What s new (and old!) in food allergy. Adelle R. Atkinson, MD, FRCPC Sea Courses May/June 2017

Transcription

1 What s new (and old!) in food allergy Adelle R. Atkinson, MD, FRCPC Sea Courses May/June 2017

2 Copyright 2017 by Sea Courses Inc. All rights reserved. No part of this document may be reproduced, copied, stored, or transmitted in any form or by any means graphic, electronic, or mechanical, including photocopying, recording, or information storage and retrieval systems without prior written permission of Sea Courses Inc. except where permitted by law. Sea Courses is not responsible for any speaker or participant s statements, materials, acts or omissions.

3 Faculty/Presenter Disclosure Faculty: Adelle Atkinson Relationships with commercial interests: Speakers Bureau/Honoraria: Nestle (unrestricted educational grant)

4 CFPC CoI Templates: Slide 2 Disclosure of Commercial Support N/A Potential for conflict(s) of interest: N/A

5 CFPC CoI Templates: Slide 3 Mitigating Potential Bias When speaking at events supported by Nestle, the grant is unrestricted and has no impact/influence on the content presented

6 Which Way is the Lady Turning?

7 7 Left Brain Counter clockwise Logic Detail Facts Language Present and past Strategies Practical math and science Comprehend Knowing Acknowledges Order/pattern perception Knows object name Reality based

8 Feeling Big picture Imagination Symbols and images Present and future Philosophy & religion Meaning Believes Appreciates Spatial perception Object function Fantasy based Presents possibilities Impetuous Risk taking 8 Right Brain Clockwise

9 Objectives By the end of this session, you will be able to: 1. Discuss the current state of food allergy in children. 2. Describe the current approach to management of food allergies including: 1. Avoidance 2. Oral challenges 3. Baked challenges 4. How and use and when to prescribe an epinephrine auto injector 3. Discuss the concept and strategy for de-labelling patients with food allergy

10 an adverse health effect arising from a specific immune response that occurs reproducibly on exposure to a given food Definition

11 Background IgE-mediated food allergies: May be life-threatening May negatively impact the quality of life for affected individuals Requires a coordinated approach between the health care team and family to keep patients safe

12 Pathogenesis

13 Signs and symptoms of an allergic reaction

14 The scope of the problem Prevalence of food allergy in US children has increased by 18% Estimated 7% of children currently have food allergies in Canada Close to 5% of adults Prevalence of peanut allergy in North America has recently tripled to 1-2% in school-aged children from 1997 to 2008 Branum AM, Lukacs SL. Pediatrics 2009; 124: Sicherer S, Sampson H. J Allergy Clin Immunol 2014;133:

15 Estimated Food Allergy Rates in North America Prevalence Infant/Child Adult Milk 2.5% 0.3% Egg 1.5% 0.2% Peanut 1.7% 0.7% Tree nuts 1.6% 1.0% Fish 0.2% 0.6% Shellfish 0.5% 1.7% Wheat, Soy 0.4% 0.3% Sesame 0.1% 0.1% Overall 5% 3-4% 1. Rona RJ et al. JACI 2007;120: Zuidmeer L et al. JACI 2008;121: Ben Shoshan M et al. JACI 2010;125:

16 Risk Factors Risk factors for the development of food allergy: Male sex Race/ethnicity increased among Asian and black children compared with white Genetics Atopy Vitamin D deficiency? Dietary fat Reduced consumption of antioxidants increased use of antacids Hygiene hypothesis

17 Natural History Allergies to milk, egg, wheat and soy typically resolve during childhood Previously thought that 85% of egg and cow s milk allergies typically resolved by 3 years of age Recent studies indicated only 11% resolved egg and 19% resolved cow s milk allergy by age 4 However, about 80% resolved these allergies by 16 years Allergies to peanut, tree nuts, fish and shellfish are usually persistent Currently, studies demonstrate that 20% can outgrow peanut allergy Savage JH et al. JACI 2007;120: Skripak JM et al. JACI 2007;120: Sicherer SH and Sampson HA. JACI 2007; 120:

18 Making the Diagnosis History specifics around the urticaria and whether there might have been a trigger (food, drug, environmental)? Associated angioedema action taken (antihistamines, epi-pen, 911) time to resolution of symptoms presence of a viral illness exercise, heat, cold or other physical triggers

19 Making the Diagnosis History continued Full review of systems for any other signs or symptoms of chronic disease thyroid disease, malignancy, autoimmunity, chronic viral infection etc. previous ingestions of the food/drug in question previous trials of therapy Personal and family history of atopy

