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Editorial
May 17, 2016

Turning the Pathogenesis of Acute Peptic Esophagitis Inside Out

Author Affiliations
  • 1Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois
JAMA. 2016;315(19):2077-2078. doi:10.1001/jama.2016.5827

In this issue of JAMA, Dunbar and colleagues1 report findings from a unique experiment in which they withdrew proton pump inhibitor (PPI) therapy from 12 patients with high-grade esophagitis whose esophageal erosions had been successfully treated by that therapy to observe the histopathological events leading to acute (recurrent) peptic esophagitis. Within 2 weeks, 11 of the patients had developed recurrent erosive esophagitis as well as a substantial worsening of reflux symptoms. All of the classic histopathological findings2 and physiological consequences of gastroesophageal reflux disease (GERD) were reproduced: basal cell hyperplasia, papillary elongation, and dilated intercellular spaces in the esophageal squamous cell epithelium; increased distal esophageal acid exposure and reduced mucosal impedance on reflux monitoring studies.

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