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GLORIA Module 6: Food Allergy Global Resources in Allergy (GLORIA™)

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Global Resources in Allergy (GLORIA™)

Global Resources In Allergy (GLORIA™) is the flagship program of the World Allergy Organization (WAO). Its curriculum educates medical professionals worldwide through regional and national presentations. GLORIA modules are created from established guidelines and recommendations to address different aspects of allergy-related patient care.


World Allergy Organization (WAO)

The World Allergy Organization is an international coalition of 77 regional and national allergy and clinical immunology societies.


WAO’s Mission

WAO’s mission is to be a global resource and advocate in the field of allergy, advancing excellence in clinical care, education, research and training through a world-wide alliance of allergy and clinical immunology societies

food allergy a gloria tm module

Food AllergyA GLORIATM Module


Prof. Cassim Motala

University of Cape Town and Red Cross Children's Hospital Cape Town, South Africa

Dr. M. Dolores Ibáñez

Hospital Nino Jesus

Madrid, Spain


Prof. Alessandro Fiocchi

Melloni University Hospital

Milan, Italy

Prof. Joaquín Sastre

Fundación Jimenez Diaz,

Department of MedicineUniversidad Autonoma de Madrid Madrid, Spain

learning objectives
Learning objectives

At the end of this presentation you will be able to:

  • Recognise the main pathogenic food allergens in adults and children
  • Differentiate between IgE-mediated, cell-mediated and mixed IgE- and cell-mediated food-related diseases in different organ systems
  • Discuss the diagnosis of food allergy and the limitations of diagnostic techniques
  • Review the treatment of food allergy
adverse reactions to food definition
Adverse reactions to food: definition

Any abnormal clinical response attributed to ingestion, contact or inhalation of any food, a food derivative or a food additive

  • Toxic
  • Non toxic or hypersensitivity

Adverse reactions to food



Non-immune mediated









Adverse Reactions to Food: Position Paper. Allergy 1995; 50:623-635


Prevalence of food allergy

Precise prevalence is unknown, but estimates are:

  • Adults: 1.4% - 2.4%
  • Children < 3 years: ~ 6%
  • Atopic dermatitis (mild/severe): ~35%
  • Asthmatic children: 6 - 8%
  • Prevalence depends on: Genetic factors, age, dietary habits, geography and diagnostic procedures

Adapted from Sampson HA. Adverse Reactions to Foods. Allergy Principles and Practice. 2003


Food allergy in children: international


Birds Nest








Tree Nuts




















second tier foods
“Second tier” foods
  • 10% reactions to foods
  • 160 foods
  • Fruits
  • Vegetables
  • Seeds (sesame, sunflower, poppy)
  • Spices
pathophysiology allergens
Pathophysiology: allergens
  • Proteins (not fat/carbohydrate)- 10-70 kD glycoproteins- Heat resistant, acid stable
  • Major allergenic foods (>85% of allergy)- Children: milk, egg, soy, wheat, other depending on geographical


- Adult: peanut, nuts, shellfish, fish

  • Single food (or related) > many food allergies
  • Characterization of epitopes underway - Linear vs conformational epitopes- B-cell vs T-cell epitopes
pathogenesis of food hypersensitivity gut barrier
Pathogenesis of food hypersensitivity: gut barrier
  • The immune system associated with this barrier is capable of discriminating among harmless foreign proteins or commensal organisms and dangerous pathogens
  • Food allergy is an abnormal response of the mucosal immune system to antigens delivered through the oral route
  • The immature state of the mucosal barrier and immune system might play a role in the increased prevalence of gastrointestinal infections and food allergy in the first few years of life

Adapted from J Allergy Clin Immunol 2004;113:808-809

pathogenesis of food hypersensitivity gut barrier16
Pathogenesis of food hypersensitivity: gut barrier
  • About 2 % of ingested food antigens are absorbed and transported throughout the body in an immunologically intact form, even through the immature gut
  • The underlying immunologic mechanisms involved in oral tolerance induction have not been fully elucidated

Adapted from J Allergy Clin Immunol 2004;113:808-809

pathophysiology immune mechanisms
Pathophysiology: immune mechanisms
  • Protein digestion
  • Antigen processing
  • Some Ag enters blood




