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

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Cytochromes P450 and Liver Injury,inal tract. Once absorbed, they circulate in blood bound to plasma proteins such as albumin, and are sequestered into fat with relative tissue: blood ratios determined by the degree of lipophilicity. For these reasons, lipophilic drugs are not readily excreted by the kidney into urine; therefore con

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Mechanisms of Drug-Induced Cholestasis,sult from accumulation in blood of compounds normally excreted in bile, such as bilirubin, bile acids, cholesterol, alkaline phosphatase,5’-nucleotidase,.-glutamyltranspeptidase,leucine amino peptidase, lipoprotein X. and immunoglobulin. The response of these compounds and the time course for elevat

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Fatty Liver and Drugs,of injury. To gain a good understanding of these mechanisms, the general scheme of triglyceride metabolism in the liver must be considered. Triglycerides (TGs), which are present in the hepatocytes, are synthesized locally from glycerol and fatty acids by TG synthetase. The liver uses TGs either to

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Choline Deficiency: An Important Model for the Study of Hepatotoxicity,als (rats have been studied very extensively) causes acute and chronic damage, not unlike, in some respects, that seen after the . of toxic drugs, e.g., carbon tetrachloride. Deprivation of no other nutrients from the diet of rats has such a fast action as choline. When rats are given a diet devoid

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Immune Mechanisms and Liver Toxicity,those that are idiosyncratic, non-dose related and non-reproducible in experimental animals. It is important to note that more idiosyncratic drug reactions are attributable predominantly or entirely to pharmacokinetic variations or enzyme polymorphisms or deficiencies than to abnormal immunological

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Hepatic Encephalopathy,a. The association of the syndrome with acute or chronic liver failure implicates a plethora of metabolic abnormalities and gut-derived toxins in its pathogenesis. Thus, it is difficult to ascribe the neurological and psychiatric manifestations of HE to the presence of a single agent or changes in a

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Liver Drug Reactions and Pregnancy,970). The epidemiologic impact of iatrogenic liver injury is considerably more important, however, when the mortality due to liver disease is considered. Specifically, the case-fatality rate for drug-induced hepatic injury ranges from a minimum figure of 10% to a high of 50% of cases, depending upon

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,Reye’s Syndrome,hy and fatty degeneration of the viscera). Manifestations of the disease included viral prodrome usually characterized by upper respiratory infection followed by severe vomiting after which mental changes and coma eventually occurred. Clinically, biochemically and histologically there was evidence o