Inhibition of gastric alcohol dehydrogenase activity by histamine H2- receptor antagonists has no influence on the pharmacokinetics of ethanol after a moderate dose.

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Abstract
Ethanol undergoes gastric first pass metabolism by alcohol dehydrogenase (ADH). We have shown that cimetidine and famotidine both cause competitive inhibition of human gastric ADH in vitro. However, in a randomized 4‐way cross‐over study in 12 healthy subjects a 7‐day course of treatment with cimetidine (800 mg day‐1), ranitidine (300 mg day‐1) or famotidine (40 mg day‐1), did not modify the pharmacokinetics of ethanol given as a post‐prandial 0.3 g kg‐1 dose. We conclude that gastric mucosal concentrations of histamine H2‐receptor blockers achieved after oral dosing are probably too low to cause significant inhibition of gastric ADH in vivo.