Mast cell




T cell

B cell

  • TNF-
  • IL-5
food allergy clinical manifestations
Food allergy: clinical manifestations

IgE IgE/Non-IgE Non-IgE


Celiac disease

Contact dermatitis

Herpetiform dermatitis

Heiner´s syndrome


Rhinitis /Asthma


Oral allergic syndrome

Gastrointestinal symptoms (GIT)

Atopic dermatitis




Adapted from J Allergy Clin Immunol. 1999;103:717-728

cutaneous food hypersensitivities atopic eczema
Cutaneous food hypersensitivities:atopic eczema
  • Generally begins in early infancy
  • Characterized by typical distribution, extreme pruritus, and chronically relapsing course
  • Allergen-specific IgE antibodies bound to Langerhans cells play a unique role as “non-traditional” receptors
  • Double blind, placebo-controlled food challenges generally provoke a markedly pruritic, erythematous, morbilliform rash
  • Food allergy plays a pathogenic role in about 35 % of moderate-to-severe atopic dermatitis in children
cutaneous food hypersensitivities
Cutaneous food hypersensitivities

Acute Urticaria and Angioedema:

  • The most common symptoms of food allergic reactions
  • The exact prevalence of these reactions is unknown
  • Acute urticaria due to contact with food is also common

Chronic Urticaria:

  • Food allergy is an infrequent cause of chronic urticaria and angioedema
ige mediated respiratory manifestations
IgE mediated: respiratory manifestations


  • An uncommon manifestation of food allergy
  • Usually seen with other food-induced symptoms
  • Vapors or steam emitted from cooking food may induced asthmatic reactions
  • Food-induced asthmatic symptoms should be suspected in patients with refractory asthma and history of atopic dermatitis, gastroesophageal reflux, food allergy or feeding problems as an infant, or history of positive skin tests or reactions to food


  • Usually seen during positive controlled challenge tests, but occasionally reported by patients
ige mediated systemic reaction anaphylaxis anaphylaxis syndrome
IgE Mediated: systemic reactionanaphylaxis/anaphylaxis syndrome
  • Food-induced anaphylaxis- Rapid-onset- Multi-organ system involvement- Potentially fatal- Any food, highest risk: peanut, nut, seafood, milk, egg
  • Food-dependent - exercise-induced- Associated with a particular food- Associated with eating any food
fatal food anaphylaxis
Fatal food anaphylaxis
  • Frequency: ~ 100 deaths/yr
  • Risk:- Underlying asthma - Delayed epinephrine- Symptom denial - Previous severe reaction
  • History: known allergic food
  • Biphasic reaction
  • Lack of cutaneous symptoms

Food-dependent, exercise-induced anaphylaxis





Mediator release

- Histamine

- Others (LTD4,PAF, etc)


Adapted from Adverse Reactions to Foods Committee.

Spanish Society of Allergy and Clinical Immunology

ige mediated git manifestation oral allergy syndrome oas
IgE-mediated: GIT manifestationoral allergy syndrome (OAS)
  • Elicited by a variety of plant proteins that cross-react with airborne allergens
  • Pollen allergic patients may develop symptoms following the ingestion of vegetable foods:

- Ragweed allergic patients: Fresh melons and bananas

- Birch pollen allergic patients: Raw potatoes,

carrots,celery, apples, pears, hazelnuts and kiwi

  • Immunotherapy for treating the pollen-induced rhinitis may reduce/eliminate oral allergy symptoms

Adapted from J Allergy Clin Immunol. 2004;


mixed ige non ige mediated git allergic eosinophilic disorders
Mixed IgE/Non-IgE mediated: GITallergic eosinophilic disorders
  • Characterized by infiltration of the esophagus, stomach and/or intestinal walls with eosinophils, basal zone hyperplasia, papillary elongation, absence of vasculitis and peripheral eosinophilia in about 50 % of patients
  • AEE can occur in children and adults. Increasing yearly incidence (23/100.000 population in Switzerland)
  • In children symptoms similar to gastroesophageal reflux and in adults dysphagia and impaction is common
  • Almost 50% of patients have other atopic diseases
  • Diagnosis is based on endoscopic findings and biopsy (>15-20 eosinophils per High Power Field)

