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*

doi:10.3969/j.issn.1672-5069.2024.01.021

Abstract

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

Zhang Yingying, Wei Kele, Ding He, et al. Risk factors of spontaneous bacterial peritonitis and peripheral blood mononuclear cell CD36/mTORC1 signal pathway expression in patients with decompensated cirrhosis[J]. Journal of Practical Hepatology, 2024, 27(1): 80-83.

References

[1] 崔丽娜,王秀芳,孙瑞青,等. 自体外周血干细胞回输对失代偿期肝硬化患者远期预后影响的研究. 中华肝脏病杂志,2022,30(3):279-284.
[2] 贾新勇,栗朋辉,郭改玲,等. 失代偿期乙肝肝硬化患者碳青霉烯类耐药大肠埃希菌医院感染的危险因素及其耐药基因. 中华医院感染学杂志,2022,32(10):1478-1481.
[3] Mattos AA, Wiltgen D, Jotz RF, et al. Spontaneous bacterial peritonitis and extraperitoneal infections in patients with cirrhosis. Ann Hepatol, 2020, 19(5):451-457.
[4] Sandmann L, Dörge P, Wranke A, et al. Treatment strategies for patients with decompensated liver cirrhosis due to hepatitis C virus infection eligible for liver transplantation: real-life data from five German transplant centers. Eur J Gastroenterol Hepatol,2019,31(8):1049-1056.
[5] Singla P, Dalal P, Kaur M,et al. Bile acid oligomers and their combination with antibiotics to combat bacterial infections. J Med Chem,2018,61(22):10265-10275.
[6] Komolafe O, Roberts D, Freeman SC, et al. Antibiotic prophylaxis to prevent spontaneous bacterial peritonitis in people with liver cirrhosis: a network meta-analysis. Cochrane Database Syst Rev, 2020 ,1(1):13125.
[7] Andrieux P, Chevillard C, Cunha-Neto E, et al. Mitochondria as a cellular hub in infection and inflammation. Int J Mol Sci, 2021, 22(21):11338.
[8] Lobo AM, Agelidis AM, Shukla D. Pathogenesis of herpes simplex keratitis: The host cell response and ocular surface sequelae to infection and inflammation. Ocul Surf, 2019, 17(1):40-49.
[9] Bhat A ,Das S ,Yadav G ,et al.Hyperoxidized albumin modulates platelets and promotes inflammation through CD36 receptor in severe alcoholic hepatitis. Hepatol Commun,2019,4(1):50-65.
[10] Deng Z, Chen M, Liu Y, et al. A positive feedback loop between mTORC1 and cathelicidin promotes skin inflammation in rosacea. EMBO Mol Med, 2021, 13(5):13560.
[11] 秦波,郭树华.自发性细菌性腹膜炎.中华肝脏病杂志,2003,11(7):439-440.
[12] 中华医学会肝病学分会. 肝硬化诊治指南.实用肝脏病杂志,2019,22(6):770-792.
[13] 周小兵,李玉鑫,高方媛,等.肝硬化合并发自发性细菌性腹膜炎133例的危险因素分析.中华消化杂志,2019,39(4):268-270.
[14] Marciano S, Díaz JM, Dirchwolf M, et al. Spontaneous bacterial peritonitis in patients with cirrhosis: incidence, outcomes, and treatment strategies. Hepat Med, 2019,11:13-22.
[15] Lotte R, Courdurié A, Gaudart A, et al. Spontaneous bacterial peritonitis: the incremental value of a fast and direct bacterial identification from ascitic fluids inoculated in blood culture bottles by MALDI-TOF MS for a better management of patients. Microorganisms, 2022, 10(6):1188.
[16] 谭志洁,赵静,刘文兴,等.肝硬化腹水患者并发自发性细菌性腹膜炎病原菌与影响因素分析.中华医院感染学杂志,2019,29(19):2953-2956.
[17] Kimmann M ,Tergast T L,Schultalbers M ,et al.Sustained impact of nosocomial-acquired spontaneous bacterial peritonitis in different stages of decompensated liver cirrhosis. PLoS ONE, 2019,14(8):e0220666.
[18] Prat L I ,Wilson P ,Freeman S C ,et al. Antibiotic treatment for spontaneous bacterial peritonitis in people with decompensated liver cirrhosis: A network meta-analysis. Cochrane Database Syst Rev,2019,16(9):CD013120.
[19] Klyachman L ,Schuster I P , Wang H,et al. S1502 a rare case of raoultella planticola-associated spontaneous bacterial peritonitis in a patient with decompensated cirrhosis. Am J Gastroenterol,2020,115(1):S757-S758.
[20] Liu K, Qiu D, Liang X, et al. Lipotoxicity-induced STING1 activation stimulates MTORC1 and restricts hepatic lipophagy. Autophagy, 2022, 18(4):860-876.

