injectable epinephrine

4.  Policies at schools and childcare centers for facilitating allergy
    avoidance and ensuring prompt treatment of food anaphylaxis

5.  Counseling of patients to inform restaurant workers about food
    allergies

6.  Counseling of patients with food-dependent exercise-induced
    anaphylaxis to avoid exercise in proximity to food consumption,
    carry self-injectable epinephrine, exercise with a \"buddy,\" and
    wear medic-alert jewelry

**Risk Assessment**

1.  Family history screening for atopy, or food allergy in particular

**Prevention**

1.  Breast feeding

2.  Maternal dietary restrictions

3.  Delayed introduction of solid or particular allergenic foods

4.  Use of supplemental hypoallergenic or reduced allergenicity infant
    formulae

5.  Avoidance of tobacco smoke

#### MAJOR OUTCOMES CONSIDERED

-   Rate of food allergy in various populations

-   Sensitivity and specificity of diagnostic tests

### METHODOLOGY

#### METHODS USED TO COLLECT/SELECT EVIDENCE

Searches of Electronic Databases

#### DESCRIPTION OF METHODS USED TO COLLECT/SELECT THE EVIDENCE

Preparation of this draft included a review of the medical literature
using a variety of search engines such as PubMed.

#### NUMBER OF SOURCE DOCUMENTS

Not stated

#### METHODS USED TO ASSESS THE QUALITY AND STRENGTH OF THE EVIDENCE

Weighting According to a Rating Scheme (Scheme Given)

#### RATING SCHEME FOR THE STRENGTH OF THE EVIDENCE

**Ia** Evidence from meta-analysis of randomized controlled trials

**Ib** Evidence from at least one randomized controlled trial

**IIa** Evidence from at least one controlled study without
randomization

**IIb** Evidence from at least one other type of quasi-experimental
study

**III** Evidence from nonexperimental descriptive studies, such as
comparative studies, correlation studies, and case-control studies

**IV** Evidence from expert committee reports, opinions or clinical
experiences of respected authorities, or both

**LB** Evidence from laboratory-based studies

#### METHODS USED TO ANALYZE THE EVIDENCE

Systematic Review

#### DESCRIPTION OF THE METHODS USED TO ANALYZE THE EVIDENCE

Published clinical studies were rated by category of evidence and used
to establish the strength of a clinical recommendation.

#### METHODS USED TO FORMULATE THE RECOMMENDATIONS

Expert Consensus

#### DESCRIPTION OF METHODS USED TO FORMULATE THE RECOMMENDATIONS

This guideline was developed by the Joint Task Force on Practice
Parameters, which has published 20 practice parameters for the field of
allergy-immunology (see list of publications in the \"Acknowledgments\"
section of the original Guideline document). The three national allergy
and immunology societies (the American College of Allergy, Asthma and
Immunology \[ACAA\], the American Academy of Allergy, Asthma, and
Immunology \[AAAAI\], and the Joint Council of Allergy, Asthma and
Immunology \[JCAAI\]) have given the Joint Task Force the responsibility
for both creating new parameters and updating existing parameters.
Although several previous parameters have addressed the diagnosis and
management of anaphylaxis, this document is the first parameter that
focuses on such reactions with respect to foods. It was written and
reviewed by specialists in the field of allergy and immunology and was
supported by the three allergy and immunology organizations noted above.

This document represents an evidence-based, broadly accepted consensus
opinion.

#### RATING SCHEME FOR THE STRENGTH OF THE RECOMMENDATIONS

A.  Directly based on category I evidence

B.  Directly based on category II evidence or extrapolated
    recommendation from category I evidence

C.  Directly based on category III evidence or extrapolated
    recommendation from category I or II evidence

D.  Directly based on category IV evidence or extrapolated
    recommendation from category I, II, or III evidence

E.  Directly based on category LB evidence

F.  Based on consensus of the Joint Task Force on Practice Parameters

#### COST ANALYSIS

A formal cost analysis was not performed and published cost analyses
were not reviewed.

#### METHOD OF GUIDELINE VALIDATION

Peer Review

#### DESCRIPTION OF METHOD OF GUIDELINE VALIDATION

The working draft of the Parameter was reviewed by a number of experts
on food allergy selected by the supporting organizations.

### RECOMMENDATIONS

#### MAJOR RECOMMENDATIONS

This practice parameter includes an algorithm on the diagnosis and
management of food allergy accompanied by annotations (numbered to
correspond with the algorithm). Guideline recommendations are presented
in the form of summary statements. After each statement is a letter in
parentheses that indicates the strength of the recommendation.
Categories of evidence (Ia, Ib, IIa, IIb, III, IV, LB) and strength of
recommendations (A-F) are defined at the end of the \"Major
Recommendations\" field.

**[Annotations]{.underline}**

1.  Adverse reactions to food are common in the population. In contrast,
    food allergy represents a small percentage of all adverse reactions
    to food. The proper diagnosis and subsequent management of food
    allergy rely heavily on historical features of the adverse reaction.
    The following historical information should be obtained: (1)
    identification of the suspect food or foods, (2) the amount of time
    between ingestion of the food and development of symptoms, (3)
    symptoms attributed to the food, (4) amount of food required for a
    reaction, (5) reproducibility of symptoms on prior or subsequent
    ingestion, (6) requirement for other cofactors (e.g., exercise),
    and (7) length of time from last reaction. After a detailed history
    has been obtained, a determination of whether the adverse reaction
    to food is likely to be immunoglobulin E (IgE) mediated or IgE
    associated is essential.

2.  There are several historical features that are suggestive of an
    IgE-mediated food reaction. Manifestations of an IgE-mediated
    reaction may include pruritus, urticaria or angioedema,
    gastrointestinal symptoms, rhinoconjunctivitis, bronchospasm, and
    anaphylaxis. Symptoms of oral allergy syndrome are usually
    restricted to the oropharynx and include pruritus, tingling, and
    angioedema of the lips, tongue, palate, and throat.
    Rhinoconjunctivitis or asthma as a sole manifestation of food
    allergy is rare; however, these symptoms occur commonly in
    association with other manifestations in food allergy. The time from
    ingestion to symptom onset in food allergy is typically rapid,
    usually within minutes, but may be delayed up to an hour and rarely
    up to a few hours. In addition, small quantities of food may elicit
    even severe reactions. Re-exposure also provokes a reaction.

> IgE-associated food reactions such as those triggering atopic
> dermatitis are more difficult to discern by history alone. The
> symptoms seen with IgE-associated reactions in atopic dermatitis are
> primarily pruritus and papulovesicular eruptions. These symptoms may
> develop minutes to hours after ingestion of the food.