Adapted from J Allergy Clin Immunol. 2006;



Mixed IgE/non-IgE mediated: GIT

allergic eosinophilic esophagitis (AEE)

  • Dysphagia
  • Abdominal pain
  • Poor response to anti - reflux drugs
  • Biopsy:Eosinophils ++++>20 eosinophils / HPF
  • Eotaxin – 3 tissue expression correlates with eosinophilia – crucial in pathogenesis of this disorder

Bullock et J Pediatr Gastroenterol Nutr. 2007


Mixed IgE/non-IgE mediated: GIT

allergic eosinophilic gastroenteritis (AEG)

  • Weight loss, FTT+/_oedema
  • Vomiting, diarrhoea (post-prandial)
  • Blood loss
  • Iron deficiency
  • Protein/iron- losing enteropathy
  • ↑ TH2 in blood and mucosa
  • ↑ Mast cells, Eosinophils in mucosa
  • Eotaxin - 3
  • Persistent food hypersensitivity at 5yr FU.

Chehade M et al JPGN 2006;42;516-521

aee and aeg
  • Food antigens have been implicated as one of the main etiologies
  • Skin prick test and atopy patch tests can be useful for food allergy diagnosis
  • Elimination diets or even amino-acid formula can be instituted on the basis of allergy testing, clinical history, biopsy and treatment response
  • Pharmacologic treatment: oral steroids and/or swallowed aerosolized fluticasone
  • ? Anti-IL-5 therapy

Adapted from J Allergy Clin Immunol. 2006;


non ige mediated git food protein induced syndromes typically milk and soy induced
Non-IgE mediated: GIT food protein induced syndromes (typically milk and soy induced)

Enterocolitis # Enteropathy Proctocolitis

Age Onset: Infant Infant/Toddler Newborn

Duration: 12-24 mo ? 12-24 mo < 12mo

Characteristics: Failure to thrive Malabsorption Bloody stools Shock Villous atrophy No systemic sx Lethargy Diarrhea Eosinophil Diarrhea

# Solid foods implicated: fish, corn, chicken, turkey, vegetables

Nowak-Wegrzyn et al Pediatrics 2003Zapatero Remon L et al. Allergol Immunopathol 2005

non ige mediated git food protein induced enterocolitis syndrome
Non IgE mediated: GIT food protein-induced enterocolitis syndrome
  • Occurs in infants prior to 8-12 months of age, but may be delayed in breast-fed babies (milk or soy protein-based formulas are implicated)
  • Symptoms may include irritability, protracted vomiting 1- 3 hours after feeding, bloody diarrhoea (leading to dehydration), anaemia, abdominal distension, failure to thrive
  • In adults and older children, fish, shellfish and cereals hypersensitivity may provoke a similar syndrome with delayed onset of severe nausea, abdominal cramps and protracted vomiting
  • Resolved: 50% at 18 months, 90% at 36 months

Adapted from J Allergy Clin Immunol. 2004;


non ige mediated git food protein induced enteropathy excluding celiac disease
Non-IgE Mediated: GIT food protein-induced enteropathy (excluding celiac disease)
  • Occurs from 0 - 24 months
  • Diarrhea (mild to moderate steatorrhea in about 80% of cases)
  • Food implicated: milk, cereals, egg, fish
  • Poor weight gain
  • Diagnosis:

-Biopsy shows patchy villous atrophy with prominent mononuclear round cell infiltrate, few eosinophils,

-Response to exclusion diet,

-Challenge test

  • Resolved at 2 - 3 years old

Adapted from J Allergy Clin Immunol. 2004;


non ige mediated git food protein induced protocolitis
Non-IgE Mediated: GIT food protein-induced protocolitis
  • Usually presents in the first few months of life and is thought to be due to food proteins passed to the infant in maternal breast milk, or to milk or soy-based formulas
  • Rectal bleeding is common
  • Diagnosis: endoscopy and colonic biopsy (eosinophils in epithelium and lamina propia)
  • Good response to extensively hydrolized formulas. Diet without dairy product in mother if lactating
  • Good prognosis with resolution at 12 months of life

