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New and Improved?

David R. Lichtenstein, MD; M. Michael Wolfe, MD

JAMA. 2000;284:1297-1299.

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

Gastrointestinal (GI) toxicity induced by nonsteroidal anti-inflammatory drugs (NSAIDs) is among the most common serious adverse drug events in the industrialized world. Gastroduodenal ulcers can be demonstrated by endoscopy in 10% to 20% of patients who take NSAIDs on a regular basis, and the annual incidence of clinically important GI complications approaches 2%.¹ The impact of NSAIDs on public health is significant and has provided the impetus to search for safer but equally effective anti-inflammatory agents.

Damage to the gastroduodenal mucosa associated with use of NSAIDs occurs as a result of both the topical and systemic properties attributed to these agents.¹ The latter appears to play the predominant role, largely through decreased synthesis of mucosal prostaglandins. These compounds are ubiquitous 20-carbon molecules that are derived from the catalytic conversion of arachidonic acid via the cyclooxygenase (COX) pathway. More than a decade has . . . [Full Text of this Article]

Author Affiliations: Section of Gastroenterology, Boston University School of Medicine, and Boston Medical Center, Boston, Mass.

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