A new study suggests that gastritis would be better treated with antibiotics than potent acid-reducing drugs, which the researchers say can do more harm than good in certain cases.
The study’s conclusion wanders astray from the common treatment for the condition – reducing acid – and left another expert with the intellectual equivalent of an upset stomach.
“When you completely block acid production, you encourage the growth of bacteria, which in turn increases stomach inflammation and sets the stage for chronic gastritis,” says study author Dr. Juanita Merchant, associate professor of internal medicine and physiology at the University of Michigan Health System.
Antibiotics, says Merchant, “address the problem at the source – the bacteria.”
Gastritis is an inflammation of the stomach lining.
Merchant says over-the-counter antacids like Tagamet (Cimetidine), Pepcid AC (famotidine), and Zantac (ranitidine) aren’t as harmful because they allow some acid production to continue. But she does take issue with powerful prescription antacids known as proton pump inhibitors – medications such as Prilosec (omeprazole), Prevacid (lansoprazole), Protonix (pantoprazole), or Aciphex (rabeprazole), which work by shutting down all acid production.
“These drugs won’t help gastritis, and they could make problems worse by creating an environment that encourages bacteria to grow,” she says.
Other doctors are not so quick to dismiss conventional wisdom.
Dr. Ali Karakurum, a gastroenterologist and assistant professor of medicine at Nassau University Medical Center in New York, finds the results “highly questionable.”
Eliminating bacteria, he says, has proven helpful only in those patients with ulcer disease caused by the bacterium Helicobacter pylori. “There are no studies showing any other type of bacteria is linked to gastritis, so I have to question the basic premise of the study,” adds Karakurum.
Merchant’s theory of bacteria-mediated gastritis revolves around a substance called gastrin, a chemical secreted by the stomach lining in response to inflammation – including the presence of bacteria. Gastrin, she says, triggers the production of excess stomach acid.
While the excess acid itself is often blamed for stomach woes, Merchant says her animal study shows it may be there for a reason. She claims that the bacteria that set gastrin into action – not the excess acid – are the real cause of the stomach problems.
More important, she believes that without treatment targeted to reduce bacteria, we could be setting ourselves up for far more severe stomach problems, including cancer.
“If you don’t treat the bacteria, you won’t get rid of the problem – at least that’s what our studies showed,” says Merchant.
Karakurum disagrees. “Most cases of gastritis are self-limiting,” he says. “They disappear on their own whether or not you find or treat any bacteria,” he says.
Merchant’s study compared the stomach linings of normal mice with those genetically altered not to produce gastrin and were thus unable to make stomach acid.
At the start of the study, researchers washed the stomach linings of all the mice, and tested the fluid for the presence of bacteria. Eliminating those mice not shown to have the ulcer-causing H. pylori bacteria – which aren’t affected by acid – they selected those that tested positive for three other types of bacteria: Lactobacillus, Enterobacter, and Staphylococcus.
The group of infected mice deficient in gastrin were treated with antibiotics for 20 days. The infected mice with normal levels of gastrin were treated for 60 days with the proton pump inhibitor omeprazole.
At the end of the study, researchers once again examined the stomach linings of the mice.
The mice given the antibiotic showed a marked reduction in inflammation and bacteria, the study found. The mice taking the acid-blocking omeprazole were shown to have increased inflammation and more bacteria than when the study started.
Further, subsequent treatment of the second group with antibiotics resulted in a similar reduction in inflammation seen in the first group – even though the mice continued on the omeprazole.
Karakurum finds an important flaw within the study design.
“H. pylori bacteria is not found in the stomach lining. It requires a biopsy of the tissue, where it hides,” he says. Not finding H. pylori in the lining is not verification that it wasn’t present, says Karakurum. And if it was, he says, then that would account for the improvement in the mice that took the antibiotic. It would also explain why the antacids didn’t work.
Sources: Interviews with Juanita L. Merchant, M.D., Ph.D., associate professor of internal medicine and physiology, University of Michigan, Ann Arbor; Ali Karakurum, M.D., assistant professor of medicine, Nassau University Medical Center, Long Island, New York; January 2002 Gastroenterology; January 2002 American Journal of Physiology