Adapted from J Allergy Clin Immunol. 2004;


non ige mediated git celiac disease
Non-Ige Mediated: GIT celiac disease
  • Extensive enteropathy leading to malabsorption
  • Associated with an immune reaction to gliadin peptides (wheat, rye and barley)
  • Highly associated with HLA-DQ2 1 *0501. 1 *0201)
  • Serology: anti-transglutaminase IgA, Anti-gliadin IgA (asymptomatic and +ve serology is common)
  • Treatment: Elimination of gluten-containing foods

Adapted from J Allergy Clin Immunol. 2004;


non ige mediated syndromes affecting the skin and lung
Non-IgE-mediated syndromes affecting the skin and lung
  • Dermatitis Herpetiformis- Vesicular, pruritic eruption- Gluten-sensitive- Associated with Celiac Disease
  • Heiner’s Syndrome- Infantile pulmonary hemosideroisis- Anemia, failure to thrive- Cow’s milk-associated- Precipitating antibodies to cow’s milk
gastrointestinal food hypersensitivity infantile colic
Gastrointestinal food hypersensitivity?Infantile colic
  • Syndrome of paroxysmal fussiness characterized by inconsolable, agonized crying
  • Generally develops in the first 2 to 4 weeks of life and persists through the third to fourth months
  • Diagnosis can be established by the implementation of several brief trials of hypoallergenic formula

Adapted from J Allergy Clin Immunol. 2004;


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
diagnosis history examination
Diagnosis: history / examination
  • 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 approach

Allergy vs intolerance

IgE-mediated vs non-IgE mediated


Diagnosing food hypersensitivity disorders: IgE-mediated

  • Identification and relationship with the food: Medical history
  • To identify specific IgE: Skin tests/serum specific IgE
  • To demonstrate that IgE sensitization is responsible for the clinical reaction: Controlled challenge tests
  • Diagnosis is based on the medical history, supported by identification of specific IgE antibodies to the incriminated food allergen and confirmed by challenge

Adapted from Adverse Reactions to Foods Committee.

Spanish Society of Allergy and Clinical Immunology

Alergol Inmunol Clin 1999; 14: 50-62.


Diagnosing IgE-mediated food hypersensitivity disorders

Medical history: Symptoms

  • Symptoms described by patient
  • Length of time between ingestion and development of symptoms
  • Severity of symptoms
  • Frequency of symptoms
  • Time from last episode

Adapted from Adverse Reactions to Foods Committee.

Spanish Society of Allergy and clinical Immunology

Alergol Inmunol Clin 1999; 14: 50-62.


Diagnosing IgE-mediated food hypersensitivity disorders

Medical history: Timing of reaction

An immediate reaction (1- 2 hours) is suggestive of an IgE mediated reaction to foods

  • It may be preceded by previous tolerance of minimal symptoms
  • It may occur apparently after the first contact

Adapted from Adverse Reactions to Foods Committee, Spanish Society of Allergy and Clinical Immunology Alergol Inmunol Clin 1999; 14: 50-62.


Diagnosing IgE-mediated food hypersensitivity disorders

Medical history: food

  • Identification of food
  • How food was prepared
  • Quantity ingested
  • Previous tolerance
  • Cross-reactions with other food
  • Hidden foods, additives, contaminants

Adapted from Adverse Reactions to Foods Committee.

Spanish Society of Allergy and clinical Immunology

Alergol Inmunol Clin 1999; 14: 50-62.


Diagnosing IgE-mediated food hypersensitivity disorders

Medical history: Patient

  • Age at onset of symptoms
  • Other factors (eg, brought on by exercise)
  • Personal and family history of atopic diseases
  • Risk factors
  • Physical examination: Atopic dermatitis, dermographism, nutritional status

Adapted from Adverse Reactions to Foods Committee.

Spanish Society of Allergy and clinical Immunology

Alergol Inmunol Clin 1999; 14: 50-62.


Diagnosing IgE-mediated food hypersensitivity disorders

  • The diagnosis of food allergy cannot be performed on the basis of a non-compatible medical history
  • No diagnostic analysis (skin tests, specific IgE in serum, etc) is of value if it is interpreted without reference to medical history

Adapted from Adverse Reactions to Foods Committee.

Spanish Society of Allergy and Clinical Immunology

Alergol Inmunol Clin 1999; 14: 50-62.


