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Acetaminophen Hepatotoxicity and Acute Liver Failure
Abstract
Acetaminophen-induced hepatotoxicity is a common consequence of acetaminophen overdose and may lead to acute liver failure (ALF). Currently acetaminophen is the most common cause of ALF in both United States and United Kingdom, with a trend to increasing incidence in the United States. N-acetylcysteine is the most effective drug to prevent progression to liver failure with acetaminophen hepatotoxicity. Liver transplantation is the only definitive therapy that will significantly increase the chances of survival for advanced ALF. This communication reviews current information regarding causes and management of acetaminophen-induced hepatotoxicity and ALF.
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Paracetamol is a major cause of drug-induced acute liver failure and has been extensively studied for its liver damage.
“Paracetamol is considered as one of the major causes for drug-induced ALF, and has been extensively studied for its liver damage. 3,4”
From Caralluma umbellata Haw. protects liver against paracetamol toxicity and inhibits CYP2E1 (2017) · cites this paper as [3]
Paracetamol is metabolized to the reactive toxic metabolite NAPQI, with generation of reactive oxygen species that augment oxidative stress.
“The mechanism behind paracetamol toxicity is mainly due to the reduction of hepatocyte GSH and increased CYP2E1 activity where paracetamol is metabolized to an extremely reactive toxic metabolite N-acetyl-p-benzoquinone imine (NAPQI) along with generation of reactive oxygen species in augmenting oxidative stress. 3,5,6”
From Caralluma umbellata Haw. protects liver against paracetamol toxicity and inhibits CYP2E1 (2017) · cites this paper as [3]
Paracetamol toxicity is mainly due to reduction of hepatocyte GSH and increased CYP2E1 activity.
“The mechanism behind paracetamol toxicity is mainly due to the reduction of hepatocyte GSH and increased CYP2E1 activity where paracetamol is metabolized to an extremely reactive toxic metabolite N-acetyl-p-benzoquinone imine (NAPQI) along with generation of reactive oxygen species in augmenting oxidative stress. 3,5,6”
From Caralluma umbellata Haw. protects liver against paracetamol toxicity and inhibits CYP2E1 (2017) · cites this paper as [3]
Citations
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Metadata
- Authors
- Chun, L. J., Tong, M. J., Busuttil, R. W., & Hiatt, J. R.
- Affiliations
- Albert Einstein College of Medicine (US)
- University of California, Los Angeles (US)
- Plastic Surgery Hospital (CN)
- Corresponding author
- Chun, Linda J.
- Venue
- Journal of Clinical Gastroenterology
- Published
- 2009-04
- Volume
- 43
- Issue
- 4
- Pages
- 342-349
- ISSN
- 0192-0790 (ISSN-L)
- OpenAlex
- W2067570070
- Cited by
- 348
- References
- 2
- Citations by year
- 2026: 9 · 2025: 12 · 2024: 31 · 2023: 14 · 2022: 12 · 2021: 18 · 2020: 17 · 2019: 16 · 2018: 11 · 2017: 23 · 2016: 26 · 2015: 21 · 2014: 25 · 2013: 27 · 2012: 31
- FWCI
- 3.45
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Clinical Gastroenterology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Drug-Induced Hepatotoxicity and Protection
- Health Sciences › Medicine › Emergency Medicine › Poisoning and overdose treatments
- Health Sciences › Medicine › Hepatology › Liver Disease and Transplantation
- Keywords
- paracetamol, hepatotoxicity, acute liver failure, acetaminophen overdose, N-acetylcysteine, liver transplantation, drug-induced liver injury, incidence trends
- MeSH terms
- Acetaminophen, Acetylcysteine, Adult, Female, United Kingdom, Humans, Male, United States, Liver Transplantation, Liver Failure, Acute, Drug Overdose, Drug-Related Side Effects and Adverse Reactions
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