摘要
目的 通过观察不同毒力型的幽门螺旋杆菌(helicobacter pylori,Hp)感染对胃液、胃蛋白酶及炎症因子的影响。方法 收集2021年12月至2023年3月收治的110例患者,根据碳13呼气试验结果,分为Hp阳性组(n=79),Hp阴性组(n=31)。其中Hp阳性组根据其Hp抗体分型,分为Ⅰ型组(n=52)、Ⅱ型组(n=11)、未定型组(n=16);Hp阴性组挑选抗体全阴者分为空白对照组(n=12)。所有患者均进行胃液pH值、钠离子(Na+)、钾离子(K+)、氯离子(Cl-)、白介素6 (Interleukin-6,IL-6)、白介素8 (Interleukin-8,IL-8)、胃泌素17 (Gastrin-17,G-17)、胃蛋白酶原Ⅰ(Pepsinogen I,PGⅠ)、胃蛋白酶原Ⅱ(Pepsinogen I,PGⅡ)检测。结果 Hp阳性组与Hp阴性组相比pH值、Na+、Cl-、K+,差异无统计学意义(P> 0.05);Hp阳性组相比Hp阴性组Cl-含量降低(P <0.05)。Hp阳性组较Hp阴性组相比IL-6、IL-8、G-17、PGⅠ、PGⅡ均有上升(P <0.05)。Ⅰ型组与Ⅱ型组、未定型组、空白对照组相比pH值、Na+、K+,差异均无统计学意义(P> 0.05)。Ⅰ型组、未定型组与空白对照组比较,Cl-含量均降低(P <0.05)。Ⅰ型组分别与Ⅱ型组、未定型组、空白对照组比较,IL-6、IL-8、PGⅠ均有上升(P <0.05)。空白对照组分别与其他各组之间PGⅡ存在明显差异(P <0.05)。Ⅰ型组与未定型组的G-17含量差异无统计学意义(P> 0.05)。Ⅰ型组与Ⅱ型组、空白对照组比较G-17均有上升(P <0.05)。结论 Ⅰ型Hp菌感染可能通过增加IL-6、IL-8、G-17的表达造成胃黏膜损伤,进而导致消化功能异常。
Objective To observe the effects of different virulence types of Helicobacter pylori on pepsin and inflammatory factors.Methods 110 patients admitted from December 2021 to March 2023 were collected and divided into HP positive group(n=79)and HP negative group(n=31)according to 13 carbon breath test results.The HP positive group was divided into type I group(n=52),type II group(n=11)and undetermined group(n=16)according to the Helicobacter pylori antibody typing.The HP negative group was selected and divided into blank control group(n=12).Gastric juice pH value,sodion(Na+),potassium(K+),chloridion(Cl-),IL-6,IL-8,gastrin 17(G-17),pepsinogenⅠ(PGⅠ)and pepsinogenⅡ(PGⅡ)were detected in all patients.Results Th-ere was no difference in pH,Na+,Cl-,K+between Hp positive group and Hp negative group(P>0.05).The content of Cl-in HP-positive group was lower than that in HP-negative group(P<0.05).The levels of IL-6,IL-8,G-17,PGⅠand PGⅡin HP-positive group were significantly higher than those in HP-negative group(P<0.05).There was no significant difference in pH,Na+and K+between type I group and type II group,undetermined group and blank control group(P>0.05).The content of Cl-in type I group and undetermined group was lower than that in blank control group(P<0.05).The levels of IL-6,IL-8 and PGⅠin type I group were higher than those in type II group,undetermined group and blank control group(P<0.05).There was a significant difference in PGⅡbetween the blank control group and the other groups(P<0.05).There was no difference in G-17 content between type I group and undetermined group(P>0.05).The level of G-17 in type I group was higher than that in type II group and blank control group(P<0.05).Conclusion Type I Hp infection may cause gastric mucosal injury by increasing the expression of IL-6,IL-8 and G-17,and then lead to abnormal digestive function.
作者
赵小青
肖嘉欣
林勇
张剑锋
王文辉
张文杰
Xiaoqing ZHAO;Jiaxin XIAO;Yong LIN;Jianfeng ZHANG;Wenhui WANG;Wenjie ZHANG(Dept.of Gastroenterology,Guangdong Provincial Hospital of Chinese Medicine,Zhuhai Guangdong 519000,China)
出处
《昆明医科大学学报》
CAS
2024年第2期148-152,共5页
Journal of Kunming Medical University
基金
珠海市科技计划医疗卫生基金资助项目(ZH2202200019HJL)。
