Paracetamol-Induced Toxicity: A Review of the Side Effects Associated with Excessive Consumption and Mishandling

Paracetamol (acetaminophen) is one of the most widely used analgesic and antipyretic medications globally, available over-the-counter in numerous formulations. Despite its perceived safety profile when used appropriately, paracetamol represents a significant cause of drug-induced liver injury and acute hepatic failure worldwide. This comprehensive review examines the mechanisms underlying paracetamol toxicity, explores the spectrum of adverse effects associated with excessive consumption and mishandling, and discusses current management strategies. The hepatotoxic potential of paracetamol is primarily mediated through the formation of the reactive metabolite N-acetyl-p-benzoquinone imine (NAPQI), which depletes glutathione stores and causes oxidative stress when the drug's normal metabolic pathways become saturated. Beyond hepatotoxicity, paracetamol overdose can result in nephrotoxicity, cardio toxicity, and metabolic acidosis. Risk factors for toxicity include chronic alcohol consumption, malnutrition, concurrent medication use, and genetic polymorphisms affecting drug metabolism. Early recognition and prompt treatment with N-acetylcysteine remain crucial for preventing irreversible organ damage. This review synthesizes current understanding of paracetamol toxicity mechanisms, clinical manifestations, risk factors, and therapeutic interventions to provide healthcare professionals with essential knowledge for managing this common yet potentially fatal poisoning.