Nov. 23, 2009 -- Stomach acid may only be part of the problem when it comes to esophagus injury related to gastroesophageal reflux disease (GERD). A new study suggests that an immune system response may be the real culprit behind reflux esophagitis.
Researchers say it's been assumed that reflux esophagitis develops when cells in the lining of the esophagus become burned and damaged by stomach acid backing up into the esophagus.
But in a rat model of GERD, researchers found that this acid reflux didn't directly damage the lining of the esophagus. Instead, the acid triggered the release of chemicals called cytokines that attract inflammatory immune cells to the area, which were responsible for the real damage.
If further studies in humans confirm these results, researchers say new GERD treatments that target this immune response may be needed to effectively manage the disease.
"Currently, we treat GERD by giving medications to prevent the stomach from making acid," says Rhonda Souza, MD, associate professor of internal medicine at the University of Texas Southwestern Medical Center, in a news release. She says "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, published in Gastroenterology, researchers created GERD in rats by performing an operation to connect the duodenum (first section of the small intestine) to the esophagus, allowing stomach acid and bile to enter the esophagus.
The results showed damage to the lining of the esophagus did not occur immediately after exposure to the stomach acids. It happened weeks later.
"That doesn't make sense if GERD is really the result of an acid burn," says researcher Stuart Spechler, MD, professor of internal medicine at UT Southwestern, in the news release. "Chemical injuries develop immediately. If you spill battery acid on your hand, you don't have to wait a month to see the damage."
Within three days after the operation, researchers found no damage to the cells on the surface layer of the esophagus, but they found inflammatory cells in the deeper layers. Those inflammatory cells rose to the surface three weeks later after the initial stomach acid exposure.