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Food Allergy

Conference Speaker: Jera Qianhui Zhang, MS, MA, RD–Diet, Microbiome and Allergy Prevention

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Jera Qianhui Zhang, MS, MA, RD

Allergy parents and patients wonder about how their gut health diet influenced their condition to begin with and what they can do going forward. Jera Qianhui Zhang will address these concerns. She is a licensed dietitian, a certified lactation counselor, and trained in the Low FODMAP Diet Protocol for Irritable Bowel Syndrome. She is also a doctoral student in Behavioral Nutrition at Teachers College, Columbia University. Her research interests include digestive health, the gluten-free diet, and immune-related disorders. She currently serves as the Chair of AAPI Professional Development Committee in the Academy of Nutrition and Dietetics.

8th East-West Integrative Medical Symposium for Immunology & Wellness–July 24th

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This conference will be brought to you via Zoom by New York Medical College (NYMC) and the laboratory of Dr. Xiu-Min Li, pioneer in the integration of Traditional Chinese

Dr. Xiu-Min Li

Medicine and Western Science. This year’s program will cover three broad areas: food allergies, eosinophilic esophagitis (EoE) and mast cell disorders, and eczema, including pernicious side effect, Topical Steroid Withdrawal. Several of the speakers have published on this website over the years. Institutions represented, in addition to NYMC, include Massachusetts General Hospital, Columbia, NYU, and Weill Cornell.

The program will run from 8:30am-3pm–eastern time

To register and/or make a donation click here.

 

Tolerance in a Test Tube Revisited: Mast Cell Activation Shows Promise As New Food Allergy Diagnostic

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By Dr. Paul Ehrlich & Henry Ehrlich

The long-time quest for a better blood test for food allergies may be closer than we thought. A letter in the Journal of Allergy and Clinical Immunology by six UK researchers headed by Alexandra Santos, MD, PhD, describes a study of the blood of children 73 of whom were diagnosed peanut allergic, 60 who were peanut-sensitized, and 41 non-allergic. Samples were subjected both to basophil activation tests (BATs), which are known to be highly predictive of allergy, and mast cell activation tests (MATs). The MATs were shown to be comparably predictive to BATs, although not precisely.

Both tests involve exposing allergenic proteins to the cells in question to see if the IgE antibodies attached to them will bind with the protein and cause them to degranulate. If it does, the patient is allergic. The problem with BAT is that since the basophils circulate in the blood, the test must be done when the sample is fresh. There is no way to achieve the economies of scale enjoyed by commercial testing services that perform other kinds (and less definitive) of allergy testing. For this reason BAT has been confined to research centers.

The MAT has a singular advantage. The key is that the mast cells aren’t taken from the individual, which would involve harvesting from tissue and the same kind of time pressure as the BAT. This would be far more intrusive than drawing blood.

Instead the lab uses something called LAD2 mast cells (or FcepsilonRI+/CD117+), which can be cultured in large quantities. They are blank slates with the high-affinity receptors ready to receive IgE antibodies. The patient’s plasma, which contains allergen-specific IgE, is drawn and shipped at low temperature to the lab where it is exposed to the cultured mast cells. The IgE binds to the receptors just as they do in the human body, and then exposed to the allergen. If they degranulate, there is an allergy. If they don’t—bingo, tolerance in a test tube.

The weaknesses of current blood tests are well known. As Santos et al write, “Peanut-specific IgE (P-sIgE) is associated with false-positive results and overdiagnosis.” And component tests have their problems too. “Measurement of Ara h 2–specific IgE is more accurate but is associated with false-negative results.” Oral food challenges, with their risks of adverse reactions, are the only definitive solution, but as we have written on this website before, many allergists won’t do them for reasons that include money, staff time, and the possibility of having to manage reactions.

The authors say that apart from diagnosis, the MAT seems to have real utility for predicting severity of reactions and would be a useful screen prior to food challenge

We have also written, and the Santos team concur, that the recent proliferation of treatments, whether things like various forms of immunotherapy, traditional Chinese medicine, or LAMP vaccine demands that there be new ways of measuring tolerance. It didn’t matter as much when there were no treatments, but now there are. Submitting patients to a continual series of challenges would be impractical and anxiety producing.

If proven for peanut and for other allergens, the mast cell activation test will be a welcome addition to the allergist tool kit.

