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Food Allergy. Againdra K. Bewtra M.B.B.S., M.D. Food Allergy: Outline. Definitions Pathophysiology Signs and Symptoms Food Allergy - Induced Diseases Prevalence and Natural History Diagnosis and Management Prevention. Introduction/Terms.

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food allergy

Food Allergy

Againdra K. Bewtra M.B.B.S., M.D.

food allergy outline
Food Allergy: Outline
  • Definitions
  • Pathophysiology
  • Signs and Symptoms
  • Food Allergy - Induced Diseases
  • Prevalence and Natural History
  • Diagnosis and Management
  • Prevention
introduction terms
  • Adverse food reaction: any aberrant reaction to food
    • toxic vs. nontoxic
  • Food intolerance: any adverse reaction due to physiologic ornonimmunologic mechanism
  • Food allergy: any adverse reaction due to an immunologic mechanism
definitions adverse reactions to food
Definitions: Adverse Reactions to Food

A. Nonimmunologic

Toxic / Pharmacologic

Non-Toxic / Intolerance

  • Bacterial food poisoning
  • Heavy metal poisoning
  • Scromboid fish poisoning
  • Caffeine
  • Alcohol
  • Histamine
  • Lactase deficiency
  • Galactosemia
  • Pancreatic insufficiency
  • Gallbladder / liver disease
  • Hiatal hernia
  • Gustatory rhinitis
  • Anorexia nervosa
definitions adverse reactions to food1
Definitions: Adverse Reactions to Food

B. Immunologic Spectrum


Non-IgE Mediated

  • Oral Allergy Syndrome
  • Anaphylaxis
  • Urticaria
  • Allergic Rhinitis
  • Acute Bronchospasm
  • Eosinophilic esophagitis
  • Eosinophilic gastritis
  • Eosinophilic gastroenteritis
  • Atopic dermatitis
  • Asthma
  • Protein-Induced Enterocolitis
  • Protein-Induced Enteropathy
  • Eosinophilic proctitis
  • Dermatitis herpetiformis
  • Food-induced Pulmonary Hemosiderosis
  • More common in atopic patients
  • One fourth of atopic adults report adverse reaction to food. (Allergy 1978;33:189-196) Will alter dietary habits
  • True prevalence unknown
    • Public perception (20-25%)> true prevalence
    • 28% mothers perceive kids to have food allergies
    • 8% of these children were DBPCFC positive (pediatrics 1987;79:683-196)
    • 1/3 of those with suggestive history have IgE mediated food allergy
    • 1-2% of adults
    • 8% of children <3 years, (worse if atopic)
pathophysiology allergens
Pathophysiology: Allergens
  • Any food can cause allergic sx
  • Protein (not fat / carbohydrate)
    • 10-70 kD water soluble glycoproteins
    • Stable to treatment with heat, acid and proteases
    • Few foods cause most of food allergy
    • Adults: peanuts, shellfish, tree nuts, fish ->85%
    • Children: eggs, peanut, milk, soy, tree nuts, fish, shellfish, wheat ->90%
    • Early introduction of foods stimulates excess IgE
  • Dyes/flavorings can also elicit allergy symptoms but rare
    • Tartrazine (FD&C yellow dye No.5), found in orange, green or yellow food
    • Flavorings: nitrites, nitrates, MSG, sulfites
  • Single food allergy> multiple food allergy
  • Characterization of epitopes underway
    • Linear vs conformational epitopes
    • B-cell vs T-cell epitopes
food allergy prevalence in specific disorders
Food Allergy Prevalence in Specific Disorders


Food Allergy Prevalence



Oral allergy syndrome

25-75% in pollen allergic

37% in children

(rare in adults)

Atopic dermatitis

20% in acute

(rare in chronic)


