Interactions between alcohol and gastric metabolizing enzymes: practical implications.
It has been demonstrated recently that some portion of ingested alcohol does not enter the systemic circulation and is not retained in the gastrointestinal tract; instead, gastric oxidation or first-pass metabolism of ethanol occurs in the stomach, catalyzed by gastric alcohol dehydrogenase. First-pass metabolism of ethanol is minimal in the fasting state; it is lower in women than in men, and in alcoholics than in nonalcoholics; and it is abolished in patients after subtotal gastrectomy. In addition, some drugs may affect first-pass ethanol metabolism. Studies of the effects of H2-receptor antagonists on blood ethanol levels are reviewed. It is concluded that some H2-receptor antagonists (cimetidine and nizatidine, in particular) can inhibit gastric ethanol oxidation and thus increase blood alcohol levels after drinking. The clinical and medicolegal implications of these findings are discussed.
Caballería
J
J
Liver Unit, Hospital Clínic i Provincial, University of Barcelona, Spain.
D000426:Alcohol Dehydrogenase / Q000187:drug effects / Q000378:metabolism*; D000818:Animals; D001682:Biological Availability; D000431:Ethanol / Q000097:blood / Q000378:metabolism*; D005753:Gastric Mucosa / Q000378:metabolism*; D006635:Histamine H2 Antagonists / Q000494:pharmacology; D006801:Humans; D007527:Isoenzymes / Q000187:drug effects / Q000378:metabolism; D051381:Rats; D013270:Stomach / Q000201:enzymology
D006635:Histamine H2 Antagonists; D007527:Isoenzymes; D000431:Ethanol; D000426:Alcohol Dehydrogenase