Hepatotoxicity

Hepatotoxicity is liver injury caused by exposure to a drug, chemical, toxin, or other harmful agent. It ranges from temporary changes in liver tests to acute liver failure.

Drug-Induced Liver Injury: Liver damage caused by prescription medicines, over-the-counter drugs, or supplements. This is the clinical form of hepatotoxicity attributed to therapeutic agents.
Alanine Transaminase: An enzyme concentrated in liver cells and measured in blood as a marker of cell injury. Its blood level often rises when toxic exposure damages hepatocytes.
Intrinsic Drug-Induced Liver Injury: Drug-induced liver injury that is predictable and related to dose or exposure level. It contrasts with unpredictable reactions to otherwise therapeutic doses.
Cirrhosis: Advanced liver scarring that distorts liver structure and impairs function. Repeated or persistent toxic injury can contribute to progressive scarring.
Reactive Metabolite: A short-lived product of metabolism that can bind to cellular molecules and cause damage. Some toxic exposures injure liver cells only after metabolic activation.
Aspartate Transaminase: An enzyme found in liver and other tissues that can rise in blood after cellular injury. It is interpreted alongside other enzymes when assessing toxic liver injury.
Idiosyncratic Drug Reaction: An uncommon, unpredictable adverse reaction that occurs in susceptible individuals. This type of drug injury is not reliably predicted by dose alone.
Liver Transplantation: Surgical replacement of a diseased or failing liver with a donor organ. Transplantation may be necessary when toxic injury causes irreversible liver failure.
Oxidative Stress: Cellular damage that occurs when reactive oxidants overwhelm antioxidant defenses. Oxidant accumulation is one pathway by which chemicals disrupt liver cells.
Alkaline Phosphatase: An enzyme found in bile ducts and other tissues, measured in blood to assess cholestasis and related conditions. A prominent rise can signal a bile-duct-centered pattern of hepatotoxicity.

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