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Walter L. Peterson, MD; Byron Cryer, MD

JAMA. 1999;282:1961-1963.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

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.

However, such inhibition may be harmful when normal gastrointestinal mucosal function is impaired and unwanted mucosal damage occurs. While such damage does not usually lead to symptoms, gastrointestinal ulceration may produce pain and, more ominously, lead to bleeding, perforation, or obstruction. A large prospective trial of more than 8000 patients with rheumatoid arthritis . . . [Full Text of this Article]

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

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