Pazgan-Simon Monika, Zuwała-Jagiełło Jolanta, Kukla Michał, Grzebyk Ewa, Simon Krzysztof
Department of Infectious Diseases and Hepatology, Wroclaw Medical University, Wroclaw, Poland.
Department of Pharmaceutical Biochemistry, Wroclaw Medical University, Wroclaw, Poland.
Clin Exp Hepatol. 2020 Sep;6(3):235-242. doi: 10.5114/ceh.2020.99517. Epub 2020 Sep 30.
Hepatotropic viruses cause metabolic disturbances such as insulin resistance and hepatosteatosis. Moreover, metabolic factors, such as insulin resistance, obesity, and type 2 diabetes mellitus, increase the risk for hepatocellular carcinoma (HCC) in patients with virus-related liver cirrhosis. Cytokines secreted by the adipose tissue (adipokines) may be implicated in these metabolic disturbances, but there is little evidence regarding the role of adipokines in virus-related cirrhosis and HCC. Thus, we studied whether serum concentrations of selected adipokines were altered in patients with virus-related liver cirrhosis, including patients with HCC.
We included 43 patients with liver cirrhosis due to chronic hepatitis B or chronic hepatitis C. Of these patients, 36 had HCC and 7 did not have any malignant lesions. In addition to routine clinical and laboratory variables, we analyzed serum concentrations of betatrophin, insulin, vaspin, visfatin, and irisin.
Compared with healthy controls, patients with HCC had significantly increased vaspin concentrations and significantly reduced irisin concentrations. Compared with controls, patients with virus-related cirrhosis, with or without HCC, had significantly increased concentrations of insulin and betatrophin. The serum visfatin concentration was non-significantly higher in patients with virus-related cirrhosis than in controls. None of the studied adipokines was a significant predictor of HCC. Serum concentrations of the studied adipokines were not related to cirrhosis severity or HCC stage.
Metabolic parameters, including serum adipokine concentrations, are altered in patients with virus-related liver cirrhosis. Adipokines might be related to the HCC risk in these patients.
嗜肝病毒会引发代谢紊乱,如胰岛素抵抗和肝脂肪变性。此外,胰岛素抵抗、肥胖和2型糖尿病等代谢因素会增加病毒相关性肝硬化患者患肝细胞癌(HCC)的风险。脂肪组织分泌的细胞因子(脂肪因子)可能与这些代谢紊乱有关,但关于脂肪因子在病毒相关性肝硬化和HCC中的作用,证据很少。因此,我们研究了包括HCC患者在内的病毒相关性肝硬化患者血清中某些选定脂肪因子的浓度是否发生了变化。
我们纳入了43例因慢性乙型肝炎或慢性丙型肝炎导致肝硬化的患者。其中有36例患有HCC,7例没有任何恶性病变。除了常规临床和实验室变量外,我们还分析了血清中β-促细胞生成素、胰岛素、内脏脂肪素、内脂素和鸢尾素的浓度。
与健康对照组相比,HCC患者的内脏脂肪素浓度显著升高,鸢尾素浓度显著降低。与对照组相比,无论有无HCC的病毒相关性肝硬化患者的胰岛素和β-促细胞生成素浓度均显著升高。病毒相关性肝硬化患者的血清内脂素浓度略高于对照组,但差异无统计学意义。所研究的脂肪因子均不是HCC的显著预测指标。所研究脂肪因子的血清浓度与肝硬化严重程度或HCC分期无关。
病毒相关性肝硬化患者的代谢参数发生了改变,包括血清脂肪因子浓度。脂肪因子可能与这些患者的HCC风险有关。