July 2002 · Vol. 14, No. 7NSAIDs: Is newer better for dysmenorrhea?
In recent years, the range of nonsteroidal anti-inflammatory drugs has broadened considerably. But when it comes to menstrual pain, the most reliable agents are not necessarily the newest.
ROGER
P.
SMITH,
MD
Jeffrey
ELLIS,
MDDr. Smith is professor of OBG at the University of Missouri–Kansas City Truman Medical Center in Kansas City, Mo. Dr. Ellis is in private practice in Plymouth, Ind.
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Key points
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Nonsteroidal anti-inflammatory drugs (NSAIDs) can prevent dysmenorrhea, unlike other agents that simply relieve symptoms.
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Although NSAIDs in one form or another have been used for centuries, agents introduced in the past 50 years have significantly improved efficacy and safety profiles.
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A greater understanding of the role of prostaglandins in physiologic and pathophysiologic processes can enhance the selection of appropriate therapeutic agents.
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Some drugs can selectively block the cyclooxygenase-2 (COX-2) isoform of the enzyme instrumental in the production of prostaglandins.
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A major shift in the way menstrual pain is viewed and treated took place in the 1970s and ’80s, with a greater understanding of the role of prostaglandins and more effective nonsteroidal anti-inflammatory drugs (NSAIDs). Subjective studies of pain and objective studies of uterine activity established a firm connection between the two. These studies also amply demonstrated the ability of NSAIDs to alter the physiology of dysmenorrhea, making it possible to prevent—rather than simply relieve—pain.
Yet, these agents still are not universally used in the treatment of dysmenorrhea, despite more than 20 years of experience with them. Moreover, the introduction of new NSAIDs has clouded rather than clarified the issue of their relative efficacy. Drugs that are welldesigned for the suppression of chronic inflammation (e.g., arthritis therapies) are not very effective for dysmenorrhea, and vice versa. Even so, it is possible to apply the findings of published studies and an understanding of the pathophysiology of dysmenorrhea to demystify the range of options.
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