Do Histamine-2 Receptor Antagonists Influence the Metabolism of Ethanol?

It has been claimed that ingested ethanol is metabolized during absorption through the gastric mucosa, and inhibition of this metabolism by certain histamine-2 (H-2) receptor antagonists enhances the blood alcohol response to small doses of ethanol. In this issue of the Annals, however, Raufman and coworkers convincingly demonstrate that none of the commercially available H-2 antagonists had a perceptible effect on blood ethanol concentrations after ingestion of 0.3 g/kg of body weight of ethanol, roughly the quantity in a bottle of 6% beer. This editorial reviews how and if ethanol metabolism might be influenced by H-2 antagonists and concludes that the stomach probably is not an important site of ethanol metabolism and that the interaction between H-2 antagonists and ethanol is clinically insignificant.

Although the liver metabolizes virtually all ethanol reaching the peripheral circulation, recent studies have suggested that an appreciable quantity of ingested ethanol may be oxidized during absorption through the gastric mucosa [1-3]. Of particular importance are claims that certain histamine-2 (H-2) antagonists inhibit this gastric metabolism and hence cause unexpectedly high blood ethanol concentrations in the imbiber [4, 5]. If correct, such findings have obvious medical, legal, and commercial implications. However, in this issue of the Annals, Raufman and coworkers [6] convincingly demonstrate that none of the commercially available H-2 antagonists influenced the blood ethanol response to ingestion of 0.3 g/kg of body weight of ethanol. This article adds fuel to an ongoing controversy regarding if and how H-2 antagonists influence alcohol metabolism.

Appreciation of the controversy concerning the interaction of H-2 antagonists and …