Hepatic Toxicity

Hydrocarbon-induced hepatic damage resulting from halogenated hydrocarbons is well described. 15 Carbon tetrachloride toxicity has been used as a model for toxin-induced hepatic dysfunction. As little as 3 mL of carbon tetrachloride has been associated with the development of fatal liver injury. 16 Other halogenated hydrocarbons, such as chloroform, are also associated with liver dysfunction. Free-radical metabolites of these agents that cause lipid peroxidation are apparently responsible for hepatocellular destruction.

Pathologic examination reveals acute fatty degeneration of the liver with areas of centrilobular necrosis. Phenobarbital, ethanol, and other agents that induce cytochrome P-450 enzymes are contraindicated because of the propensity to increase the production of the toxic metabolites. The time-course of hepatic dysfunction with acute exposures appears similar to acetaminophen hepatotoxicity. Liver function tests may be elevated within 24 h after ingestion, with the development of liver tenderness and jaundice in 48 to 96 h. Chronic exposure to carbon tetrachloride may be associated with the development of cirrhosis and hepatomas.

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