幽门螺杆菌根除治疗对肠上皮化生和萎缩性胃炎的影响  

The effect of helicobacter pylori in intestinal metaplasia and atrophic gastritis

作　　者：许兰涛[1] 陈华[1] 熊佳时[1] 唐强[1] 沈玉玲[1] 

机构地区：[1]上海交通大学附属第六人民医院奉贤分院消化内科,201400

出　　处：《疑难病杂志》2009年第12期713-715,共3页Chinese Journal of Difficult and Complicated Cases

摘　　要：目的探讨Hp感染致胃黏膜肠上皮化生和萎缩性胃炎的发病机制。方法纳入266例Hp阳性者,随机分为对照组130例和治疗组136例。观察治疗组(予Hp根除治疗)、对照组(予安慰剂)肠上皮化生程度、萎缩性胃炎进展、端粒酶活性、Survivin-mRNA表达,并进行治疗前后及组间比较。结果Survivin在肠上皮化生和萎缩性胃炎组织中高表达。对Hp感染患者进行根除治疗后促进肠上皮化生的逆转、减轻萎缩性胃炎、降低Survivin mRNA的表达、抑制端粒酶活性,与对照组比较差异有统计学意义(P<0.01)。结论对Hp感染阳性患者进行根除治疗可以通过抑制端粒酶活性、Survivin mRNA表达途径阻止肠化的发生。Objective To explore the mechanism of helicobacter pylori （Hp） infection in intestinal metaplasia of gastric mucosa and atrophic gastritis. Methods Totally 226 cases with Hp-positive were divided into treatment group （136 cases, Hp eradication therapy） and control group （130 cases, placebo therapy） randomly. To compare the degree of intestinal metaplasia, progression of atrophic gastritis, activity of telomerase, expression of Survivin mRNA between two groups. And compare pre and post treatment intragroups. Results It showed that higher expression of Survivin in intestinal metaplasia and atrophic gastritis. The Hp eradication therapy could reverse the intestinal metaplasia, release the progression of atrophic gastritis, reduce the expression of Survivin and inhibit the telomerase activity. It showed statistical significance in treatment group than control group （ P 〈 0.01 ）. Conclusion The Hp eradication therapy could help inhibit telomerase activity and expression of Survivin mRNA ,to prevent the intestinal metaplasia.

关 键 词：SURVIVIN 胃癌细胞 HP感染 凋亡 

分 类 号：R573.3[医药卫生—消化系统]