allergy testing in children: selecting tests and interpreting results...

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Allergy Testing in Children:Selecting Tests and Interpreting Results CME

Supported by an independent educational grant from Thermo Fisher Scientific.

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Allergy Testing in Children: Selecting Tests and Interpreting Results CME

This article is a CME certified activity.To earn credit for this activity visit:

www.medscape.org/roundtable/allergy

CME Released: 08/29/2014; Valid for credit through 08/29/2015

Target AudienceThis activity is intended for pediatricians, allergists, and other clinicians interested in the diagnosis of allergies in children.

GoalThe goal of this activity is to provide education on the diagnostic evaluation of allergies in children.

Learning ObjectivesUpon completion of this activity, participants will be able to:

1. List the characteristics of diagnostic testing options available for suspected food and environmental allergies

2. Summarize the challenges of interpreting allergy test results

3. Describe how to interpret the results of molecular allergy testing for common childhood allergies

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Authors and DisclosuresAs an organization accredited by the ACCME, Medscape, LLC, requires everyone who is in a position to control the content of an education activity to disclose all relevant financial relationships with any commercial interest. The ACCME defines “relevant financial relationships” as financial relationships in any amount, occurring within the past 12 months, including financial relationships of a spouse or life partner, that could create a conflict of interest.

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ModeratorRobert A. Wood, MD Professor of Pediatrics and International Health; Director, Pediatric Allergy and Immunology, John Hopkins University School of Medicine, Baltimore, Maryland

Participation by Dr Wood in the development of this product does not constitute or imply endorsement by the Johns Hopkins University or the Johns Hopkins Hospital and Health System. Disclosure: Robert A. Wood, MD, has disclosed no relevant financial relationships. Dr Wood does not intend to discuss off-label uses of drugs, mechanical devices, biologics, or diagnostics approved by the FDA for use in the United States. Dr Wood does not intend to discuss investigational drugs, mechanical devices, biologics, or diagnostics not approved by the FDA for use in the United States.

PanelistsLeonard B. Bacharier, MD Professor of Pediatrics and Medicine; Clinical Director, Division of Allergy, Immunology and Pulmonary Medicine, Washington University School of Medicine, St. Louis, Missouri

Disclosure: Leonard B. Bacharier, MD, has disclosed the following relevant financial relationships:

Served as an advisor or consultant for: Boehringer Ingelheim Pharmaceuticals, Inc.; DBV Technologies; Merck & Co., Inc.; Teva Neuroscience, Inc.

Served as a speaker or a member of a speakers bureau for: GlaxoSmithKline; Merck & Co., Inc.; Novartis Pharmaceuticals Corporation; Teva Neuroscience, Inc. Dr Bacharier does not intend to discuss off-label uses of drugs, mechanical devices, biologics, or diagnostics approved by the FDA for use in the United States. Dr Bacharier does not intend to discuss investigational drugs, mechanical devices, biologics, or diagnostics not approved by the FDA for use in the United States.


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Hugh A. Sampson, MD Professor of Pediatrics; Director, Jaffe Food Allergy Institute; Dean for Translational Biomedical Sciences, Icahn School of Medicine at Mount Sinai, New York, New York

Disclosure: Hugh A. Sampson, MD, has disclosed the following relevant financial relationships:

Served as an advisor or consultant for: Allertein Therapeutics, LLC; Danone; Regeneron Pharmaceuticals, Inc. Owns stock, stock options, or bonds from: Allertein Therapeutics, LLC; Herbal Springs LLC Dr Sampson does not intend to discuss off-label uses of drugs, mechanical devices, biologics, or diagnostics approved by the FDA for use in the United States. Dr Sampson does not intend to discuss investigational drugs, mechanical devices, biologics, or diagnostics not approved by the FDA for use in the United States.

EditorSarah Williams, PhD Senior Scientific Director, Medscape, LLC

Disclosure: Sarah Williams, PhD, has disclosed no relevant financial relationships.

CME ReviewerNafeez Zawahir, MDCME Clinical Director, Medscape, LLC

Disclosure: Nafeez Zawahir, MD, has disclosed no relevant financial relationships.