20 Making the Diagnosis Physical Examination presence of existing allergic manifestations - angioedema, hives swollen nasal mucosa signs and symptoms of atopy Evidence of manifestations of any chronic disease

21 Skin Prick Testing

22 Skin Prick Testing Histamine Saline Peanut

23 Making the Diagnosis SPT must be tailored to each individual patient, one must not do a panel of screening tests looking for a positive reaction SPT is highly reproducible, and can be used for food, penicillin and environmental allergies the negative predictive value of SPT is very high in the order of 98 to 99% the PPV of SPT is variable -- unknown for penicillin and environmental, less than 50% for some foods

24 Making the Diagnosis Intracutaneous Testing used in most centres only with penicillin, vaccines and venom not used with environmental and food used after a negative SPT by doing an intradermal injection no good evidence that it adds to the SPT, many false positives needs to be compared with the gold standard Autologous Serum Skin Test (ASST) Utility not clear, only considered for CU Currently not routinely performed

25 Intracutaneous testing

26 Making the Diagnosis Radioallergosorbent Test (RAST) in vitro test looking at specific IgE to specific allergens high negative predictive value positive predictive value low SPT more sensitive Offers some useful information and is particularly useful when SPT is not possible

27 Rast Testing

28 Rast Testing Anti-IgE Antigen IgE

29 Other up and coming tests! Component resolved diagnostic testing: Patient s specific IgE reactivity to recombinant allergenic proteins rather than whole allergens May enhance diagnostic accuracy Promising results for peanut and hazelnut Whole blood basophil activation testing May reduce need for oral food challenges

30 Making the Diagnosis Double-Blind, Placebo- Controlled Food Challenge gold standard for the diagnosis of food allergy occasional false negatives must be done under supervision in a patient with a positive SPT and a questionable history a similar protocol has not been tried with penicillin

31 Making the Diagnosis Oral food challenge (open, unblinded) Used in patients where the diagnosis is in question Used in patients who may have outgrown their allergy (eg. milk, egg, wheat) Used to de-label patients who may have falsely labeled.

32 Management Mainstay of allergy management is avoidance Food allergic individuals must be taught about: scrutinizing labels by law in Canada and the US all ingredients must be listed in plain English (top allergens) wearing a medic alert bracelet carrying an epinephrine auto-injector Avoid cross-contamination

33 Management For some patients, dietary counseling may be important: Young infants around milk source (soya is recommended for IgE mediated milk allergy but NOT for non-ige mediated milk reactions) Children with multiple food allergies who are potentially at risk for nutritional deficiencies Restaurants and travelling require preparation and caution

34 Management Heated milk and heated egg challenges: Ingestion of baked and extensively heated forms of milk and egg may hasten the development of tolerance to lesser cooked or raw forms of milk and egg Heat alters the protein confirmation QOL improvement

35 Management Anaphylaxis plan Follow-up with allergy specialist Repeat skin testing yearly to every two years Considerations of future oral food challenges may outgrow some allergens

36 Management On the horizon Desensitization (oral immunotherapy)

37 Management

38 Non-IgE Mediated Food Allergy

39 Oral Allergy Syndrome IgE cross reactivity to PR10 proteins in fruits and nuts in patients with pollen allergies Foods are tolerated in cooked or processed forms Sensitization to proteins through the respiratory tract after pollen allergy established

40 Non IgE-mediated Food Allergy FPIES FPIAP FPE Age at Onset 1 day to 1 year Days to 6 mon, usually 1 to 4 weeks Foods Implicated Symptoms Lab Findings CM, soy, rice, oat, egg (and many others) Persistent vs, diarrhea, bloody stool, shock, FTT Anemia, hypoalb, leukocytosis, thrombocytosis,?methemoglobin emia,? acidemia CM, soy, wheat, egg Bloody stools, mild diarrhea Rarely low Hg and Albumin Depends on exposure, CM and soya up to 2 years CM, soy, wheat, egg Dx, sometimes vomiting Can look like post-infectious Anemia, hypoalb, malabsorption

