AI Article Synopsis
- - Drug-induced hepatitis is rare and unpredictable, often related to the drug or its reactive metabolites that can damage liver cells through different mechanisms, including idiosyncratic and immunoallergic reactions.
- - Genetic variations in the body’s ability to detoxify drugs can affect individual susceptibility to liver damage, with deficiencies in certain enzymes like CYP 2D6 and CYP 2C19 linked to specific drug injuries.
- - Further genetic deficiencies, such as in glutathione synthetase and metabolic pathways, increase the risk of hepatotoxicity from a variety of medications, highlighting the complexity of drug interactions and individual genetics.
Article Abstract
Drug-induced hepatitis is uncommon and generally unpredictable. Hepatotoxicity may be related to the drug itself, or to chemically reactive metabolites which can bind covalently to hepatic macromolecules and may lead to either idiosyncratic, toxic hepatitis or to immunoallergic hepatitis. There is now evidence indicating that genetic variations in systems of biotransformation or detoxication may modulate either the toxic or sensitizing effects of some drugs. Thus, the genetic deficiency in a particular hepatic cytochrome P 450 isozyme (CYP 2D6) is involved in per-hexiline liver injury. The deficiency in CYP 2C19 might also contribute to Atrium hepatotoxicity. Slow acetylation related to N-acetyltransferase 2 deficiency contributes to sulfonamide hepatitis. The genetic deficiency in glutathione synthetase may increase the susceptibility to several drugs including acetaminophen. A constitutional deficiency in another cell defense mechanism, still not characterized, seems to increase significantly the risk of hepatotoxicity with halothane, phenytoin, carbamazepine, phenobarbital, sulfamides and amineptine.
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| http://dx.doi.org/10.1016/s0168-8278(97)80492-8 | DOI Listing |
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