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Robert A. Wood, MD: Hello, I am Dr Robert Wood. I am professor of pediatrics and international health and director of pediatric allergy and immunology at the Johns Hopkins University School of Medicine in Baltimore. I would like to welcome you to this program on allergy testing in children.

Two world-class experts are joining me today: Dr Leonard Bacharier, who is professor of pediatrics and clinical director of the division of allergy, immunology, and pulmonary medicine at Washington University School of Medicine in St Louis, and Dr Hugh Sampson, who is dean for translational biomedical sciences, Kurt Hirschhorn professor of pediatrics, and director of the Jaffe Food Allergy Institute at the Icahn School of Medicine at Mount Sinai in New York City.

Introduction


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We will begin with an overview of allergy testing in children. We always want to start with a careful history because we should never do any allergy test unless it is indicated by the clinical history. Many people think that they might have a food allergy, but it is the history taken by an experienced physician that will be most important in determining whether allergy testing is needed. For inhalant allergies, testing is primarily indicated for those with more severe disease, and it is especially indicated when the patient’s history is unclear. For example, somebody might have severe springtime allergies, but it is so obvious that you do not absolutely need to do a test. For someone who has chronic asthma, we do not know which allergies may be triggering the asthma, so allergy testing can be critically important in this kind of situation.

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There are 2 main ways to diagnose specific allergies.[1] Skin testing has been around a long time. It is still an incredibly valuable test. It is quick, easy, and pretty cheap, and we get results in 10 or 15 minutes. We use skin testing in the allergy clinic as a first-line, standard means of testing to get a “yes/no” answer to the question of whether the patient is allergic or not.

The second means of testing is serologic testing, which has been developed and refined over the past 30 to 40 years. With serologic testing, the allergen’s specific immunoglobulin E (IgE) level in the patient’s blood is measured. That has the advantage, especially in food allergy, of being slightly more quantitative. You get a measurement that is potentially more likely to help you determine whether a positive test result indicates a real allergy. There may also be advantages to serologic testing if the patient has severe eczema or is not able to discontinue antihistamines, in which case, skin testing may not be an option.

We are going to talk about 2 cases today: the first will focus more on food allergy, and the second will focus on inhalant allergy in an older child with asthma and allergic rhinitis.


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Case 1: Food Allergies

The first case is a 2-year-old boy, and this is a typical patient that we see in the allergy clinic or a pediatrician sees in the office on a daily or weekly basis. He comes into his pediatrician because of a history of eczema since infancy. His mother is very concerned that the eczema may be due to food allergy. She also has a concern that he may be allergic to eggs. Finally, she is most concerned because he recently had a possible reaction after eating peanut butter.

The question is: Are allergy tests needed in this situation? Are they indicated? Are they going to give us good information? We need to refer back to the history to determine the potential value of allergy testing in this child, and we need to know more. What is the real history of egg allergy? Why are they worried about that? Had he eaten eggs before, and, if so, in what form? How severe is his eczema? Severe eczema is often associated with a food allergy, whereas milder eczema is less likely to be associated with food allergy. What are the details of the possible peanut reaction? Had he eaten peanut before, or was this a first known exposure with an obvious reaction?

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The key points that we get from the history are that his eczema is persistent but relatively mild, and it has been controlled with intermittent use of low-potency topical corticosteroids. His egg history is that he had urticaria with scrambled egg at age 1, but since then has eaten eggs in baked goods without any obvious reaction. He had never eaten peanut before this recent episode, which was characterized by vomiting and hives that occurred within minutes of his first peanut exposure. He has had no apparent reaction to the other most common food allergens, such as milk, soy, or wheat.

When we examine this child, he is a very well-appearing 2-year-old. His growth rate has been normal. The only abnormality in his physical examination was mild, scattered eczema in the antecubital and popliteal fossa.


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The child came in with results of allergy testing from his pediatrician. Allergy testing is often done in a child such as this, and we want to review the results in some detail to decide whether the testing was worthwhile, which part of the results helped manage his care, and which part may have given less relevant information.