3.  Only a minority of adverse reactions to food are IgE mediated or IgE
    associated. Some adverse reactions to foods may be immune mediated
    but not involve IgE in their pathogenesis. Examples include
    gastrointestinal reactions (e.g., food-induced enterocolitis, celiac
    disease, Crohn disease), cutaneous reactions (e.g., dermatitis
    herpetiformis), and pulmonary reactions (Heiner syndrome).
    Nonimmunologic food reactions include diverse entities such as
    lactose intolerance, food poisoning, and scombroid poisoning. The
    evaluation for these non-IgE-mediated reactions may include
    diagnostic procedures such as food challenge, skin biopsy, stool
    cultures, and gastrointestinal biopsy. Specific evaluation for each
    of these non-IgE-mediated reactions is discussed in further detail
    in the \"Differential Diagnosis of Adverse Reactions to Food\"
    section of the original guideline document.

4.  If the history is consistent with an IgE-mediated or IgE-associated
    food reaction, specific IgE testing is the next step. Methods of
    testing for food-specific IgE include percutaneous skin testing
    (PSTs) (prick or puncture) and serum tests for specific IgE. Both
    methods offer high sensitivity and are therefore useful in helping
    exclude a diagnosis of food allergy. The PSTs and serum tests for
    specific IgE are only moderately specific, and therefore other
    diagnostic evaluation is typically required. Intracutaneous
    (intradermal) skin tests for foods are potentially dangerous, overly
    sensitive (increasing the rate of a false-positive test result), and
    not recommended. Commercial food extracts (except for some raw
    fruits and vegetables) typically are adequate to detect specific IgE
    in most cases of food allergy. In the case of pollen food-related
    reactions, testing with the fresh food may provide greater
    sensitivity. For example, for food reactions that involve raw fruits
    or vegetables, the PST can be performed using liquid foods, by
    creating an in-house extract, or using a prick-prick technique
    (pricking the fruit and then the patient, thereby transferring the
    soluble fruit proteins). These techniques may offer greater
    sensitivity and hence a higher negative predictive value to exclude
    food allergy.

5.  Even in a patient whose history is suggestive of an IgE-mediated
    reaction, if testing for food-specific IgE is negative, the patient
    will likely tolerate the food. In some cases of atopic dermatitis,
    particularly in infants, reactions to foods may occur in the absence
    of detectable IgE. In cases where the reaction to the food was more
    severe, an open challenge to the negatively tested food may be
    considered to definitively exclude food allergy. Oral challenges can
    elicit severe, anaphylactic reactions, so the physician should be
    prepared with appropriate emergency medications and equipment to
    promptly treat such a reaction.

6.  In patients whose food reaction was that of anaphylaxis and test
    results for food specific IgE are positive, no further evaluation is
    typically required. The risk of a potentially severe reaction on
    food challenge in such a patient warrants a more prudent approach of
    eliminating the food.

> For a few foods, increasingly higher concentrations of food specific
> IgE antibody, reflected by larger PST responses or high serum IgE
> antibody concentrations, are correlated with increasing risks for
> clinical reactions. However, for most foods, types of reactions, and
> age groups, diagnostic thresholds for clinical correlations have not
> been established.

7.  Once the diagnosis of food allergy has been established, the only
    proven therapy is strict avoidance of the specific food. Patients
    and families need to be educated to avoid unintentional ingestion of
    food allergens. Reading food labels and recognition of the
    unfamiliar terms used in labeling constituents that may indicate the
    presence of a given food allergen is essential. Vague or inaccurate
    labeling of foods and cross-contamination at the time of packaging
    or during food preparation (especially in restaurant settings) are
    other potential hazards in food avoidance. Strict food avoidance is
    usually a complex task and additional educational resources may be
    required, such as those available through the Food Allergy and
    Anaphylaxis Network (Fairfax, VA, 1-800-929-4040 or
    [http://www.foodallergy.org](http://www.foodallergy.org/)). For
    patients with a history of anaphylaxis (or reactions with
    anaphylactic potential), self-injectable epinephrine should be
    prescribed and patients should be instructed on its proper use.
    Additionally, identification of risks by cards or jewelry, such as
    MedicAlert, should be considered.

8.  In patients with a history of anaphylaxis after ingesting a specific
    food who have specific IgE to that food, food avoidance is
    recommended. If these patients continue to have anaphylactic
    reactions despite avoiding the culprit food, further evaluation is
    required. Detailed food diaries, including specific ingredient lists
    of prepared meals resulting in anaphylaxis, should be obtained by
    the patient and reviewed by the physician. Details of other
    cofactors, such as relationship to exercise, should also be
    obtained. In many cases, given the complexity of food avoidance, the
    patient may still be inadvertently ingesting the allergenic food.
    Inadvertent ingestion of \"hidden foods\" due to improper or
    imprecise labeling or cross-contamination is a well-known pitfall in
    food avoidance. In some cases, patients may be reacting to
    cross-reacting foods. Proper identification of potential
    cross-reacting foods and additional avoidance of these foods would
    also be required. In other cases, the specific IgE detected to the
    culprit food may have detected sensitization or the presence of IgE
    that is not clinically relevant. Another unidentified food allergen
    or even idiopathic anaphylaxis may be the true cause of recurrent
    anaphylaxis.

> In patients with persistent symptoms despite strict avoidance of the
> food, an oral food challenge could be considered to prove or disprove
> that the culprit food is indeed the causative allergen in the
> patient\'s recurrent symptoms. For patients with presumed food-induced
> anaphylaxis, either an open or blinded food challenge could be
> performed cautiously.
>
> In other IgE-mediated reactions to certain foods, the level of
> specific IgE or size of the wheal-and-flare reaction on PST in certain
> instances may add enough diagnostic and prognostic information to
> warrant food avoidance even in the absence of a history of
> anaphylaxis. Further evaluation is required in these patients without
> a history of food anaphylaxis who have been avoiding a food based on a
> diagnostic test yet continue to have symptoms. Given the complexity of
> food avoidance, the patient may still be inadvertently ingesting the
> allergenic food or cross-reacting food(s). In other patients without a
> history of food anaphylaxis, the diagnostic test, although highly
> predictive, may not be completely predictive and might give a
> false-positive result (e.g., sensitization without clinical
> relevance). For example, in a limited number of foods and age groups,
> a given level of food-specific IgE may yield a 95% likelihood of a
> positive challenge to that food. However, 5% of patients with this
> same level of specific IgE may be able to tolerate the food without
> symptoms.
>
> In patients without a history of food anaphylaxis who have been
> avoiding a food based on a diagnostic test, oral challenge to that
> food can also be performed. In these circumstances a blinded food
> challenge would typically be preferred. In these patients with food
> specific IgE who remain symptomatic despite avoidance, if the oral
> challenge result is positive, true food allergy is indicated and
> usually suggests that food avoidance has not been complete. Rarely,
> another food may be the causative factor and a food diary may help
> identify another culprit food allergen. In contrast, if the food
> challenge result is negative, despite the presence of food specific
> IgE, other causes of the symptoms should be sought and the negatively
> challenged food may be added back to the diet.

