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The Pathogenesis of Gastroesophageal Reflux Disease: A Challenge in Clinical Physiology

Sidney Cohen, MD
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Requests for Reprints: Sidney Cohen, MD, Department of Internal Medicine, Temple University School of Medicine, Philadelphia, PA 19140.

Temple University School of Medicine
Philadelphia, PA 19140

Ann Intern Med. 1992;117(12):1051-1052. doi:10.7326/0003-4819-117-12-1051
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This excerpt has been provided in the absence of an abstract.

Gastroesophageal reflux disease is a clinical syndrome that manifests as heartburn and the sequelae of esophagitis, ulceration, stricture, or Barrett epithelium. Adenocarcinoma of the esophagus in association with metaplastic columnar or Barrett epithelium is one of the most rapidly increasing malignancies recognized in the United States. Gastroesophageal reflux disease with its associated sequelae can now be readily diagnosed and effectively managed with histamine-2 antagonists, prokinetic agents, omeprazole, or antireflux surgery.

Despite improved diagnosis and management of gastroesophageal reflux, the pathogenesis of this condition has remained controversial. The article by Sloan and colleagues (1), in this issue of Annals, uses modern


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