It has been proposed that an appreciable fraction of ingested ethanol is metabolized in the gastric mucosa and that inhibition of this metabolism by H2‐receptor antagonists produces clinically important increases in blood ethanol. This paper reviews available data concerning gastric metabolism of ethanol and the influence of H2‐antagonists on ethanol metabolism. It concludes that very little, if any, metabolism of ethanol is likely to occur in the gastric mucosa, and the interaction between H2‐antagonists and ethanol is clinically insignificant.
|Original language||English (US)|
|Number of pages||8|
|Journal||Alimentary Pharmacology & Therapeutics|
|State||Published - Apr 1993|