Dundee, Scotland—Intestinal infections with Clostridium difficile and Campylobacter bacteria increased in patients using commonly prescribed acid-suppression medications, according to a very large population-based study from Scotland.
Use of heartburn drugs, such as proton pump inhibitors (PPIs) and H2 receptor antagonists (H2RAs), increased risks of developing C difficile by 1.7 times and Campylobacter by 3.7 times in those living in the community, compared with non-users of the medications, according to the report in the British Journal of Pharmacology.
For hospitalized patients, acid-suppression medications (ASMs) were linked to increased risks of C difficile and Campylobacter of 1.4 times and 4.5 times, respectively, added study authors, who were led by researchers from Ninewells Hospital and Medical School in Dundee.
The propensity score–matched cohort study used a record-linkage database in Tayside, Scotland, and included 188,323 patients exposed to ASMs—PPIs and H2Ras—and 376,646 controls who did not use the drugs between 1999 and 2013. Reports of positive stool tests were used to determine C difficile, Campylobacter, Salmonella, Shigella, or Escherichia coli O157.
Results indicate 22,705 positive test results—15,273 C difficile (toxin positive), 6,590 Campylobacter, 852 Salmonella, 129 Shigella and 193 E. coli O157, not mutually exclusive.
Adjusted hazard ratios for culture-positive diarrhea for the PPIs and H2Ras, exposed versus the unexposed cohort, were 2.72 during follow-up time for samples submitted from the community and 1.28 for samples submitted from hospitals.
“The results suggest that community-prescribed ASMs were associated with increased rates of C difficile and Campylobacter-positive gastroenteritis in both the community and hospital settings,” study authors conclude.
“Users of these medications should be particularly vigilant about food hygiene as the removal of stomach acid makes them more easily infected with agents such as Campylobacter, which is commonly found on poultry,” recommended senior author Thomas MacDonald, MD, MPH, PhD, of the School of Medicine at the University of Dundee.
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