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目的:了解幽门螺杆菌(Helicobacterpylori,Hp)长期感染是否促进胃黏膜肠上皮化生和异型增生的形成与发展,评价5a随访根除Hp感染对胃癌前病变的作用并探讨其机制.方法:采用前瞻性队列研究方法,对首次胃镜检查诊断为慢性胃炎而不伴有肠上皮化生和异型增生的患者作为入选病例,入选时Hp阳性患者80例,Hp阴性者30例.Hp阳性患者根据自愿原则采用根除Hp治疗或采用对照治疗.全部病例跟踪随访5a.并采用脱氧核糖核酸末端转移酶介导的缺口末端标记(TUNEL)技术及免疫组织化学染色对Hp阳性患者Hp根除前后及Hp阴性者胃黏膜上皮细胞凋亡和增生情况进行原位观察和比较.结果:Hp阳性观察组肠上皮化生的发生率(32.6%)显著高于Hp阴性对照组(12.0%,χ2=4.147,3.893,P<0.05)和Hp根除观察组(12.9%,χ2=3.869,P<0.05).Hp阳性观察组异型增生的发生率(19.6%)显著高于Hp阴性对照组(4.0%,χ2=3.893,P<0.05).Hp根除观察组肠上皮化生和异型增生的发生率与Hp阴性对照组无统计学差异.Hp阳性患者胃黏膜上皮细胞凋亡指数及PCNA指数(12.7%,14.6%)均显著高于Hp阴性患者(2.9%,8.0%,t=7.241,6.368,P<0.01),Hp根除后胃黏膜上皮细胞PCNA指数和凋亡指数(14.3%,12.9%)均显著下降(9.2%,3.6%,t=5.642,7.410,P<0.01),而Hp未根除者上述指标则无显著性变化.结论:Hp感染可能通过刺激胃黏膜上皮细胞凋亡与增生的调节紊乱,使胃黏膜的不稳定性增加,促进胃黏膜肠上皮化生和异型增生的形成与发展,从而增加患胃癌的危险性.根除Hp感染能明显降低肠上皮化生和异型增生的发生率.
Objective: To investigate whether long-term infection of Helicobacter pylori (Hp) promotes the formation and development of intestinal metaplasia and dysplasia of gastric mucosa, evaluates the effect of eradication of Hp infection on precancerous lesions in 5 years and explores its mechanism. Methods: Prospective In the cohort study, patients with chronic gastritis diagnosed as chronic gastritis without intestinal metaplasia and dysplasia were selected as inclusion cases. Eighty Hp-positive patients and 30 Hp-negative patients were enrolled. Hp-positive patients were voluntary Eradication of Hp therapy or control treatment. Follow-up of all cases 5a. End-to-end nick end labeling (TUNEL) mediated by deoxyribonuclease and immunohistochemical staining for Hp eradication in Hp-positive patients and before and after Hp-negative stomach Apoptosis and proliferation of mucosal epithelial cells were observed and compared in situ. Results: The incidence of intestinal metaplasia in Hp-positive observation group (32.6%) was significantly higher than that of Hp-negative control group (12.0%, χ2=4.147, 3.893, P <0.05) and Hp eradication observation group (12.9%, χ2=3.869, P<0.05). The occurrence rate of dysplasia in the Hp-positive observation group (19.6%) was significantly higher than that of the Hp-negative control group (4.0%, χ2=3.893, P <0.05).Hp root The incidence of intestinal metaplasia and dysplasia was not significantly different between the observation group and the Hp-negative control group. The gastric mucosal epithelial cell apoptosis index and PCNA index (12.7%, 14.6%) were significantly higher in the Hp-positive patients than in the Hp-negative patients ( 2.9%, 8.0%, t=7.241, 6.368, P<0.01). After eradication of Hp, the PCNA index and apoptotic index (14.3%, 12.9%) of gastric epithelial cells were significantly decreased (9.2%, 3.6%, t=5.642). ,7.410,P<0.01), but there was no significant change in the above indicators of Hp non-eradication. Conclusion: Hp infection may stimulate gastric mucosal instability through the stimulation of gastric mucosal epithelial cell apoptosis and proliferation of regulatory disorders, and promote The formation and development of gastric mucosal intestinal metaplasia and dysplasia increase the risk of gastric cancer. Eradication of Hp infection can significantly reduce the incidence of intestinal metaplasia and dysplasia.