When we think of food allergy in a child with eczema, we think of 5 allergens: milk, egg, soy, wheat, and peanut. The levels of these allergens that he had in his blood on ImmunoCAP® (Thermo Fisher Scientific, Uppsala, Sweden) testing were: 2.0 kUA/L for egg, 4.0 kUA/L for peanut, 5.5 kUA/L for milk, and 9.5 kUA/L for wheat. His soy test result was negative.

The pediatrician was concerned about these results and recommended to the mother that all egg, milk, and peanut be removed from his diet. Although she was worried that his eczema might be related to food allergy, this seemed like an extreme recommendation, so she came to an allergist for further advice. I would like to turn this over to Dr Sampson for his interpretation of these test results and the next steps in the approach to this patient.

Hugh A. Sampson, MD: Thank you, Bob. As you indicated, the most important issue that we need to think about is the history and exactly what happened. The first value, for egg, which is 2 kUA/L, may have significance in a very young child. The history, though, is that the boy had had a reaction at 1 year of age, but is now eating baked products that contain egg with no difficulty. The eczema is very mild and is only intermittent, which does not suggest that the ingestion of baked egg product is having any effect on his eczema, so we would not make any further recommendation for withdrawal.

Because the boy has been ingesting baked egg now for a year, we would think about doing an oral food challenge to regular egg to see whether he can tolerate it in all forms.[1-5] We would probably recommend that, in the next 6 months, he come in for an oral food challenge to standard egg. In light of the peanut sensitivity level and the history of having acute reaction—with hives and vomiting—after the ingestion of peanut, we would certainly be very concerned that this is an IgE-mediated reaction. A level of 4 kUA/L in a child of 2 years of age is significant; in this case, we would advise the mother to completely avoid peanut at this time.

The boy has been consuming milk and milk products. His eczema has been relatively well controlled and is intermittent. If we believe that milk is causing a problem, we would expect his eczema to be consistently more severe. Although the level is 5.5 kUA/L, which some might consider significant, we often see slightly elevated levels that are not clinically relevant. When we looked at a large series of children, we found that it took a level of up to 15 kUA/L to be 95% predictive that a slightly older child would react to milk.[6]

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With soy, the level was undetectable, so even though soy is one of the major allergens, it is not of concern in this case. With wheat, the level was 9.5 kUA/L, which is higher than the others. There might be some concern, but from the history, we know that the boy has been eating wheat products without any significant reaction. Also, we see significantly higher levels of IgE to wheat that do not have clinical relevance.

In this case, we would recommend that the mother continue to strictly avoid peanut in the child’s diet. We would encourage them to continue eating the baked egg products and to think about coming in for a regular egg challenge. The child can be allowed to have milk, soy, and wheat in his diet with no restriction.

One issue to think about is whether these are false-positive test results. We need to remember that the test simply tells us whether the patient has IgE antibodies to whatever it is we are testing, so the test result, per se, is not false. It accurately indicates that IgE is there. But we know that many people have low levels of IgE to foods and even to environmental allergens that are not clinically relevant.[1,2,4,7] A positive test result by itself never is an indication of a clinical allergy; you have to interpret it in the context of the clinical picture.[1,2,4,7]


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We know from a number of studies of both skin testing and measurement of serum IgE levels that the higher the level is to a particular food, the more likely it is that that individual will react to the food.[2,4,7] In a way, it gives us a sense of the likelihood that somebody will react. A number of studies have looked at various levels, and the levels may differ for individual foods. As I mentioned, with milk, the level is in the area of 15 kUA/L. With egg, it is in the neighborhood of 7 kUA/L . With peanut, it is in the range of 14 to 15 kUA/L. Different foods have different levels that provide what we call a 95% predictive value that the patient will react.[6] With younger children, we sometimes see lower levels in that 95% predictive range, so we have to take that into account.[6]

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The gold standard for determining whether someone has a clinical allergy is the oral food challenge, and this is the way we make the definitive diagnosis.[2-5] In the case we are discussing here, we do want the child to come back for an oral food challenge to egg to determine whether he has outgrown that allergy. Given the fact that he is eating baked products containing egg on a regular basis, it is highly likely that if he has not already outgrown egg allergy, he will do so in the near future.[8]

Dr Wood: Hugh, would you do a food challenge to peanut now or in the future on this child?