Diagnosing IgE-mediated food hypersensitivity disorders

Skin tests

  • Prick: Reproducible, sensitive, not irritant
  • Prick-prick: Use raw or cooked food. Highly recommended for fruits and vegetables (commercially prepared extracts are generally inadequate because of the lability of the allergens, so the fresh food must be used for skin testing)

Diagnosing IgE-mediated food hypersensitivity disorders

  • Skin Prick Tests are used to screen patients for sensitivity to specific foods
  • Allergens eliciting a wheal of at least 3 mm greater than the negative control are considered positive
  • Overall positive predictive accuracy is < 50 %
  • Negative predictive accuracy > 95 % (negative skin test results essentially confirm the absence of IgE-mediated reactions)



 3 mm


Diagnosing IgE-mediated food hypersensitivity disorders

Skin tests

  • Intradermal: Not indicated
  • Atopy Patch test (APT): Atopic dermatitis, delayed reactions

Fresh food or dry food recommended


Difficult to interpret


Specific IgE to food (CAP / Radioallergosorbent tests)

  • Sensitivity similar to skin prick tests
  • Good correlation with other procedures
  • Efficiency: Depends on the allergen
  • Indicated if SPT are contraindicated (eg, skin disease, medications)
  • Useful if discrepancy exists between history and SPT
  • The use of quantitative measurements has shown to be predictive, for some allergens, of symptomatic IgE-mediated food allergy
  • Possibility to perform component-resolved diagnosis very useful in cross-reactivity reactions: profilins (Bet v2, Phl p12), polcalcins (Bet v4, Phl p7), LPT (Pru p3, Cor a8), Gly m4, Cross-reactive Carbohydrate Determinants or CCDs
Diagnostic food-specific IgE values (CAP-system fluorescent enzyme immunoassay) of greater than 95% positive predictive value

Food Serum IgE Value (kU/L)

Egg ≥7.0

≤ 2 yr old ≥2.0*

Milk ≥15.0

≤ 2 yrs old ≥5.0**

Peanut ≥14.0

Fish ≥20.0

Tree nuts ≥15.0

From Sampson HA: JACI 107:891-896,2001.

* Boyano-Martinez T, Garcia-Ara C, Diaz-Pena JM, et al: Clin Exp Allergy 31:1464-1469,2001.

** Garcia-Ara C, Boyano-Martinez T, Diaz-Pena JM, et al:

JACI 107:185-190,2001.


Diagnosing IgE-mediated food hypersensitivity disorders

Serum specific IgE (CAP / RAST)


  • Multiple determinations with one blood sample
  • Quantitative and comparable measurements
  • Use of recombinant allergens
  • Component-resolved diagnosis


  • Cost
  • Results delayed
interpretation of laboratory tests
Interpretation of laboratory tests
  • Positive prick test or RAST / CAP

- Indicates presence of IgE antibody NOT clinical reactivity (~50% false positive)

  • Negative prick test or RAST- Essentially excludes IgE antibody (>95%)
  • Intradermal skin test with food
  • - Risk of systemic reaction & not predictive
cross reactivity among foods
Cross-reactivity among foods
  • Patients often have positive SPTs or RAST results to other members of a plant family or animal species -immunological reactivity– does not always correlate withclinical reactivity
  • Cross reactions caused primarily by “Type 1” sensitizationLegumes, tree nuts, fish, shellfish, cereal grains, mammalian and avian food products
  • Cross reactions caused by “Type 2” sensitization

- Pollen-food allergy syndrome (oral allergy syndrome),

- Latex- food syndrome

  • Proper clinical evaluation (ideally by double-blind placebo-controlled challenge testing) is necessary in patients who demonstrate immunological cross-reactivity to foods and when tolerance to food is unknown (to avoid unnecessary restriction of certain foods)
cross reactions with foods clinical implications
Cross reactions with foods: clinical implications
  • If the patient is diagnosed with allergy to a food, assessment of clinical sensitization to foods with known cross reactivity is recommended
  • If the patient is diagnosed with allergy to a food with known cross reactivity with another food which he / she is not eating (unknown tolerance) that food must be challenged to assess tolerance

