Ann Allergy Asthma Immunol 112 (2014) 85e86
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Guest Editorial
When more can be less The incidence of food allergy is increasing in the United States, with reports from the Centers for Disease Control and Prevention suggesting a tripling in the number of outpatient visits for food allergy during the past 10 to 15 years.1,2 Like it or not, as allergists, we are being thrust into a position that mandates us to appropriately order food allergy diagnostic tests and effectively interpret their results. During the last 25 years, food-specific serum IgE testing has evolved to become both a helpful companion and an appropriate alternative to skin prick testing. Unlike skin prick testing, serum IgE testing can be ordered and performed from any health care setting and measurements can be taken in patients with uncontrolled dermatitis and patients taking antihistamines. The assay clearly has a role in the diagnosis of IgE-mediated food allergy, with numerous studies reporting that the higher the value of the serum IgE, the more likely the food (if ingested) will lead to an allergic reaction.3 However, the decision on when to order the assay and which foods to test is of critical importance and will likely vary by each patient. In this issue of the Annals, Amin et al4 report their experience in cosensitization rates for select foods during 7 years from a single, hospital-based clinic. The authors report that (other than for milk) the median serum IgE values were not different whether the tested food was the culprit food that led to a reaction or whether the food was tested for other reasons (eg, testing to tree nut when peanut is the culprit food given concerns of cross-contamination and cosensitization). To know whether these results had any meaning in this cohort, one would have to know whether the incidental positive test results led to any clinically relevant outcomes. One can see that the major crux of the issue regarding foodspecific serum IgE (and skin prick testing to foods) is that sensitization does not equal clinical reactivity, and indiscriminate testing will likely lead to false-positive results in atopic individuals. However, overly selective testing may miss relevant cross-sensitizations and coreactivity not yet identified that may be clinically relevant, such as that seen amongst nuts and amongst seafood. A common clinical scenario can demonstrate this dilemma. A 1year-old child who reacts with generalized urticaria to peanut on first known ingestion presents to the allergist’s office for testing. Clearly, some form of IgE testing for peanut is warranted. However, the question arises of whether it is appropriate to test for other foods (common allergens to which the patient has not demonstrated tolerance) and, if so, which ones. To decide this appropriately, we must have an a priori understanding of what the results may show and what they are likely to mean. Data from the National Health and Nutrition Examination Survey suggest that sensitization to foods is common in the United States.5 Examining only milk, egg, peanut, and shrimp, the study reported that 1 of every 6 individuals in the United States would be expected to have at least 1 positive test result. We know, however, even from the authors of that study, that prevalence of food allergy
does not come close to approaching this frequency. Therefore, if one is going to take the “shotgun” approach to ordering serum IgE panels or random tests, undoubtedly many false-positive results will be uncovered, thus overdiagnosing food allergy and putting patients at risk for unnecessary avoidances. Selective testing, on the other hand, may be able to aid in patient care by better defining clinically relevant cross-sensitizing foods. For example, one report from the United Kingdom that offered challenges to tree nuts in all peanut allergic patients found that none reacted if their tree nut skin test result was negative, whereas only 31% reacted even if they had a positive skin test result.6 On the basis of this and similar reports, as well as issues of crosscontamination, it may be common practice for allergists to test for tree nuts when peanut is the culprit food and recommend avoidance at an early age for any sensitization. To play devil’s advocate, however, one must realize in doing so that there will clearly be inappropriate labeling of many patients who are only sensitized (but not allergic) as being tree nut allergic. As allergists, we must make cogent decisions regarding testing with our patients’ best interests in mind. Evidence-based medicine can lay the framework provided by data such as those presented above and help to improve that decision; however, we must still use the art of medicine to best decide how to use this information. Indiscriminate food panel testing is probably never warranted, but there are clearly circumstances that call for more testing than just for the single culprit food. If ordering tests to determine cosensitization, we must do so with knowledge and a plan. If we are going to consider all patients with a positive test result as allergic and not attempt confirmation of the allergy with a food challenge, there is no doubt we will overinflate the prevalence of food allergy and cause many patients unnecessary lifestyle changes. In fact, if there is a low clinical suspicion for IgE-mediated food allergy, even in the face of a positive serum food specific IgE test result, one should consider an in-office oral challenge (or referral to a center that can do this) to rule out allergy. On the contrary, if we only examine the culprit food, we may miss clinically relevant allergies before the initial exposure, thus putting our patients at risk. In the end, each situation must dictate if more is more or more is less. Jay Adam Lieberman, MD University of Tennessee Health Science Center Memphis, Tennessee
[email protected] References [1] Branum AM, Lukacs SL. Food allergy among children in the United States. Pediatrics. 2009;124:1549e1555. [2] Jackson KD, Howie LD, Akinbami LJ. Trends in Allergic Conditions Among Children: United States, 1997e2011. NCHS data brief, No. 121. Hyattsville, MD: National Center for Health Statistics; 2013.
1081-1206/13/$36.00 - see front matter Ó 2014 American College of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.anai.2013.11.009
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[3] NIAID-Sponsored Expert Panel, Boyce JA, 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): S1eS58. [4] Amin MR, Khoury JC, Assa’ad AH. Food-specific serum immunoglobulin E measurements in children presenting with food allergy. Ann Allergy Asthma Immunol. 2014;112:121e125.
[5] Liu AH, Jaramillo R, Sicherer SH, et al. National prevalence and risk factors for food allergy and relationship to asthma: results from the National Health and Nutrition Examination Survey 2005-2006. J Allergy Clin Immunol. 2010;126: 798e806. [6] Ball H, Luyt D, Bravin K, Kirk K. Single nut or total nut avoidance in nut allergic children: outcome of nut challenges to guide exclusion diets. Pediatr Allergy Immunol. 2011;22:808e812.