Dr Sampson: At this point, I would probably not do the peanut challenge. It has been a relatively short time since he had a very definitive reaction to an isolated ingestion, so, with that history, and the evidence of IgE to peanut, I would make the clinical diagnosis of peanut allergy. I would be interested in seeing this child again in 1 year or so and, at that point, would probably look at his IgE level again because it may continue to go up, which would tell me that he is less likely to outgrow the allergy. If the level comes down, he may be one of the fortunate 20% or so who does outgrow the peanut allergy.[4,5,9]

Dr Wood: Are there any other issues with his peanut allergy in terms of day-to-day management? Specifically, does his history or test result tell us anything about what his next reaction will look like?


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Dr Sampson: Many parents are concerned about IgE levels. They think that the higher the IgE level, the more severe the reaction will be. There is no evidence at this point that the level of IgE antibody to any food correlates directly with the severity of the reaction.[7] We know that the higher the IgE level, the higher the likelihood of a reaction will be, but we cannot predict the severity of that reaction. Many children with high IgE levels only have mild reactions with hives. Others who have very low IgE levels that you might think are not even diagnostic have severe reactions. The IgE level, per se, will not tell us about reaction severity.

With peanut allergy, we are much more aggressive about complete restriction of the food from the diet. We certainly educate parents and children well about how to avoid peanut where they may encounter it unknowingly, and how to recognize signs of an allergic or anaphylactic reaction. We usually provide them with an epinephrine auto-injector with instructions, including the instruction to go to a medical facility if a reaction occurs.

Another question that comes up is whether we should look for allergies to other foods. We know that approximately 35% to 40% of children who have peanut allergy also have a concomitant tree nut allergy[4];it is not uncommon. Often in our clinic we screen for allergy to several tree nuts, typically with skin tests, to determine very quickly whether there is evidence of IgE antibody to any of those tree nuts. We usually test for just a few. There are almond butters, cashew butters, and hazelnut spreads that kids like and are good substitutes for peanut butter, so we will look for allergy to some of those tree nuts. If we have a positive skin test result, especially a significant skin test result, we often will also look at the IgE level to that tree nut to give us an idea of whether this is likely to be clinically relevant and to potentially give us an idea of whether the child is likely to outgrow the allergy.

Dr Wood: Hugh, one last question for you about this case. We hear a lot lately about component testing, or component-derived testing. We did not see any results for those tests for this child. Could you comment on what those tests are and in what patients they may add something to our diagnostic measures?

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Dr Sampson: What we are able to do now with peanut component testing is look at IgE antibodies specifically to certain proteins in a food. In peanut, there are 3 storage proteins that seem to be most relevant to the likelihood of having a clinical reaction. In the part of the country where I practice, the northeast, where we have a lot of birch pollen, many children develop low-level positive test results to peanut, but this is based on the cross-reactivity of IgE antibody against the birch pollen reacting to 1 of the proteins, Ara h 8, in peanut.[4]

In this situation, it is very important to know whether this antibody is directed at 1 of the storage proteins, especially Ara h 2, which is the one most closely related to systemic reactions, or whether it is a response to the birch-related protein.

The reason that I would not do component testing in this particular case is that this is a young child -- he is 2 years old -- and we do not have a history of any respiratory allergy or seasonal symptoms. He has not been around long enough to develop much of a response to the birch pollen protein, so I would not expect that test result to be positive in this case.


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At this point, even if I were to measure that level, it would not change what I would do with this child, certainly not in the next year. In older children, especially those who have early springtime symptoms when the level of IgE to peanut is not very high, I would certainly consider measuring the component proteins. If a patient has an IgE level to peanut of 90 kUA/L, it is unlikely that the component protein antibody to Ara h 2 would not be markedly elevated; in that case, I probably would not do component testing.

Dr Wood: Thanks. Len, you have been quiet so far. You must have something to add about food allergy testing, about this case or in general.