9.  For most patients being evaluated for food allergy, there is neither
    a history of anaphylaxis nor a highly predictive, diagnostic test
    result. For these patients, further evaluation is typically required
    before diagnosing a food allergy simply based on a positive food
    specific IgE test result. Oral food challenges provide the most
    definitive means to diagnose an adverse reaction to food and are
    particularly useful in patients with episodic symptoms suggestive of
    food allergy. Although oral food challenges offer a more precise
    method for diagnosing food allergy, the complexities involved with
    oral food challenges may not be suitable for all clinical
    situations. In the evaluation of disorders with chronic symptoms
    where foods may be causal (atopic dermatitis, gastrointestinal
    symptoms), elimination of suspected causal foods may be undertaken
    to prove the concept that symptoms are diet responsive.

10. Oral food challenges provide the most definitive means to diagnose
    food allergy. These include open challenges or placebo-controlled
    blinded challenges in which the food or a placebo is masked in a
    carrier food or opaque capsules. Blinded challenges can be performed
    in a single-blind fashion, where the patient is unaware of the
    content of the test substances, or a double-blind fashion, where
    neither patient nor physician is aware of the content of the tested
    substances. Food challenges in patients with specific IgE have the
    potential to elicit serious reactions, including anaphylaxis.
    Therefore, these challenges should be performed in a controlled
    setting where emergency supplies for the treatment of anaphylaxis
    are readily available. The supplies in this setting are similar to
    those required for safe administration of allergen immunotherapy
    (see Practice Parameters for Practice Allergen Immunotherapy).

> Open challenges may be preferred in certain situations. Since they are
> the simplest to perform, in cases where multiple foods are in
> question, foods tolerated in an open challenge can be excluded. Since
> the open challenge is most prone to bias, positive results must be
> viewed with caution. Foods that result in physiologically relevant
> symptoms can be further investigated in a blinded controlled
> challenge.
>
> Single-blind challenges offer another method for food challenges.
> There are several advantages of single-blind food challenges. As
> opposed to an open challenge, the single-blind challenge helps
> eliminate patient bias. Single-blind challenges are technically easier
> to perform, since they do not involve an additional unblinded
> participant to prepare the placebo and active doses. Single-blind
> challenges have more flexibility in design, such as the addition of
> multiple initial placebo doses. This can be particularly helpful in
> patients in whom food reactions are not causally related to foods.
>
> The double-blind placebo-controlled food challenge remains the gold
> standard for the diagnosis of food allergy. Although the single-blind
> challenge helps eliminate patient bias, the individual(s) performing
> the food challenge have the potential to be biased in the
> interpretation of the results. Nevertheless, double-blind
> placebo-controlled food challenges are usually not necessary in most
> clinical situations but remain an essential tool in food allergy
> research.
>
> If a double-blind placebo-controlled food challenge result is
> positive, in most cases this indicates food allergy and food
> elimination is recommended. In contrast, a positive single-blind or
> open challenge does not necessarily indicate a true food allergy. In
> cases of a positive single-blind or open food challenge where doubt
> exists, a double-blind placebo-controlled challenge could be
> performed. Especially in cases where the positive challenge result is
> based on subjective symptoms (e.g., pruritus, dyspnea), blinded
> challenges may need to be performed to help prove causality. In
> blinded challenges, technical limitations exist, such as quantity of
> food required for reaction, ability to mask food, and if the test food
> has been eliminated for 2 weeks before the challenge (see \"Diagnosis
> of Food Allergy\" section in the original guideline document).
>
> A negative food challenge result indicates that the food-specific IgE
> is not clinically relevant and the tested food is not responsible for
> the patient\'s symptoms. In cases of negative results after blinded
> food challenges, particularly if foods are encapsulated, an open
> challenge with the food in its \"natural\" state may be required to
> ensure tolerability of the food.

11. Same as Annotation 7.

12. If a patient has no reaction on oral challenge to the incriminated
    food, the tested food is likely to be well tolerated. Nevertheless,
    to help exclude false-negative results, it has long been suggested
    to include an open feeding under supervision of a meal-size portion
    of the tested food prepared in its usual manner as a follow-up to
    any negative double-blind, placebo-controlled food challenge. It is
    also important to appreciate that certain preparation methods
    (canning, dehydration) may alter the allergens; hence, an open
    challenge with a meal-size portion of the food prepared in its
    natural state for consumption following a negative double-blind,
    placebo-controlled food challenge may be helpful.

13. Because of the poor positive predictive value of food-specific IgE
    tests, a positive test result does not always equate with clinical
    food allergy. Trial elimination diets are diagnostic and therapeutic
    procedures that may be used in patients with presumed food allergy.
    Elimination diets are particularly helpful in cases where several
    culprit allergens have been identified based on positive food
    specific IgE tests, since food challenges would need to be done
    individually to the multiple foods and can be time-consuming.

14. In patients who have symptoms suggestive of food allergy and
    specific IgE to a food or foods, improvement or resolution of
    symptoms following food elimination provides supporting evidence for
    causality. Nevertheless, a placebo effect should be considered. In
    cases where diagnostic uncertainty exists, a blinded food challenge
    may be performed to confirm a true food allergy.

15. Most children allergic to egg, milk, wheat, and/or soy lose their
    sensitivity within the first 3 to 5 years of life. Although
    food-specific IgE generally declines with the onset of clinical
    tolerance, many children who become clinically tolerant of a food
    may still have specific IgE. Food challenges may also be required to
    determine if tolerance has developed. Approximately 20% of children
    with peanut allergy may lose their sensitivity over time. Since
    peanut is a food frequently associated with anaphylaxis, care must
    be taken to select patients for peanut challenge.

