Being one of the clinicians in this course, I thought I would share some information about food allergy (which is an issue we encounter with increasing frequency):
Food allergies are adverse immunologic reactions to food proteins and run the spectrum of IgE mediated reactions to cell mediated reactions such as food protein induced enterocolitis or contact dermatitis. However, IgE mediated food reactions are the most common.
Food allergies are prevalent with reproducible symptoms in 5% of young children and 1-2% of adults. More than 90% of food allergies are caused by milk, egg, fish/shellfish, wheat, soy, peanut/tree nuts. It is estimated that 1-2% of the U.S. and European population is allergic to peanuts and/or tree nuts.
Furthermore, reactions to nuts, particularly peanut are severe and often fatal. In fact, per the United States Food Allergy & Anaphylaxis Network (FAAN) registry, peanuts are responsible for a significant percentage of food-associated deaths. Unfortunately, accidental exposure to peanuts is common, noted to occur in 14.3% of Montreal schoolchildren, and exposure to doses as small as 100 micrograms may provoke symptoms (an average peanut weighs 300-500 milligrams). Approximately 20% of children will outgrow a peanut allergy (approximately 10% outgrow tree nut allergy).
Interestingly, nearly one-third of peanut allergic patients will become tree nut allergic and this trend seems to be true of tree nut allergic patients becoming peanut allergic, at least for some tree nuts, such as cashew. So, is it that nut allergic persons are predisposed to develop allergies to multiple different nut proteins? Or are they reacting to similar epitopes in the various types of nuts? The answer is unclear for several reasons. First, and most obviously, not enough work has been done between peanut and tree nut cross reactivity. Second, how do we assess cross-reactivity? Do we use methods that denature the protein and exposure linear, but not necessarily functional epitopes, such as Western blotting? Or do we use functional assays that use structurally intact proteins such as histamine release assays (human basophils or immortalized rat basophils)? Also, how do these studies correlate with the clinical history as well as measurements of peanut or tree nut specific IgE? This is the subject of some ongoing research being conducted here as well as a few other sites in the U.S. and Europe, and perhaps elsewhere.
As a final note, there are a few articles that demonstrate transfer of allergies in the context of transplantation. The first article by Bellou et al. involves bone marrow transplantion. The second article by Phan et al. involves liver transplantation. The third article, which did not have an abstract available online reports peanut hypersensitivity transfer via fresh frozen plasma. The mechanism responsible for the transfer of allergy is undetermined but ideas include adoptive transfer of primed donor B-cells or T-cells, or the transfer of donor mast cells sensitized to peanut specific-IgE or passive transfer of donor peanut specific-IgE.
Articles:
Bellou A, et al. Tranfer of atopy following bone marrow transplantation. Ann Allergy Asthma Immunol. 1997 May;78(5):513-6.
Phan TG, et al. Passive transfer of nut allergy after liver transplantation. Arch Intern Med. 2003 Jan 27;163(2):237-9.
Arnold DM, et al. Passive transfer of peanut hypersensitivity by fresh frozen plasma. Arch Intern Med. 2007 Apr 23;167(8):853-4.
References:
Sampson H. Update on food allergy. J Allergy Clin Immunol 2004;113:805-9.
Bock S. Prospective appraisal of complaints of adverse reactions to foods in children during the first three years of life. Pediatrics 1987;79:683-8.
Hefle S, Nordlee J, Taylor S. Allergenic Foods. Crit Rev Food Sci Nutr 1996; 36:S69–S89.
Sicherer S, Furlong T, et al. A voluntary registry for peanut and tree nut allergy: Characteristics of the first 5149 registrants. J Allergy Clin Immunol 2001;108:128-32.
Sicherer S, Sampson H. Peanut allergy: Emerging concepts and approaches for an apparent epidemic. J Allergy Clin Immunol 2007;120:491-503.
Yu JW, Kagan R, Verreault N, Nicolas N, Joseph L, St Pierre Y, et al. Accidental ingestions in children with peanut allergy. J Allergy Clin Immunol 2006;118:466-72.
Roux K, Teuber S, et al. Tree nut allergens. Int Arch Allergy Immunol 2003;131:234-44.
Fleischer D, Conover-Walker M, et al. The natural history of tree nut allergy. J Allergy Clin Immunol 2005;116:1087-93.
Burks K, Bock S. Natural History of Peanut and Tree Nut Allergy: Development of Tree Nut Allergy/Sensitization. J Allergy Clin Immunol 2008;121:S235.
As a Pediatric GI physician, there are lots of parents with concerns that their children have allergy to foods. If you tested them all, chances are good the majority would be IgE negative to the food of concern. And a lot of these do not have the clinical manifestations of FPIES. Are you aware of increasing trends in non-IgE mediated food allergies/sensitivies? I think a fair number of these kids have no type of allergy at all in reality.
ReplyDeleteAlso, are there any prognosticators that you know of for someone outgrowing their food allergies?
