Guidelines for the Diagnosis and Management

of Food Allergy in the United States

Summary of the NIAID-Sponsored Expert Panel Report

National Institute of Allergy and Infectious Diseases

NIAID

U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES

National Institutes of Health

National Institute of Allergy and Infectious Diseases

Guidelines for the Diagnosis and Management 

of Food Allergy in the United States

Summary of the NIAID-Sponsored Expert Panel Report

U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES

National Institutes of Health

National Institute of Allergy and Infectious Diseases

NIH Publication No. 11-7700

December 2010

NIAID I SUMMARY OF THE NIAID-SPONSORED EXPERT PANEL REPORT

i

Authors

Primary Authors

Joshua A. Boyce, M.D.

Division of Rheumatology, Immunology 

and Allergy

Brigham and Women’s Hospital

Department of Medicine

Harvard Medical School

Boston, MA

Amal Assa’ad, M.D.

Division of Allergy and Immunology

Cincinnati Children’s Hospital Medical 

Center

University of Cincinnati

Cincinnati, OH

A. Wesley Burks, M.D.

Division of Allergy and Immunology

Department of Pediatrics

Duke University Medical Center

Durham, NC

Stacie M. Jones, M.D.

Division of Allergy and Immunology

Department of Pediatrics

University of Arkansas for Medical Sciences

Arkansas Children’s Hospital

Little Rock, AR

Hugh A. Sampson, M.D.

Elliot and Roslyn Jaffe Food Allergy Institute

Division of Allergy and Immunology

Department of Pediatrics

Mount Sinai School of Medicine

New York, NY

Robert A. Wood, M.D.

Division of Allergy and Immunology

Department of Pediatrics

The Johns Hopkins University School of 

Medicine

Baltimore, MD

Marshall Plaut, M.D.

Division of Allergy, Immunology, and 

Transplantation

National Institute of Allergy and Infectious 

Diseases

National Institutes of Health

Bethesda, MD

Susan F. Cooper, M.Sc.

Division of Allergy, Immunology, and 

Transplantation

National Institute of Allergy and Infectious 

Diseases

National Institutes of Health

Bethesda, MD

Matthew J. Fenton, Ph.D.

Division of Allergy, Immunology, and 

Transplantation

National Institute of Allergy and Infectious 

Diseases

National Institutes of Health

Bethesda, MD

NIAID-Sponsored Expert Panel Authors

S. Hasan Arshad, M.B.B.S., M.R.C.P., D.M., 

F.R.C.P.

School of Medicine

University of Southampton

Southampton, UK

The David Hide Asthma and Allergy Research 

Centre

St. Mary’s Hospital

Newport, Isle of Wight, UK

Southampton University Hospital NHS Trust

Southampton, UK
NIAID I GUIDELINES FOR THE DIAGNOSIS AND MANAGEMENT OF FOOD ALLERGY

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Sami L. Bahna, M.D., Dr.P.H.

Department of Pediatrics

Section of Allergy and Immunology

Louisiana State University Health Sciences 

Center

Shreveport, LA

Lisa A. Beck, M.D.

Department of Dermatology

University of Rochester Medical Center

Rochester, NY

Carol Byrd-Bredbenner, Ph.D., R.D., F.A.D.A.

Department of Nutritional Sciences

Rutgers University

New Brunswick, NJ

Carlos A. Camargo, Jr., M.D., Dr.P.H.

Department of Emergency Medicine

Division of Rheumatology, Allergy 

and Immunology

Department of Medicine

Massachusetts General Hospital

Harvard Medical School

Boston, MA

Lawrence Eichenfield, M.D.

Division of Pediatric and Adolescent 

Dermatology

Rady Children’s Hospital

San Diego, CA

Departments of Pediatrics and Medicine

University of California, San Diego

San Diego, CA

Glenn T. Furuta, M.D. 

Section of Pediatric Gastroenterology, 

Hepatology, and Nutrition

Digestive Health Institute

Children’s Hospital Denver

Aurora, CO

Department of Pediatrics

National Jewish Health

Denver, CO

Department of Pediatrics

University of Colorado Denver School of 

Medicine

Aurora, CO

Jon M. Hanifin, M.D.

Department of Dermatology

Oregon Health and Science University

Portland, OR

Carol Jones, R.N., A.E.-C. 

Asthma Educator and Consultant

Allergy and Asthma Network Mothers of 

Asthmatics

McLean, VA

Monica Kraft, M.D. 

Division of Pulmonary, Allergy, and Critical 

Care Medicine

Department of Medicine

Duke University Medical Center

Durham, NC

Bruce D. Levy, M.D. 

Partners Asthma Center

Pulmonary and Critical Care Medicine

Brigham and Women’s Hospital and Harvard 

Medical School

Boston, MA

Phil Lieberman, M.D.

Division of Allergy and Immunology

Department of Medicine

University of Tennessee College of Medicine

Memphis, TN

Stefano Luccioli, M.D.

Office of Food Additive Safety

U.S. Food and Drug Administration

College Park, MD

Kathleen M. McCall, B.S.N., R.N. 

Children’s Hospital of Orange County

Orange, CA

Lynda C. Schneider, M.D.

Division of Immunology

Children’s Hospital Boston

Boston, MA
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Ronald A. Simon, M.D.

Division of Allergy, Asthma and Immunology

Scripps Clinic

San Diego, CA

F. Estelle R. Simons, M.D.

Departments of Pediatrics and Child Health 

and Immunology

Faculty of Medicine

University of Manitoba

Winnipeg, Manitoba, Canada

Stephen J. Teach, M.D., M.P.H. 

Division of Emergency Medicine

Children’s National Medical Center

Washington, DC

Barbara P. Yawn, M.D., M.P.H., M.Sc.

Department of Research

Olmsted Medical Center

Rochester, MN

Department of Family and Community 

Health

University of Minnesota School of Medicine

Minneapolis, MN

Contributing Author

Julie M. Schwaninger, M.Sc. 

Division of Allergy, Immunology, and 

Transplantation

National Institute of Allergy and Infectious 

Diseases

National Institutes of Health

Bethesda, MD

Corresponding Author

Matthew J. Fenton, Ph.D. 

Division of Allergy, Immunology, and 

Transplantation

National Institute of Allergy and Infectious 

Diseases 

National Institutes of Health

Bethesda, MD

6610 Rockledge Drive, Room 3105

Bethesda, MD 20892

Phone: 301–496–8973 

Fax: 301–402–0175 

E-mail: fentonm@niaid.nih.gov

For additional copies of this document, please 

contact daitinfo@niaid.nih.gov.

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Contents*

Section 1. Introduction........................................................................................................... 1

1.1. Overview..................................................................................................................... 1

1.2. Relationship of the U.S. Guidelines to Other Guidelines............................................. 1

1.3. How the Guidelines Were Developed.......................................................................... 1

1.3.1. The Coordinating Committee ........................................................................... 1

1.3.2. The Expert Panel............................................................................................... 2

1.3.3. The Independent, Systematic Literature Review and Report............................. 2

1.3.4. Assessing the Quality of the Body of Evidence.................................................. 2

1.3.5. Preparation of the Draft Guidelines and Expert Panel Deliberations................. 2

1.3.6. Public Comment Period and Draft Guidelines Revision .................................... 3

1.4. Defining the Strength of Each Clinical Guideline ........................................................ 3

1.5. Summary..................................................................................................................... 3

Section 2. Definitions, Prevalence, and Epidemiology of Food Allergy .................................. 4

2.1. Definitions .................................................................................................................. 4

2.1.1. Definitions of Food Allergy, Food, and Food Allergens.................................... 4

2.1.2. Definitions of Related Terms ............................................................................ 4

2.1.3. Definitions of Specific Food-Induced Allergic Conditions................................. 5

2.2. Prevalence and Epidemiology of Food Allergy ............................................................ 6

2.2.1. Systematic Reviews of the Prevalence of Food Allergy ...................................... 6

2.2.2. Prevalence of Allergy to Specific Foods, Food-Induced Anaphylaxis, 

and Food Allergy With Comorbid Conditions.................................................. 6

Section 3. Natural History of Food Allergy and Associated Disorders................................... 8

3.1. Natural History of Food Allergy in Children.............................................................. 8

3.2. Natural History of Levels of Allergen-Specific IgE to Foods in Children .................... 8

3.3. Natural History of Food Allergy in Adults ................................................................. 8

3.4. Natural History of Conditions That Coexist With Food Allergy ................................ 8

3.4.1. Asthma.............................................................................................................. 8

