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    The subject of food poisoning The subject of food poisoning Document Transcript

    • THE subject of food poisoning was once largely a series of disconnected observations and records of outbreaks ; but during the last three decades the facts have been associated and the discrepancies and fallacies removed. For example, the old expression ‘ptomaine poisoning' has been shown to be without meaning and entirely incorrect. Now it is possible to give a clear account of food poisoning, including the various causal agencies, the paths of infection and the reservoirs of the various bacteria responsible. In the first edition in 1943, the author of the book under notice gave a clearly written account of the subject, and the second edition has brought it up to date. The first edition dealt very inadequately with staphylococcus food poisoning ; but this has now been remedied by the addition of a new, separate chapter of 22 pages on this subject which gives all the essential facts. An additional section (appendix I) on laboratory investigation of food poisoning cases is of doubtful utility, as this very technical subject is mainly of interest to the laboratory worker, and for him the account is barely adequate and is available elsewhere. Abstract Food poisoning is encountered throughout the world. Many of the toxins responsible for specific food poisoning syndromes are no longer limited to isolated geographic locations. With increased travel and the ease of transporting food products, it is likely that a patient may present to any emergency department with the clinical effects of food poisoning. Recognizing specific food poisoning syndromes allows emergency health care providers not only to initiate appropriate treatment rapidly but also to notify health departments early and thereby prevent further poisoning cases. This article reviews several potential food-borne poisons and describes each agent's mechanism of toxicity, expected clinical presentation, and currently accepted treatment. Abstract Although food allergy can have serious health consequences, little is currently known about people’s perceptions of food allergy. The present study examined the differences in awareness and perceptions of food allergy and anxiety between young people with and without a food allergy. Participants completed a questionnaire which asked about their perceptions and knowledge of allergies, perceived health competence and anxiety. Of the 162 participants 24 reported they were allergic to at least one food; these people perceived that their allergy had significantly less of an impact on their lives than others believed it would. Allergy status interacted with perceived health competence to affect anxiety. People with an allergy and with high health competence reported the greatest anxiety levels. Very few of the sample knew the meaning of the term ‘anaphylaxis’. Findings are discussed in terms of health education implications and possibilities.
    • Educators http://jaa.sagepub.com/ Journal of Asthma & Allergy http://jaa.sagepub.com/content/3/4/172 The online version of this article can be found at: DOI: 10.1177/2150129711431888 Journal of Asthma & Allergy Educators 2012 3: 172 originally published online 28 December 2011 Stephanie E. Hullmann, Elizabeth S. Molzon, Angelica R. Eddington and Larry L. Mullins Dating Anxiety in Adolescents and Young Adults With Food Allergies: A Comparison to Healthy Peers Published by: http://www.sagepublications.com On behalf of: Association of Asthma Educators Additional services and information for Journal of Asthma & Allergy Educators can be found at: Email Alerts: http://jaa.sagepub.com/cgi/alerts Subscriptions: http://jaa.sagepub.com/subscriptions Reprints: http://www.sagepub.com/journalsReprints.nav Permissions: http://www.sagepub.com/journalsPermissions.nav Citations: http://jaa.sagepub.com/content/3/4/172.refs.html What is This? OnlineFirst Version of Record - Dec 28, 2011 >> Version of Record - Jul 23, 2012 Downloaded from jaa.sagepub.com by guest on August 25, 2013172 Journal of asthma & allergy educators August 2012 Research Article
