Non-steroidal anti-inflammatory drugs (NSAIDs) are the most used drugs for acute and chronic pain. More than 30 billion doses of NSAIDs are consumed annually from more than 70 million prescriptions.1
Explore this issueJuly 2018
Despite their common use, NSAIDs are not free of serious toxicities. In the pre-Vioxx (rofecoxib) era, gastrointestinal toxicity was the primary concern for many NSAIDs. In 1999, Wolfe et al. demonstrated the increasing rate of hospital admissions due to NSAID toxicity, thought mostly to be due to gastrointestinal (GI) side effects.2,3
This led to the development and use of selective cyclo-oxygenase-2 (COX‑2) inhibitors, the first of which was celecoxib, released in 1998, followed soon by rofecoxib in 1999 and several others.4,5 These agents had no effect on COX-1, an enzyme responsible for production of cytoprotective prostaglandin E2 and I2 in the stomach and, hence, had reduced risk of GI side effects.6
An exponential rise in the use of these drugs occurred.5 Simultaneously, strong evidence demonstrating that many of these agents confer a risk of myocardial infarction (MI) and other cardiovascular events developed.