3.4.2. Atopic Dermatitis.............................................................................................. 9

3.4.3. Eosinophilic Esophagitis.................................................................................... 9

3.4.4. Exercise-Induced Anaphylaxis........................................................................... 9

3.5. Risk Factors for the Development of Food Allergy ..................................................... 9

3.6. Risk Factors for Severity of Allergic Reactions to Foods............................................. 9

3.7. Incidence, Prevalence, and Consequences of Unintentional Exposure to 

Food Allergens............................................................................................................ 9
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Section 4. Diagnosis of Food Allergy ................................................................................... 10

4.1. When Should Food Allergy Be Suspected? ................................................................ 10

4.2. Diagnosis of IgE-Mediated Food Allergy .................................................................. 10

4.2.1. Medical History and Physical Examination .................................................... 10

4.2.2. Methods To Identify the Causative Food........................................................ 10

4.2.2.1. Skin Prick Test................................................................................... 10

4.2.2.2. Intradermal Tests............................................................................... 12

4.2.2.3. Total Serum IgE................................................................................. 12

4.2.2.4. Allergen-Specific Serum IgE ............................................................... 12

4.2.2.5. Atopy Patch Test................................................................................ 12

4.2.2.6. Use of Skin Prick Tests, sIgE Tests, and Atopy Patch Tests 

 in Combination.................................................................................. 12

4.2.2.7. Food Elimination Diets...................................................................... 12

4.2.2.8. Oral Food Challenges ........................................................................ 12

4.2.2.9. Nonstandardized and Unproven Procedures ...................................... 13

4.3. Diagnosis of Non-IgE-Mediated Immunologic Adverse Reactions to Food............... 13

4.3.1. Eosinophilic Gastrointestinal Diseases ............................................................ 13

4.3.2. Food Protein-Induced Enterocolitis Syndrome ................................................ 13

4.3.3. Food Protein-Induced Allergic Proctocolitis.................................................... 13

4.3.4. Food Protein-Induced Enteropathy Syndrome................................................. 14

4.3.5. Allergic Contact Dermatitis............................................................................. 14

4.3.6. Systemic Contact Dermatitis ........................................................................... 14

4.4. Diagnosis of IgE-Mediated Contact Urticaria ........................................................... 14

Section 5. Management of Nonacute Allergic Reactions and Prevention of 

Food Allergy....................................................................................................... 15

5.1. Management of Individuals With Food Allergy ........................................................ 15

5.1.1. Dietary Avoidance of Specific Allergens in IgE-Mediated Food Allergy .......... 15

5.1.2. Dietary Avoidance of Specific Allergens in Non-IgE-Mediated Food Allergy.. 15

5.1.3. Effects of Dietary Avoidance on Associated and Comorbid Conditions, 

Such As Atopic Dermatitis, Asthma, and Eosinophilic Esophagitis................. 15

5.1.4. Food Avoidance and Nutritional Status.......................................................... 15

5.1.5. Food Labeling in Food Allergy Management .................................................. 15

5.1.6. When To Reevaluate Patients With Food Allergy ........................................... 15

5.1.7. Pharmacologic Intervention for the Prevention of Food-Induced Allergic

Reactions........................................................................................................ 16

5.1.7.1. IgE-Mediated Reactions..................................................................... 16

5.1.7.2. Non-IgE-Mediated Reactions............................................................. 16

5.1.8. Pharmacologic Intervention for the Treatment of Food-Induced Allergic 

Reactions........................................................................................................ 16

5.1.9. Immunotherapy for Food Allergy Management.............................................. 16

5.1.9.1. Allergen-Specific Immunotherapy ...................................................... 16

5.1.9.2. Immunotherapy With Cross-Reactive Allergens................................. 16

5.1.10. Quality-of-Life Issues Associated With Food Allergy .................................... 16

5.1.11. Vaccinations in Patients With Egg Allergy .................................................... 16
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5.1.11.1. Measles, Mumps, Rubella, and Varicella Vaccine............................ 17

5.1.11.2. Influenza Vaccine............................................................................. 17

5.1.11.3. Yellow Fever Vaccine....................................................................... 18

5.1.11.4. Rabies Vaccines ............................................................................... 18

5.2. Management of Individuals At Risk for Food Allergy .............................................. 18

5.2.1. Nonfood Allergen Avoidance in At-Risk Patients ........................................... 18

5.2.2. Dietary Avoidance of Foods With Cross-Reactivities in At-Risk Patients........ 18

5.2.3. Testing of Allergenic Foods in Patients at High Risk Prior to Introduction .... 18

5.2.4. Testing in Infants and Children With Persistent Atopic Dermatitis................. 19

5.3. Prevention of Food Allergy ....................................................................................... 19

5.3.1. Maternal Diet During Pregnancy and Lactation.............................................. 19

5.3.2. Breast-Feeding................................................................................................. 19

5.3.3. Special Diets in Infants and Young Children................................................... 19

5.3.3.1. Soy Infant Formula Versus Cow’s Milk Formula............................... 19

5.3.3.2. Hydrolyzed Infant Formulas Versus Cow’s Milk Formula 

 or Breast-Feeding............................................................................... 20

5.3.4. Timing of Introduction of Allergenic Foods to Infants.................................... 20

Section 6. Diagnosis and Management of Food-Induced Anaphylaxis and Other 

Acute Allergic Reactions to Foods...................................................................... 21

6.1. Definition of Anaphylaxis......................................................................................... 21

6.2. Diagnosis of Acute, Life-Threatening, Food-Induced Allergic Reactions................... 21

6.3. Treatment of Acute, Life-Threatening, Food-Induced Allergic Reactions.................. 21

6.3.1. First-Line and Adjuvant Treatment for Food-Induced Anaphylaxis................ 21

6.3.2. Treatment of Refractory Anaphylaxis............................................................. 24

6.3.3. Possible Risks of Acute Therapy for Anaphylaxis........................................... 24

6.3.4. Treatment To Prevent Biphasic or Protracted Food-Induced 

Allergic Reactions........................................................................................... 24

6.3.5. Management of Milder, Acute Food-Induced Allergic Reactions in 

Health Care Settings....................................................................................... 25

6.4. Management of Food-Induced Anaphylaxis.............................................................. 25

Appendix A. Primary Author Affiliations and Acknowledgments........................................ 26

Appendix B. List of Abbreviations....................................................................................... 29

* Some numbered sections found in the Guidelines are not included in this Summary because they do not include a guideline 

recommendation or an “In Summary” statement, or because the detailed information in the section was not suitable for a 

concise Summary.

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SECTION 1. Introduction

1.1. Overview

Food allergy (FA) is an important public health problem that affects adults and children 

and may be increasing in prevalence. Despite the risk of severe allergic reactions and even 

death, there is no current treatment for FA: the disease can only be managed by allergen 

avoidance or treatment of symptoms. Moreover, the diagnosis of FA may be problematic, 

given that nonallergic food reactions, such as food intolerance, are frequently confused with 

FAs. Additional concerns relate to the differences in the diagnosis and management of FA in 

different clinical practice settings. 

Due to these concerns, the National Institute of Allergy and Infectious Diseases (NIAID), part 

of the National Institutes of Health, working with more than 30 professional organizations, 

federal agencies, and patient advocacy groups, led the development of “best practice” clinical 

guidelines for the diagnosis and management of FA (henceforth referred to as the Guidelines). 

Based on a comprehensive review and objective evaluation of the recent scientific and clinical 

literature on FA, the Guidelines were developed by and designed for allergists/immunologists, 

clinical researchers, and practitioners in the areas of pediatrics, family medicine, internal 

medicine, dermatology, gastroenterology, emergency medicine, pulmonary and critical care 

medicine, and others. 

The Guidelines focus on diseases that are defined as FA (see section 2.1) and include both 

immunoglobulin E (IgE)-mediated reactions to food and some non-IgE-mediated reactions to 

food. The Guidelines do not discuss celiac disease, which is an immunologic non-IgE-mediated 

reaction to certain foods. Although this is an immune-based disease involving food, existing 

clinical guidelines for celiac disease will not be restated here.

Finally, these Guidelines do not address the management of patients with FA outside of clinical 

care settings (e.g., schools and restaurants) or the related public health policy issues. These 

issues are beyond the scope of this document.

1.2. Relationship of the U.S. Guidelines to Other Guidelines

(Not summarized here; refer to Guidelines.)

1.3. How the Guidelines Were Developed

1.3.1. The Coordinating Committee

NIAID established a Coordinating Committee (CC), whose members are listed in 

Appendix A of the Guidelines, to oversee the development of the Guidelines; review 

drafts of the Guidelines for accuracy, practicality, clarity, and broad utility of the 

recommendations in clinical practice; review the final Guidelines; and disseminate the 

Guidelines. The CC members were from 34 professional organizations, advocacy groups, 
NIAID I GUIDELINES FOR THE DIAGNOSIS AND MANAGEMENT OF FOOD ALLERGY

SECTION 1 INTRODUCTION

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and federal agencies, and each member was vetted for financial conflict of interest (COI) 

by NIAID staff. 

