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Pain in the gut? Don't blame stomach acid

Major findings from the U-M studies include:

  • Stomach cell samples from both the transgenic gastrin-deficient mice and the normal mice whose ability to produce gastric acid was inhibited by omeprazole all showed significant inflammatory changes -- including more immune cells called lymphocytes -- and greater numbers of bacteria.

  • Gastritis that developed in mice on omeprazole resolved after 20 days of antibiotic treatment, despite continued omeprazole treatment and low stomach acidity.

  • The number of acid-producing parietal cells and gastrin-secreting G-cells in the stomach increased in all mice with abnormally low levels of hydrochloric acid. Elevated numbers of parietal and G-cells correlated with the presence of inflammation, not with stomach acidity.

  • Elevated levels of gastrin during chronic inflammation suppressed production of a growth hormone called somatostatin, which inhibits parietal and G-cell function. When the inflammation subsided following antibiotic treatment, gastrin levels returned to normal releasing the hormonal brake inhibiting somatostatin.

"Our findings show that changes observed in gastrin-deficient mice are caused by inflammation triggered by an overgrowth of many bacterial species," Zavros explains. "An abnormally low level of acidity in the stomach is the factor initiating all these events."

"The bottom-line message is that a two-week course of antibiotics to treat the inflammation is essential for a successful cure," Merchant adds. "Once you get rid of the inflammation, the gastric acid levels should return to normal. It is crucial to take antibiotics for the entire two weeks exactly as your physician has prescribed, however. People often stop taking their medication early or skip doses, which helps the bacteria to develop antibiotic resistance."


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Contact: Sally Pobojewski
pobo@umich.edu
734-615-6912
University of Michigan Health System
15-Jan-2002


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