Graphic: alchemyhealth.com.au

Food Allergy Urban Myths: Two Experts Separate Fiction from Fact

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By Carina Venter, PhD, RD and David Fleischer, MD

Carina Venter, PhD, RD
David Fleischer, MD

Year after year, despite dramatic gains in research, some misconceptions are remarkably stubborn, both among patients and their doctors. We canvassed our friends in practice and research around the world to compile a list, and there was broad consensus that these are the most prevalent. (See list below of those who helped.)

1. You can’t be allergic to a food that you have not eaten
False:
Sensitization to foods can happen via the skin, particularly in children with eczema(1) During pregnancy, the fetus can be exposed to allergens their mother is eating; during breastfeeding, allergens can be passed to the infant via breast milk(2).

However, allergen avoidance during infancy when children suffer from eczema, or during pregnancy or lactation, does not seem to prevent food allergies. Allergen avoidance during pregnancy and breastfeeding is not advised until we understand the role of dietary intake better. Eating of allergens early in an infant’s life, however, seems to protect against the development of food allergies.

2. You can’t be allergic to rice, and most definitely not to banana or sweet potato!
False: Imagine the difficulties of trying to convince food allergy sceptics that your child is really peanut-allergic. Now try to imagine telling them that your child is allergic to rice! Parents who make this claim are generally met with amused condescension–“No one is allergic to rice!” Unfortunately, many of the allergens involved in food protein-induced enterocolitis syndrome (FPIES) are “atypical” allergens such as rice, sweet potato, and banana(3). (But try to explain FPIES to the average skeptic.) So yes – severe allergic reactions to foods not considered to be part of the top eight allergens are possible.

Allergic to rice: True or False?

3. The size of your skin prick test (SPT) or the level of food-specific IgE tests predicts the severity of reactions
False: The size of a SPT or the level of specific IgE to a food indicates the likelihood of being allergic but not the severity of the reaction, i.e., the larger the size of the SPT or the higher the level of serum specific IgE the more likely you may be allergic to that food(4). The reaction history remains the most important indicator.

4. Each allergic reaction to a food becomes subsequently worse
False: There is no evidence to indicate that each allergic reaction becomes worse. Many people who had only mild symptoms in the past, end up with anaphylaxis on subsequent exposure(5). There is however some evidence that a history of anaphylaxis and suffering from eczema or asthma, may increase the risk of anaphylaxis(6).

5. Everyone with food allergy develops anaphylaxis
False: Many people with IgE-mediated food allergies never develop anaphylaxis. There are a number of factors that indicate if a person may develop anaphylaxis, including(5):
– Presentation of the food allergen (e.g. baked or not, fat content*)
– Infections
– Immunological and hormonal factors
– Behavior (e.g. risk taking, alcohol)

6. If you are allergic to one peanut or a tree nut, you need to avoid all nuts
False: Individualized avoidance of nuts should be advised to those with nut allergies – taking into account the family’s preferences/needs. About one-third of patients with peanut allergy may have tree nut allergies. People with certain tree nut allergies often tolerate other tree nuts. The tree nut allergies that most often co-exist are: cashew and pistachio; walnut and pecan, although you can be allergic to one of these but not another(7).

7. My child reacts to corn starch or corn syrup in foods (most often corn syrup in infant formula)
False: Although we can find no studies to reference, personal discussions with food scientists confirm that there are only trace amounts of protein left in corn starch and undetectable amounts in corn syrup, glucose syrup, dextrose (granular) or high fructose corn syrup. Many years of clinical practice, using these products in corn-allergic individuals, have reassured us that they are perfectly safe to use from an allergy point of view, although added sugar presents other problems.

8. I tolerate soy/peanut/sesame/tree nut oils
Perhaps true: The processing of oils across the world differs a lot, and even we find it confusing. Check to find out how the oil was produced: refined/expeller/heat-pressed oils, including the big brand names, are safer to eat, but crude/cold-pressed oils are best avoided due to a higher chance of having more residual protein.

9. My/his/her food allergy is not severe as I can eat(or /my child) can eat “trace amounts” of the foods
False: Many people belief that if they have safely eaten a product that states “may contain traces”/”produced in a factory” that they are tolerant of “trace amounts” of the allergen. This is, however, not true. “May contain” is a legalism, not a guarantee that any allergen is present. Most products with some kind of “may contain” warning do not have any detectable contamination, and those that do, contain a range of different amounts. It is also important to remember that some products without a “may contain” warning may contain trace amounts of the allergen(8).

