U-M scientists show why inhibiting acid production could make gastritis worse

ANN ARBOR, Mich. - When it comes to cooling the burning pain of gastritis or an inflamed stomach lining, reducing the amount of acid in the stomach may seem like a good idea. But two new studies with laboratory mice, conducted by Howard Hughes Medical Institute scientists at the University of Michigan Medical School, indicate it could be exactly the wrong thing to do.

U-M scientists found that antibiotics were the best way to kill the bacteria that cause gastritis and eliminate stomach inflammation in their experimental mice. Mice treated with prescription drugs called proton pump inhibitors or PPIs, which block acid production, acquired more bacteria and developed more inflammatory changes in their stomach linings than untreated mice.

"These animal studies indicate that it is the inflammatory response - triggering the overproduction of hydrochloric acid - which is the stomach's primary response to bacterial colonization," says Juanita L. Merchant, M.D., Ph.D., an HHMI assistant investigator and U-M associate professor of internal medicine and physiology. "Inflammation of the stomach lining coincides with production of peptides called cytokines, which stimulate production of a hormone called gastrin. Gastrin triggers parietal cells in the stomach lining to produce more hydrochloric acid, which kills off most invading microbes. If you inhibit gastric acid production, you interfere with the stomach's natural defense mechanism."

Merchant cautions that without controlled clinical trials, it is impossible to know whether the results would be exactly the same in humans. She also emphasizes that a type of bacteria called Helicobacter pylori, the most common cause of gastritis, was excluded from these studies. Since reduced gastric acidity does appear to make the mammalian stomach more vulnerable to bacterial invasion and gastritis, however, Merch
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Contact: Sally Pobojewski
pobo@umich.edu
734-615-6912
University of Michigan Health System
15-Jan-2002