Prostaglandin metabolism in peptic ulcer disease.

Over the past decade, the physiological role of prostaglandins synthesized by the gastroduodenal mucosa has been the subject of intense research. Unfortunately, progress has been slow. Methodological problems in the identification and measurement of different prostanoids, as well as technical difficulties in performing definitive experiments, are largely to blame. Prostaglandins are not stored in tissue, can be rapidly synthesized and metabolized during tissue analysis, and appear to have multiple and sometimes conflicting biological actions on the mucosal tissues. Given these challenging problems at the biochemical and cellular levels, it is not surprising that relatively few studies have addressed potential defects in prostaglandin synthesis in patients with ulcer disease. Furthermore, the results obtained by these human studies are not always comparable because of the diverse methodological approaches chosen by different investigators. The evidence so far obtained suggests, though not conclusively, that mucosal prostaglandins play a role in the pathogenesis of ulcer disease. The most plausible hypothesis holds that defects in prostaglandin synthesis, metabolism or action on target tissues either weaken mucosal resistance to luminal acid-peptic activity or impair mucosal repair, leading to the development of chronic peptic ulcer.