الفهرس | Only 14 pages are availabe for public view |
Abstract Aim of the work Is to explore the potential relation of C. Pylori colonization and the synthesis of PG by gastric mucosa in patients with peptic ulcer and non ulcer dyspepsia. Conclusion We suggest that the pathogenesis of duodenal ulcer in patients who are not ingesting NSAIDs dose not involve sustained mucosal PGE2 deficiency which calls for further studies about the therapeutics efficacy of PG analogues in the treatment of peptic ulcer. Moreover, C. Pylori colonization did not significantly influence mucosal PGE2 concentration, but its presence correlated significantly with the severity of gastritis. So, eradication of C. Pylori infection especially in patients with histological evidence of gastritis is necessary as heavy C. Pylori colonization and C. Pylori positive active chronic gastritis are predisposing factor in ulcerogenesis. Cigarette smoking could be considered as an important factor in promoting ulcerogenesis through its effect on the gastro duodenal mucosal PGE2 concentration. |