hepatotoxic

Hepatotoxicity refers to liver injury caused by chemicals, medications, alcohol, dietary supplements, and environmental toxins. The spectrum ranges from mild enzyme elevations to acute liver failure and death, and outcomes depend on the agent, dose, and individual susceptibility.

Two broad mechanistic categories are recognized. Intrinsic hepatotoxicity is dose-dependent and predictable, as in acetaminophen overdose, where a toxic metabolite damages hepatocytes. Idiosyncratic hepatotoxicity is unpredictable and may involve immune-mediated reactions or hypersensitivity, varying between individuals and often independent of dose.

Injury patterns are usually hepatocellular, cholestatic, or mixed, reflected in laboratory tests. Elevations of ALT and AST indicate hepatocellular injury, while raised alkaline phosphatase and bilirubin suggest cholestasis. Causality assessment tools and exclusion of other liver diseases aid diagnosis; liver biopsy is rarely required but may help in uncertain cases.

Common culprits include acetaminophen, certain antibiotics, anticonvulsants, isoniazid, methotrexate, amiodarone, valproic acid, and alcohol. Herbal supplements and environmental toxins can also cause hepatotoxicity. Presentation ranges from asymptomatic enzyme elevations to jaundice, fatigue, abdominal pain, coagulopathy, or hepatic encephalopathy in severe cases.

Management centers on stopping the offending agent and providing supportive care. Acetaminophen toxicity is treated with N-acetylcysteine if indicated. Severe cases may require intensive care and liver transplantation. Prognosis varies with cause, extent of injury, and promptness of intervention.

Prevention emphasizes careful drug dosing and monitoring, particularly in at-risk populations, thorough reporting of suspected drug-induced liver injury, patient education on avoiding alcohol with hepatotoxic medications, and regulatory oversight of supplements and environmental exposures.