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.
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Michael D. Levitt (1993) studied this question.
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