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

Acetaldehyde, produced locally in the digestive tract, has recently been shown to be carcinogenic in humans. 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. 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. 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. 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.