Clinical Implications and Pathogenesis of Esophageal Remodeling in Eosinophilic Esophagitis

In eosinophilic esophagitis (EoE), remodeling changes are manifest histologically in the epithelium and subepithelium where lamina propria fibrosis, expansion of the muscularis propria, and increased vascularity occur. The clinical symptoms and complications of EoE are largely consequences of esophageal remodeling. Available therapies have demonstrated variable ability to reverse existing remodeling changes of the esophagus. Systemic therapies have the potential of addressing subepithelial remodeling. Esophageal dilation remains a useful, adjunctive therapeutic maneuver in symptomatic adults with esophageal stricture. As novel treatments emerge, it is essential that therapeutic end points account for the fundamental contributions of esophageal remodeling to overall disease activity.

Key points

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Remodeling changes in eosinophilic esophagitis include epithelial basal zone hyperplasia, lamina propria fibrosis, expansion of the muscularis propria, and increased vascularity.
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Esophageal inflammation in eosinophilic esophagitis drives the remodeling process with mediators that include IL-5, IL-13, TGFβ1, mast cells, fibroblasts, and eosinophils.
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Recent studies have provided increasing evidence that the primary symptoms of esophageal dysfunction in children and adults as well as clinical complications of eosinophilic esophagitis are consequences of esophageal remodeling and fibrostenosis.
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Esophageal remodeling in eosinophilic esophagitis can be demonstrated using widely available tests, such as histopathology, barium esophagram, upper endoscopy, and endoscopic ultrasonography.
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Clinical trials need to account for the presence and reversibility of esophageal remodeling to fully elucidate the potential benefits and limitations of therapeutic interventions.