作者: Leung , To , Chan , Lee , Chung
DOI: 10.1046/J.1365-2036.2000.00783.X
关键词:
摘要: Background: Apoptosis is associated with loss of gastric mucosal integrity and may play an important role in ulcer development. Aim: To examine how Helicobacter pylori NSAIDs interact to effect apoptosis proliferation the mucosa. Methods: Patients presenting musculoskeletal pain requiring NSAID treatment without previous exposure or pre-existing ulcers were recruited. Patients divided into three groups: (A) H. pylori-infected; (B) pylori-eradicated; (C) non-infected patients. They given naproxen for 8 weeks. non-ulcer dyspepsia infection who anti-Helicobacter therapy recruited as controls (D). Endoscopy was performed at baseline 8-weeks after receiving naproxen. Gastric antral biopsies obtained assess by terminal uridine deoxynucleotidyl nick end-labelling (TUNEL) Ki67 immunostaining. Results: A total 55 patients studied. pylori-positive had a higher index than (P < 0.0001), eradication resulted significant reduction these parameters. The induced subjects (P=0.03) whilst reduced (P=0.02). After 8 weeks NSAID, post-treatment significantly persistent (P=0.01). Conclusions: Eradication prior reduces level mucosa, which contribute maintaining mucosa preventing development.