Hepatic damage

The higher molecular weight organotin(IV)s, such as TBT and TFT, are known to be immunotoxic and to cause renal and hepatic damage. TBT at environmentally relevant concentrations increases intracellular concentration of Ca(II) ([Ca(II)],) in murine thymocytes by increasing membrane Ca(II) permeability and... 

When bifimbin in the blood exceeds 1 mg/dL (17.1 lmol/L), hyperbifimbinemia exists. Hyperbilirubinemia may be due to the production of more bilirubin than the normal fiver can excrete, or it may result from the failure of a damaged fiver to excrete bilirubin produced in normal amounts. In the absence of hepatic damage, obstmction of the excretory ducts of the fiver—by preventing the excretion of bilirubin—will also cause hyperbilirubinemia. In all these situations, bifimbin accumulates in the blood, and when it reaches a certain concentration (approximately 2-2.5 mg/dL),... 

Hepatitis E is a non-enveloped single-stranded messenger RNA virus of unclassified genus.18 The HEV is similar to HAV in that the virus is harvested in contaminated feces, thus infecting people via the fecal-oral route. High HEV levels in the bile often prompt viral shedding in the feces. The severity of hepatic damage is dependent on the HEV strain Mex 14, Sar 55, or the US 2 strain.19 No cases of chronic hepatitis E have yet been documented. 

The risk of infection may be decreased by 90% if IGIM is given within 2 weeks of being exposed to the hepatitis A virus. IGIM may still be beneficial if it is given more than 2 weeks after exposure to a known case of HAV, as it may decrease the severity of hepatic damage.1,5... 

Transaminases Hepatocellular enzymes that are released into the bloodstream after hepatic damage. 

Is the patient using herbal remedies or tisanes that are associated with hepatic damage ... 

Although hexachloroethane-induced hepatic damage can cause increases in serum levels of liver enzymes, these enzyme changes are not specific to hexachloroethane exposure (Fowler 1969b Weeks et al. 1979). In male rats, exposure to hexachloroethane is associated with the presence of granular and cellular casts in the urine (NTP et al. 1989). These effects are related to the formation of hyaline droplets in the male rat kidney. 

Hepatic Effects. Both patients described by Letz et al. (1984) (see Section 2.2.3.1) had elevated serum aspartate aminotransferase and lactic dehydrogenase, indicating severe hepatic damage. 

Conditicms that increase direct bilirubin Hepatic damage Bile duct obstruction... 

Adverse effects. Fatigue, orthostatic hypotension, extrapyramidal Parkin-son-like symptoms (p. 88), cutaneous reactions, hepatic damage, immune-hemolytic anemia... 

Chronic use of neuroleptics can, on occasion, give rise to hepatic damage associated with cholestasis. A very rare, but dramatic, adverse effect is the malignant neuroleptic syndrome (skeletal muscle rigidity, hyperthermia, stupor) that can end fatally in the absence of intensive countermeasures (including treatment with dantrolene, p. 182). 

Rifampin. Source, antibacterial activity, and routes of administration are described on p. 274. Albeit mostly well tolerated, this drug may cause several adverse effects including hepatic damage, hypersensitivity with flu-like symptoms, disconcerting but harmless red/orange discoloration of body fluids, and enzyme induction (failure of oral Liillmann, Color Atlas of Pharmacology... 

Carbon tetrachloride was fetotoxic to rats when administered on days 6-15 of gestation at 300 or 1000 ppm, 7 hours/day an increase in skeletal anomalies due to delayed development was observed in the offspring. Signs of maternal toxicity included weight loss and hepatic damage. ... 

Over a 9-year period (1967-76), 11 cases of jaundice were reported from a company that mixed preground MDA with silicon dioxide. In one instance, transient signs of myocardial damage in addition to transient signs of hepatic damage were observed after MDA exposure from a defective filter system. ... 

Intraperitoneal injection has been associated with hepatic damage in rats, causing a decrease in the activities of mixed function oxidases and in cytochrome P-450 content." ... 

Severe reactions Severe reactions including deaths caused by sulfonamides have been associated with hypersensitivity reactions, agranulocytosis, aplastic anemia, other blood dyscrasias, and renal and hepatic damage. Irreversible neuromuscular and CNS changes and fibrosing alveolitis may occur. 

Severe hepatic damage hypersensitivity acute gout. 

Severe hypersensitivity to ethionamide severe hepatic damage. 

Exposure of rats to carbon tetrachloride (up to 160 mg/kg/day for 10 days) by gavage did not alter the primary antibody response to sheep red blood cells, lymphoproliferative responses to mitogen or mixed leukocytes, natural killer cell activity, or cytotoxic T lymphocyte responses also, spleen and thymus weights were comparable to controls (Smialowicz et al. 1991). In rats exposed twice weekly for 4-12 weeks to 3,688 mg/kg/day, there was histologic evidence of hemorrhage, hemosiderin deposition, and lymphocyte depletion in the pancreaticoduodenal lymph node (Doi et al. 1991), an effect which may be secondary to induced hepatic damage. 

Haloalkanes. Certain haloalkanes and haloalkane-containing mixtures have been demonstrated to potentiate carbon tetrachloride hepatotoxicity. Pretreatment of rats with trichloroethylene (TCE) enhanced carbon tetrachloride-induced hepatotoxicity, and a mixture of nontoxic doses of TCE and carbon tetrachloride elicited moderate to severe liver injury (Pessayre et al. 1982). The researchers believed that the interaction was mediated by TCE itself rather than its metabolites. TCE can also potentiate hepatic damage produced by low (10 ppm) concentrations of carbon tetrachloride in ethanol pretreated rats (Ikatsu and Nakajima 1992). Acetone was a more potent potentiator of carbon tetrachloride hepatotoxicity than was TCE, and acetone pretreatment also enhanced the hepatotoxic response of rats to a TCE-carbon tetrachloride mixture (Charbonneau et al. 1986). The potentiating action of acetone may involve not only increased metabolic activation of TCE and/or carbon tetrachloride, but also possible alteration of the integrity of organelle membranes. Carbon tetrachloride-induced liver necrosis and lipid peroxidation in the rat has been reported to be potentiated by 1,2- dichloroethane in an interaction that does not involve depletion of reduced liver glutathione, and that is prevented by vitamin E (Aragno et al. 1992). 

Baumann M, Berauer M. 1985. Comparative study on the sensitivity of several serum enzymes in detecting hepatic damage in rats. Arch Toxicol 8 (Supplement) 370-372. 

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