This study compiled papers that addressed the effect of cimetidine, ranitidine, famotidine, and nizatidine on ethanol metabolism, first from a PubMed search and then from citations within these papers, and studies were tabulated for fasting versus fed, ethanol and H2-receptor antagonist dose, and a summary of pharmacokinetic changes.
In the 1980s-1990s, numerous studies were performed on H2-receptor antagonist inhibition of ethanol first-pass metabolism. Blood alcohol concentrations warranting possible driving under the influence citations in the United States have subsequently dropped from ≥100 mg/dL to 50 mg/dL (Utah in 2019) (30 mg/dL or zero tolerance in some parts of the world). A re-examination of these studies seemed important. The papers reviewed for the current study indicate that at doses of 0.15-0.30 mg/kg in the postprandial state (primarily after breakfast), the H2-receptor antagonists - cimetidine, ranitidine, famotidine, and nizatidine - have all been found to increase the first-pass metabolism of ethanol. With cimetidine, there were sufficient studies to suggest it might be inhibitory outside these restricted states. Although the role of inhibition of alcohol dehydrogenase has not been clearly defined, there is circumstantial evidence to support this mechanism. Further studies are required to clarify the ability of H2-receptor antagonists to inhibit first-pass metabolism of ethanol. (publisher abstract modified)
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