    • Abstract: The present study sought to examine dating anxiety and problems in social relationships and healthrelated quality of life in adolescents and young adults with food allergies compared with their healthy peers. It was hypothesized that individuals with food allergies would experience greater dating anxiety and poorer social functioning and physical and mental health–related quality of life than their healthy peers. Participants with food allergies were age, gender, and ethnicity matched to young adults without a history of allergies or any other chronic illness for analyses. The majority of adolescents and young adults with food allergies reported that their allergies interfere with physical intimacy with their current partner. Results further revealed that adolescents and young adults with food allergies reported greater dating anxiety and fear of negative evaluation than healthy peers. No differences were observed between the groups on physical or mental health–related quality of life or social functioning. For both groups, dating anxiety was a significant predictor of mental quality of life and social functioning. Keywords: food allergy; dating anxiety; quality of life A pproximately 150 individuals (adults and children) die annually due to adverse reactions to food.1 These adverse food reactions are often caused by food allergies, which affect
    • 6% to 8% of children and 2% of adults in the United States.1 Adverse food reactions are characterized by an immunological IgE reaction to the proteins on the food, with the 8 most common food allergies being fish, peanut, egg, soy, wheat, shellfish, tree nut, and cow’s milk.1 Individuals with food allergies are faced with considerable uncertainty. The severity of an allergic reaction to food can be unpredictable and depends on several factors, including an individual’s sensitivity, the type of food, and amount of food eaten.1 Exposure to food proteins can occur without an individual’s knowledge and without consuming the food. For example, individuals with peanut allergies may not be aware when peanut oil has been used in cooking, or they may have an allergic reaction to the peanut oils from peanut shells and skins that have been thrown on a restaurant floor. There is also evidence to suggest that engaging in physically intimate behaviors with a partner who has recently consumed the allergen can cause an allergic reaction.2 Peanut allergens can remain in salvia for over an hour, even after an individual has brushed his/her teeth or used mouthwash.3 Notably, research suggests that kissing can allow for the transfer of allergens through the skin, oral mucosa, or
    • saliva.2,3 As such, adults with food allergies must be diligent to avoid exposure, inquire about ingredients and food preparation when they have not prepared the food themselves, and communicate about their allergies with their partner. Whereas allergies have traditionally been thought of simply as a nuisance disease with little impact on an individual’s psychosocial functioning,4 recent research has demonstrated the mental health implications associated with having allergies. Specifically, adolescents and young adults with allergies experience higher rates of depressive and anxious symptoms and poorer mental and physical health–related quality of life (HRQOL) than their healthy peers.5 Women with allergies have also demonstrated increased levels of state and trait anxiety when compared with healthy controls.6 Additionally, researchers have examined the difference between healthy controls and individuals with allergies to understand the impact the disease has on HRQOL. Researchers have found that individuals with allergies have significantly lower HRQOL when compared with healthy controls.7,8 In an interesting allergen exposure task, DOI: 10.1177/2150129711431888. From the Department of Psychology, Oklahoma State University, Stillwater, Oklahoma. The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article. Address correspondence to: Stephanie E. Hullmann, MS, 116 North Murray Hall,
