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THE PHYSICIAN’S PERSPECTIVE ON FOOD ALLERGY NUTRITION EXCHANGE June 2, 2011 Antony Ham Pong MBBS Consultant in Allergy, Asthma & Immunology Clinical lecturer,

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Presentation on theme: "THE PHYSICIAN’S PERSPECTIVE ON FOOD ALLERGY NUTRITION EXCHANGE June 2, 2011 Antony Ham Pong MBBS Consultant in Allergy, Asthma & Immunology Clinical lecturer,"— Presentation transcript:

1 THE PHYSICIAN’S PERSPECTIVE ON FOOD ALLERGY NUTRITION EXCHANGE June 2, 2011 Antony 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

2 OBJECTIVES Define allergic and atopic disorders The Allergic March & the Allergy Epidemic What is a food allergy? How to diagnose food allergies

3 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






9 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

10 The Allergy Epidemic Atopic Eczema10-20% Hay Fever10-20% Asthma12-20% Peanut allergy 1.62%

11 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

12 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




16 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

17 Timing is everything Genetics,timing and degree of exposure to irritants, microbes and allergens will determine whether allergic sensitization or tolerance will develop

18 What is food allergy? Adverse reactions to food can be sub-divided into… Non-toxicToxic Food intolerance: non allergic (non- immune) reactions Pharmacological reactions –Eg, sulphites Food allergyToxins –Eg, salmonella, scrombroid fish IgE-mediatedNon-IgE Immediate onset Conditions include: oral allergy syndrome anaphylaxis Delayed onset Conditions include: celiac disease dietary protein enterocolitis ____________________________________________ Sicherer and Sampson JACI 2006; Food Allergy, available at

19 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





24 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

25 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) ANAPHYLAXIS Common Less common Peanut Soy Tree Nuts Wheat Fish * Mustard Shellfish: CrustaceansShellfish: Mollusks Cow’s MilkSulfites Egg Sesame

26 Factors Affecting Food Allergy Early Dietary Exposure & Food Allergy Prevalence PeanutNorth America RiceE. Asia esp. Japan FishScandinavia SesameIsrael ChickpeaIndia WheatAmerica, Europe Edible Bird’s NestSingapore (dried cave swallow saliva)

27 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)

28 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 )

29 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

30 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

31 __________________________________________ 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%)

32 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



35 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 : “ “

36 Probability Curve for Peanut

37 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 __________________________________________ Saleh Al-Muhsen et al CMAJ 2003

38 Food allergy IgE non-IgE. Food types 11 priority allergensMilk,soy,wheat SymptomsSkin, 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 Duration4-6 hoursDays to weeks

39 Food allergy IgE non-IgE. Threshold dose Single dose, small amounts eg grams Cumulative doses, usually large exposures Atopic familyYesVariable Antihistamine Rx Usually respondsNo 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

40 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

41 end

42 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

43 ____________________________________________ 1.H Sampson Food Allergy Update JACI 2004 2.Ben-Shosham et al, JACI 2009 Food Allergy: not just nuts FoodYoung ChildrenAdult Milk2.5% 1 0.3% 1 Egg1.3% 1 0.2% 1 Peanut0.8% 1 1.62% 2 0.6% 1 Tree nuts0.2% 1 0.5% 1 Fish0.1% 1 0.4% 1 Shellfish0.1% 1 2.0% 1

44 IgENon-IgE Skin Urticaria Angioedema Atopic dermatitis Respiratory Throat tightness Rhinitis Asthma Gut Vomit Diarrhea Pain Anaphylaxis Signs and Symptoms: IgE vs Non-IgE ____________________________________________ Sicherer and Sampson JACI 2006; Sampson JACI 2003

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