**[Summary Statements]{.underline}**

**Mucosal Immune Responses Induced by Foods**

1.  Mucosal adaptive immunity has dual functions of protection against
    enteric pathogens and maintenance of autotolerance against dietary
    proteins and commensal bacteria. (E)

2.  Factors that regulate gastrointestinal immune balance include the
    nature and dose of the antigen, immaturity of the host, genetic
    susceptibility, the rate of absorption of a dietary protein, and the
    conditions of antigen processing. (E)

3.  Food allergens are generally glycoproteins with molecular weights
    ranging from 10 kDa to 70 kDa. (E)

4.  The more common food allergens in infants and young children are
    cow\'s milk, hen\'s egg, peanut, tree nuts, soybeans, and wheat,
    whereas the adult counterparts are peanuts, tree nuts, fish,
    crustaceans, mollusks, fruits, and vegetables. (B)

5.  Major allergenic epitopes have been identified and genes for some of
    the major allergens have been cloned and sequenced. (E)

6.  Innate allergenicity of foods may be determined by a combination of
    factors such as solubility, resistance to pH, heat, and proteolysis
    by digestive enzymes. (E)

7.  Structural amino acid sequences, either sequential or
    conformational, account for cross-reactivity between foods.
    Sequential epitopes may be particularly important for persistence of
    allergenicity beyond childhood (e.g., casein hypersensitivity). (B)

8.  The specific factor(s) that confer allergenicity rather than
    tolerogenicity are unknown. (E)

9.  Characteristic IgE- and mast cell-mediated mechanisms occur in
    food-induced anaphylaxis, the oral allergy syndrome, and atopic
    dermatitis. (B)

10. IgE-mediated reactions to foods may occur in neonates on first
    postnatal exposure, presumably due to in utero sensitization. Since
    sensitization to dietary allergens in breast milk may occur in the
    late postnatal period, breastfeeding mothers should avoid highly
    allergenic foods if familial allergic susceptibility is present. (B)

11. Both serum and secretory specific immunoglobulin A (IgA) to dietary
    proteins may be produced in healthy subjects and allergic patients.
    (B)

12. The significance of immunoglobulin M (IgM), immunoglobulin G (IgG),
    and IgG subclass antibodies (e.g., the role of IgG4) in food allergy
    is less well understood and highly controversial. (B)

13. The role of cellular in vitro correlates as diagnostic or prognostic
    indicators of food allergy is not established. (B)

14. The role of specific cytokine profiles in serum or peripheral
    mononuclear cells of food allergic patients has not been established
    in the mechanism of food allergy. (B)

15. Certain bacterial products, viruses, parasites, and
    T-cell-independent antigens stimulate systemic immune responses
    rather than tolerance to the oral protein when coadministered with
    oral proteins. (B)

16. Sensitization to foods is much more likely to occur in the early
    neonatal period. (B)

17. Intestinal malabsorption and/or stasis may predispose patients to
    food allergy. (B)

18. Genetic susceptibility, as defined by single nucleotide
    polymorphisms or specific haplotypes, has been implicated in several
    common food allergy phenotypes. (B)

**The Clinical Spectrum of Food Allergy**

19. Allergic food reactions to foods (IgE-mediated reactions) are
    characterized by a temporal relationship between the reaction and
    prior exposure to food. Such reactions can be generalized or
    localized to a specific organ system and can be sudden, unexpected,
    severe, and life-threatening. (D)

20. Food allergens are a frequent cause of severe anaphylaxis,
    particularly in patients with concomitant asthma and allergy to
    peanut, nut, or seafood. Such reactions may be biphasic or
    protracted. Food allergy should be considered in the differential
    diagnosis of patients who have idiopathic anaphylaxis. (C)

21. The pollen-food allergy syndrome (oral allergy syndrome) is
    characterized by the acute onset of oropharyngeal pruritus,
    sometimes including lip angioedema, usually beginning within a few
    minutes after oral mucosal contact with particular raw fruits and
    vegetables during eating. (B)

22. IgE-mediated gastrointestinal reactions can present with only
    gastrointestinal symptoms or with other nongastrointestinal
    manifestations. (D)

23. Allergic eosinophilic gastroenteritis (eosinophilic
    gastroenteropathy) is characterized by postprandial gastrointestinal
    symptoms associated with weight loss in adults and failure to thrive
    in infants. (C)

24. Upper and lower respiratory tract manifestations of IgE-mediated
    reactions to foods, such as rhinoconjunctivitis, laryngeal edema,
    and asthma, can occur with or without other IgE-mediated symptoms.
    Isolated respiratory manifestations from exposure to foods are rare
    and have been reported most frequently in an occupational setting.
    (C)

25. Many inhaled food proteins in occupational settings may affect
    workers regularly exposed to such foods as flour (bakers\' asthma),
    egg white, and crustaceans. (A)

26. IgE-mediated cutaneous reactions, such as acute urticaria or
    angioedema and acute contact urticaria, are among the most common
    manifestations of food allergy. Food allergy is commonly suspected
    though rarely incriminated in chronic urticaria and angioedema but
    is implicated in at least one third of children with atopic
    dermatitis. (B)

**Prevalence and Epidemiology**

27. The prevalence of food allergy as reported in double-blind studies
    is not as great as that perceived by the public. It varies between
    2% and 5% in most studies, with definite ethnic differences. (B)

28. The prevalence of food allergy is higher in certain subgroups such
    as individuals with atopic dermatitis, certain pollen sensitivities,
    or latex sensitivity. (B)

**Natural History of Food Allergy**

29. Although sensitivity to most food allergens such as milk, wheat, and
    eggs tends to remit in late childhood, persistence of certain food
    allergies such as peanut, tree nut, and seafood most commonly
    continues throughout one\'s lifetime. (B)

30. The natural history of specific foods varies considerably. (C)

**Risk Factors and Prevention of Food Allergy**

31. The rate of observed food allergy in children born to families with
    parental asthma was approximately 4-fold higher than expected when
    compared with an unselected population. (B)

32. Food allergy prevention strategies include breastfeeding, maternal
    dietary restrictions during breastfeeding, delayed introduction of
    solid foods, delayed introduction of particular allergenic foods,
    and the use of supplemental infant formulae that are hypoallergenic
    or of reduced allergenicity. However, the effectiveness of these
    strategies for safeguarding against the development of food
    allergies has not been established. (B)

**Cross-Reactivity of Food Allergens**

33. Recent studies with molecular biological techniques have
    characterized a variety of cross-reacting allergens among foods. (C)

34. In vitro cross-reactivity to multiple shared food allergens is
    common, but clinical correlation of the cross-reactivity is
    variable. (C)

35. Cow\'s milk allergy is a common disease of infancy and childhood.
    Goat\'s milk cross-reacts with cow\'s milk. Ninety percent of cow\'s
    milk allergic patients will react to goat and/or sheep\'s milk. (A)

36. Hen\'s egg allergens cross-react with certain avian egg allergens,
    but the clinical implications of such cross-reactivity are unclear.
    (B)

