Dr. Rubenstein and his colleagues theorized that since the GERD link was not found, the mechanism of H. pylori’s negative association with Barrett’s esophagus might be from the direct impact of the bacteria on the inflammatory or mucosal response; its indirect effects on the production of leptin or ghrelin; or a confounding effect created by genetic regulation of cytokines or prior alterations in the esophageal and gastric microbiota.
The study was underwritten by the National Institutes of Health and by a senior marketing grant from the American Society for Gastrointestinal Endoscopy. Dr. Rubenstein and his associates reported no relevant disclosures.
*Correction, 9/20/2013: An earlier version of this story incorrectly identified inflammatory bowel disease.