Abstract
In most individuals, only part of the imbibed alcohol reaches the systemic blood. With doses relevant to social drinking, this is due mainly to gastric first-pass metabolism of alcohol, which acts as a barrier against toxic alcohol blood levels. The activity of gastric alcohol dehydrogenase can account for a substantial fraction of this metabolism. Fasting, female gender, old age, dilution of alcoholic beverages, chronic alcohol consumption and still undetermined factors decrease the gastric metabolism of alcohol. Aspirin and some H2-receptor antagonists also inhibit this gastric activity. In subjects with documented first-pass metabolism, these drugs increase blood alcohol levels, especially after repeated small drinks, and may result in unexpected impairment to perform complex tasks, such as driving. Thus, patients treated with these drugs should be warned of this possible side effect.
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