10. Everyone with an allergy needs to avoid even trace amounts of the food
False: We change “strict” avoidance to “individualized” avoidance in every paper we review. We have long passed the times era when all food-allergic individuals have to strictly avoid allergen exposure. We understand that some people can tolerate baked milk and egg(9). Oral and epicutaneous immunotherapies have also made it possible to tolerate allergens, either fully or to some degree(10).

11. A baby/child that who is gaining weight cannot have a food allergy
False: Many infants with food allergies have a normal, perhaps even increased weight, and just referring to the weight to make a diagnosis will lead to a lot of misdiagnosis(11). Picky eating may be a sign that the child is uncomfortable eating certain foods, and parents compensate by relying on fattening foods.

12. Breastfed babies do not develop food allergies
False: Particularly in the case of cow’s milk allergies, where over 40% of babies with milk-induced proctocolitis, a non-IgE-mediated food allergy, are exclusively breastfed.(12)

13. If you do not have IgE-mediated food allergies, it is just an intolerance
False: Although the exact mechanisms of non-IgE/gut-related food allergies are not fully understood, it is clear that the immune system is involved in non-IgE-mediated food allergy; strictly speaking, intolerances are not immune-mediated(13), most prominently lactose intolerance, which results from an enzyme deficiency.

14. Young infants will have false negative SPTs
False: SPT can be performed from any age. SPT of very young infants may be smaller than older children, but there is no lower age limit to perform SPT or food-specific IgE tests(14).

15. IgG tests are reliable to test for food intolerances
False: Our present knowledge regarding IgG indicates that IgG4 is marker of food intake or development of tolerance (it is sometimes difficult to separate the two), but there is no association with IgG to a food and food intolerance to it(15).

* High fat content allows you “tolerate” the allergen to a much higher dose BUT then have very severe reactions once you react – i.e. you miss those initial warning symptoms. Hence using low-fat peanut flour for challenges.(16)

1. du Toit G, Tsakok T, Lack S, Lack G. Prevention of food allergy. J Allergy Clin Immunol. 2016;137(4):998-1010.
2. Pastor-Vargas C, Maroto AS, Diaz-Perales A, Villalba M, Esteban V, Ruiz-Ramos M, et al. Detection of major food allergens in amniotic fluid: initial allergenic encounter during pregnancy. Pediatr Allergy Immunol. 2016.
3. Venter C, Groetch M. Nutritional management of food protein-induced enterocolitis syndrome. Curr Opin Allergy Clin Immunol. 2014;14(3):255-62.
4. Peters RL, Allen KJ, Dharmage SC, Tang ML, Koplin JJ, Ponsonby AL, et al. Skin prick test responses and allergen-specific IgE levels as predictors of peanut, egg, and sesame allergy in infants. J Allergy Clin Immunol. 2013;132(4):874-80.
5. Turner PJ, Baumert JL, Beyer K, Boyle R, Chan CH, Clark A, et al. Can we identify patients at risk of life-threatening allergic reactions to food? Allergy. 2016.
6. Flinn A, Hourihane JO. Allergic reaction to peanuts: can we predict reaction severity in the wild? Curr Allergy Asthma Rep. 2013;13(6):645-50.
7. Brough HA, Turner PJ, Wright T, Fox AT, Taylor SL, Warner JO, et al. Dietary management of peanut and tree nut allergy: what exactly should patients avoid? Clin Exp Allergy. 2015;45(5):859-71.
8. Allen KJ, Remington BC, Baumert JL, Crevel RW, Houben GF, Brooke-Taylor S, et al. Allergen reference doses for precautionary labeling (VITAL 2.0): clinical implications. J Allergy Clin Immunol. 2014;133(1):156-64.
9. Nowak-Wegrzyn A, Groetch M. Nutritional aspects and diets in food allergy. Chem Immunol Allergy. 2015;101:209-20.
10. Nowak-Wegrzyn A, Fiocchi A. Is oral immunotherapy the cure for food allergies? Curr Opin Allergy Clin Immunol. 2010;10(3):214-9.
11. Meyer R, De Koker C, Dziubak R, Venter C, Dominguez-Ortega G, Cutts R, et al. Malnutrition in children with food allergies in the UK. J Hum Nutr Diet. 2014;27(3):227-35.
12. Yilmaz EA, Soyer O, Cavkaytar O, Karaatmaca B, Buyuktiryaki B, Sahiner UM, et al. Characteristics of children with food protein-induced enterocolitis and allergic proctocolitis. Allergy Asthma Proc. 2017;38(1):54-62.
13. Boyce JA, Assa’a A, Burks AW, Jones SM, Sampson HA, Wood RA, et al. Guidelines for the diagnosis and management of food allergy in the United States: summary of the NIAID-Sponsored Expert Panel Report. Nutrition. 2011;27(2):253-67.
14. Bock SA. Diagnostic evaluation. Pediatrics. 2003;111(6 Pt 3):1638-44.
15. Du Toit G, Roberts G, Sayre PH, Bahnson HT, Radulovic S, Santos AF, et al. Randomized trial of peanut consumption in infants at risk for peanut allergy. N Engl J Med. 2015;372(9):803-13.
16. Grimshaw KE, King RM, Nordlee JA, Hefle SL, Warner JO, Hourihane JO. Presentation of allergen in different food preparations affects the nature of the allergic reaction–a case series. Clin Exp Allergy. 2003 Nov;33(11):1581-5.