1.3.2. The Expert Panel

The CC convened an Expert Panel (EP) in March 2009 that was chaired by Joshua 

Boyce, M.D. (Brigham and Women’s Hospital, Boston, MA). Panel members were 

specialists from a variety of relevant clinical, scientific, and public health areas (see 

Acknowledgments). Each member was vetted for financial COI by NIAID staff and 

approved by the CC. The charge to the EP was to use an independent, systematic 

literature review, in conjunction with consensus expert opinion and EP-identified 

supplementary documents, to develop Guidelines that provide a comprehensive 

approach for diagnosing and managing FA based on the current state of the science.

1.3.3. The Independent, Systematic Literature Review and Report

RAND Corporation prepared an independent, systematic literature review and evidence 

report on the state of the science in FA. This work was supported by an NIAID contract 

awarded in September 2008. The contract’s principal investigator was Paul G. Shekelle, 

M.D., Ph.D., an internationally recognized expert in the fields of practice guidelines 

and meta-analysis. RAND screened more than 12,300 titles, reviewed more than 1,200 

articles, abstracted nearly 900 articles, and included 348 articles in the final RAND 

report. The full version of the report with a complete list of references is available at 

http://www.rand.org/pubs/working_papers/WR757-1/.

1.3.4. Assessing the Quality of the Body of Evidence

In addition to assessing the quality of each of the included studies, RAND assessed the 

quality of the body of evidence using the Grading of Recommendations Assessment, 

Development and Evaluation (GRADE) approach, which was developed in 2004. 

GRADE provides a comprehensive and transparent methodology to develop 

recommendations for the diagnosis, treatment, and management of patients. In assessing 

the body of evidence, GRADE considers study design and other factors, such as the 

precision, consistency, and directness of the data. Using this approach, GRADE then 

provides a grade of high, moderate, or low for the quality of the body of evidence.

1.3.5. Preparation of the Draft Guidelines and Expert Panel Deliberations

All 43 clinical recommendations drafted by the EP received 90 percent (or higher) 

agreement. Sections 3, 5, and 6 of the Guidelines also contain “In Summary” 

statements. These statements are intended to provide health care professionals with 

significant information that did not warrant a recommendation, or are in place of a 

recommendation when the EP or the CC could not reach consensus. All “In Summary” 

statements received 90 percent (or higher) agreement.
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1.3.6. Public Comment Period and Draft Guidelines Revision

The draft Guidelines were posted to the NIAID Web site in March 2010 for a period 

of 60 days to allow for public review and comment. More than 550 comments were 

collected and reviewed by the CC, the EP, and NIAID. The EP revised the Guidelines 

in response to some of these comments. The final Guidelines were published in the 

December 2010 issue of the Journal of Allergy and Clinical Immunology and are 

publically available at http://www.niaid.nih.gov/topics/foodallergy/clinical/.

1.4. Defining the Strength of Each Clinical Guideline

The EP has used the verb “recommends” or “suggests” in each clinical guideline. These words 

convey the strength of the guideline, defined as follows:

•	 Recommend is used when the EP strongly recommended for or against a particular 

course of action.

•	 Suggest is used when the EP weakly recommended for or against a particular course 

of action. 

1.5. Summary

The Guidelines are intended to assist health care professionals in making appropriate decisions 

about patient care in the United States. The recommendations are not fixed protocols that 

must be followed. Health care professionals should take these Guidelines into account when 

exercising their clinical judgment. However, this guidance does not override their responsibility 

to make decisions appropriate to the circumstances of the individual patient, in consultation 

with the patient, guardian, or caregiver. Clinical judgment on the management of individual 

patients remains paramount. Health care professionals, patients, and their families need to 

develop individual treatment plans that are tailored to the specific needs and circumstances 

of the patient. This document is intended as a resource to guide clinical practice and develop 

educational materials for patients, their families, and the public. It is not an official regulatory 

document of any government agency.
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SECTION 2. Definitions, Prevalence, and 

Epidemiology of Food Allergy

2.1. Definitions

2.1.1. Definitions of Food Allergy, Food, and Food Allergens

The EP came to consensus on definitions used throughout the Guidelines.

A food allergy is defined as an adverse health effect arising from a specific immune 

response that occurs reproducibly on exposure to a given food.

A food is defined as any substance—whether processed, semiprocessed, or raw—that is 

intended for human consumption, and includes drinks, chewing gum, food additives, and 

dietary supplements. Substances used only as drugs, tobacco products, and cosmetics 

(such as lip-care products) that may be ingested are not included. 

Food allergens are defined as those specific components of food or ingredients within 

food (typically proteins, but sometimes also chemical haptens) that are recognized by 

allergen-specific immune cells and elicit specific immunologic reactions, resulting in 

characteristic symptoms. Some allergens (most often from fruits and vegetables) cause 

allergic reactions primarily if eaten when raw. However, most food allergens can still 

cause reactions even after they have been cooked or have undergone digestion in the 

stomach and intestines. A phenomenon called cross-reactivity may occur when an 

antibody reacts not only with the original allergen, but also with a similar allergen. In 

FA, cross-reactivity occurs when a food allergen shares structural or sequence similarity 

with a different food allergen or aeroallergen, which may then trigger an adverse 

reaction similar to that triggered by the original food allergen. Cross-reactivity is 

common, for example, among different shellfish and different tree nuts. 

Food oils—such as soy, corn, peanut, and sesame—range from very low allergenicity 

(if virtually all of the food protein is removed in processing) to very high allergenicity 

(if little of the food protein is removed in processing).

2.1.2. Definitions of Related Terms

Because individuals can develop allergic sensitization (as evidenced by the presence 

of allergen-specific IgE [sIgE]) to food allergens without having clinical symptoms on 

exposure to those foods, an sIgE-mediated FA requires both the presence of sensitization 

and the development of specific signs and symptoms on exposure to that food. 

Sensitization alone is not sufficient to define FA.
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These Guidelines generally use the term tolerate to denote a condition where an 

individual has either naturally outgrown an FA or has received therapy and no longer 

develops clinical symptoms following ingestion of the food. This ability to tolerate food 

does not distinguish between these two possible clinical states. Individuals may tolerate 

food only for a short term, perhaps because they have been desensitized by exposure to 

the food. Alternatively, they may develop long-term tolerance. The specific term tolerance

is used in these Guidelines to mean that an individual is symptom free after consumption 

of the food or upon oral food challenge weeks, months, or even years after the cessation 

of treatment. The immunological mechanisms that underlie tolerance in humans are 

poorly understood. 

Although many different foods and food components have been recognized as food 

allergens, these Guidelines focus on only those foods that are responsible for the 

majority of observed adverse allergic or immunologic reactions. Moreover, foods or 

food components that elicit reproducible adverse reactions but do not have established 

or likely immunologic mechanisms are not considered food allergens. Instead, these 

nonimmunologic adverse reactions are termed food intolerances. For example, an 

individual may be allergic to cow’s milk (henceforth referred to as milk) due to an 

immunologic response to milk protein, or alternatively, that individual may be intolerant 

to milk due to an inability to digest the sugar lactose. In the former situation, milk 

protein is considered an allergen because it triggers an adverse immunologic reaction. 

Inability to digest lactose leads to excess fluid production in the gastrointestinal (GI) 

tract, resulting in abdominal pain and diarrhea. This condition is termed lactose 

intolerance, and lactose is not an allergen because the response is not immune based. 

It should be noted that the words tolerance and intolerance are unrelated terms, even 

though the spelling of the words implies that they are opposites.

2.1.3. Definitions of Specific Food-Induced Allergic Conditions

The reader is referred to the Guidelines for the definitions of the following:

•	 Food-induced anaphylaxis

•	 GI food allergies and several specific syndromes

− Immediate GI hypersensitivity 

− Eosinophilic esophagitis (EoE) 

− Eosinophilic gastroenteritis 

− Food protein-induced allergic proctocolitis (AP)

− Food protein-induced enterocolitis syndrome (FPIES) 

− Oral allergy syndrome (OAS)
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•	 Cutaneous reactions to foods

− Acute urticaria

− Angioedema

− The increase in atopic dermatitis (AD) symptoms

− Allergic contact dermatitis

− Contact urticaria 

•	 Respiratory manifestations 

•	 Heiner syndrome

2.2. Prevalence and Epidemiology of Food Allergy

The true prevalence of FA has been difficult to establish for several reasons. 

•	 Although more than 170 foods have been reported to cause IgE-mediated reactions, 

most prevalence studies have focused on only the most common foods. 

•	 The incidence and prevalence of FA may have changed over time, and many studies 

have indeed suggested a true rise in prevalence over the past 10–20 years.

