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Dietary management of eosinophilic esophagitis

Seema S Aceves, MD, PhD
Section Editors
Scott H Sicherer, MD, FAAAAI
Nicholas J Talley, MD, PhD
Deputy Editor
Elizabeth TePas, MD, MS


Eosinophilic esophagitis (EoE) has been defined by a panel of experts as "a chronic, immune/antigen-mediated, esophageal disease characterized clinically by symptoms related to esophageal dysfunction and histologically by eosinophil-predominant inflammation" that is not responsive to acid blockade with a proton pump inhibitor (PPI), unlike gastroesophageal reflux disease (GERD) or PPI responsive esophageal eosinophilia [1]. The management of EoE includes dietary, pharmacologic, and endoscopic interventions. It is uncertain whether treatment of symptoms alone is sufficient or if complete resolution of eosinophilic inflammation is also required.

This topic reviews the clinical evidence for the role of food allergies in EoE and elimination and elemental diets for the treatment of EoE. The various types of allergy testing used in the diagnostic evaluation of EoE are reviewed separately. Other aspects of disease pathogenesis, clinical manifestations, general diagnostic evaluation, additional treatment options, and prognosis are also discussed elsewhere. (See "Eosinophilic esophagitis (EoE): Genetics and immunopathogenesis" and "Allergy testing in eosinophilic esophagitis" and "Clinical manifestations and diagnosis of eosinophilic esophagitis" and "Treatment of eosinophilic esophagitis" and "Patient education: Eosinophilic esophagitis (The Basics)".)


Food allergy is defined by a recurrent and predictable immune response upon ingestion of a food antigen. The mechanism of food allergy can vary from immediate immunoglobulin E (IgE)-mediated hypersensitivity to chronic autoimmune reactions driven by antigen-specific T cells. (See "Pathogenesis of food allergy", section on 'Types of reactions' and "Clinical manifestations of food allergy: An overview".)

The pathogenesis of EoE appears to depend largely upon delayed, cell-mediated hypersensitivity. Evidence for this is based both upon clinical reactions in human subjects and on animal models that rely on the presence of T cells for disease induction [2,3]. Disease induction and/or propagation have not been shown to rely on IgE-mediated mechanisms, even though IgE sensitization to foods is common in EoE and the prevalence of food-induced anaphylaxis is higher in children with EoE [4-8]. In addition, EoE triggered by a specific food has developed after resolution of IgE-mediated allergy to the same food [9].

The relationship between gastric acid/gastroesophageal reflux disease (GERD), esophageal eosinophilia, and food allergies still requires clarification. As an example, whether acid can induce epithelial barrier damage that predisposes to food sensitization or whether acid suppression allows for increased IgE sensitization remains to be systematically studied. (See "Pathogenesis of food allergy".)

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Literature review current through: Nov 2017. | This topic last updated: Aug 25, 2017.
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