The nonsteroidal anti-inflammatory drugs (NSAIDs) have enjoyed a generally laudatory press, their acronym implying neither steroid nor narcotic mechanism of action. They encompass a heterogeneous group of compounds, mostly organic acids, that appear to owe their therapeutic efficacy to an inhibition of the biosynthesis of prostaglandins. They exhibit very real analgesic and antipyretic actions as well as being anti-inflammatory (acetaminophen and phenacetin are not NSAIDs, lacking anti-inflammatory action), are surely our major pharmacologic tools in the treatment of rheumatic and arthritic disorders, and as such enjoy an expanding global utilization and popularity. The NSAIDs do, however, share certain therapeutic side effects as well as benefits.1 Aspirin, the prototype NSAID (available since 1898), indomethacin (for over 35 years), phenylbutazone, and other older NSAIDs have a long track record of clinical efficacy and "relative" safety.
Hepatotoxicity, however, is an increasingly recognized laboratory abnormality and a rare clinical side effect of the