 Carina Venter, PhD RD, is a Research Associate/Dietitian at Cincinnati Children’s Hospital Medical Center and currently the Chair of the International Network of Dietitians and Nutritionists in Allergy, a member of the AAAAI, BSACI and EAACI. She is a registered dietitian in the United Kingdom, United States and South Africa.  She has had numerous publications in international journals, and has authored book chapters and edited a book on Food Hypersensitivity. She was, until recently, working as a Senior Lecturer at the University of Portsmouth, where she was doing research into food allergies and allergy prevention, based at the David Hide Centre on the Isle of Wight. 

 Carina was a member of the Expert Panel of the National Institutes for Allergy and Infectious Diseases Peanut Allergy Prevention Guidelines, making her the only dietitian to contribute to both US and European food allergy guidelines.

 David Fleischer, MD, studied medicine at Emory University School of Medicine. He was a pediatric resident at Johns Hopkins where he also training in Pediatric Allergy/Immunology. He joined the staff of National Jewish Health in Denver in August 2005, where he worked until December 2013. In January 2014, Dr. Fleischer joined the new Allergy Section at Children’s Hospital Colorado (CHCO), where he is currently an Associate Professor of Pediatrics and the University of Colorado Denver School of Medicine.

Dr. Fleischer’s clinical interests include food allergy, eosinophilic gastrointestinal disease, and atopic dermatitis. His research has focused on the natural history of food allergy and novel treatments for food allergy, including oral, sublingual, and epicutaneous immunotherapies. He has been involved in several projects examining the primary prevention of allergy, including as a member of the 2015-16 National Institutes for Allergy and Infectious Diseases (NIAID) Expert Panel that is updating the 2010 NIAID Food Allergy Guidelines on the topic of the Prevention of Peanut Allergy.

Dr. Fleischer has published many peer-reviewed articles, review articles, and book chapters on food allergy and eosinophilic gastrointestinal disease.

 

{Note, the authors would like to thank those who helped to put their list together: Marion Groetch (USA), Berber Vlieg-Boerstra (The Netherlands), Rosan Meyer (France), Hannah Hunter (UK), Lianne Reeves (UK), Marianne Williams (UK), Paul Turner (UK), Isabel Skypala (UK), Fallon Schultz (USA), Raquel Durban (USA)}

 

 

 

 

The LEAP Trial 12 Months Later: Are We Ready to LEAP-On?

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Jesse owensBy David Stukus, MD

What Do We Know About the Prevention of Peanut Allergy?

For decades, the belief among allergists and pediatricians was that avoidance of allergenic foods would prevent the development of allergy. Previous clinical guidelines published in 2000 by the American Academy of Pediatrics recommended avoidance of all milk products until 1 year of age, egg until 2, and peanut, tree nuts, and seafood until 3. Lo and behold, just 8 years later, the authors realized that there was no evidence to support this approach and the guidelines were not just revised, but also completely reversed, in 2008 to recommend introduction of solid foods, including allergenic foods, into the diet between 4-6 months of age. This stark contrast was met with confusion and reluctance to change the paradigm without solid evidence in support. Pediatricians and parents were left in limbo. Then, in March 2015 The Learning Early About Peanut Allergy (LEAP) study was published in the New England Journal of Medicine. For the first time, the LEAP study very strongly demonstrated that early introduction of peanut to high risk infants does indeed prevent the development of peanut allergy.

