根除幽门螺杆菌对胃窦黏膜萎缩的逆转作用

Follow-up study on reversal of antrum mucosal atrophy after eradication of Helicobacter pylori

目的评价5a随访根除幽门螺杆菌(Helicobacterpylori,Hp)感染对胃窦黏膜萎缩的逆转作用并探讨其机制。方法采用前瞻性队列研究方法,选择110例慢性萎缩性胃窦炎患者作为观察对象。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。采用TUNEL技术及免疫组化染色检测胃黏膜上皮细胞凋亡和增殖情况。结果Hp阳性观察组患者胃黏膜萎缩程度在5a中加重的比例高达43%,显著高于Hp根除观察组及Hp阴性对照组(13%和20%,P<0.05)。Hp根除观察组胃窦黏膜萎缩程度减轻的病人比率为29%,显著高于Hp阳性观察组(9%,P<0.01)。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%,P<0.01),Hp根除后胃黏膜上皮细胞PC-NA指数和凋亡指数(14.3%,12.9%)均显著下降(9.2%,3.6%,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殖的调节紊乱,促进胃窦黏膜萎缩的形成与发展。根除Hp治疗可以使胃窦黏膜萎缩程度减轻和逆转。

[Objective] To observe the long term effects of Helicobacter pylori （H. pylori） infection on gastric mucosa , to explore the effect of H. pylori eradication in patients with antrum atrophic gastritis. [Methods] 110 recruited patients were those diagnosed as chronic atrophic gastritis endoscopically and pathologically. H. pylori-posirive patients were given H. pylori eradication therapy according to their willingness. All patients were followed-up for 5 years. Meanwhile, using terminal deoxynucleotidyl transferase-mediated nick end labeling （TUNEL） technique and immunohistochemical staining, we observed the apoptotic cells and proliferative cells. [Results] After 5 years follow-up, 43% of patients the antrum mucosal atrophy was aggravated in the infection group, which was significantly higher than that in the H. pylori negative group and in the H. pylori eradication group（20%, 13%, P〈0.05）. 29% of patients the antrum mucosal atrophy was reduced in the H. pylori eradication group, which was significantly higher than that in the infection group （9%, P 〈0.01）. The apoptotic index and PCNA index of gastric epithelial in the patients infected with H. pylori（12.7%, 14.6%） were significantly higher than those of H. pylori negative gastric epithelial（2.9%, 8.0%, P〈0.01 ）. After eradication of H. pylori with triple therapy, the PCNA index and apoptotic index fell from 14.3% and 12.9% to 9.2% and 3.6%（P〈0.01）. In the persisting H. pylori infected patients, the apoptotic index and PCNA index were not statistically decreased. [Conclusions] H. pylori infection may play a promotional role in the formation and development of antrum atrophic gastritis, possibly by inducing gastrc epithelial apoptosis and proliferation in paralle. The antrum mucosal atrophy can be reduced or even reversed by the eradication of H. pylori.