Titlebook: Drug-Induced Hepatotoxicity; Ross G. Cameron,George Feuer,Felix A. Iglesia Book 1996 Springer-Verlag Berlin Heidelberg 1996 Hepatotoxizit?

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Molecular Biology of Hepatic Drug Reactions,echanisms of drug toxicity has been carried out in animal models or in vitro systems using cultures of non-hepatocyte cell lines. The limitations and pitfalls of extrapolating from non-human data to the clinical situation are well recognised.

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Cytochromes P450 and Liver Injury,ivery to the liver before the drug is distributed throughout the body and exerts its therapeutic effects, (b) trans cellular pores or fenestrations in the endothelial cells lining the sinusoidal spaces are unique to the liver and are sufficiently large to permit most plasma proteins to diffuse into

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Mechanisms of Drug-Induced Cholestasis, bile pigments in the canaliculi andhepatocytes, dilation of the canalicular space with a reduction of microvilli,feathery degeneration, accumulation of copper, and Mallory body-like cytoplasmicinclusions. Finally, the simplest functional definition of cholestasis is adecrease in bile flow. Cholesta

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Liver Reactions to Tacrine,rine administration was shown to produce statistically significant improvements in several measures of cognitive function (. et a1. 1992; . et a1. 1994). As a result of these clinical trials, tacrine has been approved by the United States Food and Drug Administration for the treatment of mild to mod

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0171-2004 ho- sis and even malignancy. Hence the possibility of adverse drug effects must be considered in the differential diagnosis of many patients with liver disease.978-3-642-64657-7978-3-642-61013-4Series ISSN 0171-2004 Series E-ISSN 1865-0325