    • Oklahoma State University, Stillwater, OK 74078; e-mail: stephanie.hullmann@okstate.edu. For reprints and permissions queries, please visit SAGE’s Web site at http://www.sagepub.com/journalsPermission.nav. © 2011 The Author(s) Dating Anxiety in Adolescents and Young Adults With Food Allergies A Comparison to Healthy Peers stephanie e. hullmann, ms, elizabeth s. molzon, Ba, angelica r. eddington, ms, and larry l. mullins, Phd Downloaded from jaa.sagepub.com by guest on August 25, 2013
    • IMP Food Allergy Seminar.Lecture.ClassPresentation Transcript 1. Food Allergy Update: Overview for SCAFP Suzanne S. Teuber, M.D. [email_address] Professor of Medicine Training Program Director, Allergy and Immunology 2. Sometimes tough to avoid… 3. Definitions 4. Adverse Food Reactions Bacterial food poisoning Heavy metal poisoning Scombroid fish poisoning Caffeine Alcohol Histamine Toxic / Pharmacologic Non-Toxic / Intolerance Non-immunologic Lactase deficiency Galactosemia Pancreatic insufficiency Gallbladder / liver disease Hiatal hernia Gustatory rhinitis Anorexia nervosa Idiosyncratic Adapted from Sicherer S, Sampson H. J Allergy ClinImmunol 2006;117:S470-475. 5. Adverse Food Reactions Systemic (Anaphylaxis) Oral Allergy Syndrome Immediate gastrointestinal allergy Asthma/rhinitis UrticariaMorbilliform rashes and flushing Contact urticariaEosinophilic esophagitis Eosinophilic gastritis Eosinophilic gastroenteritis Atopic dermatitis IgE-Mediated (most common) Non-IgE Mediated Cell-Mediated Immunologic Protein-Induced Enterocolitis Protein-Induced EnteropathyEosinophilicproctitis Dermatitis herpetiformis Contact dermatitis Sampson H. J Allergy ClinImmunol 2004;113:805-9, Chapman J et al. Ann Allergy Asthma &Immunol 2006;96:S51-68. 6. Pathophysiology 7. Allergens Proteins or glycoproteins (not fat or carbohydrate as primary immunogens) Generally heat resistant, acid stable Major allergenic foods
    • (>85% of allergy) Children: milk, egg, soy, wheat, peanut, tree nuts Adults: peanut, tree nuts, shellfish, fish , fruits and vegetables commonly stated that “ 90% of food allergies are caused by the “Big 8 ””, this was true for children with atopic dermatitis, not the general population with anaphylaxis. ER studies in US: FRUITS and VEGGIES same % as peanut, crustaceans highest 8. Emergency Department Visits for Food Allergy (Clark et al. JACI 2004;113:347) Crustaceans: 19% Peanuts: 12% Fruits and Veggies: 12% Are these counted in food allergy prevalence estimates? -NO 9. CASE: Crustacean Allergy: IgE Towards Protein in the Food, NOT Iodine 79 year old man had anaphylaxis to shrimp at age 20, 25 Doctors told him he was allergic to iodine in seafood Avoided seafood, iodized salt for years Age 70: retirement dinner, hostess picked shrimp out of his portion and gave it to him --- ER visit for anaphylaxis At age 79, specific IgE measurement extremely high to shrimp: >100 kU/L On follow-up after education on avoidance, happily consuming foods with iodized salt because he didn’t have to screen salt source any more 10. Pan-allergens Proteins in food, pollen or plants that possess homologous IgE binding epitopes across species Tropomyosins: crustacea, dust mites, cockroach, mollusks Storage mites in flour: anaphylaxis reported! Parvalbumins: fish Bovine IgG: beef, lamb, venison, cow’s milk Lipid transfer protein: fruits (peach, apple), vegetables, peanut, tree nuts Profilin: fruits, vegetables Class 1 chitinases: fruits, wheat, latex 11. Immune Mechanisms IgE-Mediated IgE-receptor Histamine Protein digestion Antigen processing Some Ag enters blood Mast cell APC B cell T cell TNF- IL-5 Non-IgE Mediated 12. Risk Factors 13. Risk Factors for Development of Food Allergy Chapman J et al. Ann Allergy Asthma &Immunol 2006;96:S51-68. Local Factors (Rodent Models)