Leonard B. Bacharier, MD: We see many patients who come in for a variety of health concerns, and food allergy is often thought of as a potential contributor to many of these problems. It is important to recognize which problems are highly related to food allergy and which are less tightly related or not at all related, because, as we have heard, we can get into trouble by performing testing in children for whom the history is unlikely to truly reflect IgE-mediated food allergy.

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The typical manifestations of food allergy come in a variety of classes. Probably the common are cutaneous-derived manifestations, such as atopic dermatitis. Food allergy is most likely to be related to atopic dermatitis that is on the more severe end of the spectrum rather than minimal isolated patches of atopic dermatitis. Children with food allergy can develop acute episodes of urticaria and/or angioedema, which are clear symptoms that would prompt a food allergy evaluation. Gastrointestinal symptoms, such as vomiting and/or diarrhea, are also quite common in acute food reactions and should be followed up with a further history and appropriate testing.

Respiratory symptoms can occur in combination with cutaneous and/or gastrointestinal symptoms or can infrequently occur as isolated symptoms of food allergy. Symptoms such as cough, wheeze, or laryngeal edema that occur in close approximation to a food exposure could be considered indicators of food allergy. Multisystem reactions or anaphylaxis with an appropriate food exposure should be considered for further evaluation of food allergy.


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Those contrast with other conditions that are very prevalent and are generally poorly understood, and often families want to explore food allergy as a potential cause of those conditions. The literature does not support the idea that conditions such as hyperactivity, developmental delay, autism, behavioral abnormalities, or recurrent upper respiratory tract infections are related to IgE-mediated food allergy. When those are the presenting complaints, further testing for food allergy seems to be inappropriate.

Dr Wood: Any last points, Len?

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Dr Bacharier: One additional point that is worth noting and is highlighted by this case is that we are often given the opportunity to test for food allergy by using panels of diagnostics, which include multiple foods. There are clear pitfalls in the panel approach, in that you might be testing for allergy to foods that have no clinical relevance to the case. Therefore, it is important to recognize the negative elements of panel testing and recognize that if the child comes in with a clear history of reaction to a single food, you can test to just that single food and not be tempted to see what other allergies might exist when there is no history to support additional testing.


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Case 2: Inhalant Allergies

Dr Wood: Thank you. Let us move on to our second case, which is another very typical child. This is an older child, a 10-year-old girl. She has symptoms of allergic rhinitis -- nasal congestion, sneezing, and pruritus -- that are particularly prominent at the height of the spring pollen season. She also carries a diagnosis of moderate, persistent asthma, which has been treated with an inhaled corticosteroid and short-acting β-agonist as needed.

Despite these maintenance medications, she typically experiences exacerbations twice yearly, especially in the spring and shortly after return to school in the fall. She now has worsening of her daily symptoms that seems to be temporarily related to her younger sister obtaining a pet cat. Len, could you go through the steps you would take as an initial approach to this patient?

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Dr Bacharier: It is important to recognize that in children who have persistent asthma, allergy is almost a given coexisting condition. In children with mild to moderate asthma, 80% to 90% will demonstrate allergic sensitization to at least 1 inhalant allergen.[10] We know that that allergic sensitization when combined with ongoing exposure to those allergens is clearly associated with greater disease activity and increased airway reactivity, so the combination of exposure and sensitization is a risk factor for more severe disease. The reason to look for allergic sensitization in children who have allergic rhinitis with asthma is that it helps us guide important elements of their care, including environmental controls and potential proactive escalation of asthma medications during periods of increased risk, and it may help guide the prescription of allergen immunotherapy.


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The testing methods that we have available for inhalant allergy are identical to those that are available for food allergy, with skin testing typically serving as our first-line approach. In vitro testing also allows us to identify inhalant allergen sensitivity and provides very comparable sensitivity and specificity with skin testing. This approach may be of value, especially in children who live in areas where access to allergists may not be very proximate, and they may benefit from in vitro testing that does not require subspecialty consultation.

Dr Wood: How do you approach testing? Is that a panel approach or not?

