Carbon tetrachloride hepatotoxicity
Last reviewed: 23.04.2024
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Carbon tetrachloride can enter the body by accident or as a result of admission with a suicidal purpose. In this case, it can be gaseous (for example, during dry cleaning or when filling a fire extinguisher) or mixed with drinks.
Damage to the liver is due to a toxic metabolite that acts on cytochrome P450-dependent monooxidase located in the smooth endoplasmic reticulum of perivennular hepatocytes. Its action is enhanced by enzyme inducers, for example, alcohol and barbiturates, and is weakened by protein starvation, leading to a decrease in the activity of enzymes metabolizing drugs.
[Morphological changes
In the hepatocytes of zone 3, hydropic dystrophy is revealed in the form of a transparent cytoplasm and a pycnotic nucleus. Fatty degeneration can be expressed in varying degrees - from single fat drops to diffuse involvement of hepatocytes. There is a slight infiltration of portal zones with polymorphonuclear leukocytes. Fibrosis is not characteristic. As they recover, the morphological picture in the liver returns to normal.
Symptoms
Poisoning is characterized by vomiting, abdominal pain and diarrhea. During the 2nd day jaundice joins. There may be an increase and pain in the liver. Due to severe hypoprothrombinemia, spontaneous bleeding is possible. The activity of serum transaminases is significantly increased; the level of serum albumin is reduced.
In severe cases, acute renal failure is at the forefront. Expressed acute hemorrhagic gastritis. Due to the fact that carbon tetrachloride is an anesthetic, there is increasing drowsiness.
Substances similar in structure to carbon tetrachloride
Adolescents who smell glue containing toluene, or a pair of household fluids containing trichlorethylene, may develop jaundice with liver necrosis and kidney failure.
The picture, similar to poisoning with carbon tetrachloride, develops with the production poisoning with the solvent 1,1,1-trichloroethane.
Benzene derivatives - trinitrotoluene, dinitrophenol and toluene - mainly affect the bone marrow, causing its aplasia. There may be acute liver damage, but chronic changes are rare.
Contact with industrial organic solvents can lead to an increase in the level of transaminases. A short contact (less than 3 months) with a dimethylformamide solvent leads to digestive disorders, a significant increase in the level of transaminases, focal hepatic cell necrosis and small-droplet obesity. With more prolonged contact (more than 1 year), clinical manifestations are minimal, and the level of transaminases is increased moderately. With liver biopsy, small-droplet obesity and proliferation of a smooth endoplasmic reticulum are revealed.
Electron microscopy of biopsy specimens shows SHIK-positive inclusions and pathological changes in mitochondria.
The production contact with 2-nitropropane can lead to death.
Perhaps not all cases of industrial liver damage can be identified. The prognostic value of prolonged industrial contact with toxic substances is not known.
Treatment
In the preventive examination of workers in contact with carbon tetrachloride, attention should be paid to the size and tenderness of the liver, the level of urobilinogen in the urine, and the activity of serum transaminases and GGTP.
In acute poisoning, a high-calorie, carbohydrate rich food is prescribed; with signs of acute liver-kidney failure, appropriate treatment, including hemodialysis. The early administration of acetylcysteine can minimize damage to the liver and kidneys.
Forecast
In the acute stage, the cause of death is renal failure. If the victim does not die in the acute stage, later complications from the liver do not develop. In experiments on rats it was shown that repeated intoxications lead to cirrhosis. In humans such effects are not observed; with prolonged contact, hepatocytes can even become more resistant to this intoxication. Carbon tetrachloride is not an etiological factor of liver cirrhosis in humans.