Liver disease drug treatment

Sailer R et al The use of silymarin In the treatment of liver diseases. Drugs 2001 61(14) 2035-2063. [PMID 11735632] (Review Of the literature on the efficacy and safety of silymarin tor treatment of chronic hepatitis and cirrhosis.)... 

Plasma-derived antithrombin concentrates have been used medically since the 1980s for the treatment of hereditary and acquired antithrombin deficiency. Hereditary (genetic) deficiency is characterized by the presence of little/no native antithrombin activity in plasma and results in an increased risk of inappropriate blood clot/emboli formation. Acquired antithrombin deficiency can be induced by drugs (e.g. heparin and oestrogens), liver disease (decreased antithrombin... 

Contraindications to heparin therapy include hypersensitivity to the drug, active bleeding, hemophilia, severe liver disease with elevated prothrombin time (PT), severe thrombocytopenia, malignant hypertension, and inability to meticulously supervise and monitor treatment. 

Cell Specific Delivery of Anti-Inflammatory Drugs to Hepatic Endothelial and Kupffer Cells for the Treatment of Inflammatory Liver Diseases... 

Hepatotoxicity Hepatotoxicity, primarily of the hepatocellular type, has been associated with ketoconazole, including rare fatalities. Measure liver function before starting treatment and frequently during treatment. Monitor patients receiving ketoconazole concurrently with other potentially hepatotoxic drugs, particularly those patients requiring prolonged therapy or those with a history of liver disease. 

Hepatotoxicity Itraconazole has been associated with rare cases of serious hepatotoxicity, including liver failure and death. Some of these cases had neither pre-existing liver disease, nor a serious underlying medical condition. If liver function tests are abnormal, discontinue treatment. In patients with raised liver enzymes or an active liver disease or who have experienced liver toxicity with other drugs, do not start treatment unless the expected benefit exceeds the risk of hepatic injury. In such cases, liver enzyme monitoring is necessary. 

For these reasons, a mild elevation of this type during treatment with mirtazapine does not necessarily mean that the drug should be discontinued but rather that repeated monitoring should be done to determine whether it resolves. The drug should be discontinued if the elevation exceeds 3.0 times the upper limit of normal. A workup may be indicated to determine whether the elevation is symptomatic of an underlying liver disease (e.g., hepatitis C) rather than necessarily assuming it is due to mirtazapine. 

A number of medicinal plants including Glycyrrhiza glabra, Silybum marianum, Picrorrhiza kurroa and Artemisia capillar is have been traditionally used for the treatment of hepatitis. These plants contain various compounds with unique structures such as alkaloids, terpenoids and polyphenols. To study the hepatoprotective phytoconstituents of medicinal plants is of value to provide a scientific basis for the traditional use. Additionally, the active constituents could be used as pharmacological tools for the study of the mechanisms underlying liver disease or as lead compounds for the development of new drugs for hepatitis. In fact,... 

Rost KL, Brockmoller J, Esdom F, et al. Phenocopies of poor metabolizers of omeprazole caused by liver disease and drug treatment. J Hepatol 1995 23 268-277. 

All the scenarios describe why each of the five patients has different issues that should be taken into account when considering drug choice, thus demonstrating the importance of knowing as much as you can about the patient s liver disease. The scenarios are not all-encompassing and do not include all potential drug treatments. Drugs are included in the options purely to demonstrate some of the principles involved. 

Based on their pharmacokinetic profile alone, the safest statins in chronic compensated liver disease and a history of decompensation are prohahly pravastatin and rosnvastatin. However, clinical experience with rosnvastatin in liver disease is lacking, and so it cannot be recommended. In addition, the true rate of post-marketing adverse drug reactions is not yet clear. Pravastatin is therefore the drug of choice in these patients, where treatment is deemed necessary. It should, however, be avoided in acute episodes until liver function or transaminases stabilise/return to normal. 

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