Mechanism of the aspirin-induced rise in blood alcohol levels

Aspirin increases blood alcohol levels after post-prandial alcohol consumpt ion in men. This was attributed to a decrease in first pass metabolism seco ndary to inhibition of gastric alcohol dehydrogenase. Since accelerated gas tric emptying, decreased volume of distribution or delayed elimination coul d also result in higher blood alcohol levels, we investigated the effect of aspirin (1 g taken with a meal) on these parameters. Aspirin did not chang e the volume of ethanol distribution or the rate of its elimination. Moreov er, it did not have a significant effect on gastric emptying. The half-time of Tc-99m-DTPA loss was 65.5+/-5.4 minutes without and 71.3+/-6.5, with as pirin. Despite a trend for slower gastric emptying with aspirin, the alcoho l bioavailability increased and was associated with a 39% decrease in the f irst pass metabolism of alcohol (from 106+/-4 to 65+/-19 mg/kg, p<0.05), co nsistent with the inhibition of gastric ADH activity. In keeping with this interpretation, the effect of aspirin was virtually absent in women, who ha ve a much smaller first pass metabolism available for inhibition by aspirin .