实用肝脏病杂志 ›› 2024, Vol. 27 ›› Issue (1): 80-83.doi: 10.3969/j.issn.1672-5069.2024.01.021

• 肝硬化 • 上一篇    下一篇

失代偿期肝硬化并发自发性细菌性腹膜炎患者危险因素和PBMC CD36/mTORC1信号通路变化研究*

张迎迎, 魏珂乐, 丁鹤, 郭慧杰, 崔轶, 王昳   

  1. 451191 郑州市 河南省第二人民医院消化内科(张迎迎,魏珂乐,丁鹤,郭慧杰,崔轶);郑州大学第一附属医院消化内科(王昳)
  • 收稿日期:2023-03-22 出版日期:2024-01-10 发布日期:2024-01-04
  • 通讯作者: 魏珂乐,E-mail:1121164315@qq.com
  • 作者简介:张迎迎,女,36岁,大学本科。E-mail:juzi20022@163.com
  • 基金资助:
    *河南省医学科技攻关计划联合共建项目(编号:LHGJ20191027)

Risk factors of spontaneous bacterial peritonitis and peripheral blood mononuclear cell CD36/mTORC1 signal pathway expression in patients with decompensated cirrhosis

Zhang Yingying, Wei Kele, Ding He, et al   

  1. Department of Gastroenterology, Second Provincial Hospital, Zhengzhou 451191, Henan Province, China
  • Received:2023-03-22 Online:2024-01-10 Published:2024-01-04

摘要: 目的 探讨失代偿期肝硬化患者并发自发性细菌性腹膜炎(SBP)的危险因素,分析患者外周血单个核细胞(PBMC)分化抗原(CD)36/哺乳动物雷帕霉素靶蛋白1(mTORC1)信号通路水平变化。方法 2020年7月~2023年12月我院诊治的失代偿期肝硬化患者82例,其中并发SBP者43例。取腹水培养,进行细菌鉴定,采用PCR法检测PBMC CD36/mTORC1 mRNA水平。应用多因素Logistic回归分析影响失代偿期肝硬化患者并发SBP的危险因素。结果 在本组43例SBP患者中,分离出病原菌8株(9.8%),其中科氏葡萄球菌和溶血葡萄球菌各1株,大肠埃希菌2株,肺炎克雷伯菌2株和阴沟杆菌2株;SBP患者既往SBP发生史、血清总胆红素、血清白蛋白、INR、MELD评分及PBMC CD36和mTORC1 mRNA水平分别为51.2%、(45.7±5.2)μmol/L、(21.7±3.1)g/L、(1.5±0.5)、(24.9±7.5)、(3.2±0.8)和(2.4±0.7),与肝硬化组【分别为18.0%、(12.3±1.4)μmol/L、(35.3±5.4)g/L、(1.2±0.3)、(12.8±3.7)、(1.4±0.5)和(1.1±0.4)】比,差异显著(P<0.05);多因素Logistic回归分析结果显示,SBP发生史、血清总胆红素、ALB、MELD评分及PBMC CD36和mTORC1水平为影响失代偿期肝硬化并发SBP的独立危险因素(P<0.05)。结论 失代偿期肝硬化并发SBP患者PBMC CD36/mTORC1信号通路表达上调,其在SBP发生过程中的作用还有待于进一步研究。

关键词: 失代偿期肝硬化, 自发性细菌性腹膜炎, 分化抗原36/哺乳动物雷帕霉素靶蛋白1信号通路

Abstract: Objective The purpose of this study was to investigate the risk factors of spontaneous bacterial peritonitis (SBP) and peripheral blood mononuclear cell (PBMC) cluster of differentiation (CD) 36/mammalian target of rapamycin 1 (mTORC1) signal pathway expression in patients with decompensated cirrhosis. Methods 82 patients with decompensated liver cirrhosis were encountered in our hospital between July 2020 and December 2023. Ascites bacteria was cultured and characterized routinely. The PBMCs were separated and the CD36/mTORC1 mRNA was detected by real-time fluorescent quantitative PCR. The multivariate Logistic regression analysis was applied to screen the risk factors for SBP occurrence in patients with decompensated cirrhosis. Results The complications of SBP was found in 43 cases out of our patients with decompensated liver cirrhosis and eight strains (9.8%)of bacteria were successfully isolated, including one strain of Staphylococcus coriolis, one strain of Hemolytic Staphylococcus, two strains of Escherichia coli, two strains of Klebsiella pneumonia and two strains of Enterobacter cloacae; the incidence of past SBP, serum total bilirubin, albumin, international normalized ratio, the model of end-stage liver disease score, the PBMC CD36 mRNA and mTORC1 mRNA in patients with SBP were 51.2%, (45.7±5.2)μmol/L, (21.7±3.1)g/L, (1.5±0.5), (24.9±7.5), (3.2±0.8) and (2.4±0.7), all significantly different compared to [18.0%,(12.3±1.4)μmol/L, (35.3±5.4)g/L, (1.2±0.3), (12.8±3.7), (1.4±0.5) and (1.1±0.4), respectively, P<0.05] in patients with liver cirrhosis; the multivariate Logistic regression analysis showed that the past SBP, serum bilirubin, albumin, MELD score as well as PBMC CD36 and mTORC1 levels were all the independent risk factors for the occurrence of SBP in patients with decompensated liver cirrhosis (P<0.05). Conclusion The PBMC CD36/mTORC1 signal pathway is up-regulated in patients with decompensated cirrhosis and complicated SBP, and the mechanism involved in the pathogenesis needs further investigation.

Key words: Decompensated liver cirrhosis, Spontaneous bacterial peritonitis, Cluster of differentiation 36/mammalian target of rapamycin 1 signal pathway