Antiviral therapy effectively improves liver hemodynamics as evidenced by serum biomarker and contrast-enhanced ultrasound examinations in patients with hepatitis B cirrhosis

PeerJ

article

Xiaoyong Xu¹  Chaoxue Zhang²  Chen Shi¹  Naizhong Hu¹  Bin Sun¹  Derun Kong¹  Jianming Xu¹ 

[1] Department of Gastroenterology, The First Affiliated Hospital of Anhui Medical University;Department of Ultrasound, The First Affiliated Hospital of Anhui Medical University

关键词: Hepatitis B virus;    Cirrhosis;   

DOI  :  10.7717/peerj.5484

学科分类：社会科学、人文和艺术（综合）

来源: Inra

【 摘 要 】

Background and AimsTo prospectively evaluate the effects of antiviral therapy on liver hemodynamics in patients with hepatitis B cirrhosis.MethodsSeventy consecutive eligible HBV-related cirrhotic inpatients were enrolled in the prospective study. Fifty-two received different nucleoside analogs monotherapy and 18 denied antiviral therapy. Their liver biochemistry profiles and HBV-DNA were measured at the baseline and every 3 months. Peripheral blood vWF and sCD163, as well as liver ultrasound Doppler parameters including portal vein diameter (PVD), portal vein velocity (PVV), portal vein congestion index (PV-CI), hepatic vein damping index (HV-DI), hepatic arterial arrival time (HAAT), hepatic vein arrival time (HVAT) and intrahepatic cycle time (HV-HA), were measured at the baseline and the follow-up periods.ResultsIn the antiviral group, all patients achieved complete virologic and liver biochemical responses after 3-month antiviral treatment. Furthermore, the response states were maintained till the follow-up endpoint. However, in the non-antiviral group, HBV DNA replication resulted in higher levels of ALT and AST compared to the baseline values (P < 0.05). In the antiviral group, PVD, PV-CI, HV-DI, vWF-Ag and sCD163 were all significantly reduced than the baseline values (P < 0.05), and PVV was significantly increased than the baseline value (P < 0.05).ConclusionsAntiviral therapy could effectively suppress hepatocyte inflammation and alleviate the dysfunction of intrahepatic vascular endothelial and hepatic macrophages, which might improve hepatic hemodynamic function in HBV-related cirrhosis.

【 授权许可】

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