Gastroesophageal reflux disease (GERD) may not develop as a direct result of acid reflux into the esophagus as previously thought, but may instead be an autoimmune disorder.
In a new animal study performed at UT Southwestern Medical Center, it appears the acid reflux triggers the esophagus to release chemicals called cytokines, which in turn attract inflammatory cells to the esophagus.It is these inflammatory cells that cause the characteristic esophageal damage of GERD. The symptoms of this inflammatory include heartburn.
The study was performed on rats, and involved connecting the first part of the small intestine (duodenum) directly to the esophagus. This operation would allow stomach acid and bile to enter the esophagus of the rats, in a situation similar to acid reflux in people. The results were not as expected.
Soon after the operation, the researchers expected to see the death of surface cells of the esophagus, and they expected to see the injury progress later to the deeper layers. Instead, they found the opposite. Three days after the surgery, there was no damage to surface cells, but the researchers did find inflammatory cells in the deeper layers of the esophagus. Those inflammatory cells didn't rise to the surface layer until three weeks after the initial acid exposure.
"That doesn't make sense if GERD is really the result of an acid burn, as we all were taught in medical school," said Dr. Stuart Spechler, professor of internal medicine at UT Southwestern and senior author of the study. "Chemical injuries develop immediately. If you spill battery acid on your hand, you don't have to wait a month to see the damage."
Dr. Souza, staff physician at the Dallas Veterans Affairs Medical Center and part of the Harold C. Simmons Comprehensive Cancer Center at UT Southwestern, noted, "In animal models of reflux esophagitis designed to mimic the human disease, researchers hadn't looked at the early events in the development of esophageal injury. Most of those investigators have been interested in the long-term consequences of GERD, and we found virtually no published data about what happens later that induces gastroesophageal reflux."
The next step for researchers is to conduct additional studies in humans.
The study was supported by the Dallas VA Medical Center and the National Institutes of Health, and appears in the November issue of Gastroenterology.