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Eosinophilic esophagitis (EoE) is a chronic immune-mediated inflammatory disease of the esophagus that affects an estimated 34.4/100 000 people in Europe and North America. EoE affects both children and adults, and causes dysphagia, food impaction of the esophagus, and esophageal strictures.
EoE is defined by symptoms of esophageal dysfunction, such as vomiting, dysphagia, or feeding difficulties, in a patient with an esophageal biopsy demonstrating at least 15 eosinophils per high-power field in the absence of other conditions associated with esophageal eosinophilia such as gastroesophageal reflux disease or achalasia. Genetic factors and environmental factors, such as exposure to antibiotics early in life, are associated with EoE. Current therapies include proton pump inhibitors; topical steroid preparations, such as fluticasone and budesonide; dietary therapy with amino acid formula or empirical food elimination; and endoscopic dilation. In a systematic review of observational studies that included 1051 patients with EoE, proton pump inhibitor therapy was associated with a histologic response, defined as less than 15 eosinophils per high-power field on endoscopic biopsy, in 41.7% of patients, while placebo was associated with a 13.3% response rate. In a systematic review of 8 randomized trials of 437 patients with EoE, topical corticosteroid treatment was associated with histologic remission in 64.9% of patients compared with 13.3% for placebo. Patients with esophageal narrowing may require dilation. Objective assessment of therapeutic response typically requires endoscopy with biopsy.
Conclusions and Relevance
EoE has a prevalence of approximately 34.4/100 000 worldwide. Treatments consist of proton pump inhibitors, topical steroids, elemental diet, and empirical food elimination, with esophageal dilation reserved for patients with symptomatic esophageal narrowing.
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CME Disclosure Statement: Unless noted, all individuals in control of content reported no relevant financial relationships. If applicable, all relevant financial relationships have been mitigated.
Corresponding Author: Gary W. Falk, MD, MS, Division of Gastroenterology, University of Pennsylvania Perelman School of Medicine, Perelman Center for Advanced Medicine, 3400 Civic Center Blvd, 7th Floor, South Pavilion, Philadelphia, PA 19104 (firstname.lastname@example.org).
Accepted for Publication: August 17, 2021.
Author Contributions: Drs Muir and Falk had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis.
Concept and design: Both authors.
Acquisition, analysis, or interpretation of data: Both authors.
Drafting of the manuscript: Both authors.
Critical revision of the manuscript for important intellectual content: Both authors.
Administrative, technical, or material support: Both authors.
Conflict of Interest Disclosures: Dr Muir reported receiving research funding from Allakos. Dr Falk reported receiving research funding from Allakos, Arena, Adare/Ellodi, Bristol Myers Squibb, Celgene, Lucid, Regeneron, and Shire/Takeda and is a consultant for Allakos, Adare/Ellodi, Bristol Myers Squibb/Celgene, Lucid, Sanofi, and Shire/Takeda.
Funding/Support: This work was supported in part by the National Institutes of Health (NIH)/National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Center for Molecular Studies in Digestive and Liver Disease (P30DK050306) and by the Consortium for Eosinophilic Gastrointestinal Disease Research (CEGIR) (U54 AI117804), which is part of the Rare Disease Clinical Research Network (RDCRN), an initiative of the Office of Rare Diseases Research, National Center for Advancing Translational Sciences (NCATS), and is funded through collaboration between the National Institute of Allergy and Infectious Diseases, NIDDK, and NCATS. CEGIR is also supported by patient advocacy groups including the American Partnership for Eosinophilic Disorders, Campaign Urging Research for Eosinophilic Diseases, and Eosinophilic Family Coalition. As a member of the RDCRN, CEGIR is also supported by its data management and coordinating center (U2CTR002818). Dr Muir is funded by NIH grants R01 DK124266-01 and R21TR00303902.
Role of the Funder/Sponsor: The funders had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication.
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