    • Pepsin digestion Gastrointestinal infections? Malabsorption Rate of absorption Antigen processing Nature and dose of Ag Transdermal exposure Host Factors Age (esp neonates) Genetic susceptibility FHx of atopyFHx of food allergy Atopic dermatitis Transdermal food exposure (peanut) 14. Food Allergy Disorders 15. Anaphylaxis Syndromes Food-induced anaphylaxis Food allergy = #1 cause of anaphylaxis in the ED Rapid-onset, up to 30% biphasic May be localized (single organ) or generalized Potentially fatal Do DNA Allergy Relief Treatments for these high risk foods: peanut, tree nut, seafood (cow’s milk and egg in young children) Food-dependent, exercise-induced: 2 forms Specific foods (wheat, celery most common) Any food (post- prandial) 16. Fatal Food Anaphylaxis Frequency: ~ 150 deaths / year Clinical features: Biphasic reaction can contribute –initially better, then recurs Cutaneous symptoms may not be present Respiratory symptoms prominent Risk factors : Underlying asthma – Delayed epinephrine Symptom denial – Previous severe reaction Adolescents, young adults History: known food allergen Key foods: peanuts and tree nuts dominate (~90% of fatalities) , fish,crustaceans, few milk, few misc. Most events occurred away from home Bock SA, et al. J Allergy ClinImmunol 2001;107:191-3. 17. Cutaneous Reactions Acute urticaria/angioedema – common Contact urticaria - common Food allergy rarely causes chronic urticaria/angioedema 1/3 of kids with moderate to severe atopic dermatitis may have food allergy (especially cow’s milk, egg, soy, wheat). Morbilliform rashes may be seen in these children upon food challenge. Contact dermatitis (food handlers) 18. Respiratory Responses Upper and lower respiratory tract symptoms may be seen (rhinoconjunctivitis, laryngeal edema, asthma) Rarely
    • isolated, usually accompany skin and GI symptoms Inhalational exposure may cause respiratory symptoms that can be severe Occupational Restaurants Kitchen/Home Example: crabs to be boiled 19. Pollen-Food Syndrome or Oral Allergy Syndrome Clinical features: rapid onset oral pruritus, rarely progressive Epidemiology: prior sensitization to pollens Key foods: raw fruits and vegetables Allergens: Profilins and pathogenesis–related proteins Heat labile (cooked food usually OK) Cause: cross reactive proteins pollen/food Birch Apple, carrot, celery, cherry, pear, hazelnut Ragweed Banana, cucumber, melons Grass Melon, tomato, orange Mugwort Melon, apple, peach, cherry 20. GI Syndromes of Children and Adults: Celiac Disease (Gluten-sensitive enteropathy) In children: FTT, or weight loss Malabsorption, diarrhea, abdominal pain May be subtle In adults, average 10 years of nonspecific symptoms: Diarrhea, abdominal pain GERD Malabsorption May present atypically with osteoporosis, infertility, neurologic sx Pathophysiology: an immune-mediated enteropathy triggered by gluten peptides in genetically predisposed patients (DQ2 or DQ8) Lymphocytic infiltration of small bowel Villus atrophy 21. Celiac Disease (Gluten-sensitive enteropathy) Cont’d: Diagnosis ~1/133 people in US have celiac disease – many are currently undiagnosed IgA anti-tissue transglutaminase (IgG if IgA-deficient), anti- endomysialAb, little role for anti-gliadinAb currently due to poor specificity Upper endoscopy with biopsy; Management Strict, lifelong, gluten avoidance (wheat, barley, rye) Rare risk of GI lymphoma Oats almost always OK Link with resources: dietician, local support groups, national organizations (listed at www.celiac.nih.gov) 22. GI Syndromes of Children and Adults Gastrointestinal Anaphylaxis or Immediate Gastrointestinal Allergy IgE-mediated Acute emesis/diarrhea/abdominal pain Can present without other signs or symptoms of an allergic reaction to food
