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Rheumatology Advance Access originally published online on October 31, 2006
Rheumatology 2006 45(12):1458-1460; doi:10.1093/rheumatology/kel353
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© The Author 2006. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

EDITORIALS

Non-steroidal anti-inflammatory drugs—changes in prescribing may be warranted

R. Madhok, O. Wu1, G. McKellar and G. Singh2

Centre for Rheumatic Diseases, Glasgow Royal Infirmary, Castle St, 1Division of Developmental Medicine, University of Glasgow, Glasgow, UK and 2Division of Gasterenterology and Hepatology, Department of Medicine, Stanford University School of Medicine, California, USA

Correspondence to: Rajan Madhok, Centre for Rheumatic Diseases, Glasgow Royal Infirmary, Castle St, Glasgow, UK. E-mail: gcl103@clinmed.gla.ac.uk

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Non-steroidal anti-inflammatory drugs (NSAIDs) are among one of the most frequently prescribed classes of drugs. Both their benefits and harms arise due to inhibition of cycloxygenase (COX) of which there are two isoenzymes, COX 1 and 2. Both COX isoenzymes have a hydrophobic tunnel, through which the substrate accesses the active site. The tunnel is larger in the COX 2 isoenzyme with a side pocket, a property exploited in the development of specific COX 2 inhibitors [1]. The premise of the initial, COX 2 hypothesis was that the gastrointestinal side effects arose due to inhibition of COX 1 whereas their anti-inflammatory or analgesic properties were COX 2 mediated. Although now appreciated to be rather naïve, the superiority of the selective COX 2 inhibitors in preventing . . . [Full Text of this Article]


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