•	 Studies of FA incidence, prevalence, and natural history are difficult to compare 

because of inconsistencies and deficiencies in study design and variations in the 

definition of FA. 

2.2.1. Systematic Reviews of the Prevalence of Food Allergy

(Not summarized here; refer to Guidelines.)

2.2.2. Prevalence of Allergy to Specific Foods, Food-Induced Anaphylaxis, and Food Allergy 

With Comorbid Conditions

The following is a summary of prevalence data for the most common food allergies and 

anaphylaxis:

Peanut

•	 Prevalence of peanut allergy in the United States is about 0.6 percent of the 

population.

•	 Prevalence of peanut allergy in France, Germany, Israel, Sweden, and the United 

Kingdom varies between 0.06 and 5.9 percent.
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Tree nuts

•	 Prevalence of tree nut allergy in the United States is 0.4–0.5 percent of the 

population.

•	 Prevalence of tree nut allergy in France, Germany, Israel, Sweden, and the 

United Kingdom varies between 0.03 and 8.5 percent.

Seafood

•	 Prevalence rates in the United States are significantly lower for children than 

for adults: fish allergy, 0.2 percent for children versus 0.5 percent for adults; 

crustacean shellfish allergy, 0.5 versus 2.5 percent; any seafood allergy, 0.6 

versus 2.8 percent. 

•	 Prevalence rates in the United States are higher for women than for men: 

crustacean shellfish allergy, 2.6 percent for women versus 1.5 percent for men; 

any fish, 0.6 versus 0.2 percent. 

Milk and hen’s egg

•	 In a Danish cohort, allergy to milk was confirmed in 2.2 percent. Of these, 

54 percent had IgE-mediated allergy, and the remaining 46 percent were 

classified as non-IgE mediated. 

•	 In a Norwegian cohort, the prevalence of hen’s egg (henceforth referred to as 

egg) allergy was estimated to be 1.6 percent, and most egg reactions were IgE 

mediated. 

Food-induced anaphylaxis

•	 Several studies in the United States assessed the incidence of anaphylaxis 

related to food. These studies found wide differences in the rates (from 

1/100,000 population to as high as 70/100,000 population) of hospitalization 

or emergency department visits for anaphylaxis, as assessed by International 

Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM) 

codes or medical record review. 

•	 The proportion of anaphylaxis cases thought to be due to foods also varied 

between 13 and 65 percent, with the lowest percentages found in studies that 

used more stringent diagnostic criteria for anaphylaxis. 

The EP agreed that any estimate of the overall U.S. incidence of anaphylaxis is unlikely 

to have utility because such an estimate fails to reflect the substantial variability in 

patient age, geographic distribution, criteria used to diagnose anaphylaxis, and the study 

methods used.
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SECTION 3. Natural History of Food Allergy and

Associated Disorders

The EP reviewed the literature on the natural history of FA and summarized the available 

data for the most common food allergens in the United States: egg, milk, peanut, tree nuts, 

wheat, crustacean shellfish, and soy. Natural history data for fish allergy were unavailable as 

of the completion of the systematic literature review (September 2009). It should be noted 

that many published studies addressing the natural history of FA typically come from selected 

populations (e.g., from a single clinic or hospital) that may not be representative of the general 

or community-based patient population with a specific FA condition. Thus, the findings of 

these studies may not necessarily be extrapolated to all patients with the condition. 

3.1. Natural History of Food Allergy in Children

In Summary: Most children with FA eventually will tolerate milk, egg, soy, and wheat; 

far fewer will eventually tolerate tree nuts and peanut. The time course of FA resolution in 

children varies by food and may occur as late as the teenage years. A high initial level of sIgE 

against a food is associated with a lower rate of resolution of clinical allergy over time. 

3.2. Natural History of Levels of Allergen-Specific IgE to Foods in Children

In Summary: For many patients, sIgE antibodies to foods appear within the first 2 years of 

life. Levels may increase or decrease; a decrease is often associated with the ability to tolerate 

the foods.

3.3. Natural History of Food Allergy in Adults

In Summary: FA in adults can reflect persistence of pediatric FAs (e.g., milk, peanut, and 

tree nuts) or de novo sensitization to food allergens encountered after childhood. Although 

there is a paucity of data from U.S. studies, FA that starts in adult life tends to persist.

3.4. Natural History of Conditions That Coexist With Food Allergy

In Summary: FA may coexist with asthma, AD, EoE, and exercise-induced anaphylaxis. 

In patients with asthma, the coexistence of FA may be a risk factor for severe asthma 

exacerbations. Moreover, food may be a trigger for exercise-induced anaphylaxis. Elimination 

of food allergens in sensitized individuals can improve symptoms of some comorbid 

conditions.

3.4.1. Asthma

In Summary: Asthma and FA often coexist in pediatric and adult patients. FA is 

associated with severe asthma.
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3.4.2. Atopic Dermatitis

In Summary: AD and FA are highly associated. When tolerance develops to a food, 

the reintroduction of the food in the diet will not result in recurrence or worsening of 

the AD. 

3.4.3. Eosinophilic Esophagitis

In Summary: EoE is commonly associated with sensitization to foods. The natural 

history of EoE is that of a chronic condition that resolves spontaneously or with therapy, 

and then relapses. There are insufficient data to judge the impact of food sensitization 

on the natural history of EoE, and vice versa. Only retrospective data exist that support 

a beneficial effect of dietary changes on the histopathologic changes in the esophagus in 

EoE.

3.4.4. Exercise-Induced Anaphylaxis

In Summary: Exercise-induced anaphylaxis in adults is triggered by foods in about 

one-third of patients and has a natural history marked by frequent recurrence of the 

episodes.

3.5. Risk Factors for the Development of Food Allergy

In Summary: Family history of atopy and the presence of AD are risk factors for the 

development of both sensitization to food and confirmed FA.

3.6. Risk Factors for Severity of Allergic Reactions to Foods

In Summary: The severity of allergic reactions to foods is multifactorial and variable. The 

severity of a reaction cannot be accurately predicted by the degree of severity of past reactions 

nor by the level of sIgE or the size of the wheal from the skin prick test (SPT). The factor most 

commonly identified with the most severe reactions is the coexistence of asthma.

3.7. Incidence, Prevalence, and Consequences of Unintentional Exposure to 

Food Allergens

In Summary: Self-reported reactions to food frequently occur in patients with a known 

diagnosis of FA. Although a subset of these reactions is due to intentional exposure, most 

are due to unintentional exposure. Both types of exposure can be life-threatening. There is 

no evidence that unintentional or intentional exposures to the food allergen alter the natural 

history of the FA.
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SECTION 4. Diagnosis of Food Allergy

4.1. When Should Food Allergy Be Suspected?

Guideline 1: The EP recommends that FA should be considered:

•	 In individuals presenting with anaphylaxis or any combination of symptoms listed 

in table I that occur within minutes to hours of ingesting food, especially in young 

children and/or if symptoms have followed the ingestion of a specific food on more 

than one occasion

•	 In infants, young children, and selected older children diagnosed with certain 

disorders, such as moderate to severe AD, EoE, enterocolitis, enteropathy, and AP 

•	 In adults diagnosed with EoE

4.2. Diagnosis of IgE-Mediated Food Allergy

4.2.1. Medical History and Physical Examination

Guideline 2: The EP recommends using medical history and physical examination to 

aid in the diagnosis of FA.

•	 Medical history: The EP recommends using a detailed medical history to help 

focus the evaluation of an FA. Although the medical history often provides 

evidence for the type of food-induced allergic reaction and the potential 

causative food(s) involved, history alone cannot be considered diagnostic of FA.

•	 Physical examination: The EP recommends performing a focused physical 

examination of the patient, which may provide signs consistent with an allergic 

reaction or disorder often associated with FA. However, by itself, the physical 

examination cannot be considered diagnostic of FA.

Guideline 3: The EP recommends that parent and patient reports of FA must be 

confirmed, because multiple studies demonstrate that 50–90 percent of presumed FAs 

are not allergies. 