    • 23. GI Syndromes of Children and Adults Eosinophilic Gastrointestinal Disorders: eosinophilic esophagitis/gastritis/gastroenteritis Prevalence increasing, eosinophilic esophagitis is the most common syndrome, all rare in adults Symptoms Post-prandial N/V/D/abdominal pain, weight loss FTT in infants and young children, irritability, sleep disturbance GER, often refractory, may be seen In teens/adults: dysphagia, food impaction 24. Eosinophilic Gastrointestinal Disorders: eosinophilic esophagitis/gastritis/gastroenteritis cont’d: Diagnosis Biopsy: eos infiltration (mucosa serosa): >15/HPF Presence of eos doesn’t necessarily invoke food allergy May affect esophagus to rectum Response to specific food elimination found in a subset of patients (especially eosinophilic esophagitis): can screen for food allergy with prick/in vitro IgE, patch testing with food is currently under investigation 25. Disorders Not Proven to be Related to Food Allergy Migraines Behavioral / Developmental disorders Arthritis Seizures Inflammatory bowel disease 26. Prevalence and Natural History 27. Prevalence of Food Allergy Perception by public: 20-25% Confirmed allergy (oral challenge) Adults: 3-4% Infants/young children: 6-8% Specific Allergens Dependent upon societal eating and cooking patterns Prevalence higher in those with: Atopic dermatitis Certain pollen allergies Latex allergy Prevalence seems to be increasing 28. Estimated Prevalence of Food Allergy Sampson H. J Allergy Clin Immunol;113:805-19. Food Children (%) Adults (%) Cow’s milk 2.5 0.3 Egg 1.3 0.2 Soy 0.3-0.4 0.04 Peanut 0.8 0.6 Tree nut 0.2 0.5 Crustaceans Fish 0.1 0.1 2.0 0.4 29. Prevalence of Clinical Cross Reactivity Among Food “Families” Food Allergy Prevalence of Allergy to > 1 Food in Family Fish 30% -100% Tree
    • Nut 15% - 40% Grain 25% Legume 5% Any 11% Sicherer SH. J Allergy ClinImmunol. 2001 Dec;108(6):881-90. 30. Natural History Dependent on food &immunopathogenesis ~ 85% of cases of cow milk, soy, egg and wheat allergy remit by age 3 yrs – numbers may be worse now for milk and egg Declining/low levels of specific-IgE favorable IgE binding to conformational epitopes favorable Non-IgE-mediated GI allergy Infant forms resolve in 1-3 years Toddler / adult forms more persistent 31. Natural History (cont’d) Allergies to peanuts, tree nuts, seafoods, and seeds typically persist ~20% of cases of peanut allergy resolve by age 5 years. Prognostic factors include : PST <6mm ≥ 2 years avoidance History of mild reaction Few other atopic diseases Low levels of peanut-specific IgE Rarely re-develop allergy: role for regular ingestion? 32. Diagnosis and Management 33. Evaluation: History & Physical Exam History: most important Symptoms, timing, reproducibility, treatment and outcome Concurrent exercise, NSAIDs, EtOH Diet details / symptom diary Subject to recall “ Hidden” ingredient(s) may be overlooked Physical exam: assess for other allergic and alternative disorders Identify general mechanism Allergy vs intolerance IgE versus non-IgE mediated 34. Evaluation of Food Allergy Suspect IgE-mediated Panels/broad screening should NOT be done without supporting history because of high rate of false positives. Prick skin tests (prick-prick with fresh food if pollen- food syndrome) In vitro tests for food-specific IgE Suspect non-IgE- mediated Consider biopsy of gut, skin Suspect non-immune, consider: Breath hydrogen Sweat test Endoscopy 35. Interpretation of Laboratory Tests Positive prick test or specific IgE Indicates presence of IgE antibody NOT clinical reactivity ~90% sensitivity ~50% specificity ~ 50% false positives Larger skin tests/higher
