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幽门螺杆菌感染对胃黏膜病理变化的影响
引用本文:王吉耀,王瑞娟,徐永正,刘天舒,乐凡,董玲. 幽门螺杆菌感染对胃黏膜病理变化的影响[J]. 胃肠病学, 2003, 8(1): 25-28
作者姓名:王吉耀  王瑞娟  徐永正  刘天舒  乐凡  董玲
作者单位:1. 复旦大学附属中山医院消化内科,200032
2. 复旦大学附属金山医院消化内科
3. 上海市奉贤区人民医院内科
摘    要:背景:幽门螺杆菌(H.pylori)感染已被公认为慢性胃炎和消化性溃疡的重要危险因素,根除H.pylori能加速消化性溃疡的愈合,但其对胃黏膜病理变化的影响尚有待进一步探索。目的:了解根除H.pylori对慢性胃炎胃黏膜病理变化和癌前状态的影响。方法:采用多中心随机对照临床试验和回顾性队列研究,样本选自胃癌高发区:上海郊区的金山区和奉贤区。共纳入360例经内镜检查证实有H.pylori感染的慢性胃炎伴或不伴十二指肠溃疡患者,随机分为两组。治疗组用三联疗法(质子泵抑制剂或Hz受体阻滞剂加两种抗生素)治疗,对照组单纯慢性胃炎患者予西沙必利、十二指肠溃疡患者予西米替丁治疗。在第1年和第4年末随访胃镜,根据H.pylori是否根除将患者分为两组:H.pylori阳性组和H.pylori阴性组。所有胃黏膜活检标本由两位病理科医师统一复读。结果:至第4年末,有120例患者完成全部随访,其中H.pylori持续根除组54例,阳转组5例;H.pylori持续未根除组45例,阴转组16例。持续根除组第1年随访时,活动性炎症比例减少(P<O.05);第4年随访时,慢性炎症和肠化程度以及活动性炎症比例减少(P<O.05)。持续未根除组第1年随访时,慢性炎症程度增加(P<O.05);第4年随访时,慢性炎症和肠化程度以及活动性炎症比例增加(P<O.05),萎缩程度较第1年随访时增加(P<O.05)。结论:根除H.pylori可以减轻慢性胃炎的炎症程度,防止肠化的发生和发展。

关 键 词:幽门螺杆菌感染 胃黏膜 病理 慢性胃炎 消化性溃疡
修稿时间:2002-10-24

Effect of Helicobacter pylori Infection on Pathologic Changes of Gastric Mucosa
WANG Jiyao,WANG Ruijuan,XU Yongzheng,LIU Tianshu,LE Fan,DONG Ling. Effect of Helicobacter pylori Infection on Pathologic Changes of Gastric Mucosa[J]. Chinese Journal of Gastroenterology, 2003, 8(1): 25-28
Authors:WANG Jiyao  WANG Ruijuan  XU Yongzheng  LIU Tianshu  LE Fan  DONG Ling
Abstract:Background: Helicobacter pylori (H. pylori) infection has been regarded as an important risk factor of chronic gastritis and peptic ulcer. Eradication of H. pylori can accelerate the healing of peptic ulcer, but whether it can affect the pathologic changes of gastric mucosa needs to be investigated. Aims: To evaluate the effect of eradication of H. pylori on the pathologic changes of gastric mucosa and its precancerous status in patients with chronic gastritis. Methods: Multicentre randomized controlled clinical trial and retrospective cohort study were conducted. All samples were selected from two rural areas of Shanghai, Jinshan and Fengxian districts, with high incidence of gastric cancer. 360 patients endoscopically diagnosed as chronic gastritis and/or duodenal ulcer with H. pylori infection were recruited and randomly divided into two groups. In the treatment group triple therapy (proton pump inhibitor or H2-receptor antagonist plus two antibiotics) was used, and in the control group cisapride was given to patients with chronic gastritis, and cimetidine to patients with duodenal ulcer. All patients were followed-up by endoscopy at the end of 1 and 4 years. Two cohorts were determined basing on the results of positive and negative H. pylori tested histologically. The biopsied specimens of gastric mucosa were reviewed by two pathologists. Results: At the end of 4 years 120 patients were followed up. Among them, 54 patients were H. pylori eradicated and 5 patients were H. pylori positive again, while 45 patients were H. pylori positive and 16 were H. pylori negative. In those who were persistent H. pylori positive, at the end of first year the proportion of active inflammation decreased (P<0.05). At the end of fourth year, the degree of chronic inflammation and intestinal metaplasia, as well as the proportion of active inflammation decreased (P<0.05). In those H. pylori were persistently positive, the degree of chronic inflammation increased at the end of first year (P<0.05), the degree of chronic inflammation, intestinal metaplasia and the proportion of active inflammation increased at the end of fourth year (P<0.05). At the end of fourth year the degree of atrophy was more significant than that at the end of first year (P<0.05). Conclusions: Eradication of H. pylori can mitigate the degree of chronic gastritis and impede the development and progress of intestinal metaplasia.
Keywords:Helicobacter pylori  Pathologic Processes  Gastric Mucosa
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