GLORIA Module 6: Food Allergy - PowerPoint PPT Presentation

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GLORIA Module 6: Food Allergy

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  1. GLORIA Module 6: Food Allergy

  2. Sponsored by: GLORIA™ is supported by unrestricted educational grants from

  3. 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 and local training programs. GLORIA modules are created from established guidelines and recommendations to address different aspects of allergy-related patient care.

  4. US GLORIA Program In conjunction with the American College of Allergy, Asthma and Immunology (ACAAI), GLORIA is now presented for CME Credit in the US to Regional, State and Local Societies. The GLORIA educational materials are available for download on WAO’s website www.worldallergy.org/gloria

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

  6. 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

  7. Food AllergyA GLORIATM Module Authors 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 Reviewer Prof. Alessandro Fiocchi Melloni University Hospital Milan, Italy Prof. Joaquín Sastre Fundación Jimenez Diaz, Department of MedicineUniversidad Autonoma de Madrid Madrid, Spain

  8. 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

  9. 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

  10. Adverse reactions to food TOXIC Nontoxic Non-immune mediated Immune-mediated Intolerance Allergy Enzymatic Pharmacologic Undefined Non-IgE-mediated IgE-mediated Adverse Reactions to Food: Position Paper. Allergy 1995; 50:623-635

  11. 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

  12. SINGAPORE Birds Nest Seafood Egg Milk USA & UK Milk Egg Peanut Tree Nuts Seafood ITALY Milk Egg Seafood AUSTRALIA Milk Egg Peanuts Sesame FRANCE Egg Peanuts Milk Mustard ISRAEL Milk Egg Sesame Food allergy in children: International

  13. “Second tier” foods • 10% reactions to foods • 160 foods • Fruits • Vegetables • Seeds (sesame, sunflower, poppy) • Spices

  14. 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 area - 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

  15. 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

  16. 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

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

  18. Food Allergy: clinical manifestations IgE IgE/Non-IgE Non-IgE Protein-inducedproctocolitis/enterocolitis Celiac disease Contact dermatitis Herpetiform dermatitis Heiner´s syndrome Urticaria/angioedema Rhinitis /Asthma Anaphylaxis Oral allergic syndrome Gastrointestinal symptoms (GIT) Atopic dermatitis Eosinophilic gastro-intestinal disorders Adapted from J Allergy Clin Immunol. 1999;103:717-728

  19. 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

  20. IgE Mediated: respiratory manifestations Asthma • 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 Rhinoconjunctivitis • Usually seen during positive controlled challenge tests, but occasionally reported by patients

  21. 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

  22. 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

  23. Food-dependent, exercise-induced anaphylaxis Exercise Wheat Temperature Gastrin Mediator release - Histamine - Others (LTD4,PAF, etc) ANAPHYLAXIS Adapted from Adverse Reactions to Foods Committee. Spanish Society of Allergy and Clinical Immunology

  24. 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; 113:808-809

  25. 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

  26. Food allergy prevalence in specific disorders

  27. Mixed IgE/Non-IgE mediated: GIT allergic 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; 118:1054-9

  28. 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

  29. Allergic eosinophilic esophagitis endoscopic findings White plaques (eosinophils) Rings

  30. 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

  31. 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; 118:1054-9

  32. Non-IgE mediated: GIT food protein induced syndromes (typically milk and soy induced) Enterocolitis #EnteropathyProctocolitis 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

  33. 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; 113:808-809

  34. 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; 113:808-809

  35. 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; 113:808-809

  36. 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; 113:808-809

  37. Non-IgE-mediated syndromesaffecting 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

  38. 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; 113:808-809

  39. Disorders not proven to be related to food allergy • Migraines • Behavioral/Developmental disorders • Arthritis • Seizures • Inflammatory bowel disease

  40. 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

  41. 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.

  42. 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.

  43. 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.

  44. 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.

  45. 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.

  46. 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.

  47. 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)

  48. 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) + Diameter  3 mm

  49. Diagnosing IgE-mediated food hypersensitivity disorders • In infants younger than 2 years, skin prick tests to milk, egg, or peanut with wheal diameters of at least 8 mm are more than 95% predictive of reactivity • In general, negative skin prick test results are extremely useful for excluding IgE-mediated food allergies, but positive skin test results are only suggestive of presence of clinical food allergies • There is no correlation between the size of wheal and the clinical sensitivity in individual patients