    • IgEcorrelates with likelihood of reaction but not severity Negative prick test or specific IgE Essentially excludes IgE antibody (>95% specific) 36. Unproven/Experimental Tests Intradermal skin test with food Risk of systemic reactions and death Not predictive (high false positive rate) Provocation/neutralization, cytotoxic tests, applied kinesiology (muscle response testing), hair analysis, electrodermal testing, food-specific IgG or IgG4 (IgG “RAST”) Note: industry/restaurants have no way of ascertaining whether a consumer was “diagnosed” by these methods or has a true food allergy. Science does not enter until a lawsuit is filed…. 37. Diagnosis: Elimination Diets & Food Challenges Elimination diets (1 - 6 weeks) most useful for chronic disease ( eg. AD, GI syndromes) Eliminate suspected food(s) or Prescribe limited “eat only” diet or Elemental diet Oral challenge testing (MD supervised, emergency meds available) Open Single-blind Double-blind, placebo-controlled (DBPCFC) 38. Diagnostic Approach: IgE-Mediated Allergy If test for specific-IgE antibody is Negative: reintroduce food* Positive: start elimination diet If elimination diet is associated with No resolution: reintroduce food* Resolution Open / single-blind challenges to “screen” DBPCFC for equivocal open challenges * Unless convincing history warrants supervised challenge 39. Treatment of Food Allergy Complete avoidance of specific food trigger Ensure nutritional needs are being met Education Anaphylaxis Emergency Action Plan if applicable most accidental exposures occur away from home This frozen dessert could have peanut, tree nut, cow’s milk, egg, wheat 40. Peanut allergen exposure through saliva: assessment and interventions to reduce exposure. Maloney JM et al. JACI 2006:118:719-24 . In our UC Davis group of patients with severe tree nut or peanut allergy, 5.3% volunteered that they had a reaction from kissing, sometimes several hours after partner had eaten food. 1/3 in dating situation . This study: Waiting 60 min, then brushing still did not remove peanut allergen
    • completely Authors suggest waiting several hours and ingesting a peanut- free meal to be more effective than tooth-brushing or gum-chewing. 41. Treatment: Dietary Elimination Education Hidden ingredients in restaurants/homes (peanut in sauces,egg rolls) Labeling issues (“spices”, changes, errors) Cross contact (shared equipment) Seeking assistance Food allergy specialist Registered dietitian: (www.eatright.org) Food Allergy & Anaphylaxis Network (www.foodallergy.org; 800-929-4040) and local support groups 42. Treatment: Dietary Elimination Education Hidden ingredients in restaurants/homes (peanut in sauces,egg rolls) International products Restaurants: outsourced dressings/desserts a problem Woman with near- fatal reaction after patisserie cake Secret ingredients 43. FALCPA won’t help this: “No Nuts in It!” swore the chef -- Meal served. Told specifically that there were no nuts in it 36 yr old woman with tree nut allergy – peanuts OK Upscale bistro; chef in charge Told waitress of life- threatening allergy – asked to check with chef to make sure dishes she was ordering were safe. Was told, “No problem.” Highly Educated Expert Chef 44. Ate a few bites and started to have tingling in the mouth Called the waitress over and asked if there was any way there were nuts in the dish – was told “No” Reaction progressed over minutes, trouble breathing and speaking, used her Epi-Pen, 911 called Hospitalized Jambalaya 45. After discharge, she spoke to the chef, who repeatedly denied to her that there were nuts in the dish Important to find out the cause, because if it was a new allergy she would have to track it down to avoid it in future along with tree nuts Threatened a lawsuit Chef only then disclosed ground cashews were used as a secret ingredient 46. “ Didn’t know it could be so serious” The chef maintained that he had been residing on planet earth despite an address in San Francisco
