UT Southwestern Medical Center researchers have found in an animal study that a condition called gastroesophageal reflux disease (GERD) might not develop as a direct result of acidic digestive juices burning the esophagus.
Rather, gastroesophageal reflux spurs the esophageal cells to release chemicals called cytokines, which attract inflammatory cells to the esophagus. It is those inflammatory cells, drawn to the esophagus by cytokines, that cause the esophageal damage that is characteristic of GERD. The condition is manifested by symptoms such as heartburn and chest pain.
"Currently, we treat GERD by giving medications to prevent the stomach from making acid," said Dr. Rhonda Souza, associate professor of internal medicine at UT Southwestern and lead author of the study appearing the November issue of
Gastroenterology. "But if GERD is really an immune-mediated injury, maybe we should create medications that would prevent these cytokines from attracting inflammatory cells to the esophagus and starting the injury in the first place."
In the study, researchers created GERD in rats by connecting the duodenum to the esophagus. This operation allows stomach acid and bile to enter the esophagus. Researchers were surprised to learn that esophagitis didn't develop for a number of weeks after the operation.
"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."