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乙型肝炎病毒DNA复制水平及抗HBV治疗对肝细胞癌微血管侵犯的影响

Effect of hepatitis B virus DNA replication level and anti-HBV therapy on microvascular invasion of hepatocellular carcinoma.

作者信息

Qu Chao, Huang Xinyu, Liu Kui, Li Kun, Tan Bin, Qu Linlin, Cao Jingyu, Zhu Chengzhan

机构信息

1Department of Hepatobiliary and Pancreatic Surgery, the Affiliated Hospital of Qingdao University, No.16 Jiangsu Road, Qingdao City, 266003 Shandong Province China.

3Medical College of Qingdao University, No.308 Ningxia Road, Qingdao City, 266071 Shandong Province China.

出版信息

Infect Agent Cancer. 2019 Jan 21;14:2. doi: 10.1186/s13027-019-0219-8. eCollection 2019.

DOI:10.1186/s13027-019-0219-8
PMID:30679943
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6341680/
Abstract

BACKGROUND

Chronic hepatitis B virus (HBV) infection is a major risk factor for the occurrence and development of cirrhosis and hepatocellular carcinoma (HCC). Microvascular invasion (MVI) of HCC is closely related to postoperative recurrence. We aimed to investigate the effect of HBV DNA replication levels and anti-HBV treatment on the occurrence of MVI in HCC.

METHODS

A retrospective analysis of the clinical and pathological data of 660 patients undergoing hepatectomy for hepatocellular carcinoma at the Affiliated Hospital of Qingdao University from January 2015 to December 2017 is included in this study.

RESULTS

This study involved a total of 660 patients with an MVI incidence rate of 46.8% (309/660). Univariate analysis revealed that positive HBV surface antigen (HBsAg), detectable HBV DNA load, and administration of antiviral treatment were significantly associated with the formation of MVI. Multivariable logistic regression analysis in patients with positive seral HBsAg showed that detectable HBV DNA load (OR = 5.33,  < 0.001) was an independent risk factor for MVI. Antiviral treatment for more than six months (OR = 0.37,  = 0.002) was an independent protective factor against MVI. Patient groups with severe MVI had significantly higher rates of HBV infection ( = 0.017), a detectable HBV DNA load (> 100 IU/ml) rate ( < 0.001), and obvious low antiviral treatment rate ( = 0.021).

CONCLUSIONS

HBV DNA replication level is an independent risk factors for the formation of HCC MVI, and anti-hepatitis B virus treatment has an inhibitory effect on MVI formation.

摘要

背景

慢性乙型肝炎病毒(HBV)感染是肝硬化和肝细胞癌(HCC)发生发展的主要危险因素。HCC的微血管侵犯(MVI)与术后复发密切相关。我们旨在研究HBV DNA复制水平和抗HBV治疗对HCC中MVI发生的影响。

方法

本研究纳入了2015年1月至2017年12月在青岛大学附属医院接受肝细胞癌肝切除术的660例患者的临床和病理数据,进行回顾性分析。

结果

本研究共纳入660例患者,MVI发生率为46.8%(309/660)。单因素分析显示,HBV表面抗原(HBsAg)阳性、可检测到的HBV DNA载量以及抗病毒治疗的使用与MVI的形成显著相关。对血清HBsAg阳性患者进行多变量逻辑回归分析显示,可检测到的HBV DNA载量(OR = 5.33,< 0.001)是MVI的独立危险因素。抗病毒治疗超过6个月(OR = 0.37,= 0.002)是预防MVI的独立保护因素。MVI严重的患者组HBV感染率(= 0.017)、可检测到的HBV DNA载量(> 100 IU/ml)率(< 0.001)明显更高,而抗病毒治疗率明显较低(= 0.021)。

结论

HBV DNA复制水平是HCC中MVI形成的独立危险因素,抗乙型肝炎病毒治疗对MVI形成有抑制作用。

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Hepatitis B virus infection and active replication promote the formation of vascular invasion in hepatocellular carcinoma.乙型肝炎病毒感染和活跃复制促进肝细胞癌中血管侵犯的形成。
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