PubMed · 5869874
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V K Nielsen, J Larsen. 1965-07-15. [Carbon tetrachloride].. https://pubmed.ncbi.nlm.nih.gov/5869874/
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Carbon tetrachloride induces diffuse fatty degeneration and centrilobular necrosis in the liver and the severity of liver injury is roughly proportional to the dosage administered. Nonetheless, the incidence of cirrhosis by this agent is rare. Several drugs, including methyldopa, methotrexate, isoniazid and vitamin A, have occasionally been reported to cause chronic active hepatitis, fibrosis and cirrhosis. There is no question that continued administration of the drug in the presence of clinically apparent hepatitis can lead to chronic active hepatitis, fibrosis and cirrhosis. Early recognition that a therapeutic drug is the probable cause of liver injury, followed by prompt withdrawal of such a drug, generally suffices in the management of drug-induced chronic liver disease.
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1. The acute toxicity of many volatile compounds is similar, being more related to physical properties than to chemical structure. 2. Volatile substance abusers experiences euphoria and disinhibition but this may be followed by nausea and vomiting, dizziness, coughing and increased salivation; cardiac arrhythmias, convulsions, coma and death occur in severe cases. 3. Laboratory analysis of blood and urine samples collected up to 24 h post-exposure may be helpful if the diagnosis of volatile substance abuse is in doubt. 4. There is only a weak correlation between blood toluene and 1,1,1-trichloroethane concentrations and the clinical features of toxicity, possibly because of rapid initial tissue distribution and elimination. 5. Recovery normally occurs quickly once exposure has ceased but support for respiratory, renal or hepatic failure may be needed as well as treatment for cardiac arrhythmias. Therapy with intravenous acetylcysteine should be considered in cases of acute carbon tetrachloride poisoning.