Abstract
<h3>In Reply.—</h3> We appreciate the comments of Hall and colleagues. We believe our patient had superimposed acetaminophen hepatotoxicity because of the laboratory features and charac teristic centrilobular injury. She was taking no other hepatotoxic drugs (except alcohol) and had not knowingly been exposed to any other toxins. We agree that chronic liver disease alone does not predispose patients to hepatotoxicity from therapeutic acetaminophen use. She did not have any histologic or clinical evidence of cirrhosis. Rather, this case report describes an alcohol-abusing patient who developed centrilobular fibrosis while ingesting what she perceived to be a routine dose of acetaminophen—two extra-strength acetaminophen capsules every four hours. Potentiation of acetaminophen toxicity in chronic alcoholics receiving small doses of acetaminophen has been previously described.<sup>1,2</sup>Fasting also enhances experimental acetaminophen hepatotoxicity<sup>3</sup>and her dietary intake may have been poor. Other enzyme-inducing agents such as phenobarbital have also been shown to potentiate acetaminophen
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