{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T10:03:39Z","timestamp":1791194619235,"version":"4.1.0"},"reference-count":53,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"1","license":[{"start":{"date-parts":[[2015,9,1]],"date-time":"2015-09-01T00:00:00Z","timestamp":1441065600000},"content-version":"tdm","delay-in-days":4079,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2004,7]]},"abstract":"<jats:sec><jats:title\/><jats:p>Examination of the pharmacokinetics of acetaminophen can decrease misconceptions involved in clinical evaluation. Enzyme patterns and acetaminophen levels must be related to time and known metabolic phenomena. A careful look at ethanol and nutrition, especially fasting demonstrates that therapeutic doses of acetaminophen do not place patients at a greater risk in either of these instances. An overdose of acetaminophen in a chronic alcohol abuser may result in more severe hepatotoxicity than in the nonalcoholic. CYP2E1 and glutathione must be evaluated simultaneously rather than in isolation. Glucuronidation capacity in humans is not a factor except in massively overdosed patients. 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