37. In vitro cross-reactivity between soybean and other legume foods is
    extensive, but oral food challenges demonstrate that clinical
    cross-reactivity to other legumes in soy bean sensitive children is
    uncommon and generally transitory. (B)

38. Patients with peanut allergy generally tolerate other beans (95%),
    even soy. Evaluation of legume allergy in a patient with peanut
    allergy should be individualized but avoidance of all legumes is
    generally unwarranted. (B)

39. There is significant cross-reaction between different species of
    fish. Although there is limited investigation of the clinical
    relevance of such cross-reactivity, patients who are clinically
    allergic to any species of fish should be cautious about eating fish
    of another species until the clinical relevance of such
    cross-reactions to that species can be demonstrated by an accepted
    food challenge. (B)

40. Crustaceans, such as shrimp, crab, crawfish, and lobster, are a
    frequent cause of adverse food reactions, including life-threatening
    anaphylaxis. There is considerable risk of cross-reactivity between
    crustaceans. Less well defined is cross-reactivity between mollusks
    and crustaceans. (C)

41. Crustaceans do not cross-react with vertebrate fish. (B)

42. Seafood allergy is not associated with increased risk of
    anaphylactoid reaction from radiocontrast media. (F)

43. Patients with wheat allergy alone show extensive in vitro
    cross-reactivity to other grains that is not reflected clinically.
    Therefore, elimination of all grains from the diet (i.e., wheat,
    rye, barley, oats, rice, corn) of a patient with grain allergy is
    clinically unwarranted and may be nutritionally detrimental. (B)

44. Evaluation of cross-reactivity among tree nuts (walnut, hazelnut,
    Brazil nut, pecan) is characterized by shared allergens among tree
    nuts and between tree nuts and other plant-derived foods and pollen.
    Clinical reactions to tree nuts can be severe and potentially fatal
    and can occur from the first exposure to a tree nut in patients
    allergic to other tree nuts. In most cases, elimination of all tree
    nuts from the diet is appropriate. (C)

45. Since the proteins of cacao nut undergo extensive modification into
    relatively nonallergenic complexes during the processing of
    commercial chocolate, clinical sensitivity to chocolate is
    vanishingly rare. (D)

46. Although IgE-mediated reactions to fruits and vegetables are
    commonly reported, clinically relevant cross-reactivity resulting in
    severe reactions is uncommon. (C)

47. The latex-fruit syndrome is the result of cross-reactivity between
    natural rubber latex proteins and fruit proteins. Class 1 chitinases
    (Hev b 6, hevein-like proteins), profilins (Hev b 8), beta-1,
    3-gluconases (Hev b 2), and other cross-reactive polypeptides have
    been implicated. The most commonly reported cross-reactive foods
    include banana, avocado, kiwi, and chestnut, but many other fruits
    and some nuts have been identified in cross-reactivity studies. (D)

48. Seed storage proteins appear to be the main allergens in the edible
    seeds; in particular, 2S albumin family proteins (part of the cereal
    prolamin superfamily) have been demonstrated as allergens in sesame,
    mustard, sunflower, and cottonseed. Cross-reactivity has not been
    well-studied. (E)

**Adverse Reactions to Food Additives**

49. The number of additives used by the food industry is extensive. Only
    a small number of additives have been implicated in IgE-mediated or
    other (immunologic or nonimmunologic) adverse reactions. Adverse
    reactions to food additives, therefore, are rare. (C)

50. Food additives may cause anaphylaxis, urticaria or angioedema, or
    asthma. These reactions can be severe or even life-threatening;
    fatalities have been described. (C).

51. Tartrazine (Federal Food, Drug, and Cosmetic Act \[FD&C\] yellow
    No. 5) sensitivity is extremely rare. There is no convincing
    evidence to support the contention that tartrazine \"cross-reacts\"
    with cyclooxygenase-inhibiting drugs. (B)

52. Monosodium glutamate (MSG) sensitivity is a rare cause of urticaria
    or angioedema. (C) It is also a rare cause of bronchospasm in
    patients with asthma. (B)

53. Sulfites produce bronchospasm in 5% of the asthmatic population, in
    most cases due to generation of sulfur dioxide in the
    oropharynx. (A) Sulfite-induced anaphylaxis has also been described.
    (B)

54. \"Natural\" food additives, including annatto, carmine, and saffron,
    as well as erythritol (ERT; 1,2,3,4-butanetetrol), a sweetener, may
    be rare causes of anaphylaxis. (C)

55. Adverse reactions (anaphylaxis, urticaria or angioedema, or
    bronchospasm) from food additives should be suspected when symptoms
    after food or beverage consumption occur some but not all the time,
    suggesting that the reaction occurs only when an additive is
    present. (C)

56. Management entails avoiding foods or beverages that contain the
    implicated additive and using self-injectable epinephrine for
    life-threatening reactions, especially for individuals who are
    sulfite sensitive. (B)

**Genetically Modified Foods**

57. Many of the major food groups have undergone modification by gene
    manipulation or replacement, and several of these food products are
    currently on grocery store shelves. (C)

58. The possibility exists that transgenic plant proteins in novel
    genetically modified foods could cause severe food allergy,
    including anaphylactic shock, if allergenic determinants (amino acid
    sequences) in the transgenic proteins share a high degree of
    homology to those of known food allergens. (E)

59. As illustrated by recent introduction of corn engineered to contain
    a pesticide, gamma endotoxin (derived from *Bacillus
    thuringiensis*), into the human food chain, food allergy to such
    engineered foods could occur in workers previously exposed and
    sensitized to this endotoxin or in other highly susceptible atopic
    patients. (A)

60. The potential allergenicity of newly developed genetically modified
    foods should be investigated on a case-by-case basis by individual
    commercial developers and appropriate regulatory agencies. (D)

**Diagnosis of Food Allergy**

61. The primary tools available to diagnose adverse reactions to foods
    include history (including diet records), physical examination, skin
    prick or puncture tests, serum tests for food specific IgE
    antibodies, trial elimination diets, and oral food challenges. (B)

62. A detailed dietary history, at times augmented with written diet
    records, is necessary to determine the likelihood that food is
    causing the disorder, identify the potential triggers, and determine
    the potential immunopathophysiology. (D)

63. A physical examination may reveal the presence of atopic disorders,
    such as asthma, atopic dermatitis, and allergic rhinitis, that
    indicate an increased risk for food allergy or reveal alternative
    diagnoses that may reduce the likelihood of food allergy. (C)