Cross reactivity in food allergy:

clinical relevance

OAS = Oral Allergy Syndrome

CMA = Cow’s Milk Allergy

Scott H. Sicherer. AAAAI San Francisco 2004:Seminar 3508.

diagnosing ige mediated food hypersensitivity disorders
Diagnosing IgE-mediated food hypersensitivity disorders

Other Techniques

  • Histamine release with foods:

Similar sensitivity and specificity to serum specific IgE

  • Sulphidoleukotrienes released from basophils with food: Not well studied
  • For monitoring food challenges:

- Plasma and urinary histamine: High sensitivity, low


- Serum tryptase: High specificity, low sensitivity

unproven experimental tests useless
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 - 6 weeks):- Eliminate suspected food/s, or- Prescribe limited “eat only” diet, or- Elemental diet
  • Oral challenge testing:- Physician supervised- Emergency room medications must be available
basic elimination diet allowed foods
Basic elimination diet: ALLOWED foods
  • Rice
  • Fruit:Pear, Apple, Grape
  • Meat:Lamb, Chicken
  • Vegetables:Asparagus, Beetroot, Carrots, Lettuce, Sweet potatoes, Butternut Squash
  • Other:Black Tea, Rooibos
  • Olive oil, Sunflower oil, Sugar, Salts

NB: No Preservatives, no tinned or packet foods

types of challenge testing
Types of challenge testing
  • Double -blind
  • Single-Blind
  • Open
  • Exercise + oral challenge
  • Inhalation challenge

Controlled food challenges: double-blind, placebo-controlled (DBPCFC)

  • DB is the procedure generally recommended, especially if a positive challenge outcome is expected
  • DB is the method of choice for scientific protocols
  • DB is the method of choice when studying late reactions or chronic symptoms, such as atopic eczema, isolated digestive late reactions, or chronic urticaria
  • DB is the only way to conveniently study subjective food-induced complaints, such as acute subjective adverse reactions, chronic fatigue syndrome, multiple chemical sensitivities, migraine or joint complaints

EAACI Position Paper. Allergy

2004; 59: 690-697

double blind placebo controlled food challenge testing limitations
Double-blind, placebo-controlled food challenge testing: limitations
  • Tedious
  • Time-consuming and expensive
  • Potential risk requires specialist unit (research)
  • IgE-mediated or non-IgE-mediated?
controlled food challenges single blind challenge
Controlled food challenges: single-blind challenge
  • Single-blind challenge carries the same difficulties for blinding foods as for double-blind, and introduces subjective bias of the observer
  • It needs additional work (cross-over by an external technician)
  • The recommendation of the European Academy of Allergology and Clinical Immunology is to always perform double-blind food challenge

EAACI Position Paper. Allergy 2004;

59: 690-697

controlled food challenges open challenge
Controlled food challenges: open challenge
  • A negative double-blind challenge should always be followed by an open challenge
  • A positive open challenge could be sufficient when dealing with IgE-mediated acute reactions manifesting with objective signs
  • For practical reasons, an open challenge can be the first approach when the probability of anegative outcome is estimated to be very high

EAACI Position Paper. Allergy 2004:

59: 690-697

diagnostic approach non ige mediated disease
Diagnostic approach:non-IgE-mediated disease
  • Includes disease with unknown mechanisms- Food additive intolerance
  • Elimination Diets (may need elemental diet)
  • Oral Challenges- Timing / dose / approach individualized for disorder - Enterocolitis syndrome can elicit shock- Enteropathy / eosinophilic gastroenteritis-prolonged feedings to develop symptoms
  • May require ancillary testing (endoscopy / biopsy)
food allergy treatment
Food allergy: treatment
  • Correct diagnosis
  • Treatment of reactions
  • Avoidance
  • Role of dietician
  • Tolerance assessment
  • Prevention
  • Immunotherapeutic strategies

Adapted from Adverse Reactions to Foods Committee.

