幽门螺杆菌感染与胃癌前病变演化的关系

Relationship between Helicobacter pylori infection and gastric precancer-ous lesions:a follow-up study

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.

AIM: To observe long-term effects of Helicobacter pylori(H. pylori) infection on gastric mucosa , to explore the roleand mechanisms of H. pylori in the histogenesis and devel-opment of gastric precancerous lesions by following-up 110patients with H. pylori-related gastritis for 5 years.METHODS: The patients were those diagnosed as chronicgastritis without intestinal metaplasia and gastric dysplasiaendoscopically and pathologically. H. pylori-positive patientswere given H. pylori eradication therapy according to theircontent. All patients were followed-up for 5 years.Meanwhile, using terminal deoxynucleotidyl transferase-mediated nick end labeling (TUNEL) technique and immu-nohistochemical staining, the authors observed the apoptoticcells and proliferative cells in situ in H. pylori negative gas-tric mucosa , H. pylori positive gastric mucosa before andafter H. pylori eradication.RESULTS: After 5 years follow-up, the incidence of intes-tinal metaplasia in H. pylori positive group (32.6%) wassignificantly higher than that in H. pylori negative group(12.0%,χ2= 4.147, 3.893, P <0.05) and H. pylori eradica-tion group (12.9%,χ2 =3.869, P <0.05. The incidence ofgastric dysplasia in H. pylori positive group (19.6%) wassignificantly higher than that in H. pylori negative group (4.0%,χ2=3.893, P <0.05). The incidences of intestinal meta-plasia and gastric dysplasia in H. pylori eradication groupwere not significantly different from those in H. pylori nega-tive group. The apoptotic index and PCNA index of gastricepithelia in the patients infected with H. pylori (12.7%,14.6%) were significantly higher than those of H. pylori nega-tive gastric epithelia (2.9%,8.0%, t =7.241,6.368,P <0.01). After eradication of H. pylori with triple therapy, PCNAindex and apoptotic index fell from 14.3% and 12.9% to 9.2% and 3.6% (t =5.642,7.410, P <0.01). In persistent H.pylori infected patients, apoptotic index and PCNA indexwere not statistically decreased.CONCLUSIONS: H. pylori infection may play a promo-tional role in the histogenesis and development of intestinalmetaplasia and gastric dysplasia, possibly by inducing gastrcepithelial apoptosis and proliferation in parallel. Eradicationof H. pylori can reduce the incidence of intestinal metapla-sia and gastric dysplasia.