Abstract

Non-aspirin nonsteroidal anti-inflammatory drugs (NSAIDs) are frequently used to treat pain, fever, and inflammation. Historically, NSAIDs have been categorized as traditional NSAIDs and newer cyclooxygenase (COX)-2 inhibitors (coxibs). However, traditional NSAIDs also inhibit the COX-1 and COX-2 enzyme isoforms to a varying degree. This diversity of COX-1 and COX-2 selectivity within the class of traditional NSAIDs has proven clinically important, with evidence accumulating on the cardiovascular risks associated with selective COX-2 inhibition. Thus, the relative COX-2 selectivity of traditional NSAIDs correlates with their cardiovascular risk profile, being more favourable for non-selective NSAIDs, such as naproxen and low-dose ibuprofen, and less favourable for more COX-2 selective agents, such as diclofenac. To enhance clinically relevant terminology, we advocate categorizing all non-aspirin NSAIDs—including traditional NSAIDs—according to their relative COX-1 and COX-2 selectivity as either COX-1 inhibitors, non-selective NSAIDs, or COX-2 inhibitors. We further recommend subcategorizing COX-2 inhibitors as newer COX-2 inhibitors (coxibs) or older COX-2 inhibitors. Finally, we recommend examining the effects of the individual NSAIDs included in each of the proposed categories. Adhering to these recommendations will align future studies, advance interpretation of COX-specific adverse cardiovascular effects, and provide better guidance to clinicians prescribing NSAIDs.

Highlights

  • RESUME Les anti-inflammatoires non steroïdiens (AINS) differents de l’aspirine sont frequemment utilises pour traiter la douleur, la fievre et l’inflammation

  • The 2 major COX enzyme isoforms are COX-1, which is continuously expressed in most tissues, and COX-2, which is upregulated in response to inflammatory processes.[6]

  • The analgesic and antipyretic effects of Nonsteroidal anti-inflammatory drugs (NSAIDs) derive mainly from inhibition of COX-2 and the resulting decrease in proinflammatory prostaglandins E2 and I2,2 whereas the gastrointestinal complications[7] derive mainly from inhibition of COX-1 and the resulting inhibition of gastrointestinal protective prostaglandins E2 and I2.2 The increased risk of gastrointestinal complications associated with COX-1 inhibition promoted the development of newer COX-2 inhibitors in the late 1990s

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Summary

Introduction

RESUME Les anti-inflammatoires non steroïdiens (AINS) differents de l’aspirine sont frequemment utilises pour traiter la douleur, la fievre et l’inflammation. Correlates with their cardiovascular risk profile, being more favourable for non-selective NSAIDs, such as naproxen and low-dose ibuprofen, and less favourable for more COX-2 selective agents, such as diclofenac.

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