Spanish Society of Allergy and Clinical Immunology

treatment emergency medicines
Treatment emergency medicines
  • 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 siblings / friends
  • Emergency identification bracelet
treatment avoidance
Treatment: avoidance
  • Mainstay of treatment
  • Must be considered as a therapeutic approach
  • Risk-benefit must be assessed

- Correct diagnosis is essential

    • Very restrictive diets can lead to malnutrition
  • Dietician’s role is crucial
treatment dietary elimination
Treatment: dietary elimination
  • Hidden ingredients
  • Labelling issues
  • Cross contamination (shared equipment)
  • “Code words” (“Natural flavor” may be cow’s milk)
  • Seeking assistanceRegistered dietician: (
  • Food Allergy Network ( (800-929-4040)
hidden foods
Hidden foods

Some foods (allergens) are masked and may be taken

un-noticed during diagnostic procedure:

  • Spices: Mustard, pepper, sesame
  • Legumes and tree nuts: Peanut, soy
  • Milk protein (protein supplements): Caseine, caseinates
  • Vaccines
  • Kitchen tools, volatile allergens
  • Transgenic foods with new proteins

Parasitized food:

  • Mites in flour ( pasta, pizzas)
  • Anisakis simplex in fish


example milk elimination
Example: milk elimination

Artificial butter flavor, butter fat, buttermilk, casein, caseinates (sodium, calcium, etc), cheese, cream, cottage cheese, curds, custard, Half&Half®, hydrolysates (sasein, 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®

substitute infant formulas
Substitute infant formulas
  • Soy (confirm soy IgE negative)<15% soy allergy among IgE-cow’s milk allergy~50% soy allergy among non-IgE cow’s milk allergy
  • Cow’s milk protein hydrolysates:90% tolerance in IgE-cow’s milk allergy
  • Partial hydrolysates: Not hypoallergenic!
  • Amino acid-based formulas: Lack allergenicity
natural history
Natural history
  • Dependent on food & immunopathogenesis
  • IgE-mediated allergy:- CM 85% remit by 8 yrsSaarinen et al JACI 2005- Egg 66% remit after 5 yrsBovano-Martinez et al JACI 2002- Peanut 20% may remit (8% may recur)Fleischer et alJACI 2004- Treenut, seafood typically persist
  • Declining/low levels of specific-IgE predictive
  • Non-IgE-associated GI allergy- Infant forms resolve 1- 3 years- Toddler/adult forms more persistent
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/CAP may remain positive- Reduced concentration specific-IgE encouraging
food specific ige cut off levels which predict 50 pass rate for challenge tests
Food specific IgE cut off levels which predict 50% pass rate for challenge tests

Food IgE level (KUA/l)

Milk 2

Egg 2

Peanut 2

Wheat ?

Soy ?

Perry et al. JACI 2004

prevention of food allergy allergic disease
Prevention of food allergy / allergic disease
  • Identify patients at risk (difficult)
    • There is no reliable or genetic immunological marker
    • Atopic background in parents, siblings
  • Dietary restriction (milk, egg, fish, nut)
    • In pregnancy: No benefit
    • Adverse effects on maternal-fetus nutrition
    • Hydrolyzed formula (HF): Variable effect (Cochrane Database Syst Rev. 2006 Oct 18); GINI Study, JACI Mar 2007; extensively HF & partially HF reduce incidence of AD, but not that of asthma
    • Delayed introduction of solid food: Variable effect (Ann Allergy Asthma Immunol. 2006;97:10-20)
  • Prolonged breast feeding?
  • Probiotics??
future immunomodulatory therapies
Future immunomodulatory therapies
  • Humanized anti-IgE monoclonal antibody therapy
  • “Engineered (mutated) allergen protein immunotherapy
  • Antigen-immunostimulatory sequence (CpG)-modulated immunotherapy
  • Peptide immunotherapy
  • Plasmid-DNA immunotherapy
  • Cytokine-modulated immunotherapy
  • Induction of tolerance or oral immunotherapy (milk, egg, hazelnut…….)
  • IgE & non-IgE mediated food allergy conditions exist
  • History and examination paramount
  • Diagnosis is by elimination and challenge testing
  • Avoidance / education / preparation for emergencies are current therapies
  • Periodic re-challenge to monitor tolerance as indicated by history, allergen, and level of food specific-IgE

World Allergy Organization (WAO)

For more information on the

World Allergy Organization (WAO),

please visit www.worldallergy.orgor contact:

WAO Secretariat

555 East Wells Street, Suite 1100

Milwaukee, WI 53202

United States

Tel: +1 414 276 1791

Fax: +1 414 276 3349