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JOURNAL ARTICLE
REVIEW

Pharmacotherapies for the Treatment of Eosinophilic Esophagitis: State of the Art Review

Willemijn E de Rooij, Evan S Dellon, Claire E Parker, Brian G Feagan, Vipul Jairath, Christopher Ma, Albert J Bredenoord
Drugs 2019 July 27
31352605
Eosinophilic esophagitis (EoE), a chronic allergic disorder of the esophagus, is characterized by symptoms of esophageal dysfunction and eosinophil-predominant inflammation. The incidence of EoE has increased substantially over the past two decades, coinciding with the so-called allergy epidemic. Current treatment options consist of dietary intervention, endoscopic dilatation, and pharmacotherapy. Given that EoE is a chronic progressive disease that is prone to relapse after cessation of therapy, these treatment options are suboptimal for long-term management. Persistent, uncontrolled esophageal inflammation is associated with esophageal remodeling and stricture formation, thus, the creation and/or discovery of alternative treatments is of paramount importance. The pathogenesis of EoE is currently under intense investigation, and recent insights concerning cellular and molecular etiology have led to the development of therapies that target specific pathophysiological pathways. This article provides an overview of established EoE pharmacotherapies, which include proton pump inhibitors and swallowed topical steroids. Additionally, anti-allergic targets, immunosuppressives, and monoclonal antibodies (such as mepolizumab, reslizumab, QAX576, RPC4046, dupilumab, omalizumab, and infliximab) that have been evaluated as treatments for EoE are summarized. Finally, several promising therapeutic agents (e.g., sialic acid-binding immunoglobulin-like lectin 8 antibodies, the transforming growth factor-β1 signal blocker losartan, CC chemokine receptor type 3 antagonists, thymic stromal lymphopoietin antibodies, antibodies targeting the α4β7 integrin, anti-interleukin-9 antibodies, and anti-interleukin-15 antibodies) that target specific molecules or cells implicated in the pathogenesis of EoE are proposed.

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