Liver injury induced by paracetamol and challenges associated with intentional and unintentional use

Figure 1 Paracetamol metabolism pathways and breakdown into N-acetyl-p-benzoquinone imine, by cytochrome P450 2E1. N-acetyl-p-benzoquinone imine is the toxic metabolite produced from paracetamol metabolism when the other two conjugation pathways become over-saturated. The resultant toxic N-acetyl-p-benzoquinone imine byproduct is converted into nontoxic metabolites by glutathione, which is regenerated by N-acetylcysteine. NAPQI: N-acetyl-p-benzoquinone imine; CYP2E1: Cytochrome P450 2E1; NAC: N-acetylcysteine.

Figure 2 Factors that pre-dispose patients to increased paracetamol toxicity.

Figure 3 Flowchart depicting the management pathway for acute paracetamol overdose/ toxicity. ALT: Aminotransferase; AST: Aspartate aminotransferase.