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Editorial
November 24, 1999

COX-1–Sparing NSAIDs—Is the Enthusiasm Justified?

Author Affiliations

Author Affiliations: Medical Service, Department of Veterans Affairs Medical Center, and Department of Internal Medicine, University of Texas Southwestern Medical Center at Dallas, Dallas.

JAMA. 1999;282(20):1961-1963. doi:10.1001/jama.282.20.1961

Nonsteroidal anti-inflammatory drugs (NSAIDs) are among the most widely used therapeutic agents today, with nearly $2 billion spent in the United States yearly on prescription NSAIDs alone.1 By inhibiting the enzyme cyclooxygenase (COX) and decreasing prostaglandin synthesis, these agents provide effective analgesia and suppress inflammation. Most NSAIDs (nonselective) inhibit not only prostaglandins at sites of inflammation but also prostaglandins that serve important functions in other parts of the body. This inhibition may be beneficial when, for example, these drugs are prescribed to impair normal platelet function to prevent cardiovascular events.

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