THE PHYSICIAN’S PERSPECTIVE ON FOOD

ALLERGYNUTRITION EXCHANGE

June 2, 2011Antony Ham Pong MBBS

Consultant in Allergy, Asthma & Immunology

Clinical lecturer, Pediatrics, Univ of Ottawa; Consultant, Chest Clinic, CHEO

Co-Chair, Infection/Immunology/Allergy Block, U of Ottawa School of Medicine

OBJECTIVES

• Define allergic and atopic disorders

• The Allergic March & the Allergy Epidemic

• What is a food allergy?

• How to diagnose food allergies

ATOPY & ALLERGY• ATOPY is the genetic predisposition to

produce IgE on allergen exposure, resulting from an imbalance between TH1 and TH2 helper lymphocytes

• Specific IgE produced attaches to the surface of mast cells

• Subsequent allergen exposure causes mast cell inflammatory mediator release

• ALLERGY is the clinical hypersensitivity which occurs as a manifestation of atopy

Childhood asthma : Blame your parents

• Both parents asthmatic : 75% risk

• One parent asthmatic : 30% risk

• One parent & one sibling : 40% risk

• No one with asthma : 5–10% risk

The Allergy Epidemic• Atopic Eczema 10-20%

• Hay Fever 10-20%

• Asthma 12-20%

• Peanut allergy 1.62%

The Allergic March

• Atopic eczema onset age 0 - 2 yrs

• Food allergy onset age 0 - 2 yrs

• Asthma onset age 2 - 5 yrs

• Allergic rhinitis onset age > 5 yrs

The Allergy Epidemic

• The Hygiene Theory proposes that the major increase in allergies, which is seen only in well-developed countries, is due to excess cleanliness. Our immune system does not have enough work to do, therefore it begins to react to harmless things in our environment, causing allergies.

• This may explain in part why 70% of allergic children have no family history of atopic disease

Microbial exposures associated with less allergy and

asthma: Clinical studies • Older siblings / large family size• Early day care• Less antibiotic use• Lactobacillus ingestion• Infections

– Respiratory tract: measles, tuberculosis, tuberculin positivity– Gastrointestinal : Hep A, H. pylori,

• Being brought up on a farm– Animal exposure / Stables exposure– Drinking unpasteurized milk ( higher endotoxin levels)– Endotoxin levels higher

• Keeping a dog/cat ( unless one is allergic to it!)– Home environment contaminated with endotoxin

Timing is everything

Genetics ,timing and degree of exposure to irritants, microbes and allergens will determine

whether allergic sensitization or tolerance will develop

What is food allergy?Adverse reactions to food can be sub-divided into…

Non-toxic Toxic

• Food intolerance: non allergic (non-immune) reactions

• Pharmacological reactions

– Eg, sulphites

Food allergy • Toxins

– Eg, salmonella, scrombroid fish

IgE-mediated Non-IgE

• Immediate onset

Conditions include:

• oral allergy syndrome

• anaphylaxis

• Delayed onset

Conditions include:

• celiac disease

• dietary protein enterocolitis

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Sicherer and Sampson JACI 2006; Food Allergy, available at www.worldallergy.org

Features of IgE-mediated food induced allergic reactions

• Onset within 30 mins, rarely up to 4 hrs

• Duration < 4-6 hours

• Reactions recur reliably with re-exposure

• Threshold dose (usually small amount)

• Anaphylaxis can occur with a small amount of a potent allergen or a larger amount of a ‘milder’ allergen

ANAPHYLAXIS: OVERVIEW

• Anaphylaxis is a severe, potentially fatal systemic allergic reaction that occurs suddenly (minutes to hours) after contact with an allergy-causing substance

• Death can occur in minutes, usually due to closure of airways

• Allergic reaction affects many body systems : rash & swelling, breathing difficulties, vomiting & diarrhoea, heart failure & low blood pressure ANAPHYLACTIC SHOCK

Common Allergenic Foods and their Labeling in Canada – A

Review(Zarkadas M., Scott F, Salminen J, Ham Pong AJ.Can J Allergy Clin Immunol 1999, 4: 118-141)

ANAPHYLAXISCommon Less commonPeanut SoyTree Nuts WheatFish * MustardShellfish: Crustaceans Shellfish: MollusksCow’s Milk SulfitesEggSesame

Factors Affecting Food AllergyEarly Dietary Exposure & Food Allergy

Prevalence

Peanut North America

Rice E. Asia esp. Japan

Fish Scandinavia

Sesame Israel

Chickpea India

Wheat America, Europe

Edible Bird’s Nest Singapore(dried cave swallow saliva)

How much is too much?

