Hypochlorhydria induced by a proton pump inhibitor leads to intragastric microbial production of acetaldehyde from ethanol

Background:Acetaldehyde, produced locally in the digestive tract, has recently been shown to be carcinogenic in humans.Aim:To examine the effect of iatrogenic hypochlorhydria on intragastric acetaldehyde production from ethanol after a moderate dose of alcohol, and to relate the findings to the changes in gastric flora.Methods:Eight male volunteers ingested ethanol 0.6 g/kg b.w. The pH, acetaldehyde level and microbial counts of the gastric juice were then determined. The experiment was repeated after 7 days of lansoprazole 30 mg b.d.Results:The mean (± S.E.M.) pH of the gastric juice was 1.3 ± 0.06 and 6.1 ± 0.5 (P < 0.001) before and after lansoprazole, respectively. This was associated with a marked overgrowth of gastric aerobic and anaerobic bacteria (P < 0.001), by a 2.5‐fold (P=0.003) increase in gastric juice acetaldehyde level after ethanol ingestion, and with a positive correlation (r=0.90, P < 0.001) between gastric juice acetaldehyde concentration and the count of aerobic bacteria.Conclusions:Treatment with proton pump inhibitors leads to hypochlorhydria, which associates with intragastric overgrowth of aerobic bacteria and microbially‐mediated acetaldehyde production from ethanol. Since acetaldehyde is a local carcinogen in the concentrations found in this study, long‐term use of gastric acid secretory inhibitors is a potential risk‐factor for gastric and cardiac cancers.