Hp感染对慢性胃炎患者胃泌素、胃蛋白酶原水平的影响及其临床意义
作者: |
1潘园,
1张保国,
2徐贝
1 宣城市中心医院消化内科,安徽 宣城 242000 2 宣城市中心医院检验科,安徽 宣城 242000 |
通讯: |
潘园
Email: pyzxyy@sina.cn |
DOI: | 10.3978/j.issn.2095-6959.2021.11.005 |
摘要
目的:研究幽门螺杆菌(Helicobacter pylori,Hp)感染对慢性胃炎患者胃泌素(gastrin)、胃蛋白酶原(pepsinogen,PG)的影响及其临床意义。方法:选取2017年12月至2020年11月宣城市中心医院收治的80例慢性胃炎患者,并将其分为Hp阳性组与Hp阴性组,每组各40例,比较两组患者的胃泌素17(G-17)、PG-I、PG-II水平,分析慢性胃炎患者Hp感染的影响因素。结果:Hp阳性患者的G-17、PG-II水平高于Hp阴性患者,而PG-I水平低于Hp阴性患者(P<0.05);饮食方式、G-17、PG-I、PG-II水平均为慢性胃炎患者Hp感染的影响因素(P<0.05);饮食方式(共餐)(OR=1.595)、G-17水平(OR=1.632)、PG-II水平(OR=1.768)是影响慢性胃炎患者Hp感染的独立因素,差异有统计学意义(P<0.05)。结论:Hp感染可导致慢性胃炎患者血清G-17、PG-II异常分泌。
关键词:
幽门螺杆菌;胃泌素;蛋白酶原;慢性胃炎
Effects of Helicobacter pylori infection on the levels of gastrin and pepsinogen in patients with chronic gastritis and its clinical significance
CorrespondingAuthor: PAN Yuan Email: pyzxyy@sina.cn
DOI: 10.3978/j.issn.2095-6959.2021.11.005
Abstract
Objective: To study effects and clinical significance of Helicobacter pylori (Hp) infection on gastrin and pepsinogen (PG) in patients with chronic gastritis and. Methods: A total of 80 patients with chronic gastritis admitted to the hospital from December 2017 to November 2020 were enrolled and divided into Hp positive group and Hp negative group, with 40 cases in each group. The levels of G-17, PG-I and PG-II, between the two groups were compared. The influencing factors of Hp infection in patients with chronic gastritis were analyzed. Results: The levels of G-17 and PG-II in Hp-positive patients were higher than those in Hp-negative patients, while PG-I level was lower than that in Hp-negative patients (P<0.05). The diet mode, G-17, PG-I and PG-II levels were all influencing factors of Hp infection in patients with chronic gastritis (P<0.05). The diet mode (interdine) (OR=1.595), G-17 level (OR=1.632) and PG-II level (OR=1.768) were independent influencing factors of Hp infection in patients with chronic gastritis (P<0.05). Conclusion: Hp infection may cause abnormal secretion of serum G-17 and PG-II in patients with chronic gastritis.
Keywords:
Helicobacter pylori; gastrin; pepsinogen; chronic gastritis