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When isoniazid, a drug used in the treatment of tuberculosis, is given to patients receiving phenytoin, phenytoin intoxication develops in some patients with the slow-acetylator phenotype.1 This interaction is presumably a result of isoniazid's ability to inhibit liver microsomal p-hydroxylation, the major route of inactivation of phenytoin.The most serious adverse effect of isoniazid, hepatotoxicity, is thought to result from microsomal metabolism of the metabolite, acetylhydrazine, to a reactive intermediate.2 Carbamazepine is an antiepileptic drug that is eliminated by microsomal metabolism in the liver. It is a microsomal-enzyme-inducing agent, and it induces its own metabolism.3 Carbamazepine intoxication has been . . .
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Wright et al. (1982) studied this question.
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