5-6% in asthmatic or food allergic



Chronic rhinitis


pathogenesis of food allergy
Pathogenesis of Food Allergy
  • Gut barriers: Physical
    • defensive barrier against pathogens; tolerate food protein
    • gastric acid, proteolytic enzymes, mucus, peristalsis
      • digest protein to make it less antigenic by: reduce size, alter the structure
  • Gut barrier: Immunologic - Dominant response is tolerance
    • GALT [Peyer’s patches, appendix, IELC (Intraepithelial lymphocytic cells), LC, plasma cells, mast cells - lamina propria, mesenteric LN]
    • Food ingestionAb release (sIgA) (IgG, IgM, IgE)
      • sIgA: binds protein, forms complexes = decreased absorption
      • 2% macromolecules are absorbed-to these oral tolerance devel.
pathogenesis of food allergy1
Pathogenesis of Food Allergy
  • Dominant response of GALT is suppression/tolerance
  • Oral tolerance induction occurs by IELC and GALT
  • IEC: Soluble Ag(food) presented primarily by IELC leading to immune suppression
    • Central APC for immunosuppression in the gut
    • Have MHC-II and present Ag to CD8+ by (CD1d)
  • GALT: Pathogens selectively presented to M cells in the (GALT)
    • bacteria, viruses, parasites
    • sampled by M cells (Peyer’s patches)  IgA
barrier immaturity in the infant
Barrier immaturity in the Infant
  • Low basal acid output
  • Immature intestinal proteolytic activity
  • Immature microvilli-> Ag transport into IEC
  • Newborns lack sIgA and IgM in exocrine secretion
  • Early introduction of numerous food Ag stimulates excess IgE
pathogenesis of food allergy2
Pathogenesis of Food Allergy
  • Genetic predisposition to lack of oral tolerance
  • Food-specific IgE bind to FcRI on mast cells/basophils and FcRII on macrophages, monocytes, lymphocytes, eosinophils and platelets
  • Release of mediators which produce: vasodilation, smooth muscle contraction, mucus secretion.
  • Non-IgE: possibly Type III, Type IV
pathophysiology immune mechanisms
Pathophysiology: Immune Mechanisms
  • Protein digestion
  • Antigen processing
  • Some Ag enters blood




Mast cell

Non-IgE Mediated


  • TNF-
  • IL-5

T cell

B cell

signs and symptoms
Signs and Symptoms

IgE Non-IgE Acute Chronic




Atopic dermatitis


Throat tightness








clinical disorders signs and symptoms
Clinical Disorders-Signs and Symptoms
  • IgE vs. non-IgE
  • GI, cutaneous, respiratory
  • IgE:
    • GI: vomit, diarrhea, pain
    • Resp: throat tightness, rhinitis, asthma
    • Skin: urticaria, angioedema, atopic dermatitis
    • Other GI Findings: gastric hypotonia, retention of meal, pylorospasm, peristaltic changes
  • Non-IgE
    • GI: vomiting, diarrhea, pain
    • Resp: asthma
    • Skin: atopic dermatitis
oral allergy syndrome
Oral Allergy Syndrome
  • ? Contact urticaria
  • Rapid onset, IgE-mediated, rarely progressive
  • Oral pruritis, tingling, AE of lips, tongue, palate, throat
  • Usually fresh fruits and vegetables
  • Heat labile: cooked forms: no reaction
  • Cause: cross reactive proteins in pollen/food (fruit or vegetables)



