Liver Hepatotoxicity

Isolated liver segments from starved rats exposed to 100 mg KCN/L Oxygen consumption reduced 80%, and evidence of hepatotoxicity as judged by enzyme release, glutathione depletion, and calcium accumulation in liver. Hepatotoxicity prevented by feeding rats fructose 39... 

Billings, R.E. Colorado State University Mechanisms of toxic chemical interaction in the liver-hepatotoxicity NIEHS... 

Liver (hepatotoxicity) [77] Twenty-one drugs or reference compounds with known hepatoxicity have been screened in 6-dpf zebrafish larvae. 

D-MS Methapyrilene cyproterone Rat liver Hepatotoxic drugs compared for protein signa-tures of toxicity... 

Apart from their acute and chronic toxicity, mycotoxins may possess carcinogenic, mutagenic, and teratogenic properties. They may act primarily on the liver (hepatotoxicity), kidney (nephrotoxicity), nervous (neurotoxicity), and immune systems (immunotoxicity or immunosuppression), on the uterus (uterotropism), and on the skin (dermatotoxicity), or they may act as... 

Liver Hepatotoxic and liver tumor-inducing effects of long-term danazol prophylaxis have been investigated in 92 patients with hereditary angioedema, 46 of whom were taking danazol [34 ]. There were no... 

Liver Hepatotoxicity associated with transdermal rivastigmine use has been reported [134 ]. 

Liver Hepatotoxicity has again been attributed to sertraline (SEDA-30, 16) [40 ]. In this case report, it presented within 6 months of treatment in a 17-year-old boy with no other demonstrable explanation. 

Liver Hepatotoxicity related to the consumption of noni juice, prepared from the fruits of Morinda dtrifolia, has again been reported [71 ]. 

Liver Hepatotoxicity was retrospectively evaluated in a cohort study in 105 lung transplant recipients taking voriconazole [25 ]. Age less than 40 years, cystic fibrosis, use of azathioprine, history of liver disease and early initiation of voriconazole were associated with hepatotoxicity and in multivariable logistic regression analysis, perioperative initiation of voriconazole was independently associated with hepatotoxicity. 

Liver Hepatotoxic events occasionally have been reported when ezetimibe is used in conjunction with a statin, as in the case of a 70-year-old woman who developed fulminant hepatic failure, necessitating liver transplantation 10 weeks after switching from simvastatin to simvastatin 4- ezetimibe[25]. A study with 32 subjects with nonalcoholic fatty liver disease pathology showed that ezetimibe improved hepatic fibrosis but increased hepatic long-chain fatty acids and HbA c [26]. 

As regards toxicity, pyrazole itself induced hyperplasia of the thyroid, hepatomegaly, atrophy of the testis, anemia and bone marrow depression in rats and mice (72E1198). The 4-methyl derivative is well tolerated and may be more useful than pyrazole for pharmacological and metabolic studies of inhibition of ethanol metabolism. It has been shown (79MI40404) that administration of pyrazole or ethanol to rats had only moderate effects on the liver, but combined treatment resulted in severe hepatotoxic effects with liver necrosis. The fact that pyrazole strongly intensified the toxic effects of ethanol is due to inhibition of the enzymes involved in alcohol oxidation (Section 4.04.4.1.1). 

Yellow phosphorus was the first identified liver toxin. It causes accumulation of lipids in the liver. Several liver toxins such as chloroform, carbon tetrachloride, and bromobenzene have since been identified. I he forms of acute liver toxicity are accumulation of lipids in the liver, hepartxiellular necrosis, iii-trahepatic cholestasis, and a disease state that resembles viral hepatitis. The types of chrome hepatotoxicity are cirrhosis and liver cancer. 

Liver cancer can also be a consequence of exposure to hepatotoxic chemicals. Natural hepatocarcinogens include fungal aflatoxins. Synthetic hepato-carcinogens include nitrosoamines, certain chlorinated hydrocarbons, polychlorinated biphenyls (PCBs), chloroform, carbon tetrachloride, dimethyl-benzanthracene, and vinyl chloride.Table 5.15 lists the chemical compounds that induce liver cancer or cirrhosis in experimental animals or... 

A number of quinolones had to be taken off the market due to toxic effects on the liver, heart, or other organs, that became recognized only after marketing (e.g. temafloxacin, trovafloxacin, grepafloxacin). A risk for severe cardiotoxicity, hepatotoxicity, or phototoxicity is... 

PYRAZINAMIDE Patients should have baseline liver functions tests to use as a comparison when monitoring liver function during pyrazinamide therapy. The nurse should monitor the patient closely for symptoms of a decline in hepatic functioning (ie, yellowing of the skin, malaise, liver tenderness, anorexia, or nausea). The primary health care provider may order periodic liver function tests. Hepatotoxicity appears to be dose related and may appear at any time during therapy. 

When administering acetaminophen, the nurse assesses the overall health and alcohol usage of the patient before administration. fatients who are malnourished or abuse alcohol are at risk of developing hepatotoxicity (damage to the liver) with the use of acetaminophen. 

Tacrine is particularly damaging to the liver and can result in hepatotoxicity. Because tacrine is more likely to cause adverse reactions and drug interactions, it must be administered more frequently (4 times a day) and is rarely used in current therapy. Donepezil has fewer and milder side effects than tacrine It is considered the agent of first choice However, some patients may achieve a better response with one drug than another. Additional adverse reactions are listed in the Summary Drug Table Cholinesterase Inhibitors. 

Diarrhea, cramps, nausea, and vomiting are die more common adverse drug reactions. A reduction in die dose may reduce or eliminate these problems. Prolonged use of tiiese drugs may result in hepatotoxicity (toxic to die liver). 

The purpose of this study was to compare hepatotoxic effects of monobromo-benzene, 3 dibromobenzene isomers, hexabromobenzene and tetrabromobisphenol A with special attention paid to the dynamics of changes of selected indicators of liver necrosis during acute poisoning. 

At the doses used, there is blockage of the effects of as much as 25 mg of injected heroin. Toxicity in heroin addicts is low, but some reported subtle adverse effects of naltrexone such as decreased energy (Hollister et al. 1981). Nonaddicted obese subjects have been known to develop markedly elevated transaminase levels at doses of 300 mg/day (Mitchell et al. 1987). The inference has been drawn that high doses are potentially hepatotoxic (Pfohl et al. 1986), and the drug is contraindicated in liver failure or acute hepatitis. 

In vitro studies on isolated cells including hepatocytes, erythrocytes, fibroblasts, and alveolar cells continue to demonstrate the specificity of action that these toxins have for liver cells (83,86,93). This specificity has led Aune and Berg (94) to use isolated rat hepatocytes as a screen for detecting hepatotoxic waterblooms of cyanobacteria. 

Nelson, S.D. (1990). Molecular mechanisms of the hepatotox-icity caused by acetaminophen. Semin. Liver Dis. 10, 267-278. 

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