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Normal gastric acidity protects against development of bacterial gastroenteritis (GE); achlorhydric patients have higher risk for GE. Limited data suggest that acid-reduction therapy also confers higher risk for GE. To evaluate this possibility further, investigators in the U.K. used the General Practice Research Database to identify 6414 patients who presented with bacterial GE from 1992 through 2001. These patients were matched with 50,000 controls from the same database by age, sex, and calendar year.
Logistic regression analysis showed that patients with GE were more likely than controls to be taking proton-pump inhibitors (PPIs) but not histamine-2–receptor antagonists (H2RAs). PPI users were significantly more likely to develop GE than were nonusers (relative risk, 2.9; 95% CI, 2.4–3.5). Risk increased when PPI doses were doubled (RR, 5.0; 95% CI, 2.7–9.3). H2RA use was not associated with bacterial GE (RR, 1.1; 95% CI, 0.9–1.4). Omeprazole and lansoprazole conferred similar risk for GE, and the specific bacterium responsible for diarrhea (campylobacter or salmonella) did not affect the relative risks associated with the drugs. GE was associated with alcoholism, low body-mass index, recent use of antidiarrheals, and use of antibiotics during the prior week. The authors concluded that PPI therapy, but not H2RA therapy, led to higher risk for campylobacter- or salmonella-associated GE.
García-Rodríguez LA et al. Use of acid-suppressing drugs and the risk of bacterial gastroenteritis. Clin Gastroenterol Hepatol 2007 Dec; 5:1418.
Comment
These findings are consistent with those of other studies: Spontaneous or therapeutic reduction of gastric acid lowers the number of bacteria that are required to produce clinical GE. The inability of H2RAs to produce effects similar to those of PPIs could be due to their less-potent acid-reduction capability or to some additional effect of PPIs. The conclusions of the study are limited to campylobacter- and salmonella-associated disease because these species were responsible for 94% of GE in this study; clostridium species caused fewer than 1% of the cases. The population-based clinical magnitude of this association cannot be determined, as these researchers did not evaluate the incidence of GE among patients who take PPIs.