    • 47. Hospitality literature Wait staff: majority thought it was OK to pick an allergen off a dish and serve it to the customer 80% of managers said they were familiar with food allergy but only about 50% could define it. Others gave examples of things like spoiled food. 48. Treatment: Dietary Elimination Education Hidden ingredients in restaurants/homes (peanut in sauces,egg rolls) Labeling issues (“spices”, changes, errors) Cross contact (shared equipment) Seeking assistance Food allergy specialist Registered dietitian: (www.eatright.org) Food Allergy & Anaphylaxis Network (www.foodallergy.org; 800-929-4040) and local support groups 49. Contain cow’s milk: 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 ® . AS of January 1, 2006, all food containing “Big Eight Allergens” (cow’s milk, peanut, tree nut, hen’s egg, soy, wheat, fish, crustacean) in the U.S. MUST declare the ingredient on the label in COMMON language. Does NOT apply to non-Big 8 allergens (e.g., sesame). Label reading used to be very challenging Example: Cow’s Milk Food Allergen Labeling and Consumer Protection Act of 2004 (P.L. 108- 282) (FALCPA) 50. Geographic Unit United States (U.S. Public Law 2004) European Union (European Commission 2003) Australia-New Zealand (Australia New Zealand Food Authority 2001) Canada (pending law, Health Canada 2008) Japan (Ministry of Health 2001) Cow’s milk √ √ √ √ √ Hen’s egg √ √ √ √ √ Wheat √ √ √ √ √ Soy √ √ √ √ Peanut √ √ √ √ √ Tree nuts √ √ √ √ Fish √ √ √ √
    • Crustacean √ √ √ √ Molluscs √ √ Sesame √ √ √ Mustard seed √ celery √ buckwheat √ 51. Undeclared food (allergens) Current laws don’t help people with allergy to less common food allergens that are present in small amounts. Example: spices. UCD: personally have patients with oregano, cumin, garlic allergy. Virtually any food can be an allergen Prefer not to experiment with finding a threshold in an uncontrolled setting! FULL disclosure of all ingredients would be helpful Gets back to fact that we need more data on meaningful thresholds for a reaction E.g., soy lecithin 52. May Contain.. FDA mandated to publish results of follow-up studies on utility and consumer preferences for “may contain” labeling. Should be available soon. Consumers “hate it” As detection kits improve, can the use of these terms decrease? Need thresholds 53. Treatment: Dietary Elimination Education Hidden ingredients in restaurants/homes (peanut in sauces,egg rolls) Labeling issues (“spices”, changes, errors) Cross contact (shared equipment) Seeking assistance Food allergy specialist Registered dietitian: (www.eatright.org) Food Allergy & Anaphylaxis Network (www.foodallergy.org; 800-929-4040) and local support groups 54. Cross-Contact We need to do a better job teaching patients And restaurant staff Utensils Surfaces Pans/pots Deep fryers Scatter No need to “eliminate” allergens when there is a “safe” area for all and knowledgeable staff. 55. Treatment: Dietary Elimination Education Hidden ingredients in restaurants/homes (peanut in sauces,egg rolls) Labeling issues (“spices”, changes, errors) Cross contact (shared equipment) Seeking assistance Food allergy specialist Registered dietitian: (www.eatright.org) Food Allergy & Anaphylaxis Network (www.foodallergy.org; 800-929-4040) and local support groups
    • 56. Emergency Treatment: Anaphylaxis Epinephrine: drug of choice Self- administered epinephrine readily available at all times If administered, seek medical care IMMEDIATELY Train patients, parents, contacts: indications/technique Anti-histamines: secondary therapy only: WILL NOT STOP ANAPHYLXAXIS Written Anaphylaxis Emergency Action Plan Schools, spouses, caregivers, mature sibs / friends Emergency identification bracelet 57. MYTH: Prior Episodes Predict Future Reactions No predictable pattern Severity depends on: Sensitivity of the individual Dose of the allergen Other factors (e.g., food matrix effects, exercise, concurrent medications, airway hyperresponsiveness) Must always be prepared for an emergency . 58. Patients with severe food allergy may not receive education on avoidance, self-injectable epinephrine or referral to an allergist at emergency department visits. It is imperative for primary care doctors and allergists to recognize the risks and help patients avoid a future accident. Emergency Department Management of Food Allergy Clark S, et al. J Allergy ClinImmunol 2004;113:347-352. 