Paracetamol Poisoning and Liver Transplantation: An Updated Review Publisher

Summary: How can severe paracetamol poisoning be assessed? A review highlights blood acidity, clotting and kidney markers as warning signs of liver failure, and care options. #Toxicology #LiverHealth

Tolou Ghamari Z
Source: Current Chemical Biology Published:2026

Abstract

Introduction: Regarding clinical recovery and survival of patients with severe paracetamol-induced acute liver failure and hepatic encephalopathy, liver transplantation is recommended as a good approach to management. This review summarizes the findings of previous studies associated with paracetamol-induced hepatotoxicity and liver transplantation. Methods: All relevant articles (n=113) were searched systematically between the relevant record initiation and 14 October 2025 (the date of our final search), across PubMed and Web of Science. The search terms included the main concepts and their synonyms, including the problem: “paracetamol-over-dose”, “paracetamol poisoning”, the intervention “assessment of hepatotoxicity”, and the outcome “liver transplantation”, combined with the AND, OR operators. Synonyms for this concept were extracted from thesauri such as Medical Subject Headings (MeSH). Results: An arterial pH lower than 7.3 or all three of the following: 1) International Normalized ratio of Prothrombin Time > 6.5, 2) Creatinine > 3.39 mg/dl, and a grade 3 or 4 hepatic encephalopathy should be considered as poor prognosis criteria in the patient. To avoid the need for liver transplantation associated with end-stage liver disease as the most available treatment nowadays, attention to the other new therapeutics approach such as: procalcitonin serum levels, vitamin K1, sustained c-Jun N-terminal kinase (JNK) activation, targeted metabolomics method based on the metabolic profiling of fatty acids, initial verification of keratin-18 and high-mobility group box-1 protein molecular, combination of adult stem cell transplantation with conservative medication recommended. Discussion: The creation of N-acetyl-p-benzoquinone imine by cytochrome P450 and the generation of reactive oxygen species by paracetamol overdose could cause severe hepatic failure. The escalation in cellular and mitochondrial glutathione disulfide levels after paracetamol overdose suggests the participation of oxidative stress in the pathophysiology. Conclusion: With the advancements in technology and immunotherapies, the cost of liver transplantation continues to increase. Therefore, consideration should be given to further restrictions on paracetamol due to its availability as an over-the-counter drug. 2026, Bentham Science Publishers