Prevention Of Nsaidinduced Peptic Ulcers

This is particularly relevant for the elderly and other high-risk patients (see above). The synthetic prostaglandin misoprostol in a dose of 800 micrograms daily in 2-4 divided doses reduces the incidence of gastric and duodenal ulceration and their complications by about 40% when coadministered with NSAIDs. Abdominal pain and diarrhoea limit its use; halving the dose reduces the incidence of adverse effects, but at the expense of a reduced protective effect. The proton pump inhibitors, in healing doses, are similar in efficacy to the higher dose of misoprostol. H2 receptor antagonists offer some protection against duodenal ulcers but none against gastric ulcers.

Evidence for the benefit of Helicobacter pylori eradication is controversial.

Selective inhibition of COX-2 has the objective of preserving anti-inflammatory activity whilst avoiding gastric mucosal toxicity. Rofecoxib, celecoxib and meloxicam vary in their selectivity for COX-2. The incidence of peptic ulcers and their complications with rofecoxib is similar to that seen when proton pump inhibitors are co-administered with nonselective NSAIDs. The adverse effect profile of these drugs remains fully to be evaluated.

Transient gastro-oesophageal reflux occurs in almost everybody and it is only when episodes become frequent, with prolonged exposure of the oesophageal mucosa to acid and pepsin, that problems develop. Factors contributing to pathological reflux include:

• Incompetence of the gastro-oesophageal sphincter

• Delayed oesophageal clearance of acid

• Delayed gastric emptying.

The commonest symptom is heartburn, and as many as 15% of people in Western populations experience this regularly. Approximately 50% will have oesophagitis, the severity of which does not correlate with symptoms. The other main complications are acute or chronic bleeding, oesophageal stricture and Barrett's metaplasia, which carries an increased risk of oesophageal carcinoma. There is no evidence that Helicobacter pylori is involved in pathogenesis of GORD.

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