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. 2012 Jul;36(1):48-56.
doi: 10.1111/j.1365-2036.2012.05118.x. Epub 2012 May 3.

The relative contribution of NSAIDs and Helicobacter pylori to the aetiology of endoscopically-diagnosed peptic ulcer disease: observations from a tertiary referral hospital in the UK between 2005 and 2010

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The relative contribution of NSAIDs and Helicobacter pylori to the aetiology of endoscopically-diagnosed peptic ulcer disease: observations from a tertiary referral hospital in the UK between 2005 and 2010

C Musumba et al. Aliment Pharmacol Ther. 2012 Jul.

Abstract

Background: Recent data from Western countries indicate that the aetiology of peptic ulcer disease (PUD) is changing as the prevalence of Helicobacter pylori is decreasing while the use of low-dose aspirin (LDA, ≤325 mg/day) is increasing.

Aim: To investigate the changing aetiology and demographics of PUD in a well-characterised patient cohort at a large tertiary hospital in the UK between July 2005 and June 2010.

Methods: Patients diagnosed with PUD following endoscopy were categorised as non-steroidal anti-inflammatory drug (NSAID)-users or non-users, and their H. pylori status determined. Comparisons between NSAID-users and non-users, and between non-aspirin NSAID-users and LDA-users were summarised using counts and corresponding percentages (for categorical variables) and means and standard deviations (for continuous variables).

Results: Overall, 386 patients were enrolled; 57% used NSAIDs (51% LDA only) and 43% were non-users. 57% of the whole cohort was H. pylori-positive (including 66% with duodenal ulcers and 47% with gastric ulcers). Compared with non-users, NSAID-users were older (mean age 68 vs. 61 years) and fewer were H. pylori-positive (52% vs. 63%). LDA-users were older (mean age 71 vs. 62 years) and more likely to be H. pylori-positive (61% vs. 41%) than those using non-aspirin NSAIDs. Twelve per cent of the patients were neither using NSAIDs nor were H. pylori-positive.

Conclusions: The NSAIDs, particularly LDA, were most commonly associated with PUD in this cohort. Our findings are compatible with the decline in the prevalence of H. pylori-positive PUD and increase in non-NSAID, non-H. pylori PUD previously reported.

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