Original articleSystemic allergic disorderSerum IgE measurement and detection of food allergy in pediatric patients with eosinophilic esophagitis
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.
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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
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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.