64. Tests for food specific IgE antibody include PSTs (prick or
    puncture) and serum assays. These tests are highly sensitive
    (generally \>90%) but only modestly specific (approximately 50%) and
    therefore are well suited for use when suspicion of a particular
    food or foods is high but are poor for the purpose of screening
    (e.g., using panels of tests without consideration of likely
    causes). (B)

65. Intracutaneous (intradermal) skin tests for foods are potentially
    dangerous, overly sensitive (increasing the rate of a false-positive
    test result), and not recommended. (D)

66. Results of PSTs and serum tests for food specific IgE antibody may
    be influenced by patient characteristics (e.g., age), the quality
    and characteristics of reagents (e.g., variations in commercial
    extracts, cross-reacting proteins among food extracts), and
    techniques (e.g., assay types, skin test devices, location of test
    placement, mode of measurement). (B)

67. Increasingly higher concentrations of food specific IgE antibodies
    (reflected by increasingly larger PST response size and/or higher
    concentrations of food-specific serum IgE antibody) correlate with
    an increasing risk for a clinical reaction. (C)

68. A trial elimination diet may be helpful to determine if a disorder
    with frequent or chronic symptoms is responsive to dietary
    manipulation. (D)

69. Graded oral food challenge is a useful means to diagnose an adverse
    reaction to food. (B)

70. A number of additional diagnostic tests are under investigation,
    including atopy patch tests, basophil activation assays, and tests
    for IgE binding to specific epitopes. (E)

71. Some tests, including provocation neutralization, cytotoxic tests,
    IgG antibodies directed to foods, and hair analysis, are either
    disproved or unproven; therefore, they are not recommended for the
    diagnosis of food allergy. (C)

72. Ancillary tests may be needed to confirm the diagnosis of food
    intolerance or immune reactions to foods, such as breath hydrogen
    tests for lactose intolerance or gastrointestinal biopsy to
    determine eosinophilic inflammation or atrophic villi. (D)

73. The rational selection, application, and interpretation of tests for
    food-specific IgE antibodies require consideration of the
    epidemiology and underlying immunopathophysiology of the disorder
    under investigation, the importance of making a definitive
    diagnosis, estimation of prior probability that a disorder or
    reaction is attributable to particular foods, and an understanding
    of the test utility. (D)

**Food-Dependent Exercise-Induced Anaphylaxis (EIA)**

74. Individuals with food-dependent EIA develop neither anaphylaxis with
    ingestion of food without subsequent exercise nor anaphylaxis after
    exercise without temporally related ingestion of food. (A)

75. Two subsets of patients with food-dependent EIA have been described
    (Bock 1987): one subset may develop anaphylaxis when exercising in
    temporal proximity to ingestion of any type of food (Young et al.,
    1994); another subset may experience anaphylaxis with exercise in
    conjunction with ingestion of a specific food. (A)

76. Management of food-dependent EIA entails avoiding exercising in
    proximity to food consumption, carrying self-injectable epinephrine,
    exercising with a \"buddy,\" and wearing medic-alert jewelry. (C)

**Differential Diagnosis of Adverse Reactions to Foods**

77. Non-IgE-mediated immunologic reactions to foods have been implicated
    in such entities as (1) food-induced enterocolitis and colitis, (2)
    malabsorption syndromes (e.g., celiac disease), (3) cow\'s
    milk-induced syndromes, and (4) dermatitis herpetiformis. (C)

78. Food-induced enterocolitis and colitis are most commonly seen in
    infants several hours after ingestion of food proteins, most notably
    those in cow\'s milk or soy formulas. Infants with food-induced
    enterocolitis develop severe protracted vomiting and diarrhea
    compared with infants with food-induced colitis who usually appear
    healthy. Both groups of patients present with blood and eosinophils
    in the stool, although colitis more often presents with gross blood.
    (C)

79. Immune-mediated malabsorption syndromes that result in diarrhea and
    weight loss (or lack of weight gain) may occur secondary to
    intolerance to a variety of food proteins, including those in cow\'s
    milk, soy, wheat, other cereal grains, and eggs. (C)

80. Celiac disease is a severe form of malabsorption characterized by
    total villous atrophy and extensive cellular infiltrates due to an
    immunologic reaction to gliadin, a component of gluten found in
    wheat, oat, rye, and barley. The diagnosis of the disease is
    crucial, since the removal of gluten from the diet can lead to
    reversal of histopathologic changes and recovery of gastrointestinal
    function. (C)

81. In a subset of infants, colic and gastroesophageal reflux disease
    have been attributed to adverse reactions to cow\'s milk. However,
    an immunologic basis for these conditions has not been clearly
    established. (A)

82. Dermatitis herpetiformis is characterized by a chronic, intensely
    pruritic, papulovesicular rash symmetrically distributed over the
    extensor surfaces of the extremities and the buttocks associated
    with gluten ingestion and often with gluten-sensitive enteropathy.
    Direct immunofluorescence or specific immunologic assays may be
    helpful in making the diagnosis. (B)

83. Cow\'s milk-induced pulmonary hemosiderosis (Heiner syndrome) is an
    extremely rare condition in infants and toddlers that also may be
    related to egg or pork hypersensitivity and for which the
    immunopathology is poorly understood. It is characterized clinically
    by recurrent episodes of pneumonia associated with pulmonary
    infiltrates, hemosiderosis, gastrointestinal blood loss,
    iron-deficiency anemia, and failure to thrive. The presence of
    precipitating antibodies to the responsible antigen is necessary but
    not sufficient to make the diagnosis. (C)

84. Toxic food reactions, bacterial contamination of food, and
    pharmacologic food reactions may mimic IgE-mediated reactions and
    should be considered early in the differential diagnosis because of
    the serious nature of such reactions. (C)

85. Pharmacologic adverse food reactions occur after ingestion of foods
    with pharmacologically active substances, such as vasoactive amines,
    in particular histamine (scombroid poisoning), and produce a wide
    range of clinical manifestations, especially gastrointestinal and
    central nervous system in nature. Patients may present with
    flushing, sweating, nausea, vomiting, diarrhea, headache,
    palpitations, dizziness, swelling of the face and tongue,
    respiratory distress, and shock. (C)

86. Enzymatic food reactions are caused by the ingestion of normal
    dietary amounts of foods in individuals susceptible to such
    reactions because of medications, disease states, malnutrition, or
    inborn errors of metabolism (e.g., lactose intolerance). (C)

87. Reactions not related to specific food ingestion but due to the act
    of eating that can be misdiagnosed as reactions to foods include
    gustatory or vasomotor rhinitis, carcinoid syndrome, idiopathic
    anaphylaxis, systemic mastocytosis, inflammatory bowel disease, and
    irritable bowel syndrome. (C)

