Original article
Systemic allergic disorder
Serum IgE measurement and detection of food allergy in pediatric patients with eosinophilic esophagitis

https://doi.org/10.1016/j.anai.2010.03.018Get rights and content

Background

Although associated allergies are common and the mechanism may include long-term exposure to allergens, measurement of serum specific IgE levels has not been studied in pediatric eosinophilic esophagitis (EE).

Objective

To compare the results of serum IgE testing, patch testing, and epicutaneous skin testing to measure allergic sensitization in pediatric patients with EE.

Methods

In a cross-sectional study of 53 pediatric patients with EE, relevant history was obtained by questionnaire, and patch testing to foods was performed. Food and inhalant sensitivities were also assessed using skin prick testing and serum specific IgE measurement. Streptavidin CAP was used to measure specific IgE to cross-reactive carbohydrate determinants and Helicobacter pylori.

Results

The overall prevalence of food and inhalant sensitization was 80%, with higher total IgE levels in sensitized vs nonsensitized patients (median, 150 vs 13 IU/mL; P < .001). For foods, serum IgE measurement detected more positive results than did skin prick testing. Specific IgE to milk was most common (43%). Inhalants were implicated as frequently as were foods. In keeping with this, 32% of patients had a cluster of multiple sensitivities that included pollens, soy, grains, peanut, and tree nuts and had higher total IgE levels (P = .001). Patch test results were interpreted as positive in 39% of patients (rye, wheat, and soy were the most common).

Conclusions

Most, but not all, patients with EE are highly atopic individuals with frequent allergic sensitivities. Thus, serum IgE measurement of low-titer IgE antibody may be useful in identifying relevant food sensitivities and in distinguishing subgroups of patients with EE, making a more directed approach to food avoidance possible.

Introduction

Eosinophilic esophagitis (EE) is an increasingly recognized disorder characterized by an abnormal accumulation of eosinophils in the esophageal mucosa in patients with symptoms of refractory gastroesophageal reflux and dysphagia.1 Although its pathogenesis remains unknown, initial studies2, 3 in mice exposed to the aeroallergen Aspergillus fumigatus suggested a role for T cells and interleukin 5. A recent study4 of RNA in human biopsy specimens suggested a role for interleukin 13 and eotaxin-3 in the recruitment of eosinophils. Once present, eosinophils may act in an autocrine manner to perpetuate inflammation and decrease epithelial barrier function.5 An allergic trigger for this inflammation is suspected because a large proportion of patients have identifiable allergic sensitivities.6, 7 Despite the high prevalence of specific allergic sensitivities and associated atopic diagnoses frequently found in patients with EE, the relationship between EE and allergic sensitization is not straightforward.

The role of allergic sensitization in EE seems to mimic that seen in atopic dermatitis and asthma rather than in traditional food allergy. To start with, the inciting food or inhaled allergen cannot be identified from the patient's history. Individuals with EE who have IgE antibody to food allergens do not usually report immediate symptoms, such as oral allergy syndrome, urticaria, or anaphylaxis. Although seasonal fluctuations in symptoms and eosinophil counts have been observed, the role of inhalant allergic triggers remains less clear.8, 9 The mechanism of EE may not be a result of preformed mediator release from cross-linking of mast cell–bound IgE antibodies, and food (and inhalant) sensitivities have not been found in some patients. However, almost all patients have been shown to improve with complete dietary avoidance.10, 11 This makes the proper identification of allergic triggers highly desirable.

Typically, serum IgE antibody measurements have not been used in the measurement of food sensitivities in pediatric patients with EE.1 The objective of the present study was to characterize the allergic sensitization found in pediatric patients with EE by measuring specific IgE antibodies to common food and inhalant allergens (using CAP-FEIA [Phadia, Uppsala, Sweden]) and comparing the results with those of patch testing to foods and standard epicutaneous skin tests to foods and inhalants.

Section snippets

Methods

Between January 15, 2007, and June 29, 2009, patients referred to the Allergy Clinic at Nationwide Children's Hospital with positive biopsy findings for EE, defined as at least 15 eosinophils per high-power field (eos/hpf), were randomly approached for participation in a cross-sectional study. All the parents (and patients) (n = 55) agreed to participate; however, blood could not be collected from 2 patients, so they were not included in the analysis. This study was approved by the

Results

The demographic profile of the pediatric patients with EE included in this analysis is similar to that reported in other groups.14 Patients ranged in age from 7 months to 18 years, with a median age at diagnosis of 9.0 years. A predilection for male sex was observed (75%), and a history of allergy medication use or a diagnosis of asthma was reported in 70% of patients. The most frequently observed EE symptoms were dysphagia (51%), abdominal pain (45%), and vomiting (45%). Food impaction was

Discussion

As a group, patients with EE have an atopic phenotype with associated allergic rhinitis, asthma, or both and frequent allergic sensitivities.1, 6, 7, 16 Some investigators have suggested the importance of food triggers and others inhalants.2, 9, 16 The results of this study emphasize that a large proportion of pediatric patients with EE have specific IgE to milk and that subgroups of patients with EE can be identified and distinguished based on IgE responses. In this cohort of pediatric

References (31)

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Disclosures:Phadia has provided grant support to Thomas A.E. Platts-Mills.

Funding Sources: This study was funded by grant K23AI059317 from the National Institutes of Health and by a Davis/Bremer grant from the The Ohio State University.

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