GERD may be due to immune reaction rather than acid burn.
Gastroesophageal reflux (Risk factors)
Gastroesophageal reflux (Diagnosis)
Gastroesophageal reflux (Care and treatment)
Heartburn (Risk factors)
|Publication:||Name: Australian Journal of Medical Herbalism Publisher: National Herbalists Association of Australia Audience: Academic Format: Magazine/Journal Subject: Health Copyright: COPYRIGHT 2009 National Herbalists Association of Australia ISSN: 1033-8330|
|Issue:||Date: Winter, 2009 Source Volume: 21 Source Issue: 4|
|Geographic:||Geographic Scope: Australia Geographic Code: 8AUST Australia|
Souza RF et al 2009. Gastroesophageal reflux might cause
esophagitis through a cytokine-mediated mechanism rather than caustic
acid injury. Gastroenterol 137:5;1776-84.
Gastroesophogeal reflux disease (GERD) is a relatively recent but growing condition characterised by symptoms such as heartburn and chest pain, with much research being produced in pursuit of treatment options. Until now the popular explanation has been that GERD develops as a direct result of acidic digestive juices burning the esophageal epithelial cells. However this study, using an animal model, refutes that assumption discovering that while caustic chemical injuries develop rapidly, esophagitis might not appear until weeks after the induction of reflux.
Instead they found that 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.
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 and is a reasonable representation of how GERD develops in humans--acidic digestive juices from the stomach surge into the esophagus. Soon after the operation they expected to see the death of surface cells of the esophagus and the injury progress later to the deeper layers. Surprisingly they found the opposite. Three days after the surgery there was no damage to surface cells but they did find inflammatory cells in the deeper layers of the esophagus. Those inflammatory cells did not 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," considers Dr Stuart Spechler, a 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."
Previous studies have shown that if an animal esophagus is perfused with highly concentrated acid, esophageal damage develops quickly. In humans however the large majority of reflux episodes do not contain such highly concentrated acid. Dr Souza, another of the study's authors, commented that "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".
GERD is currently treated by giving medications to prevent the stomach from making acid. If GERD is in fact an immune mediated injury, it may be that treatment needs to include medications that would prevent these cytokines from attracting inflammatory cells to the esophagus and starting the injury in the first place.
Kim Hunter MNHAA
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