88. Conditions incorrectly identified as being related to food ingestion
    include multiple sclerosis, attention-deficit disorder, autism and
    other behavioral conditions, chronic fatigue syndrome, and the
    \"yeast connection.\" (C)

**General Management of Food Allergy**

89. The key to the management of patients with food allergy is avoidance
    of foods known to have or suspected of having caused a reaction. (F)

90. Since elimination diets may lead to malnutrition or other serious
    adverse effects (e.g., personality change), every effort should be
    made to ensure that the dietary needs of the patient are met and
    that the patient and/or caregiver(s) are fully educated in dietary
    management. Once the diagnosis of food allergy is confirmed, the
    patient should be advised to avoid eating the food. (D)

91. In some cases, severe allergic reactions may be seen in patients who
    only inhale or come in contact with food allergens, thereby making
    avoidance even more difficult. (D)

92. The successful avoidance of food allergens relies on (1)
    identification in each patient of the specific food that caused the
    reaction; (2) recognition of cross-reacting allergens in other
    foods; (3) education of the patient and/or caregiver about avoidance
    measures, with particular emphasis on hidden food allergens or
    additives; and (4) willingness of the educated patient and/or
    caregiver to read labels carefully, inquire at restaurants, and take
    other measures to prevent inadvertent exposure to known or suspected
    allergens. (D)

93. In selected cases, reevaluation of patients with food allergy may be
    important to determine if food allergy has been lost over time. (F)

94. If there is a history of suspected or proven IgE-mediated systemic
    reactions to foods, injectable epinephrine should be given to
    patients and/or caregivers to carry with them and they should be
    instructed in its use. (F)

95. Prophylactic medications have not been shown to be effective in
    consistently preventing severe, life-threatening reactions to foods
    and may mask a less severe IgE-mediated reaction to a food,
    knowledge of which could prevent a more severe reaction to that food
    in the future. (D)

**Management in Special Settings and Circumstances**

96. Fatal and near-fatal food anaphylactic reactions tend to occur away
    from home after an unintentional ingestion of a food allergen by
    individuals with a known allergy to the same food. (C)

97. Delay in the administration of injectable epinephrine is a common
    feature of fatal food allergic reactions. (C)

98. Peanut and tree nuts account for most fatal and near-fatal food
    allergic reactions in the United States. (C)

99. Allergic reactions that result from direct skin contact with food
    allergens are generally less severe than reactions due to allergen
    ingestion. Reactions that result from inhalation of food allergens
    are generally less frequent and less severe than reactions caused by
    either direct skin contact or ingestion. Exceptions to these
    generalizations are more likely in occupational environments and
    other settings in which food allergen sensitization occurred via
    either inhalation or skin contact. (B)

100. Schools and childcare centers should have policies for facilitating
     food allergen avoidance, including staff education regarding label
     reading and cross-contamination, prohibition of food or utensil
     sharing, and increased staff supervision during student meals. (D)

101. Schools and childcare centers should have policies ensuring prompt
     treatment of food anaphylaxis, including a requirement for
     physician-prescribed treatment protocols for food allergic
     students, staff education regarding recognition and treatment of
     anaphylaxis, and the ready availability of injectable epinephrine.
     (D)

102. It is important to inform workers in a restaurant or other food
     establishment about a history of a systemic food allergic reaction,
     although this does not ensure that the meal will be free of the
     offending food. (C)

103. Allograft transplant recipients may acquire specific food allergic
     sensitivities from organ donors. (B)

104. Patients with latex allergy have an increased risk of experiencing
     IgE-mediated food-induced symptoms, including anaphylaxis,
     particularly when ingesting banana, avocado, kiwi, or chestnut. (C)

**[Definitions]{.underline}**:

**Category of Evidence**

**Ia** Evidence from meta-analysis of randomized controlled trials

**Ib** Evidence from at least one randomized controlled trial

**IIa** Evidence from at least one controlled study without
randomization

**IIb** Evidence from at least one other type of quasi-experimental
study

**III** Evidence from nonexperimental descriptive studies, such as
comparative studies, correlation studies, and case-control studies

**IV** Evidence from expert committee reports, opinions or clinical
experiences of respected authorities, or both

**LB** Evidence from laboratory-based studies

**Strength of Recommendation**

A.  Directly based on category I evidence

B.  Directly based on category II evidence or extrapolated
    recommendation from category I evidence

C.  Directly based on category III evidence or extrapolated
    recommendation from category I or II evidence

D.  Directly based on category IV evidence or extrapolated
    recommendation from category I, II, or III evidence

E.  Directly based on category LB evidence

F.  Based on consensus of the Joint Task Force on Practice Parameters

#### CLINICAL ALGORITHM(S)

\"Algorithm for Diagnosis and Management of Food Allergy\" is provided
in the original guideline document.

### EVIDENCE SUPPORTING THE RECOMMENDATIONS

#### REFERENCES SUPPORTING THE RECOMMENDATIONS

[References open in a new
window](http://www.guideline.gov/summary/select_ref.aspx?doc_id=9218)

#### TYPE OF EVIDENCE SUPPORTING THE RECOMMENDATIONS

The type of supporting evidence is identified and graded for each
summary statement (see \"Major Recommendations\" field).

### BENEFITS/HARMS OF IMPLEMENTING THE GUIDELINE RECOMMENDATIONS

#### POTENTIAL BENEFITS

-   Improved quality of care in the prevention, diagnosis, and
    management of food allergies

-   Reduced morbidity and mortality related to food allergy or
    misdiagnosis of food allergy

#### POTENTIAL HARMS

Elimination diets may lead to malnutrition or other serious adverse
effects (e.g., personality change). Every effort should be made to
ensure that the dietary needs of the patient are met and that the
patient and/or caregiver(s) are fully educated in dietary management.

### QUALIFYING STATEMENTS

#### QUALIFYING STATEMENTS

-   This is a complete and comprehensive document at the current time.
    These clinical guidelines are designed to assist clinicians by
    providing a framework for the evaluation and treatment of patients
    and are not intended to replace a clinician\'s judgment or establish
    a protocol for all patients. The medical environment is a changing
    environment and not all recommendations will be appropriate for all
    patients. Because this document incorporated the efforts of many
    participants, no single individual, including those who served on
    the Joint Task Force, is authorized to provide an official American
    Academy of Allergy, Asthma and Immunology (AAAAI) or American
    College of Allergy, Asthma and Immunology (ACAAI) interpretation of
    these practice parameters. Any request for information about or an
    interpretation of these practice parameters by the AAAAI or the
    ACAAI should be directed to the Executive Offices of the AAAAI, the
    ACAAI, and the Joint Council of Allergy, Asthma and Immunology.
    These parameters were developed by the Joint Task Force on Practice
    Parameters, representing the American Academy of Allergy, Asthma and
    Immunology, the American College of Allergy, Asthma and Immunology,
    and the Joint Council of Allergy, Asthma and Immunology. These
    parameters are not designed for use by pharmaceutical companies in
    drug promotion.

