慢性胃炎镜下病理特点与幽门螺杆菌血清抗体类型的相关性研究

目的探讨不同菌型幽门螺杆菌(Hp)血清抗体类型与慢性胃炎发生率及其病理特点的关系。方法选取该院2014年11月-2016年11月收治疗的上腹部不适的患者650例作为研究对象,所有患者均行胃镜检查,所有患者均行Hp呼气实验检查Hp,并采用酶联免疫吸附法检查患者血清中Hp抗体类型,采用Logistic分析Hp感染与慢性胃炎发生及其病理特点的关系。结果 650例患者中慢性胃炎93例,以Hp(-)为对照组,Hp(+)组患者慢性胃炎风险是Hp(-)患者的1.6倍,Hp(+)Cag A-Ig G+患者慢性胃炎是Hp(-)患者的2.3倍,Hp(+)Cag A-Ig G-患者慢性胃炎是Hp(-)患者的1.8倍。慢性萎缩性胃炎(CAG)患者27例中,以Hp(-)为参照,Hp(+)组患者CAG是Hp(-)患者的2.1倍,Hp(+)Cag A-Ig G-患者CAG是Hp(-)患者的1.9倍,Hp(+)Cag A-Ig G+患者CAG是Hp(-)患者的2.9倍;CAG伴不典型增生(Dys)患者13例中,以Hp(-)为参照,Hp(+)组患者是Hp(-)患者的2.4倍,Hp(+)Cag A-Ig GCAG伴Dys是Hp(-)患者的3.5倍,Cag A-Ig G+的慢性胃炎患者炎症反应程度明显比Hp(-)及Cag A-Ig G-的患者高,且炎症活动度明显更高。结论 Hp(+)Cag A-Ig G+感染加重慢性胃炎患者胃黏膜患者的炎症反应,同时促进慢性胃炎向CAG伴Dys发展。

Correlation between pathological features of chronic gastritis and serum antibody types of Helicobacter pylori

Abstract: Objective?To investigate the relationship between the types of serum antibodies against Helicobacter pylori (Hp) and the incidence of chronic gastritis and its pathological features.?Methods?650 patients from November 2014 to November 2016 were selected. All the patients underwent Helicobacter pylori breath test to check the throttle, and the throttle pylori antibody examined by ELISA, logistic analysis were used to the relationship between the risk and the pathological features of Hp infection and chronic gastritis.?Results?93 of 650 patients were diagnosed with chronic gastritis, 1.6 times Hp (-), Hp (+) CagA + IgG + patients with chronic gastritis were 1.8 times Hp (-), 27 patients with Hp (-), 27 patients with chronic atrophic gastritis. CAG was 2.1 times in patients with Hp (-) >in 13 patients with chronic atrophic gastritis with Hp (-), CAG was 2.4 times in patients with Hp (-), compared with Hp (+) CagA IgG + patients Hp (-) patients with chronic gastritis were 3.5 times more likely to be Hp (-) patients, and the degree of inflammatory response in patients with chronic gastritis (CagA-IgG+) was significantly higher than that in patients with Hp- and CagA-IgG-, and the inflammatory activity was significantly higher.?Conclusion?Hp (+) CagA-IgG+ infection aggravates the inflammatory response in patients with chronic gastritis and promotes the development of chronic gastritis to atrophic gastritis and dysplasia.