21.   Animal studies have shown a correlation between the bastric mucosal injury induced by ethanol or acid and increased synthesis of leukotrienes.

22.   Previous studies in humans have shown that synthesis of leukotrienes correlates with gastroduodenal mucosal injury.

23.   If NSAIDs directly enhance leukotriene synthesis this may also contribute to mucosal injury.

24.   Inhibition of prostaglandin synthesis by NSAIDs is the major established mechanism by which NSAIDs render the gastric mucosa vulnerable to mucosal injury.

25.   Endoscopically ingestion of NSAIDs is associated with a high prevalence of superficial mucosal injury.

26.   In theory the increased prostaglandin synthesis seen with Helicobacter pylori might explain such a reduction in minor mucosal injury.

27.   In our study, however, although there was a trend to higher prostaglandin concentrations in Helicobacter pylori positive patients with lower levels of mucosal injury this was weak.