• MILK – fatality from 2.5ml ( ½ tsp)

• EGG – anaphylaxis from 10mg (1/3,000 oz)

• FISH - anaphylaxis from 1 gm (1/30 0z)

• SHRIMP – anaphylaxis from 1 gm (1/4 shrimp)

Threshold Doses:How much peanut is too much?

• Dose of peanut causing a subjective reaction eg itchy mouth = 10 ug or 1/50,000 peanut

• Objective reaction in challenge studies = 0.25 to 2mg ( 1/2,000 to 1/250 peanut )

• Usual starting dose in challenge studies = 100mg peanut flour ( 1/5 peanut )

Can the smell or touch of peanut cause anaphylaxis?

• Possibility that high level peanut dust can provoke anaphylaxis in airplanes ( Sicherer 1999)

• Smell of peanut butter does not cause allergic reactions– reactions to this are most likely due to intense dislike of the smell ( the smell is due to volatile organic molecules and not allergenic proteins), or inadvertent ingestion

• Anaphylaxis has been induced inhalation of steam carrying food particles eg shrimp, fish, milk

FOOD ALLERGY : ROUTE OF EXPOSURE

• Ingestion – directly or indirectly (eg maternal dietary proteins via breast mlk)

• Inhalation eg boiling foods (eg shrimp, milk), food dust (eg peanut, egg, wheat, psyllium), ?milk contaminated lactose in asthma dry powder inhalers

• Musosal contact : eye (eg shrimp), rectal (eg milk enema)

• Skin : abraded skin eg milk containing ointment or lactobacillus capsules; egg lecithin containing creams

• Parenteral : drug & intralipid formulations

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Sampson et al. JACI 2003

Diagnosis of Food Allergy

• Positive Allergy Skin Prick Test (SPT) or blood test (CAP IgE)– Indicates presence of IgE antibody NOT

clinical reactivity – Must be interpreted in the context of clinical

history

• Negative SPT and CAP IgE– Essentially excludes IgE antibody (>95%)

Allergy Skin tests

• Prick/puncture – most common technique, introduces allergen into the very superficial skin (epicutaneous layer) usually flexor surface of forearm, sometimes on back; is more specific but not as sensitive as intradermal

• Intradermal – introduces a larger quantity of allergen into a deeper layer of skin of upper forearm; more sensitive but less specific than prick

• Scratch – old technique, not used now as too variable

ALLERGY PRICK SKIN TEST “SIZE DOES MATTER”

Peanut PST > 6mm : ½ will be allergic

Peanut PST > 8mm : Most likely allergic

Cow’s Milk PST > 8mm : “ “

Egg PST > 7mm : “ “

Probability Curve for Peanut

Food Challenge

• Reasons to challenge:– Confirm reactivity– Confirm non-reactivity– Follow for tolerance

• Oral challenge testing (MD supervised, ER meds available)– Open– Single-blind– Double-blind, placebo-controlled (DBPCFC)

• Sensitivity, Specificity, PPV, NPV ~ 100%

• Limitations:– Risk to patient– Dose– Duration of challenge– Success of blinding

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Saleh Al-Muhsen et al CMAJ 2003

Food allergyIgE non-IgE

.Food types

11 priority allergens Milk,soy,wheat

Symptoms Skin, respiratory, GI, systemic

GI, Failure to thrive, Eczema, anemia, hypo-

albuminemia

Time to onset of symptoms

Acute: minutes to 4 hours

Subacute to chronic: days to weeks

Duration 4-6 hours Days to weeks

Food allergyIgE non-IgE

.Threshold dose

Single dose, small amounts eg grams

Cumulative doses, usually large exposures

Atopic family Yes VariableAntihistamine Rx Usually responds No response

Lab Blood eosinophils, elevated IgE

Stool mucus, WBC

Biopsy-flattened villi, eosinophilia

Allergy tests/

Specific IgE

Often positive with good clinical correlation

Variable-clinical correlation often not as dramatic

FOOD ALLERGY PROGNOSIS

• Onset before age 3 years esp cow’s milk (age 2-3), egg(age 5-7), soy & wheat (age 2-3) : usu outgrown

• Onset after age 3 years : usu lifelong

• Peanut allergy : up to 20% reported to be outgrown ( probably optimistic)

• Usually lifelong : Peanut, tree nuts, fish, shellfish, seeds

• end

ACTIONS OF HISTAMINE

• Peripheral vasodilation

• Increased vascular permeability

• Altered cardiac conduction

• Bronchial/intestinal smooth muscle contraction

• Nerve stimulation-Cutaneous pruritus/pain

• Increased glandular mucus secretions

IgE Non-IgE Skin

UrticariaAngioedemaAtopic dermatitis

RespiratoryThroat tightnessRhinitisAsthma

GutVomitDiarrheaPain

Anaphylaxis

Signs and Symptoms: IgE vs Non-IgE

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Sicherer and Sampson JACI 2006; Sampson JACI 2003