The LEAP trial enrolled 640 infants all between 4-11 months of age and randomized them to two groups: one group avoided any peanut until 5 years of age and the other group consumed 2 grams of peanut 3 times a week until 5 years of age. All participants had moderate-to-severe eczema and/or egg allergy and underwent skin prick testing and food challenge at enrollment. The LEAP trial demonstrated a significant reduction in peanut allergy at 5 years of age for infants who consumed compared with those who avoided, including an 86% relative reduction in those with negative skin tests and 70% relative reduction in those with a mild skin test wheal size of 1-4 mm at enrollment. This was the first large-scale study demonstrating the possibility of prevention of food allergy through early introduction.

It is important to understand that the LEAP study findings are not generalizable for several reasons. First, the participants all had moderate-to-severe eczema and/or egg allergy. It remains unknown what effect early introduction of peanut would have for infants without eczema, for those with food allergies other than egg, or for those with a family history of peanut allergy. There is no reason to believe anyone would react differently than this well-chosen cohort of at-risk infants, but we also have no data. Second, the LEAP protocol was very strict with consumption of at least 2 grams of peanut three times per week for 4 years. It remains unknown what the effect would be from eating less amounts less frequently. Third, all infants in LEAP were less than 11 months old, mean age 7.8 months. It remains unknown what would happen if peanut were introduced at 12 months of age or later. However, LEAP data clearly demonstrates an increased risk of larger peanut skin test or failed oral challenge with increasing age. Lastly, LEAP excluded any infants with a wheal size 5 mm. or greater on skin prick testing. 8 mm. is well regarded as the size of wheal on skin testing associated with a 95% likelihood of having a peanut allergy. It is possible that a group of infants with wheal skin test size to peanut between 5-8 mm. would also be able to tolerate and then prevent development of peanut allergy.

Since LEAP was published, not everyone has been a fan of the results. This has no bearing on anyone who already has a peanut allergy, as this is a study looking at prevention. In addition, many parents became upset as they specifically avoided giving their children peanut until later in life only to see their children still develop peanut allergy, and LEAP now shows that this could have potentially (likely) been avoided. All I can say is that recommendations are made based upon the best available current evidence. Hindsight is 20/20, and I share the burden with all of my colleagues that perhaps we gave the wrong advice for a period of time. Physicians make treatment recommendations based upon the best available evidence and current treatment guidelines, both of which are moving targets. One can observe the seemingly constant changes to screening procedures (see: mammograms) or dietary recommendations (see: trans fats, carbohydrates, sugars, etc) to begin to understand how knowledge gaps become filled in by research over a course of years and decades.

Some have screamed that a conflict of interest occurred due to partial funding for the study from the National Peanut Board. However, there were several funding sources for this study, not to mention that trial design, implementation, and interpretation of results was performed by the investigators, not the funders. In a nearly unprecedented manner within the field of allergy/immunology, the study authors made all of their study data available for free to the entire world through TrialShare, which literally allows anyone with interest the capability of pouring through and then re-analyzing all of the data. Lastly, some have taken issue with certain exclusion criteria in LEAP, but careful review of study protocol shows that the authors did a thorough and comprehensive job of studying the possibility of primary prevention of peanut allergy in a cohort of at-risk infants and excluded infants with possible confounding factors such as other co-morbid conditions (extremely common in research studies).

Did LEAP Truly Prevent Peanut Allergy or Just Lead to Desensitization?

One of the unanswered questions from LEAP is in regards to mechanism of action. While there was a dramatic reduction in peanut allergy at 5 years of age for infants who consumed regularly versus those who avoided, the study was not designed to investigate why this occurred. Oral immunotherapy for food allergy is not a cure, but offers a way to desensitize and potentially develop tolerance or prevent severe reactions from occurring with accidental ingestion. Oral immunotherapy requires daily ingestion of the food allergen in very small amounts in order to maintain desensitization. Missed doses or prolonged periods of time in between doses can cause a loss of the desensitized state and lead to allergic reaction with the next exposure. This is an extremely important concept not well understood by many seeking the ‘food allergy cure’ that does not yet exist. Is it possible that LEAP merely led to prolonged desensitization? The authors were determined to find out.