Birch Apple, apricot, carrot, cherry, kiwi, plum

Ragweed Banana, cucumber, melon, watermelon

Grass Cherry, peach, potato, tomato

fatal food anaphylaxis
Fatal Food Anaphylaxis
  • Frequency: ~ 150 deaths / year
  • Risk:
    • Underlying asthma – Delayed epinephrine
    • Symptom denial – Previous severe reaction
  • History: known allergic food
  • Key foods: peanut / nuts / shellfish
  • Biphasic reaction
  • Lack of cutaneous symptoms
anaphylaxis anaphylaxis syndromes
Anaphylaxis / Anaphylaxis Syndromes
  • Food-induced anaphylaxis (IgE mediated)
    • Rapid-onset
    • Multi-organ system involvement
    • Potentially fatal
    • Any food, highest risk: peanut, nut, seafood
  • Symptoms: cutaneous, respiratory, hypotension, vascular collapse, dysrythmias
  • Pts usually have the following in common:
    • Asthma, accidental ingestion of the food allergen,previous allergic reaction to the same food, immediate symptoms
  • Food-associated, exercise-induced (usually within 2-4 hours after ingestion of food)
    • Associated with a particular food
    • Associated with eating any food
prevalence of clinical cross reactivity among food families
Prevalence of Clinical Cross Reactivity Among Food “Families”

Prevalence of Allergy to > 1 Food in Family

Food Allergy


30% -100%

Tree Nut

15% - 40%







disorders not proven to be related to food allergy
Disorders Not Proven to be Related to Food Allergy
  • Migraines
  • Behavioral / Developmental disorders
  • Arthritis
  • Seizures
  • Inflammatory bowel disease
natural history
Natural History
  • Dependent on food & immuno-pathogenesis
  • ~ 85% CM, egg, wheat, soy allergy remit by 3 yrs
    • Declining/low levels of specific-IgE predictive
    • IgE binding to conformational epitopes predictive
  • Allergy to peanut, nuts, seafood typically persist
  • Non-IgE-mediated GI allergy
    • Infant forms resolve 1-3 years
    • Toddler / adult forms more persistent
diagnosis history physical
Diagnosis: History / Physical
  • History: symptoms, timing, reproducibility
    • Acute reactions vs chronic disease
  • Diet details / symptom diary
    • Specific causal food(s)
    • “Hidden” ingredient(s)
  • Physical examination: evaluate disease severity
  • Identify general mechanism
    • Allergy vs intolerance
    • IgE versus non-IgE mediated
diagnosis laboratory evaluation
Diagnosis: Laboratory Evaluation
  • Suspect IgE-mediated
    • Prick skin tests (fresh extract if oral allergy)
    • RAST
  • Suspect non-IgE-mediated
    • Consider biopsy of gut, skin
  • Suspect non-allergic, consider:
    • Breath hydrogen
    • Sweat test
    • Endoscopy
  • Adjunctive tests
    • Endoscopy,/biopsy, stool analysis (heme, leukocytes, eosinophils)
  • Elimination diet  proof of reactivity
  • Oral food challenge: DBPCFC
    • Gold standard
interpretation of laboratory tests
Interpretation of Laboratory Tests
  • Positive prick test or RAST
    • Indicates presence of IgE antibody NOT clinical reactivity (~50% false positive)
  • Negative prick test or RAST
    • Essentially excludes IgE antibody (>95%)
  • ID skin test with food
    • Risk of systemic reaction & not predictive
    • Contraindicated
  • Unproven/experimental tests (useless)
    • Provocation/neutralization, cytotoxic tests, applied kinesiology, hair analysis, IgG4
diagnosis elimination diets and food challenges
Diagnosis: Elimination Diets and Food Challenges
  • Elimination diets (1 to 6 weeks)
    • Eliminate suspected food(s), or
    • Prescribe limited “eat only” diet, or
    • Elemental diet
  • Oral challenge testing (MD supervised, ER meds available)
    • Open
    • Single-blind
    • Double-blind, placebo-controlled (DBPCFC)
diagnostic approach ige mediated allergy
Diagnostic Approach: IgE-Mediated Allergy
  • Test for specific-IgE antibody
    • Negative: reintroduce food*
    • Positive: start elimination diet
  • Elimination diet
    • No resolution: reintroduce food*
    • Resolution
      • Open / single-blind challenges to “screen”
      • DBPCFC for equivocal open challenges