4.2.2. Methods To Identify the Causative Food

4.2.2.1. Skin Prick Test

Guideline 4: The EP recommends performing an SPT (also known as a skin 

puncture test) to assist in the identification of foods that may be provoking IgEmediated food-induced allergic reactions, but the SPT alone cannot be considered 

diagnostic of FA.
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Table I. Symptoms of Food-Induced Allergic Reaction

Target Organ Immediate Symptoms Delayed Symptoms

Cutaneous Erythema

Pruritus

Urticaria

Morbilliform eruption

Angioedema

Erythema 

Flushing 

Pruritus 

Morbilliform eruption

Angioedema

Eczematous rash

Ocular Pruritus 

Conjunctival erythema

Tearing 

Periorbital edema

Pruritus

Conjunctival erythema

Tearing

Periorbital edema

Upper respiratory Nasal congestion

Pruritus

Rhinorrhea

Sneezing

Laryngeal edema

Hoarseness

Dry staccato cough

  

Lower respiratory Cough

Chest tightness

Dyspnea

Wheezing

Intercostal retractions

Accessory muscle use

Cough, dyspnea, and wheezing

GI (oral) Angioedema of the lips, tongue, 

or palate

Oral pruritus

Tongue swelling

  

GI (lower) Nausea

Colicky abdominal pain

Reflux

Vomiting 

Diarrhea

Nausea

Abdominal pain

Reflux

Vomiting

Diarrhea 

Hematochezia

Irritability and food refusal with 

weight loss (young children)

Cardiovascular Tachycardia (occasionally bradycardia in anaphylaxis)

Hypotension

Dizziness

Fainting 

Loss of consciousness

  

Miscellaneous Uterine contractions 

Sense of “impending doom”   

GI, gastrointestinal.

Note: This table is presented as table IV in the Guidelines.
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4.2.2.2. Intradermal Tests

Guideline 5: The EP recommends that intradermal testing should not be used to 

make a diagnosis of FA.

4.2.2.3. Total Serum IgE

Guideline 6: The EP recommends that the routine use of measuring total serum 

IgE should not be used to make a diagnosis of FA.

4.2.2.4. Allergen-Specific Serum IgE

Guideline 7: The EP recommends sIgE tests for identifying foods that 

potentially provoke IgE-mediated food-induced allergic reactions, but alone these 

tests are not diagnostic of FA.

4.2.2.5. Atopy Patch Test

Guideline 8: The EP suggests that the atopy patch test (APT) should not be used 

in the routine evaluation of noncontact FA.

4.2.2.6. Use of Skin Prick Tests, sIgE Tests, and Atopy Patch Tests in Combination

Guideline 9: The EP suggests not using the combination of SPTs, sIgE tests, and 

APTs for the routine diagnosis of FA.

4.2.2.7. Food Elimination Diets

Guideline 10: The EP suggests that elimination of one or a few specific foods 

from the diet may be useful in the diagnosis of FA, especially in identifying foods 

responsible for some non-IgE-mediated food-induced allergic disorders, such as 

FPIES, AP, and Heiner syndrome, and some mixed IgE- and non-IgE-mediated 

food-induced allergic disorders, such as EoE. 

4.2.2.8. Oral Food Challenges

Guideline 11: The EP recommends using oral food challenges for diagnosing 

FA. The double-blind placebo-controlled food challenge is the gold standard. 

However, a single-blind or an open-food challenge may be considered diagnostic 

under certain circumstances: If either of these challenges elicits no symptoms (i.e., 

the challenge is negative), then FA can be ruled out; but when either challenge 

elicits objective symptoms (i.e., the challenge is positive) and those objective 

symptoms correlate with medical history and are supported by laboratory tests, 

then a diagnosis of FA is supported.
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4.2.2.9. Nonstandardized and Unproven Procedures

Guideline 12: The EP recommends not using any of the following 

nonstandardized tests for the routine evaluation of IgE-mediated FA:

•	 Basophil histamine release/activation 

•	 Lymphocyte stimulation

•	 Facial thermography

•	 Gastric juice analysis

•	 Endoscopic allergen provocation

•	 Hair analysis

•	 Applied kinesiology

•	 Provocation neutralization

•	 Allergen-specific IgG4

•	 Cytotoxicity assays

•	 Electrodermal test (Vega)

•	 Mediator release assay (LEAP diet)

4.3. Diagnosis of Non-IgE-Mediated Immunologic Adverse Reactions to Food

4.3.1. Eosinophilic Gastrointestinal Diseases

Guideline 13: The EP suggests that SPTs, sIgE tests, and APTs may be considered to 

help identify foods that are associated with EoE, but these tests alone are not sufficient 

to make the diagnosis of FA. The role of these tests in the diagnosis of other eosinophilic 

GI disorders has not been established.

4.3.2. Food Protein-Induced Enterocolitis Syndrome

Guideline 14: The EP recommends using the medical history and oral food challenge 

to establish a diagnosis of FPIES. However, when history indicates that infants or 

children have experienced hypotensive episodes or multiple reactions to the same food, 

a diagnosis may be based on a convincing history and absence of symptoms when the 

causative food is eliminated from the diet. 

4.3.3. Food Protein-Induced Allergic Proctocolitis

Guideline 15: The EP recommends using the medical history, resolution of symptoms 

when the causative food is eliminated from the diet, and recurrence of symptoms 

following an oral food challenge to diagnose AP. 
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4.3.4. Food Protein-Induced Enteropathy Syndrome

(Not summarized here; refer to Guidelines.)

4.3.5. Allergic Contact Dermatitis

Guideline 16: The EP recommends using the medical history, including the absence 

of symptoms while the causative food is avoided, and positive patch tests to diagnose 

allergic contact dermatitis. 

4.3.6. Systemic Contact Dermatitis

Guideline 17: The EP suggests using the medical history, including the resolution of 

symptoms while the causative food is avoided, and positive patch tests to establish the 

diagnosis of systemic contact dermatitis. 

4.4. Diagnosis of IgE-Mediated Contact Urticaria

Guideline 18: The EP suggests using the medical history, including the absence of 

symptoms while the causative food is avoided, positive sIgE tests or SPTs, and positive 

immediate epicutaneous skin tests (e.g., positive immediate responses to APTs), to establish 

the diagnosis of food-induced IgE-mediated contact urticaria. 

Contact urticaria can be of two types, either IgE mediated or non-IgE mediated. In IgEmediated contact urticaria, substances present in foods interact with sIgE bound to cutaneous 

mast cells, leading to the release of histamine and other inflammatory mediators. Localized 

or generalized urticaria, as well as systemic symptoms, may result. sIgE-mediated contact 

urticaria may be assessed with APTs, SPTs, or sIgE tests, although there is no standardization 

of diagnostic methodology. In non-IgE-mediated contact urticaria to food, systemic symptoms 

are rarely seen.
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SECTION 5. Management of Nonacute Allergic 

Reactions and Prevention of Food Allergy

5.1. Management of Individuals With Food Allergy

5.1.1. Dietary Avoidance of Specific Allergens in IgE-Mediated Food Allergy

Guideline 19: The EP recommends that individuals with documented IgE-mediated 

FA should avoid ingesting their specific allergen or allergens. 

5.1.2. Dietary Avoidance of Specific Allergens in Non-IgE-Mediated Food Allergy

Guideline 20: The EP recommends that individuals with documented non-IgEmediated FA should avoid ingesting their specific allergen or allergens. 

5.1.3. Effects of Dietary Avoidance on Associated and Comorbid Conditions, Such As Atopic 

Dermatitis, Asthma, and Eosinophilic Esophagitis

Guideline 21: In individuals with documented or proven FA who also have one or 

more of the following—AD, asthma, or EoE—the EP recommends avoidance of their 

specific allergen or allergens. 

Guideline 22: In individuals without documented or proven FA, the EP does not

recommend avoiding potentially allergenic foods as a means of managing AD, asthma, 

or EoE. 

5.1.4. Food Avoidance and Nutritional Status

Guideline 23: The EP recommends nutritional counseling and regular growth 

monitoring for all children with FA.

5.1.5. Food Labeling in Food Allergy Management

Guideline 24: The EP suggests that individuals with FA and their caregivers receive 

education and training on how to interpret ingredient lists on food labels and how to 

recognize labeling of the food allergens used as ingredients in foods. The EP also suggests 

that products with precautionary labeling, such as “this product may contain trace 

amounts of allergen,” be avoided.

5.1.6. When To Reevaluate Patients With Food Allergy

Guideline 25: The EP suggests follow-up testing for individuals with FA depending 

on the specific food to which the individual is allergic. Whether testing is done annually 

or at other intervals depends on the food in question, the age of the child, and the 

intervening medical history.
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5.1.7. Pharmacologic Intervention for the Prevention of Food-Induced Allergic Reactions

5.1.7.1. IgE-Mediated Reactions

Guideline 26: There are no medications currently recommended by the EP 

to prevent IgE-mediated food-induced allergic reactions from occurring in an 

individual with existing FA. 

5.1.7.2. Non-IgE-Mediated Reactions

Guideline 27: There are no medications currently recommended by the EP to 

prevent non-IgE-mediated food-induced allergic reactions from occurring in an 

individual with existing FA.