59. Future Immunomodulatory Therapies Recombinant anti-IgE antibody Mutated B-cell epitopes Minimal T-cell epitopes Immune-modulating adjuvants (ISS) Probiotics T lymphocyte manipulation to induce tolerance Heat-killed E. coli encoding mutated allergens Chinese herbal remedies (Food Allergy Herbal Formula) Oral tolerance induction 60. Induction of tolerance after establishment of peanut allergy by the food allergy herbal formula-2 is associated with up-regulation of IFN- γ .Qu et al. CEA 2007;37:846 . Murine model of peanut anaphylaxis Treatment by gavage bid x 6 weeks started AFTER mice allergic completely blocks reactions Still blocked reactions to peanut 4 weeks after treatment stopped IL-4, IL-5, IL-13 significantly decreased in mesenteric lymph nodes of treated mice IFN- γ significantly increased in mesenteric lymph nodes of
    • treated mice An apparently synergistic combination of phytochemicals is present 61. Phamacological and immunological effects of individual herbs in the Food Allergy Herbal Formula-2 (FAHF-2) on peanut allergy. Kattan JD et al. Phytotherapy Res 2008;epub ahead of print 4/08 The nine separate “herbs” were individually tested as in the previous studies in the murine model No single herb offered full protection One offered statistically signif (but only 4 mice) protection (only ¼ mice had a reaction to peanut): Huang Bai: Phellodendron bark Huang Bai also reduced plasma histamine levels, but no change in IgE or specific IgG2a levels, whereas FAHF-2 results in decreased IgE and increased IgG2a Tried a simplified formula with only Huang Bai and 2 other “herbs”, but 2/5 mice had anaphylactic reactions to peanut Best results with full formula 62. Food Allergy Initiative and NIH-NIAID Food Allergy Consortium Funding to Xiu-Min Li and Hugh Sampson at Mt. Sinai. Food Allergy Herbal Formula 2 is a bitter-tasting decoction/tea. Now, a tablet form has been developed (12 small tablets tid is the human dose). Phase I trial scheduled to start now – announced that patients were now being enrolled at 2008 AAAAI meeting: just tolerability/safety. They plan to seek FDA approval via Phase II, III trials. 63. If the safety profile is good, since it is an herbal supplement, it could be available OTC with no health claims by the end of 2008 according to a recent Food Allergy Initiative mailer. This needs to be thought through very carefully though Knock-offs could proliferate with claims for all kinds of allergies Lead, arsenic, cadmium, adulteration (remember Zencor/sildenafil??) Takes time for FTC to catch up with those who illegally make claims 64. A randomized, double-blind, placebo-controlled study of Milk Oral Immunotherapy (MOIT) for cow’s milk allergy. Skripak JM et al. JACI 2008;S137 20 randomized to milk or placebo (2:1 ratio) after baseline
    • studies Build up day: started with 0.4 mg milk protein, final dose 50 mg Daily dosing with eight weekly dose increases to maintenance of 500 mg Continued daily for 3-4 mo 11 completed, 5 active, 6 placebo Baseline OFC: all 11 reacted to 40 mg milk protein (the initial dose) 65. Cont’d: MOIT Post OFC active group: cumulative median dose to elicit reaction in active group: 5,140 mg (range 2,540 – 6,140) 1 patient tolerated final dose of 8,140 mg with no symptoms. Post OFC placebo group: still reactive at 40 mg 968 total active MOIT doses: 9.9% local reactions, 3.8% systemic, epi given in 2 reactions 994 placebo doses: 11.3% local reactions, 1.2% systemic, no epi given. 66. Rush specific oral tolerance induction in peanut allergic patients at high risk of anaphylactic reactions. Blumchen K et al. JACI 2008:S136 . 6 children, ages 3-10 Peanut ImmunoCAP range 85->100 kU/l, median >100 All asthmatic, all “high risk” DBPCFC median provoking dose 470 mg peanut Inpatient rush protocol, allergic symptoms appeared at 96 mg to 480 mg, 3/6 had lower respiratory symptoms, multiple reactions requiring treatment Discharged after 6 days: on maintenance doses from 24 mg to 160 mg of peanut NOT protective doses! Conclusion: not a good approach for this type of pt.