Prostaglandins in peptic ulcer disease: effect of nonsteroidal anti-inflammatory compounds (NOSAC).
This study shows that human fundic mucosa generates various PGs, particularly PGE2, and thromboxanes and this generation appears to be significantly lower in gastric ulcer than in duodenal ulcer patients or normal subjects. Non-steroidal antiinflammatory compounds (NOSAC), such as aspirin and indomethacin, greatly reduce the PG biosynthesis and cause mucosal damage including mucosal erosions and haemorrhages observed at endoscopy, increased gastric microbleeding and DNA loss. In contrast, carprofen, a novel NOSAC with good antiinflammatory properties and gastric tolerance, failed to affect mucosal generation of PGs and did not influence gastric mucosal integrity. This study indicates that the deficiency of endogenous PGs may play a role in the pathogenesis ulcer and that the degree of gastric mucosal damage by NOSAC is closely related to the alteration in the capability of the mucosa to generate PGs.
D000328:Adult; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D001241:Aspirin / Q000494:pharmacology; D002227:Carbazoles / Q000494:pharmacology; D004381:Duodenal Ulcer / Q000378:metabolism*; D005753:Gastric Mucosa / Q000187:drug effects / Q000378:metabolism*; D006801:Humans; D007213:Indomethacin / Q000494:pharmacology; D011448:Prostaglandin Antagonists / Q000494:pharmacology; D011453:Prostaglandins / Q000096:biosynthesis*; D011863:Radioimmunoassay; D013276:Stomach Ulcer / Q000378:metabolism*; D013931:Thromboxanes / Q000096:biosynthesis
D000893:Anti-Inflammatory Agents; D002227:Carbazoles; D011448:Prostaglandin Antagonists; D011453:Prostaglandins; D013931:Thromboxanes; C007005:carprofen; D001241:Aspirin; D007213:Indomethacin