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Inhibition of gastric alcohol dehydrogenase activity by histamine H2‐ receptor antagonists has no influence on the pharmacokinetics of ethanol after a moderate dose.
Author(s) -
Mallat A,
RoudotThoraval F,
Bergmann JF,
Trout H,
Simonneau G,
Dutreuil C,
Blanc LE,
Dhumeaux D,
Delchier JC
Publication year - 1994
Publication title -
british journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.216
H-Index - 146
eISSN - 1365-2125
pISSN - 0306-5251
DOI - 10.1111/j.1365-2125.1994.tb04263.x
Subject(s) - famotidine , cimetidine , ranitidine , pharmacokinetics , histamine h2 receptor , histamine , alcohol dehydrogenase , pharmacology , ethanol , in vivo , chemistry , first pass effect , oral administration , stomach , medicine , endocrinology , receptor , antagonist , biology , biochemistry , microbiology and biotechnology
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.