5.1.8. Pharmacologic Intervention for the Treatment of Food-Induced Allergic Reactions

Allergen avoidance is the first line of treatment for FA, and use of antihistamines, as 

needed, remains the mainstay of managing (as opposed to preventing) symptoms of 

nonsevere food-induced allergic reactions. However, drug therapy has been used to 

treat FA in cases where allergen avoidance is extremely difficult or results in nutritional 

deficiencies. Drugs that alter the immune response to the allergen are commonly 

considered the most likely candidates for such therapy in the future, but these treatments 

are not currently recommended (see Guideline 28). 

5.1.9. Immunotherapy for Food Allergy Management

5.1.9.1. Allergen-Specific Immunotherapy

Guideline 28: The EP does not recommend using allergen-specific 

immunotherapy to treat IgE-mediated FA.

5.1.9.2. Immunotherapy With Cross-Reactive Allergens

Guideline 29: The EP does not recommend immunotherapy with cross-reactive 

allergens for treating IgE-mediated FA.

5.1.10. Quality-of-Life Issues Associated With Food Allergy

Guideline 30: The EP recommends that patients with FA and their caregivers be 

provided with information on food allergen avoidance and emergency management that 

is age and culturally appropriate.

5.1.11. Vaccinations in Patients With Egg Allergy

In Summary: Patients who have generated IgE antibodies to an allergen are at risk 

for anaphylaxis with systemic exposure to that allergen. Thus, patients who have IgEmediated egg allergy are at risk for anaphylaxis if injected with vaccines containing egg 
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protein. More detailed information about specific egg-containing vaccines (measles, 

mumps, and rubella [MMR], MMR with varicella [MMRV], influenza, yellow fever, and 

rabies) is provided in sections 5.1.11.1–5.1.11.4 of the Guidelines.

The EP recognizes that changes in these recommendations may occur in the future 

as there is an increased understanding of the risk factors for allergic reactions and as 

vaccine manufacturing processes improve and decrease the final egg protein content of 

vaccines. For the most current recommendations, health care professionals should refer 

to the Web sites of the American Academy of Pediatrics (AAP) and Advisory Committee 

for Immunization Practices (ACIP):

•	 http://aapredbook.aappublications.org/

•	 http://www.cdc.gov/vaccines/recs/acip/

5.1.11.1. Measles, Mumps, Rubella, and Varicella Vaccine

Guideline 31: The EP recognizes the varying consensus recommendations of the 

different organizations on this particular vaccine and recommends that children 

with egg allergy, even those with a history of severe reactions, receive vaccines 

for MMR and MMRV. The safety of this practice has been recognized by ACIP 

and AAP and is noted in the approved product prescribing information for these 

vaccines.

5.1.11.2. Influenza Vaccine

In Summary: The EP concludes that insufficient evidence exists to recommend 

administering influenza vaccine, either inactivated or live-attenuated, to patients 

with a history of severe reactions to egg proteins. Severe reactions include a history 

of hives, angioedema, allergic asthma, or systemic anaphylaxis to egg proteins (or 

chicken proteins). Less severe or local manifestations of allergy to egg or feathers 

are not contraindications. However, the EP notes that egg allergy is relatively 

common among the very patients who would highly benefit from influenza 

vaccination. Such patients include children and young adults (from 6 months to 

18 years old for seasonal influenza, and from 6 months to 24 years old for H1N1 

influenza) and all patients with asthma. It should be noted that live-attenuated 

vaccine is not licensed for use in patients with asthma.

Although ACIP and AAP, and also the vaccine manufacturers, do not recommend 

influenza vaccination in patients who are allergic to egg, several publications have 

described different approaches to giving the influenza vaccine to patients with 

severe allergic reactions to egg. These approaches, which depend on the ovalbumin 

content and the results of SPTs or intradermal tests with the vaccine, include 

a single dose of vaccine, two doses of vaccine, or multiple doses. However, the 

evidence supporting these approaches is limited by the small numbers of patients 
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included in each study. Moreover, data indicate that, although the vaccines are 

relatively safe, there remains some, albeit low, risk of systemic reactions. Also, 

negative SPT results do not accurately predict safety of vaccination, in that 

5 percent of patients with negative SPTs had systemic reactions to vaccination. 

5.1.11.3. Yellow Fever Vaccine

In Summary: The EP recognizes the current guidelines from the different 

organizations and recommends against administering yellow fever vaccine 

to patients with a history of hives, angioedema, allergic asthma, or systemic 

anaphylaxis to egg proteins, unless an allergy evaluation and testing with the 

vaccine is done first. This approach has been recognized by ACIP and AAP and is 

noted in the approved product prescribing information for this vaccine.

5.1.11.4. Rabies Vaccines

In Summary: The EP recognizes the current guidelines from the different 

organizations and recommends against administering rabies vaccines to patients 

with a history of hives, angioedema, allergic asthma, or systemic anaphylaxis to 

egg proteins, unless an allergy evaluation and testing with the vaccine is done first. 

This approach has been recognized by ACIP and AAP and is noted in the approved 

product prescribing information for these vaccines.

5.2. Management of Individuals At Risk for Food Allergy

5.2.1. Nonfood Allergen Avoidance in At-Risk Patients

Guideline 32: The EP suggests that patients at risk for developing FA do not limit 

exposure to potential nonfood allergens (e.g., dust mites, pollen, or pet dander). Patients 

at risk for developing FA are defined as those with a biological parent or sibling with 

existing, or history of, allergic rhinitis, asthma, AD, or FA. This definition of “at risk” is 

used throughout sections 5.2 and 5.3.

5.2.2. Dietary Avoidance of Foods With Cross-Reactivities in At-Risk Patients

Guideline 33: The EP suggests that patients at risk for developing FA do not need to 

limit exposure to foods that may be cross-reactive with the eight major food allergens in 

the United States (milk, egg, peanut, tree nuts, soy, wheat, fish, and crustacean shellfish).

5.2.3. Testing of Allergenic Foods in Patients at High Risk Prior to Introduction

In Summary: The EP concludes that insufficient evidence exists to recommend 

routine FA testing prior to the introduction of highly allergenic foods (such as milk, 

egg, and peanut) in children who are at high risk of reacting to the introduction of such 

foods. The definition of children at high risk, in this specific situation, is children with 

preexisting severe allergic disease and/or a family history of FA. Nevertheless, there 
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may be some value in FA evaluations that include an oral food challenge for a select 

group of patients with certain risk factors, such as having a sibling with peanut allergy 

or evidence of another underlying FA (e.g., testing for tree nut allergy in a child with 

peanut allergy). It is possible that an FA evaluation prior to introduction of a food could 

potentially prevent allergic reactions. However, widespread SPTs and sIgE tests are not 

recommended because of their poor predictive value. These tests would lead to many 

clinically irrelevant results and unnecessary dietary restrictions, especially if unconfirmed 

by oral food challenges. Overall, the risk-to-benefit ratio of FA evaluation should be 

considered on an individual basis, especially for the highly allergenic foods in high-risk 

young children.

Guideline 34: The EP suggests that the general population of children not be tested 

for FA to highly allergenic foods prior to their introduction into the diet. The general 

population of children does not have preexisting severe allergic disease and also does not 

have a family history of FA.

5.2.4. Testing in Infants and Children With Persistent Atopic Dermatitis

Guideline 35: The EP suggests that children less than 5 years old with moderate 

to severe AD be considered for FA evaluation for milk, egg, peanut, wheat, and soy, if 

at least one of the following conditions is met:

•	 The child has persistent AD in spite of optimized management and topical 

therapy. 

•	 The child has a reliable history of an immediate reaction after ingestion of a 

specific food.

5.3. Prevention of Food Allergy

5.3.1. Maternal Diet During Pregnancy and Lactation

Guideline 36: The EP does not recommend restricting maternal diet during pregnancy 

or lactation as a strategy for preventing the development or clinical course of FA. 

5.3.2. Breast-Feeding

Guideline 37: The EP recommends that all infants be exclusively breast-fed until 

4 to 6 months of age, unless breast-feeding is contraindicated for medical reasons. 

5.3.3. Special Diets in Infants and Young Children

5.3.3.1. Soy Infant Formula Versus Cow’s Milk Formula

Guideline 38: The EP does not recommend using soy infant formula instead of 

cow’s milk infant formula as a strategy for preventing the development of FA or 

modifying its clinical course in at-risk infants (“at risk” is defined in Guideline 32).
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5.3.3.2. Hydrolyzed Infant Formulas Versus Cow’s Milk Formula or Breast-Feeding

Guideline 39: The EP suggests that the use of hydrolyzed infant formulas, as 

opposed to cow’s milk formula, may be considered as a strategy for preventing the 

development of FA in at-risk infants who are not exclusively breast-fed (“at risk”

is defined in Guideline 32). Cost and availability of extensively hydrolyzed infant 

formulas may be weighed as prohibitive factors. 

