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Non-steroidal anti-inflammatory drugs in athletes

G Lippi, M Franchini, G C Guidi

Department of Morphological-Biomedical Science, Institute of Chemical and Clinical Microscopy, University of Verona, Verona, Italy

Correspondence to:
Correspondence to:
Professor Lippi
Istituto di Chimica e Microscopia Clinica, Dipartimento di Scienze Morfologico-Biomediche, Università degli Studi di Verona, Ospedale Policlinico G B Rossi, Piazzale Scuro, 10, 37134 Verona, Italy; ulippi@tin.it

Keywords: aspirin; bleeding; injury; non-steroidal anti-inflammatory drugs

The first 150 words of the full text of this article appear below.

Aspirin and the non-steroidal anti-inflammatory drugs (NSAIDs) have been commercially available for decades, and their ability to reduce pain and inflammation is well established. It was first shown nearly 30 years ago that aspirin strongly inhibits platelet function by acetylation of platelet cyclo-oxygenase (COX) at the functionally important amino acid serine 529. This prevents access of the substrate (arachidonic aid) to the catalytic site of the enzyme at tyrosine 385 and results in irreversible inhibition of platelet dependent formation of thromboxane, a powerful promoter of aggregation, for the lifetime of the platelet (7–10 days). Aspirin is about 150–200-fold more potent as an inhibitor of the constitutive isoform of the platelet enzyme (COX-1) than the inducible isoform (COX-2), which is expressed by cytokines, inflammatory stimuli, and some growth factors.¹ This explains the different dose requirements of aspirin as an antithrombotic (COX-1) and an anti-inflammatory drug (COX-2).² Non-aspirin NSAIDs inhibit the activity . . . [Full text of this article]

W F Kean

Correspondence to:
Correspondence to:
W F Kean

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