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 rece ntly been shown to be carcinogenic in humans. Aim: To examine the effect of iatrogenic hypochlorhydria on intragastric ac etaldehyde 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, aceta ldehyde level and microbial counts of the gastric juice were then determine d. 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 ba cteria (P < 0.001), by a 2.5-fold (P=0.003) increase in gastric juice aceta ldehyde level after ethanol ingestion, and with a positive correlation (r=0 .90, P < 0.001) between gastric juice acetaldehyde concentration and the co unt of aerobic bacteria. Conclusions: Treatment with proton pump inhibitors leads to hypochlorhydria , which associates with intragastric overgrowth of aerobic bacteria and mic robially-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 gas tric and cardiac cancers.