Download Drug-Induced Liver Disease (2nd Edition) by Neil Kaplowitz, Laurie D. DeLeve PDF

By Neil Kaplowitz, Laurie D. DeLeve

ISBN-10: 0824708113

ISBN-13: 9780824708115

That includes greater than 4100 references, Drug-Induced Liver affliction might be a useful reference for gastroenterologists, hepatologists, kinfolk physicians, internists, pathologists, pharmacists, pharmacologists, and medical toxicologists, and graduate and clinical institution scholars in those disciplines.

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Additional info for Drug-Induced Liver Disease (2nd Edition)

Example text

As noted in Table 1, omeprazole treatment should have resulted in induction of CYP1A2 activity, especially since the investigators only studied subjects who were CYP2C19 poor metabolizers and who would therefore have had relatively high blood levels of omeprazole (14). The absence of an increase in NAPQI production after omeprazole treatment therefore suggests that CYP1A2 is not a substantial contributor to NAPQI production in humans receiving therapeutic doses of acetaminophen. Likewise, rifampin pretreatment did not produce a detectable increase in NAPQI production (48), indicating that CYP3A4 is likely to be at best a minor pathway for production of NAPQI from therapeutic doses of acetaminophen.

Oxidation of acetaminophen to its toxic quinone imine and nontoxic catechol metabolites by baculovirus-expressed and purified human cytochromes P450 2E1 and 2A6. Chem Res Toxicol 1998; 11:295–301. The Role of Cytochrome P450s 31 47. Sarich T, Kalhorn T, Magee S, et al. The effect of omeprazole pretreatment on acetaminophen metabolism in rapid and slow metabolizers of S-mephenytoin. Clin Pharmacol Ther 1997; 62:21–28. 48. Manyike PT, Kharasch ED, Kalhorn TF, Slattery JT. Contribution of CYP2E1 and CYP3A to acetaminophen reactive metabolite formation.

With some drugs, a single P450 is involved in the majority of the metabolism. This is illustrated in Fig. 1 by drug A, which is only capable of binding to, and being metabolized by, CYP2D6. The resulting metabolite generally then undergoes phase II conjugation and the conjugated metabolite is frequently excreted back into the space of Disse, now more water soluble and more readily eliminated by the kidneys. Alternatively, the metabolite can be sorted to the bile canaliculus (not shown in Fig. 1) to be excreted in bile into the small intestine, now less likely to undergo enterohepatic cycling.

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Drug-Induced Liver Disease (2nd Edition) by Neil Kaplowitz, Laurie D. DeLeve

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