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

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[1]	Ding Rong, Ji Wenli, Chen Tingting, et al. Distribution and drug resistance of pathogens in patients with decompensated hepatitis B cirrhosis and spontaneous bacterial peritonitis [J]. Journal of Practical Hepatology, 2024, 27(3): 398-401.
[2]	Qiu Wanchun, Mao Xiaorong, Deng Lefeng, et al. Sarcopenia in hospitalized patients with liver cirrhosis and its impact on the occurrence of spontaneous bacterial peritonitis [J]. Journal of Practical Hepatology, 2023, 26(5): 674-677.
[3]	Feng Dongxia, Xi Jing, Yang Zhenbin, et al. Predictive performance of peripheral blood mononuclear cell NLRP3 and caspase-1 mRNA levels in patients with hepatitis B cirrhosis and complicated spontaneous bacterial peritonitis [J]. Journal of Practical Hepatology, 2023, 26(5): 682-685.
[4]	Shen Yipeng, Zhu Junfeng. Spontaneous bacterial peritonitis in patients with liver cirrhosis [J]. Journal of Practical Hepatology, 2022, 25(6): 909-912.
[5]	Luo Nan, Li Rongkuan. Spontaneous bacterial peritonitis in patients with liver cirrhosis [J]. Journal of Practical Hepatology, 2022, 25(5): 616-619.
[6]	Wang Jing, Bi Ning, Fang Liang, et al. Correlation of blood CD64 index to intestinal mucosal barrier functions in patients with hepatitis B cirrhosis and spontaneous bacterial peritonitis [J]. Journal of Practical Hepatology, 2022, 25(1): 79-82.
[7]	Liu Yuling, Zhen Zengguo, Wang Huijuan, et al. Effects of probiotics on intestinal barrier function of patients with liver cirrhosis complicated by spontaneous bacterial peritonitis [J]. Journal of Practical Hepatology, 2021, 24(6): 867-870.
[8]	Li Cuiru, Wu Li, Ping Caiyan, et al. Clinical efficacy of microecological agents in the treatment of patients with hepatitis B liver cirrhosis complicated by spontaneous bacterial peritonitis [J]. Journal of Practical Hepatology, 2020, 23(6): 845-848.
[9]	Hu Dengcai, Du Li, Cao Chenhong, et al.. Serum procalcitonin and C-reactive protein levels in predicting spontaneous bacterial peritonitis in patients with decompensated liver cirrhosis [J]. Journal of Practical Hepatology, 2020, 23(5): 699-702.
[10]	Wu Wenhao, Fu Hanguang, Chen Zhaoqin. Clinical features,pathogenic distribution and drug susceptibility in patients with liver cirrhosis complicated by spontaneous bacterial peritonitis [J]. JOURNAL OF PRACTICAL HEPATOLOGY, 2018, 21(3): 356-359.
[11]	Zhao Yu, Zhu Yu, Zhang Daizhong. Efficacy of intrahepatic transplantation of human umbilical cord mesenchymal stem cells combined with matrine in the treatment of patients with decompensated hepatitis B cirrhosis [J]. JOURNAL OF PRACTICAL HEPATOLOGY, 2018, 21(3): 360-363.
[12]	Liu Yuling, Feng Zhenqing, Jia Qiulong, et al.. Changes of serum liver fibrosis index in patients with hepatitis B-induced liver cirrhosis complicated by spontaneous bacterial peritonitis [J]. JOURNAL OF PRACTICAL HEPATOLOGY, 2017, 20(3): 356-357.
[13]	Cen Yu，Su Sibiao，et al.. IL-22 expression and its clinical significance in patients with hepatitis B virus-induced decompensated liver cirrhosis [J]. JOURNAL OF PRACTICAL HEPATOLOGY, 2016, 19(6): 734-735.
[14]	Ju Chaoxia, Chen Judi, Zhou Meifang, et al. Peritoneal intubation lavage in cirrhotic patients with spontaneous bacterial peritonitis [J]. JOURNAL OF PRACTICAL HEPATOLOGY, 2016, 19(4): 482-483.
[15]	Zhou Jing,Su Fei. Clinical features of 100 patients with acute exacerbation of cirrhosis with liver function decompensation [J]. JOURNAL OF PRACTICAL HEPATOLOGY, 2016, 19(3): 314-317.