Generation of prostaglandins in gastric mucosa of patients with peptic ulcer disease: effect of nonsteroidal antiinflammatory compounds.
Human fundic mucosa generates various prostaglandins (PGs), particularly PGE2, and tromboxanes. This generation appears to be significantly lower in gastric ulcer patients than in duodenal ulcer patients or normal subjects. Nonsteroidal antiinflammatory compounds (NOSAC), such as aspirin or indomethacin, greatly reduce the PG biosynthesis and cause mucosal damage, including mucosal erosions and hemorrhages observed at endoscopy, increased gastric microbleeding and DNA loss. In contrast, paracetamol or carprofen, a novel NOSAC, fails to affect mucosal generation of PGs and does not influence gastric mucosal integrity. This study indicates that endogenous PGs may be involved in the pathogenesis of gastric ulcer and that normal generation of mucosal PGs is essential for the mucosal integrity.
D000328:Adult; D000893:Anti-Inflammatory Agents / Q000009:adverse effects / Q000494:pharmacology*; D015232:Dinoprostone; D005744:Gastric Acid / Q000378:metabolism; D005753:Gastric Mucosa / Q000187:drug effects / Q000378:metabolism*; D006801:Humans; D010437:Peptic Ulcer / Q000139:chemically induced / Q000378:metabolism*; D011458:Prostaglandins E / Q000096:biosynthesis* / Q000378:metabolism
D000893:Anti-Inflammatory Agents; D011458:Prostaglandins E; D015232:Dinoprostone