Dr Bacharier: In contrast to the food allergy approach, allergy testing to inhalants tends to involve the panel approach. It is important that those panels are determined geographically because, depending on local geography, the pollens, molds, and other exposures may vary. Appropriate testing would include the geographically relevant allergens and exclude those that may not be of local importance.

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Finally, it is important that children with persistent asthma have such an evaluation for allergy because it may not be entirely evident, as it was in this case, that an allergen such as cat might be a driving force in their disease. More subtle allergen sensitization, such as sensitization to house dust mites or mold, may be important environmental allergies that would warrant further modification.

Dr Wood: Hugh, before we go on to the test results in this patient, do you have any other comments?

Dr Sampson: I would just reiterate what Len said about the panel approach. We are using panels of certain allergens, but if we have a child who has no symptoms in the fall, for example, we would not be looking for weeds in a panel. We use panels that are associated with particular times of the year and with geographic areas.


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Dr Wood: Going back to the 10-year-old girl, after performing some allergy tests, she turned out to be quite highly sensitive to outdoor allergens, including trees, grasses, and weeds; to indoor allergens, including dust mites and that pet cat; and to mold allergens, which can be both indoor and outdoor, including Alternaria and Aspergillus species. Len, what would we do with this information? How can we take these test results and actually improve her allergy and asthma care?

Dr Bacharier: It is relevant to note that this child has evidence of allergic sensitization to both seasonal and year-round inhalant allergens. Her sensitization to the tree pollen likely explains a large part of the springtime symptomatology, whereas the sensitization to ragweed and/or molds is a likely contributor to the symptoms that tend to recur when she returns to school. In addition, the sensitization to cat helps us confirm that this is, indeed, an important trigger that the developed after the recent addition of the cat to the home.

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All of these might lead us to recommend environmental modifications aimed at reducing these exposures, which should help reduce her symptom burden both for allergic rhinitis and asthma. These modifications include the springtime and fall-time closure of the windows, the constant running of the air conditioning, and the very simplistic but probably effective approach of a nightly shower to remove the pollen burden before it gets transmitted to the pillow. There will always be a discussion of removal of the cat from the home, which is a complicated discussion for sure, and in children who have allergic sensitization to dust mites, the addition of dust mite-impermeable bedding may reduce their exposure and contribute to some degree of asthma improvement.

Dr Wood: Can you use this information at all in managing her medications?


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Dr Bacharier: It is important that we recognize that these allergenic sensitizations help predict periods of increased risk of asthma; therefore, knowing what she is allergic to may allow some proactive escalation or initiation of therapy for her allergic rhinitis before the beginning of the spring and fall pollen seasons. It may allow us to consider a step-up of asthma medications during these vulnerable times to minimize the risk of exacerbation during the spring and when the child returns to school.

Dr Wood: If skin testing was not available for this child, would you do in vitro or IgE testing to obtain similar information?

Dr Bacharier: You certainly can, and I think that these 2 approaches are comparable in their sensitivity and specificity and provide very comparable discussion points for the provision of care.

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Dr Wood: We just have a few minutes left, and I would like to take those to discuss not just the 2 cases but also the other children we see in our practices and the challenges and possible improvements that allergy testing may provide in the future. We have seen a huge benefit and better in vitro testing, but we also hear a clear message that these tests are far from perfect science and we need to use the clinical history and our clinical judgment in their interpretation. I will pass it back to Hugh and Len for a few additional comments.

Dr Sampson: One point is exemplified by our first case, the young child with eczema. One of the rules I typically give to our fellows is that the younger the child and the worse the eczema, the more likely there is food involvement. If you have an older patient, the chance that food allergy is a major contributor is much lower; you want to focus on the younger child and the child with moderate to severe atopic dermatitis.

Another point is that several studies have shown is that egg allergy is the most common food allergy we see in children with atopic dermatitis, so if you are dealing with a patient who has moderate to severe atopic dermatitis, egg would be 1 of the foods that you would test.[11,12] Often, especially with more severe disease, the history is not quite as clear as what we saw in the first case we discussed.

Dr Wood: Len, could you comment on other types of allergy testing that are out in the community now?

