Abstract

Non-steroidal anti-inflammatory drug (NSAID) ingestion is associated with erosions, petechiae, type C gastritis, ulceration, interference with ulcer healing, ulcer complications and injury to the small and large intestines. In the UK, NSAIDs can probably be linked to approximately 1200 deaths per year, mainly in the elderly. Inhibition of prostaglandin synthesis plays a major part in NSAID-induced gastric mucosal injury, whilst inhibition of thromboxane synthesis by platelets and impaired platelet aggregation may contribute to ulcer bleeding. There is evidence to show that the impairment of healing of gastric and duodenal ulcer that is associated with concomitant NSAID therapy can be overcome by the use of omeprazole. Acid inhibition has been shown to be effective in prophylaxis of NSAID-induced duodenal lesions. Studies on the prevention of NSAID-associated gastric lesions have indicated that ranitidine is less effective than misoprostol, but that treatment with the latter is associated with a number of side effects, principally in the gastrointestinal tract (e.g. diarrhoea). Whether omeprazole will prevent gastric and duodenal ulceration due to NSAID ingestion is the subject of ongoing research, but studies of acute ulceration have shown efficacy against erosions and microbleeding.

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