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Rheumatology Advance Access originally published online on July 8, 2008
Rheumatology 2008 47(9):1265-1266; doi:10.1093/rheumatology/ken229
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© The Author 2008. 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

Safer NSAID strategies: consensus or contentious?

C. J. Hawkey

Wolfson Digestive Diseases Centre, University of Nottingham, Nottingham, UK

Correspondence to: C. J. Hawkey, Wolfson Digestive Diseases Centre, University Hospital, Nottingham, NG7 2UH, UK. E-mail: cj.hawkey@nottingham.ac.uk

The first 10% of the full text of this article appears below.

Helicobacter pylori and NSAIDs, including increasingly aspirin, account for the vast majority of ulcers and ulcer complications of which bleeding is the most common. Whilst a simplistic view would predict that risks would be higher if both causes were present, pharmacological considerations might suggest otherwise. The principal mechanism of NSAID damage involves inhibition of the synthesis of prostaglandins that underlie protective mechanisms—mucosal blood flow, mucus and bicarbonate secretion—that adapt the stomach and duodenum to resist the harmful effects of gastric contents.

Helicobacter pylori acts differently. In the gastric mucosa and at sites of duodenal gastric metaplasia and the duodenum, it subverts host signalling mechanisms and induces a persistent ‘acute’ neutrophilic inflammatory . . . [Full Text of this Article]


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