Conclusions


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Dr Bacharier: It is important to recognize that not all allergy tests measure the same variable, provide comparable information, or have a scientific basis to clarify how they contribute to the clinical manifestations of disease. When testing for allergy, practitioners need to make sure that they are doing tests that measure IgE directed against either inhalants or food allergens. There are many commercial tests that measure IgG antibodies directed against foods and/or inhalants, and although these do appropriately identify the presence of such antibodies, there is little to no evidence to link those antibodies to the clinical manifestations of disease.[7] Therefore, they provide very little in the way of actionable clinical care, but they often provide anxiety and confusion for families who are trying to interpret the results of multiple positive results that have no clinical correlates.

Dr Wood: Thanks. Hopefully, in this brief time we have given you a sense of available allergy testing, their pros and cons, and the best way to use them for our patients. Allergy is incredibly common. Between 15% and 25% of all children in the United States are affected by some allergic disease, so this is something that has a great effect on the lives of children. Making the right diagnosis and treating patients appropriately can provide enormous value to their quality of life.

I would like to thank my colleagues, Dr Hugh Sampson and Dr Len Bacharier, for taking the time to do this today. I meant at the beginning these are world class colleagues and we are very lucky to have them here on this valuable program.

Dr Sampson: Thanks for having us, Bob. It was a pleasure.

Dr Bacharier: It was a great pleasure. Thank you so much.

Dr Wood: I would like to thank you all for participating in this activity. You may now take the CME posttest by clicking on the earn-CME-credit link. Please also take a moment to complete the program evaluation that follows.

This transcript has been edited for style and clarity.

This article is a CME-certified activity. To earn credit for this activity visit: http://www.medscape.org/viewarticle/830273

Pg.30


AbbreviationsIgE = immunoglobulin E

References 1. Bernstein IL, Li JT, Bernstein DI, et al. Allergy diagnostic testing: an updated practice parameter. Ann Allergy Asthma Immunol. 2008;100(3 suppl 3):S1-S148.2. Boyce JB, Assa’ad A, Burks AW, et al. Guidelines for the diagnosis and management of food allergy in the United States: report of the NIAID-Sponsored Expert Panel. J Allergy Clin Immunol. 2010;126(6 suppl):S1-S58.3. Sicherer SH, Sampson HA. Food allergy: epidemiology, pathogenesis, diagnosis, and treatment. J Allergy Clin Immunol. 2014;133:291-307. 4. Sicherer SH, Wood RA. Advances in diagnosing peanut allergy. J Allergy Clin Immunol Pract. 2013;1:1-13. 5. Wood RA. The likelihood of remission of food allergy in children: when is the optimal time for challenge? Curr Allergy Asthma Rep. 2012;12:42-47.6. Sampson HA. Update on food allergy. J Allergy Clin Immunol. 2004;113:805-819. 7. Sicherer SH, Wood RA; American Academy of Pediatrics Section on Allergy and Immunology. Allergy testing in childhood: using allergen-specific IgE tests. Pediatrics. 2012;129:193-197. 8. Sicherer SH, Wood RA, Vickery BP, et al. The natural history of egg allergy in an observational cohort. J Allergy Clin Immunol. 2014;133:492-499.9. Neuman-Sunshine DL, Eckman JA, Keet CA, et al. The natural history of peanut allergy. Ann Allergy Asthma Immunol. 2012;108:326-331. 10. Nelson HS, Szefler SJ, Jacobs J, et al. The relationships among environmental allergen sensitization, allergen exposure, pulmonary function, and bronchial hyperresponsiveness in the Childhood Asthma Management Program. J Allergy Clin Immunol. 1999;104(4 Pt 1):775-785.11. Savage JH, Matsui EC, Skripak JM, Wood RA. The natural history of egg allergy. J Allergy Clin Immunol. 2007;120:1413-1417. 12. Salehi T, Pourpak Z, Karkon S, et al. The study of egg allergy in children with atopic dermatitis. World Allergy Organ J. 2009;2:123-127.

allergy testing in children: selecting tests and interpreting results...

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