HELICOBACTER INFECTION AND GASTRIC ETHANOL-METABOLISM

The organism frequently colonizing the stomach of patients suffering f rom chronic active gastritis and peptic ulcer disease-Helicobacter pyl ori-possesses marked alcohol dehydrogenase (ADH) activity. Consequentl y, Helicobacter infection may contribute to the capacity of the stomac h to metabolize ethanol and lead to increased acetaldehyde production. To study this hypothesis, we first determined ADH activity in a varie ty of H. pylori strains originally isolated from human gastric mucosal biopsies. ADH activity was also measured in endoscopic gastric mucosa l specimens obtained from H. pylori-positive and -negative patients. F urthermore, we used a mouse model of Helicobacter infection to determi ne whether infected animals exhibit more gastric ethanol metabolism th an noninfected controls. Most of the 32 H. pylori strains studied poss essed clear ADH activity and produced acetaldehyde. In humans, gastric ADH activity of corpus mucosa did not differ between H. pylori positi ve and -negative subjects, whereas in antral biopsies ADH activity was significantly lower in infected patients. In mice, gastric ADH activi ty was similar or even lower in infected animals than in controls, dep ending on the duration of infection, despite the fact that the infecti ous agent used-Helicobacter felis-showed ADH activity in vitro. In acc ordance with this, Helicobacter infection tended to decrease rather th an increase gastric ethanol metabolism in mice. In humans, it remains to be established whether the observed decrease in antral ADH activity associated with H. pylori infection can lead to reduced gastric first -pass metabolism of ethanol.