The Persistence of Oral Tolerance to Peanut (LEAP-On) study was published in the New England Journal of Medicine in March 2016 and used the same participants from LEAP. LEAP-On asked all children in both the avoidance and consumption groups to strictly avoid peanut for 12 months, after their oral challenge at 60 months of age. This was to try and determine whether peanut allergy was truly prevented through early introduction, or whether these infants were being desensitized, similar to oral immunotherapy.

LEAP-On enrolled 88.5% of participants from the original trial (556 children). Study authors monitored adherence to peanut avoidance during the 12 months of subsequent avoidance and noted high rates in both groups, with 90.4% in the original peanut avoidance group continuing avoidance compared with 69.3% in the peanut consumption group. (Kudos to the 70% of parents who agreed to remove peanut from their children’s diet not knowing whether they may develop peanut allergy after 4 years of tolerance.)

After 12 months of peanut avoidance, there was no significant increase in children developing peanut allergy from the group that previously consumed; 3.6% at 5 years of age, compared with 4.8% at 6 years. There were a total of 3 new cases of peanut allergy in both groups. In addition, the original peanut consumption group continued to have much lower rates of peanut allergy after completion of LEAP-On, 4.8% vs 18.6%.

Does LEAP-ON Change Anything?

So what does this all mean? According to the new data from LEAP-On, early introduction of peanut to infants at high risk for development of peanut allergy not only dramatically reduces rates of peanut allergy at 5 years of age, but also shows this effect to be sustained after one year of avoidance. This is likely due to true prevention, as opposed to a prolonged desensitization.

We still do not know the exact duration or amount of consumption necessary to induce sustained tolerance. LEAP participants consumed 2 grams of peanut 3 times per week for 4 years. Is it possible that eating peanut ad lib or for shorter duration will have the same effect? This remains unknown. However, we have clear and strong evidence that early and sustained consumption of peanut in high risk infants is effective in preventing the development of food allergy, and now in sustaining unresponsiveness.

Currently, when I meet a parent (or expectant mother) with a 4-11 month old infant who has moderate-to-severe eczema and/or egg allergy, I am thrilled to have the opportunity to discuss the LEAP study findings and implications. I offer skin prick testing to peanut and have had tremendous success introducing peanut butter to infants in my office setting. Every single one has a look of wide-eyed wonderment at the new experience for their taste buds. Significant breakthroughs such as this do not come along frequently in medicine. Being able to offer families a likely preventative strategy brings great joy to these parents (many of whom have older children with existing peanut allergy) and myself as well.

Information from the original LEAP and new LEAP-On studies will be used to formulate new guidelines to help pediatricians and allergists encourage the introduction of peanut to all infants, with recommendations to test and/or challenge first for those at high risk. The National Institute of Allergy and Infectious Disease is coordinating these guidelines, with input from food allergy experts from across North America and Europe. Goal for publication is sometime in 2016.

In the meantime, we must continue to help parents and pediatricians understand exactly what the data from these research studies has taught us. Parents of newborns should discuss these implications with their child’s pediatrician or allergist prior to introducing peanut. Pediatricians should start discussing this with parents at the 4-month well child visit. Allergists need to continue educating everyone as to what this all means.

It has been suggested that it takes approximately 10-15 years before new guidelines are adopted into clinical practice. Let’s all hope it doesn’t take that long to prevent a new generation of infants from developing peanut allergy.

 

David Stukus, MD, is board certified in Allergy/Immunology and is an Assistant Professor of Pediatrics at Nationwide Children’s Hospital and The Ohio State University in Columbus, Ohio. His clinical and research interests focus on asthma and food allergies, especially improving education and adherence for patients and families. As part of his research, Dr. Stukus has created novel technology and educational tools using mobile health apps to improve the care of patients, for which he was recognized with the Nationwide Children’s Hospital Department of Pediatrics Junior Faculty Award in November 2013. Dr. Stukus has been an active member of the medical advisory team for Kids with Food Allergies since 2009 and was elected to the Board of Directors for the Asthma and Allergy Foundation of America in 2014. Lastly, Dr. Stukus actively engages with food allergy support groups and participates in social media on twitter through @AllergyKidsDoc.

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