-   This parameter was edited by Dr. Nicklas in his private capacity and
    not in his capacity as a medical officer with the Food and Drug
    Administration. No official support or endorsement by the Food and
    Drug Administration is intended or should be inferred.

### IMPLEMENTATION OF THE GUIDELINE

#### DESCRIPTION OF IMPLEMENTATION STRATEGY

An implementation strategy was not provided.

#### IMPLEMENTATION TOOLS

Clinical Algorithm

For information about
[availability](#identifying-information-and-availability), see the
\"Availability of Companion Documents\" and \"Patient Resources\" fields
below.

### INSTITUTE OF MEDICINE (IOM) NATIONAL HEALTHCARE QUALITY REPORT CATEGORIES

#### IOM CARE NEED

Getting Better\
Living with Illness\
Staying Healthy

#### IOM DOMAIN

Effectiveness\
Patient-centeredness

### IDENTIFYING INFORMATION AND AVAILABILITY

#### BIBLIOGRAPHIC SOURCE(S)

American College of Allergy, Asthma, & Immunology. Food allergy: a
practice parameter. Ann Allergy Asthma Immunol 2006 Mar;96(3 Suppl
2):S1-68. \[682 references\]
[PubMed](http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16597066)

#### ADAPTATION

Not applicable: The guideline was not adapted from another source.

#### DATE RELEASED

2006 Mar

#### GUIDELINE DEVELOPER(S)

American Academy of Allergy, Asthma and Immunology - Medical Specialty
Society\
American College of Allergy, Asthma and Immunology - Medical Specialty
Society\
Joint Council of Allergy, Asthma and Immunology - Medical Specialty
Society

#### SOURCE(S) OF FUNDING

Funded by the American Academy of Allergy, Asthma, and Immunology
(AAAAI), the American College of Allergy, Asthma, and Immunology
(ACAAI), and the Joint Council of Allergy, Asthma and Immunology
(JCAAI).

#### GUIDELINE COMMITTEE

Joint Task Force on Practice Parameters

#### COMPOSITION OF GROUP THAT AUTHORED THE GUIDELINE

*Chief Editors*: Jean A. Chapman, MD, Cape Girardeau, MO; I. Leonard
Bernstein, MD, Departments of Medicine & Environmental Health,
University of Cincinnati College of Medicine, Cincinnati, OH; Rufus E.
Lee, MD, Dothan, AL; John Oppenheimer, MD, Department of Medicine,
UMDNJ-New Jersey Medical School, New Brunswick, NJ

*Associate Editors*: Richard A. Nicklas, MD, Department of Medicine,
George Washington Medical Center, Washington, DC; Diane E. Schuller, MD,
Department of Pediatrics, Pennsylvania State University, Milton S.
Hershey Medical College, Hershey, PA; Sheldon L. Spector, MD, Department
of Medicine, University of California, Los Angeles; David Lang, MD,
Allergy/Immunology Section, Division of Medicine, and Allergy/
Immunology Fellowship Training Program, Cleveland Clinic Foundation,
Cleveland, OH; Ronald A. Simon, MD, Division of Allergy, Asthma and
Immunology, Scripps Clinic and Research Foundation, La Jolla, CA; David
Kahn, MD, Department of Internal Medicine, Division of Allergy &
Immunology, University of Texas Southwestern Medical Center, Dallas, TX;
Jay M. Portnoy, MD, Section of Allergy, Asthma & Immunology, The
Children\'s Mercy Hospital, Professor of Pediatrics, University of
Missouri-Kansas City, School of Medicine, Kansas City, MO; Stephen A.
Tilles, MD, Department of Medicine, University of Washington School of
Medicine, Seattle, WA; Joann Blessing-Moore, MD, Department of Medicine
& Pediatrics, Stanford University Medical Center, Palo Alto, CA; Scott
H. Sicherer, MD, Department of Pediatrics, Jaffe Food Allergy Institute,
Mount Sinai School of Medicine, New York, NY: Dana V. Wallace, MD, Nova
Southeastern University, Davie, FL; Suzanne S. Teuber, MD, Department of
Medicine, Training Program Director, Allergy and Immunology, University
of California \-- Davis, School of Medicine, Division of Rheumatology,
Allergy and Clinical Immunology, Genome and Biomedical Sciences
Facility, Davis, CA

*Reviewers*: Eyassu Abegaz, MD; Sami Bahna, MD, Shreveport, LA; Wesley
Burks, MD, Durham, NC; Nugyek Camara, MD, Hinsdale, IL; Alessandro
Fiocchi, MD, Milan, Italy; Marianne Frieri, East Meadow, NY; Raif Geha,
Boston, MA; Paul Hannaway, MD, Salem, MA; John Kelso, MD, San Diego, CA;
Myngoc T. Nguyen, MD, Piedmont, CA; Barbara E. Magera, MD, PharmD,
Charleston, SC; Hugh A. Sampson, MD, New York, NY; Jonathan Spergel, MD,
Philadelphia, PA; and Robert S. Zeiger, MD, PhD, San Diego, CA

#### FINANCIAL DISCLOSURES/CONFLICTS OF INTEREST

Not stated

#### GUIDELINE STATUS

This is the current release of the guideline.

#### GUIDELINE AVAILABILITY

Electronic copies: Available in Portable Document Format (PDF) from the
[Joint Council of Allergy, Asthma, and Immunology (JCAAI) Web
site](http://www.jcaai.readyportal.net/file_depot/0-10000000/20000-30000/27387/folder/63948/Food_Allergy_2006.pdf).

Print copies: Available from JCAAI, 50 N. Brockway, Ste 3-3 Palatine, IL
60067

#### AVAILABILITY OF COMPANION DOCUMENTS

None available

#### PATIENT RESOURCES

None available

#### NGC STATUS

This NGC summary was completed by ECRI on June 12, 2006. The information
was verified by the guideline developer on July 18, 2006.

#### COPYRIGHT STATEMENT

This NGC summary is based on the original guideline, which is subject to
the guideline developer\'s copyright restrictions. Please contact the
Joint Council of Allergy, Asthma, and Immunology for more information.

### DISCLAIMER

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