Hepatic toxicity of nonsteroidal anti-inflammatory drugs.

  • 1 March 1984
    • journal article
    • review article
    • Vol. 3  (2) , 128-38
Abstract
The hepatic toxicity associated with the use of nonsteroidal anti-inflammatory drugs (NSAIDs) is reviewed. NSAIDs include agents in more than 10 classes of compounds, many of which are capable of producing hepatic injury. When NSAIDs are used to treat rheumatic disease, the hepatic effects of the disease itself may complicate the diagnosis of NSAID-induced hepatic injury. Hepatotoxicity caused by drugs may be either intrinsic or idiosyncratic in nature and may be manifested by hepatocellular injury, cholestasis, or a combination of both types of injury. Intrinsic hepatotoxins, such as salicylates, produce injury in a large percentage of exposed individuals that is often dose related and occurs after a short, fixed latent period. Idiosyncratic injury, such as that caused by sulindac, occurs in unusually susceptible persons, usually after a variable latent period. Injury is not dose related. In most cases of hepatocellular injury, the prognosis of those patients who survive the acute phase of injury is good. Fatalities rarely result from cholestatic injury. Monitoring of serum hepatic-enzyme concentrations is recommended for patients receiving NSAIDs from the indole, pyrazolone, and propionic acid classes since these agents have been associated with the greatest incidence of adverse hepatic reactions. Enzyme monitoring is advisable for high-risk individuals receiving NSAIDs from other classes. Enhance vigilance on the part of clinicians, patients, and pharmaceutical manufacturers is needed to reduce the incidence of hepatotoxicity associated with the use of NSAIDs.

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