Steve, thanks for the response. The prevalence of FPIES is frequently stated as "unknown" due to variability of presentation, under-recognition, lack of diagnostic challenge, etc. (http://www.allergysa.org/journals/2009/june/food-protein-induced-enterocolitis.pdf).
ReplyDeleteAn Austrialian group did note an increased number of diagnoses over the years but did not know if this was a true signal or the result of increased awareness (Mehr S, et al. Food Protein-Induced Enterocolitis Syndrome: 16-Year Experience. Pediatrics 2009;123(3): e459-e464.
With respect to food allergy evaluations, yes we are seeing a definite increase in evaluation and many of these are without a supportive clinical history and are non-immunologic reactions (IgE or non-IgE mediated).
The difficulty with diagnosing food allergy is that skin tests to foods have a high false positive rate (meaning positive reaction but the patient tolerates the food without difficulty and thus is not clinically allergic). With respect to food specific IgE in general, a negative number is reassuring but a "low" or "moderate" specific IgE level is not informative. Similarly, a "high" specific IgE is suggestive, but again must be clinically correlated. However, work done by Sampson did determine specific IgE thresholds for certain foods that "predict clinical reactivity in this population with greater than 95% certainty, were identified: egg, 6 kilounits of allergen-specific IgE per liter (kU[A]/L); milk, 32 kU(A)/L; peanut, 15 kU(A)/L; and fish, 20 kU(A)/L. " (Sampson H, et al. Relationship between food-specific IgE concentrations and the risk of positive food challenges in children and adolescents. J Allergy Clin Immunol 1997;100(4):444-51.)
Yet, even in the setting of a documented food allergy, there is poor correlation between specific IgE levels and severity of reaction.
With respect to prognostics, annual tracking of food specific IgE is the best prognosticator. First, a decreasing specific IgE is a good sign. And, if the specific IgE level reaches 2 kUA/L (ImmunoCAP) or below, the patient may be suitable for a food challenge (age appropriate). Of this population 9-20% seem to pass the challenge and thus "outgrow" their allergy.
Hope this helps.
I have a general question/concern as I have a 9 week old son. I had read that introducing solids too early can produce food allergies.Is this true? I have not introduced anything other than formula at this point but I am curious. Also, when is a good time to test my child for possible food allergies/ and or respiratory allergies? I am very allergic to pollen, ragweed, etc... and am wondering if my child will be the same.
ReplyDeleteJennifer, thanks for the response. Previous "expert" recommendations recommended avoiding certain foods such as peanuts/tree nuts, strawberries, etc. until 2 years of age. These were not founded on any data, but rather a consensus opinion. However, a recent study demonstrated an association with lower peanut allergy and exposure within the first year of life for a genetically similar cohort (Du Toit G, et al. Early consumption of peanuts in infancy is associated with a low prevalence of peanut allergy. J Allergy Clin Immunol. 2008 Nov;122(5):984-91.). Thus early avoidance doesn't seem to make sense.
ReplyDeleteIn terms of testing for food allergies, you should not test unless you have a clinical suspicion in general. This means that if your child reacts adversely to a food then certainly test. The issue with broad non-specific testing is the high rate of false positive skin tests.
With respect to testing for seasonal aeroallergens such as grass or tree pollen or weeds, the (variable) recommendation tends to be testing at 2 years of age at the earliest. The thinking being that a person would need a season of exposure to become sensitized and then experience symptoms the following season. This is not a hard and fast rule, but is a majority approach.
In terms of perennial aeroallergens like mold, cat, dog, dust mite. Testing can be performed as early as 1 year of age. Again, this varies among physicians and some may do it sooner or later.
There is a genetic disposition for atopy, thus your child may develop allergies, or may not. It is more likely if both mother and father are allergic.
Hope this helps.
You had mentioned 'More than 90% of food allergies are caused by milk, egg, fish/shellfish, wheat, soy, peanut/tree nuts.' What makes these food items different from food items that we do not develop an allergy to?
ReplyDeleteHolly, thanks for the question. Unfortunately the answer to your question is unknown. Speculation includes a possible multifactorial etiology including inherent allergenicity or the food protein, route of first exposure, amount of exposure, etc. What is known is that some food allergies are more likely to resolve including milk and egg. To the contrary, some other food allergies are difficult less likely to resolve such as shellfish and nut. Why this is the case is also unknown.
ReplyDeleteI had a question regarding atopy and development of food allergy--can skin exposure to (for example) peanut trigger sensitization during infancy--specifically, during a severe bout of eczema? If so, should caregivers be carefully about exposing peanut oils to infants?
ReplyDeleteAlso, I suppose that since just about everything is passed along through breastmilk, should breastfeeding mothers avoid higher allergenic foods (especially if there is a genetic predisposition to allergy/atopy/asthma)?
These are probably difficult questions to answer, but I would enjoy hearing your thoughts...