DOMINIQUE LARREY, M.D.; JEAN HENRION, M.D.; FRANCIS HELLER, M.D.; GERARD BABANY, M.D.; CLAUDE DEGOTT, M.D.; DOMINIQUE PESSAYRE, M.D.; JEAN-PIERRE BENHAMOU, M.D.
LARREY D, HENRION J, HELLER F, BABANY G, DEGOTT C, PESSAYRE D, et al. Metoprolol-lnduced Hepatitis: Rechallenge and Drug Oxidation Phenotyping. Ann Intern Med. 1988;108:67-68. doi: 10.7326/0003-4819-108-1-67
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Published: Ann Intern Med. 1988;108(1):67-68.
Metoprolol is a widely used beta-adrenoreceptor antagonist. To our knowledge, there is no report of hepatitis involving this drug as well as other beta-adrenoreceptor antagonists (1). Metoprolol is metabolized by three major oxidation pathways (2); two of them, O-dealkylation and alpha-hydroxylation, undergo genetically controlled polymorphisms correlated with that of debrisoquine oxidation (2-4). This finding strongly suggests that metoprolol oxidation depends at least partly on the same isozyme of cytochrome P-450 involved in the genetic polymorphism of oxidation of debrisoquine and many other drugs such as sparteine, perhexiline, and several other beta-adrenoreceptor antagonists (5). Poor metabolizers of debrisoquine and metoprolol exhibit
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Cardiology, Coronary Risk Factors, Gastroenterology/Hepatology, Hypertension, Liver Disease.
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