5.3.4. Timing of Introduction of Allergenic Foods to Infants

Guideline 40: The EP suggests that the introduction of solid foods should not be 

delayed beyond 4 to 6 months of age. Potentially allergenic foods may be introduced at 

this time as well.
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SECTION 6. Diagnosis and Management of FoodInduced Anaphylaxis and Other Acute Allergic 

Reactions to Foods

6.1. Definition of Anaphylaxis

Anaphylaxis is defined as a serious allergic reaction that is rapid in onset and may cause death. 

Typically, IgE-mediated food-induced anaphylaxis is believed to involve systemic mediator 

release from sensitized mast cells and basophils. The term anaphylactoid has been used in 

the past to indicate adverse reactions that are not IgE mediated and typically are not lifethreatening. This term is imprecise and will not be used in these Guidelines. 

6.2. Diagnosis of Acute, Life-Threatening, Food-Induced Allergic Reactions

Guideline 41: The EP recommends that the health care professional considering a diagnosis 

of food-induced anaphylaxis should understand: 

•	 The signs and symptoms characteristic of anaphylaxis

•	 The timing of symptoms in association with food ingestion/exposure

•	 Comorbid conditions, such as asthma, that may affect treatment and outcome

•	 The limited utility of laboratory parameters in the acute-care setting

6.3. Treatment of Acute, Life-Threatening, Food-Induced Allergic Reactions

6.3.1. First-Line and Adjuvant Treatment for Food-Induced Anaphylaxis

Guideline 42: The EP recommends that treatment for food-induced anaphylaxis 

should focus on the following:

•	 Prompt and rapid treatment after onset of symptoms (see table II)

•	 Intramuscular (IM) epinephrine as first-line therapy

• Other treatments, which are adjunctive to epinephrine dosing
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TABLE II. Summary of the Pharmacologic Management of Anaphylaxis (Modified)

Note: These treatments often occur concomitantly, and are not meant to be sequential, with 

the exception of epinephrine as first-line treatment.

In the Outpatient Setting

•	 First-line treatment:

− Epinephrine, IM; auto-injector or 1:1,000 solution

` Weight 10–25 kg: 0.15 mg epinephrine autoinjector, IM (anterior-lateral thigh)

` Weight >25 kg: 0.3 mg epinephrine autoinjector, IM (anterior-lateral thigh)

` Epinephrine (1:1,000 solution) (IM), 0.01 mg/kg per dose; maximum dose, 0.5 mg per dose 

(anterior-lateral thigh)

− Epinephrine doses may need to be repeated every 5–15 minutes

•	 Adjunctive treatment:

− Bronchodilator (β2-agonist): albuterol 

` MDI (child: 4–8 puffs; adult: 8 puffs) or

` Nebulized solution (child: 1.5 ml; adult: 3 ml) every 20 minutes or continuously as needed

− H1

 antihistamine: diphenhydramine

` 1–2 mg/kg per dose

` Maximum dose, 50 mg IV or oral (oral liquid is more readily absorbed than tablets) 

` Alternative dosing may be with a less-sedating second generation antihistamine 

− Supplemental oxygen therapy

− IV fluids in large volumes if patient presents with orthostasis, hypotension, or incomplete 

response to IM epinephrine

− Place the patient in recumbent position if tolerated, with the lower extremities elevated

In the Hospital-Based Setting

•	 First-line treatment:

− Epinephrine IM as above, consider continuous epinephrine infusion for persistent hypotension 

(ideally with continuous non-invasive monitoring of blood pressure and heart rate); alternatives 

are endotracheal or intra-osseous epinephrine

•	 Adjunctive treatment:

− Bronchodilator (β2

-agonist): albuterol 

` MDI (child: 4–8 puffs; adult: 8 puffs) or

` Nebulized solution (child: 1.5 ml; adult: 3 ml) every 20 minutes or continuously as needed

− H1 antihistamine: diphenhydramine

` 1–2 mg/kg per dose

` Maximum dose, 50 mg IV or oral (oral liquid is more readily absorbed than tablets) 

` Alternative dosing may be with a less-sedating second generation antihistamine 
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TABLE II. Summary of the Pharmacologic Management of Anaphylaxis (Modified) (continued)

In the Hospital-Based Setting (continued)

− H2 antihistamine: ranitidine

` 1–2 mg/kg per dose

` Maximum dose, 75–150 mg oral and IV

− Corticosteroids

` Prednisone at 1 mg/kg with a maximum dose of 60–80 mg oral or

` Methylprednisolone at 1 mg/kg with a maximum dose of 60–80 mg IV

− Vasopressors (other than epinephrine) for refractory hypotension, titrate to effect

− Glucagon for refractory hypotension, titrate to effect

` Child: 20–30 μg/kg

` Adult: 1–5 mg

` Dose may be repeated or followed by infusion of 5–15 μg/min

− Atropine for bradycardia, titrate to effect

− Supplemental oxygen therapy

− IV fluids in large volumes if patients present with orthostasis, hypotension, or incomplete 

response to IM epinephrine

− Place the patient in recumbent position if tolerated, with the lower extremities elevated

Therapy for the Patient at Discharge 

•	 First-line treatment:

− Epinephrine auto-injector prescription (2 doses) and instructions

− Education on avoidance of allergen

− Follow-up with primary care physician

− Consider referral to an allergist

•	 Adjunctive treatment: 

− H1 antihistamine: diphenhydramine every 6 hours for 2–3 days; alternative dosing with a 

nonsedating second-generation antihistamine

− H2 antihistamine: ranitidine twice daily for 2–3 days

− Corticosteroid: prednisone daily for 2–3 days

IM, intramuscular; IV, intravenous; MDI, metered-dose inhaler.

Note: This table is presented as table VI in the Guidelines.

Epinephrine is the first-line treatment in all cases of anaphylaxis. All other drugs have 

a delayed onset of action. When there is suboptimal response to the initial dose of 

epinephrine, or if symptoms progress, repeat epinephrine dosing remains first-line 

therapy over adjunctive treatments. 
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The cornerstones of initial management should begin with the following concurrent 

steps: 

•	 Elimination of additional allergen exposure

•	 IM injection of epinephrine 

•	 Call for help (summon a resuscitation team in the hospital setting, call 9–1–1 or 

an equivalent service in the community setting), although attempts to summon 

help should not delay use of epinephrine

These actions should be quickly followed by these additional steps: 

•	 Placement of the patient in a recumbent position (if tolerated), with the lower 

extremities elevated

•	 Provision of supplemental oxygen

•	 Administration of intravenous (IV) fluid (volume resuscitation) 

In Summary: The use of antihistamines is the most common reason reported for not 

using epinephrine and may place a patient at significantly increased risk for progression 

toward a life-threatening reaction. 

6.3.2. Treatment of Refractory Anaphylaxis

No published prospective studies exist on the optimal management of refractory 

anaphylactic shock. Repeated use of epinephrine, as well as IV fluids, corticosteroids, 

and vasopressor agents, may be needed. Prompt transfer to an acute-care facility and 

intensive-care unit for treatment and monitoring is essential.

6.3.3. Possible Risks of Acute Therapy for Anaphylaxis

There are no absolute contraindications to epinephrine use in anaphylaxis. However, 

there are subgroups of patients who might theoretically be at higher risk for adverse 

effects during epinephrine therapy. Because the risk of death or serious disability from 

anaphylaxis itself usually outweighs other concerns, existing evidence clearly favors 

the benefit of epinephrine administration in most situations. Some level of decision 

making regarding the risk-to-benefit ratio may be warranted for patients under specific 

circumstances (described in the Guidelines).

6.3.4. Treatment To Prevent Biphasic or Protracted Food-Induced Allergic Reactions

Very little information exists that defines the mechanism of biphasic or protracted 

allergic reactions. Similarly, little information exists to support specific therapy to 

prevent biphasic or protracted food-induced allergic reactions. In general, induction 

and recruitment of inflammatory cells and release of preformed, long-acting mediators 

from mast cells have been implicated as mechanisms. Due to their anti-inflammatory 
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properties, systemic corticosteroids are often recommended to prevent biphasic or 

protracted food-induced allergic reactions, but little data support their use.

6.3.5. Management of Milder, Acute Food-Induced Allergic Reactions in Health Care Settings

Milder forms of allergic reactions, such as flushing, urticaria, isolated mild angioedema, 

or symptoms of OAS, can be treated with H1

 and H2 antihistamine medications. When 

antihistamines alone are given, ongoing observation and monitoring are warranted to 

ensure a lack of progression to more significant symptoms of anaphylaxis. If progression 

or increased severity is noted, epinephrine should be administered immediately. 

Additionally, if there is a history of a prior severe allergic reaction, epinephrine should be 

administered promptly and earlier in the course of treatment (e.g., at the onset of even 

mild symptoms).