41 Non IgE-mediated Food Allergy Treatment Natural History Comments FPIES FPIAP FPE Food elimination, 80% respond to a hydrolysate, rechallenge in 12 to 24 months CM resolves age 3 to 5, rice 50% resolved by age 5 Up to 40% with CM induced also react to soy Up to 35% transition to IgE positivity Food elimination from maternal diet, hypoallergenic formula, reintroduce after 12 months Majority resolve by 12 months No transition to IgE disease Overall milder than FPIES Food elimination, rechallenge and biopsy in 1 to 2 years Most resolve in 24 to 36 months No transition to IgE disease Overall milder than FPIES

42 Anaphylaxis and the Epinephrine Autoinjector

43 Anaphylaxis opposite of protection term first coined by Ortier and Richet in 1902 a pathologic phenomenon that occurs on subsequent re-exposure to a particular antigen causing an overwhelming immune response 43

44 Anaphylaxis the reaction occurs due to exposure of an individual with specific IgE antibodies to a specific allergens this results in activation of mast cells and release of the mediators of inflammation clinical symptoms ensue anaphylaxis is on a the most severe end of a spectrum 44

45 Risk Factors Peanuts and tree nuts Delay in administration of epinephrine Teen or young adult Poorly controlled asthma Use of β-blocker medications Absence of skin symptoms Denial of symptoms Bock SA et al. JACI 2007;119:

46 Anaphylaxis Etiology o food - peanuts and shellfish o insect stings - Hymenoptera including yellow jackets, yellow hornet, white-faced hornet, wasp and honeybee o medications - antibiotics, ASA, NSAID s o exercise o vaccines o latex o immunotherapy 46

47 Anaphylaxis Clinical Features Skin and Mucosa: Hives, swelling (lips, tongue, uvula), itching, warmth, redness/flushing, rash Respiratory system: Cough, wheezing, dyspnea, chest pain/tightness, throat tightness, stridor, hoarse voice, nasal congestion or hayfever-like symptoms (rhinorrhea, nasal itching, sneezing, watery eyes), hypoxemia, reduced PEF 47

48 Anaphylaxis Gastrointestinal system: Nausea, pain/cramps, vomiting, diarrhea, dysphagia Cardiovascular system: Pale/blue colour, weak pulse, faintness, syncope, dizziness/lightheaded, shock, collapse, tachycardia/arrhythmias Other: Anxiety, impending doom, headache, uterine cramps, metallic taste, incontinence Note: Anaphylaxis can occur without hives 48

49 Anaphylaxis Clinical Course usually uniphasic but can be biphasic or protracted biphasic reaction occurs in approximately 15 to 30% of cases within 4 to 8 hours 49

50 Anaphylaxis Diagnosis comprehensive history and physical examination (if not acute) detail into the apparent inciting event, foods, drugs, insect stings, association with exercise history of atopy skin testing if appropriate 50

51 Anaphylaxis highly likely when any one of these 3 criteria fulfilled Acute onset of illness (minutes to several hours) with involvement of skin and/or mucosal tissue AND AT LEAST ONE OF THE FOLLOWING: a) Respiratory compromise b) Reduced blood pressure or associated symptoms of end-organ dysfunction Two or more of the following that occur rapidly after exposure to a likely allergen for that patient (minutes to several hours) a) Involvement of the skin-mucosal tissue b) Respiratory compromise c) Reduced blood pressure or associated symptoms d) Persistent gastrointestinal symptoms Reduced blood pressure after exposure to known allergen for that patient (minutes to several hours) a) Infants and children: low systolic blood pressure (age-specific) or greater than 30% decrease in systolic blood pressure b) Adults: systolic blood pressure of less than 90 mmhg or greater than 30% decrease from baseline

52 Anaphylaxis Management acute A B C s 2 large bore IV s epinephrine 0.01 mg/kg (0.01 cc/kg) of 1:1000 concentration given IM IV epinephrine may be used in the critically ill patient as long as the patient is highly monitored diphenhydramine 1-2 mg/kg steroids 52

53 Anaphylaxis after the acute event - observation period for at least 12 hours those who have severe respiratory distress or hypotension should be observed for a minimum of 24 hours after resolution of symptoms patient should be referred to an allergist/immunologist for evaluation prevention, epinephrine auto-injector, MedicAlert bracelet 53

54 Management

55 Resources

56 Now you do it

57 Summary and wrap-up Here is what we said we would do: By the end of this session, you will be able to: 1. Discuss the current state of food allergy in children. 2. Describe the current approach to management of food allergies including: 1. Avoidance 2. Oral challenges 3. Baked challenges 4. How and use and when to prescribe an epinephrine auto injector 3. Discuss the concept and strategy for de-labelling patients with food allergy

58 Thank you