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Food Allergy

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

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  1. Food Allergy Againdra K. Bewtra M.B.B.S., M.D.

  2. Food Allergy: Outline • Definitions • Pathophysiology • Signs and Symptoms • Food Allergy - Induced Diseases • Prevalence and Natural History • Diagnosis and Management • Prevention

  3. 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

  4. 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

  5. Definitions: Adverse Reactions to Food B. Immunologic Spectrum IgE-Mediated 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

  6. Prevalence • 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)

  7. 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

  8. Food Allergy Prevalence in Specific Disorders Disorder Food Allergy Prevalence Anaphylaxis 35-55% Oral allergy syndrome 25-75% in pollen allergic 37% in children (rare in adults) Atopic dermatitis 20% in acute (rare in chronic) Urticaria 5-6% in asthmatic or food allergic children Asthma Chronic rhinitis Rare

  9. 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.

  10. 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

  11. 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

  12. 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

  13. Pathophysiology: Immune Mechanisms • Protein digestion • Antigen processing • Some Ag enters blood IgE-Mediated IgE-receptor APC Mast cell Non-IgE Mediated Histamine • TNF- • IL-5 T cell B cell

  14. Signs and Symptoms IgE Non-IgE Acute Chronic Skin Urticaria Angioedema Atopic dermatitis Respiratory Throat tightness Rhinitis Asthma Gut Vomit Diarrhea Pain Anaphylaxis

  15. 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

  16. 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) Pollen Foods Birch Apple, apricot, carrot, cherry, kiwi, plum Ragweed Banana, cucumber, melon, watermelon Grass Cherry, peach, potato, tomato

  17. 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

  18. 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

  19. Prevalence of Clinical Cross Reactivity Among Food “Families” Prevalence of Allergy to > 1 Food in Family Food Allergy Fish 30% -100% Tree Nut 15% - 40% Grain 25% Legume 5% Any 11%

  20. Cross Reactivity of Foods

  21. Disorders Not Proven to be Related to Food Allergy • Migraines • Behavioral / Developmental disorders • Arthritis • Seizures • Inflammatory bowel disease

  22. 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

  23. 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

  24. Signs and Symptoms of Food Allergy

  25. 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

  26. 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

  27. CAP-RAST FEIA

  28. 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)

  29. 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

  30. 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)

  31. Diagnostic Approach to Evaluating Food Allergy

  32. Strict avoidance Difficult Of 32 peanut allergic patients studied by bock et al. Only 8 were successful at peanut avoidance for 5 years. Impossible Peanut allergens on airplanes. Medicine 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

  33. 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: (www.eatright.org) • Food Allergy Network (www.foodallergy.org; 800-929-4040)

  34. 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®.

  35. 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

  36. 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

  37. Allergy Prevention Pollutants, Tobacco smoke Food allergens early Infections ? Genes Gender Inflammation Sensitization Primary Damage Secondary Tertiary

  38. Possibly effective Immunotherapy Treatment of peanut allergy with rush I.T. Oppenheimer JJ et al. JACI 1992;90:256-262 Oral allergen gene immunization Mice Roy et al Horner et al reported decreased anaphylaxis with DNA vaccine Generally found not effective H1 and H2 antihistamines Oral Cromolyn sodium Ketotofin Antiprostaglandins Other Treatments

  39. Future Immunomodulatory Therapies • Recombinant anti-IgE antibody • Gene (naked DNA) immunization • Mutated B-cell epitopes • Minimal T-cell epitopes • Immune-modulating adjuvants (ISS) • Probiotics

  40. Reasons for Allergy Referral • Identification of causative food • Institution of elimination diet • Education on food avoidance • Development of action plan • Prevention of other allergies

  41. Guidelines for Food Allergy

  42. Conclusion • 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

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