Abstract
Paracetamol (acetaminophen) is a worldwide used analgesic and antipyretic drug. It is metabolised via several metabolic pathways, including glucuronidation, sulfation, oxidation, hydroxylation, and deacetylation: Hepatic and other organ damage may occur, especially in overdose, because of the accumulation of a toxic metabolite. Intersubject and ethnic differences have been reported in paracetamol metabolism activation, suggesting possible differences in susceptibility to toxicity and in pain alleviation, linked to different pharmacogenetic profiles. This article aims at reviewing, in the literature, the links between paracetamol metabolism and enzyme genotypes in the context of toxic side effects and efficacy of paracetamol in therapeutics.
MeSH terms
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Acetaminophen / chemistry
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Acetaminophen / metabolism*
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Acetaminophen / toxicity
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Amidohydrolases / genetics
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Amidohydrolases / metabolism
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Antipyretics / chemistry
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Antipyretics / metabolism*
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Antipyretics / toxicity
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Cytochrome P-450 Enzyme System / genetics
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Cytochrome P-450 Enzyme System / metabolism
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Genetic Variation*
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Glucuronosyltransferase / genetics
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Glucuronosyltransferase / metabolism
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Glutathione Transferase / genetics
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Glutathione Transferase / metabolism
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Humans
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Liver / drug effects
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Liver / enzymology
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Molecular Structure
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Sulfotransferases / genetics
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Sulfotransferases / metabolism
Substances
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Antipyretics
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Acetaminophen
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Cytochrome P-450 Enzyme System
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Glucuronosyltransferase
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Glutathione Transferase
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Sulfotransferases
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Amidohydrolases
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fatty-acid amide hydrolase