6.4. Management of Food-Induced Anaphylaxis

Guideline 43: The EP recommends that the management of food-induced anaphylaxis 

should focus on the following:

•	 Dosing with IM epinephrine followed by transfer to an emergency facility for 

observation and possible further treatment

• Observation for 4 to 6 hours or longer based on severity of the reaction

•	 Education for patient and family on:

− Allergen avoidance

− Early recognition of signs and symptoms of anaphylaxis

− Anaphylaxis emergency action plan implementation

− Appropriate IM epinephrine administration

− Medical identification jewelry or an anaphylaxis wallet card

•	 Epinephrine auto-injector prescription and training provided at the time of discharge

•	 Continuation of adjunctive treatment after patient discharge:

− H1 antihistamine: diphenhydramine every 6 hours for 2–3 days; alternative dosing 

with a nonsedating second-generation antihistamine

− H2

 antihistamine: ranitidine twice daily for 2–3 days

− Corticosteroid: prednisone daily for 2–3 days

•	 Follow-up appointment with primary health care professional (after the food-induced 

anaphylactic reaction), with consideration for additional follow-up with a clinical 

specialist such as an allergist/immunologist
NIAID I GUIDELINES FOR THE DIAGNOSIS AND MANAGEMENT OF FOOD ALLERGY

26

APPENDIX A. Primary Author Affiliations and 

Acknowledgments

Primary Authors

*Joshua A. Boyce, M.D. 

Division of Rheumatology, Immunology 

and Allergy

Brigham and Women’s Hospital

Department of Medicine

Harvard Medical School

Boston, MA

*Amal Assa’ad, M.D. 

Division of Allergy and Immunology

Cincinnati Children’s Hospital Medical 

Center

University of Cincinnati

Cincinnati, OH

*A. Wesley Burks, M.D. 

Division of Allergy and Immunology

Department of Pediatrics

Duke University Medical Center

Durham, NC

*Stacie M. Jones, M.D. 

Division of Allergy and Immunology

Department of Pediatrics

University of Arkansas for Medical Sciences

Arkansas Children’s Hospital

Little Rock, AR

*Hugh A. Sampson, M.D. 

Elliot and Roslyn Jaffe Food Allergy Institute

Division of Allergy and Immunology

Department of Pediatrics

Mount Sinai School of Medicine

New York, NY

*Robert A. Wood, M.D. 

Division of Allergy and Immunology

Department of Pediatrics

The Johns Hopkins University School of 

Medicine

Baltimore, MD

Marshall Plaut, M.D. 

Division of Allergy, Immunology, and 

Transplantation

National Institute of Allergy and Infectious 

Diseases 

National Institutes of Health

Bethesda, MD

Susan F. Cooper, M.Sc. 

Division of Allergy, Immunology, and 

Transplantation

National Institute of Allergy and Infectious 

Diseases

National Institutes of Health

Bethesda, MD

Matthew J. Fenton, Ph.D. 

Division of Allergy, Immunology, and 

Transplantation

National Institute of Allergy and Infectious 

Diseases

National Institutes of Health

Bethesda, MD

Authors who are members of the Expert Panel are denoted with an asterisk (*) in this list.

For additional information, please contact the National Institute of Allergy and Infectious Diseases at 

daitinfo@niaid.nih.gov.
NIAID I SUMMARY OF THE NIAID-SPONSORED EXPERT PANEL REPORT

27

APPENDIX A

27

PRIMARY AUTHOR AFFILIATIONS AND ACKNOWLEDGMENTS

Acknowledgments

NIAID-Sponsored Expert Panel

S. Hasan Arshad, M.B.B.S., M.R.C.P., D.M., 

F.R.C.P. 

School of Medicine

University of Southampton

Southampton, UK

The David Hide Asthma and Allergy Research 

Centre

St. Mary’s Hospital

Newport, Isle of Wight, UK

Southampton University Hospital NHS Trust

Southampton, UK

Sami L. Bahna, M.D., Dr.P.H. 

Department of Pediatrics

Section of Allergy and Immunology

Louisiana State University Health Sciences 

Center

Shreveport, LA

Lisa A. Beck, M.D. 

Department of Dermatology

University of Rochester Medical Center

Rochester, NY

Carol Byrd-Bredbenner, Ph.D., R.D., F.A.D.A. 

Department of Nutritional Sciences

Rutgers University

New Brunswick, NJ

Carlos A. Camargo, Jr., M.D., Dr.P.H. 

Department of Emergency Medicine

Division of Rheumatology, Allergy and 

Immunology

Department of Medicine

Massachusetts General Hospital

Harvard Medical School

Boston, MA

Lawrence Eichenfield, M.D. 

Division of Pediatric and Adolescent 

Dermatology

Rady Children’s Hospital

San Diego, CA

Departments of Pediatrics and Medicine

University of California, San Diego

San Diego, CA

Glenn T. Furuta, M.D. 

Section of Pediatric Gastroenterology, 

Hepatology, and Nutrition

Digestive Health Institute

Children’s Hospital Denver

Aurora, CO

Department of Pediatrics

National Jewish Health

Denver, CO

Department of Pediatrics

University of Colorado Denver School of 

Medicine

Aurora, CO

Jon M. Hanifin, M.D. 

Department of Dermatology

Oregon Health and Science University

Portland, OR

Carol Jones, R.N., A.E.-C. 

Asthma Educator and Consultant

Allergy and Asthma Network Mothers of 

Asthmatics

McLean, VA

Monica Kraft, M.D. 

Division of Pulmonary, Allergy, and Critical 

Care Medicine

Department of Medicine

Duke University Medical Center

Durham, NC
NIAID I GUIDELINES FOR THE DIAGNOSIS AND MANAGEMENT OF FOOD ALLERGY

28

APPENDIX A

28

PRIMARY AUTHOR AFFILIATIONS AND ACKNOWLEDGMENTS

Bruce D. Levy, M.D. 

Partners Asthma Center

Pulmonary and Critical Care Medicine

Brigham and Women’s Hospital and 

Harvard Medical School

Boston, MA

Phil Lieberman, M.D. 

Division of Allergy and Immunology

Department of Medicine

University of Tennessee College of Medicine

Memphis, TN

Stefano Luccioli, M.D. 

Office of Food Additive Safety

U.S. Food and Drug Administration

College Park, MD

Kathleen M. McCall, B.S.N., R.N. 

Children’s Hospital of Orange County

Orange, CA

Lynda C. Schneider, M.D. 

Division of Immunology

Children’s Hospital Boston

Boston, MA

Ronald A. Simon, M.D. 

Division of Allergy, Asthma and Immunology

Scripps Clinic

San Diego, CA

F. Estelle R. Simons, M.D. 

Departments of Pediatrics and Child Health 

and Immunology

Faculty of Medicine

University of Manitoba

Winnipeg, Manitoba, Canada

Stephen J. Teach, M.D., M.P.H. 

Division of Emergency Medicine

Children’s National Medical Center

Washington, DC

Barbara P. Yawn, M.D., M.P.H., M.Sc.

Department of Research

Olmsted Medical Center

Rochester, MN

Department of Family and Community 

Health

University of Minnesota School of Medicine

Minneapolis, MN

NIAID Staff

Julie M. Schwaninger, M.Sc. 

Division of Allergy, Immunology, and 

Transplantation

National Institute of Allergy and Infectious 

Diseases

National Institutes of Health

Bethesda, MD
NIAID I SUMMARY OF THE NIAID-SPONSORED EXPERT PANEL REPORT

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APPENDIX B. List of Abbreviations

AAP: American Academy of Pediatrics 

ACIP: Advisory Committee on Immunization Practices 

AD: Atopic dermatitis 

AP: Allergic proctocolitis 

APT: Atopy patch test 

CC: Coordinating Committee 

COI: Conflict of interest 

EoE: Eosinophilic esophagitis 

EP: Expert Panel 

FA: Food allergy 

FPIES: Food protein-induced enterocolitis syndrome 

GI: Gastrointestinal 

GRADE: Grading of Recommendations Assessment, Development and Evaluation 

ICD-9-CM: International Classification of Diseases, Ninth Revision, Clinical Modification 

IgE: Immunoglobulin E

IM: Intramuscular 

IV: Intravenous

MDI: Metered-dose inhaler

MMR: Measles, mumps, and rubella 

MMRV: Measles, mumps, rubella, and varicella 

NIAID: National Institute of Allergy and Infectious Diseases 

OAS: Oral allergy syndrome 

sIgE: Allergen-specific IgE 

SPT: Skin prick test 


U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES

National Institutes of Health

National Institute of Allergy 

and Infectious Diseases

NIH Publication No. 11-7700

December 2010

www.niaid.nih.gov