* Unless convincing history warrants supervised challenge

diagnostic approach non ige mediated disease
Diagnostic Approach: Non-IgE-Mediated Disease
  • Includes disease with unknown mechanisms
    • Food additive allergy
  • Elimination diets (may need elemental diet)
  • Oral Challenges
    • Timing/dose/approach individualized for disorder
      • Enterocolitis syndrome can elicit shock
      • Enteropathy / eosinophilic gastroenteritis may need prolonged feedings to develop symptoms
    • DBPCFCs preferred
    • May require ancillary testing (endoscopy / biopsy)
Strict avoidance


Of 32 peanut allergic patients studied by bock et al. Only 8 were successful at peanut avoidance for 5 years.


Peanut allergens on airplanes.


Epi-pen carried at all times

Instructed use in office

Use and go to E.R.

Observe 4 hours

Risk of fatality increases with delay in epinephrine administration

1/3 of pts with fatal or near fatal anaphylaxis had biphasic reaction

treatment dietary elimination
Treatment: Dietary Elimination
  • Hidden ingredients (peanut in sauces or egg rolls)
  • Labeling issues (“spices”, changes, errors)
  • Cross contamination (shared equipment)
  • “Code words” (“Natural flavor” may be CM)
  • Seeking assistance
    • Registered dietitian: (
    • Food Allergy Network (; 800-929-4040)
example milk elimination
Example: Milk Elimination

Artificial butter flavor, butter, butter fat, buttermilk, casein, caseinates (sodium, calcium, etc.), cheese, cream, cottage cheese, curds, custard, Half&Half®, hydrolysates (casein, milk, whey), lactalbumin, lactose, milk (derivatives, protein, solids, malted, condensed, evaporated, dry, whole, low-fat, non-fat, skim), nougat, pudding, rennet casein, sour cream, sour cream solids, sour milk solids, whey (delactosed, demineralized, protein concentrate), yogurt. MAY contain milk: brown sugar flavoring, natural flavoring, chocolate, caramel flavoring, high protein flour, margarine, Simplesse®.

treatment emergency medications
Treatment: Emergency Medications
  • Epinephrine: drug of choice for reactions
    • Self-administered epinephrine readily available
    • Train patients: indications/technique
  • Antihistamines: secondary therapy
  • Emergency plan in writing
    • Schools, spouses, caregivers, mature sibs / friends
  • Emergency identification bracelet
treatment follow up
Treatment: Follow-Up
  • Re-evaluate for tolerance periodically
  • Interval and decision to re-challenge:
    • Type of food allergy
    • Severity of previous symptoms
    • Allergen
  • Ancillary testing
    • Skin prick test/RAST may remain positive
    • Reduced concentration food specific-IgE encouraging
allergy prevention
Allergy Prevention

Pollutants, Tobacco smoke

Food allergens early











other treatments
Possibly effective


Treatment of peanut allergy with rush I.T. Oppenheimer JJ et al. JACI 1992;90:256-262

Oral allergen gene immunization


Roy et al

Horner et al reported decreased anaphylaxis with DNA vaccine

Generally found not effective

H1 and H2 antihistamines

Oral Cromolyn sodium



Other Treatments
future immunomodulatory therapies
Future Immunomodulatory Therapies
  • Recombinant anti-IgE antibody
  • Gene (naked DNA) immunization
  • Mutated B-cell epitopes
  • Minimal T-cell epitopes
  • Immune-modulating adjuvants (ISS)
  • Probiotics
reasons for allergy referral
Reasons for Allergy Referral
  • Identification of causative food
  • Institution of elimination diet
  • Education on food avoidance
  • Development of action plan
  • Prevention of other allergies
  • 2% of the population have food allergy
  • Children: milk, eggs, peanuts, soy, wheat
  • Adults: peanuts, shellfish, nuts, fish
  • History and physical
  • IgE and non-IgE mediated conditions exist
  • Dx by elimination and challenge
  • Tx avoidance, education, preparation for emergencies
  • Periodic re-challenge to monitor tolerance