DALLAS—A small, single-center study led by researchers from the Dallas VAMC suggests that gastroesophageal reflux disease (GERD) might be caused by an immune reaction, rather than direct chemical injury from stomach acids.
Results were published online recently as a “Preliminary Communication” online by the Journal of the American Medical Association.1
“In this preliminary study of 12 patients with severe reflux esophagitis successfully treated with PPI therapy, stopping PPI medication was associated with T lymphocyte–predominant esophageal inflammation and basal cell and papillary hyperplasia without loss of surface cells,” wrote first author Kerry Dunbar, MD, PhD, from the Dallas VAMC and colleagues. “If replicated, these findings suggest that the pathogenesis of reflux esophagitis may be cytokine-mediated rather than the result of chemical injury.”
“Although this radical change in the concept of how acid reflux damages the esophagus of GERD patients will not change our approach to its treatment with acid-suppressing medications in the near future, it could have substantial long-term implications,” said senior author Stuart Spechler, MD, chief of gastroenterology at the Dallas VAMC.
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