乙型肝炎病毒DNA复制水平和抗HBV治疗对肝细胞癌微血管侵犯

StephenW

Infect Agent Cancer. 2019 Jan 21;14:2. doi: 10.1186/s13027-019-0219-8. eCollection 2019.
Effect of hepatitis B virus DNA replication level and anti-HBV therapy on microvascular invasion of hepatocellular carcinoma.
Qu C1,2, Huang X3,2, Liu K1, Li K1, Tan B1, Qu L1, Cao J1, Zhu C1.
Author information

1
    1Department of Hepatobiliary and Pancreatic Surgery, the Affiliated Hospital of Qingdao University, No.16 Jiangsu Road, Qingdao City, 266003 Shandong Province China.
2
    3Medical College of Qingdao University, No.308 Ningxia Road, Qingdao City, 266071 Shandong Province China.
3
    2Department of Infectious Diseases, the Affiliated Hospital of Qingdao University, No. 1677 Wutaishan Road, Qingdao City, 266555 Shandong Province China.

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, P < 0.001) was an independent risk factor for MVI. Antiviral treatment for more than six months (OR = 0.37, P = 0.002) was an independent protective factor against MVI. Patient groups with severe MVI had significantly higher rates of HBV infection (P = 0.017), a detectable HBV DNA load (> 100 IU/ml) rate (P < 0.001), and obvious low antiviral treatment rate (P = 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.
KEYWORDS:

Hepatitis B virus DNA; Hepatocellular carcinoma; Microvascular invasion; Postoperative recurrence

PMID:
    30679943
PMCID:
    PMC6341680
DOI:
    10.1186/s13027-019-0219-8

StephenW

感染癌症。 2019年1月21日; 14：2。 doi：10.1186 / s13027-019-0219-8。 eCollection 2019。
乙型肝炎病毒DNA复制水平和抗HBV治疗对肝细胞癌微血管侵犯的影响。
曲C1,2，黄X3,2，刘K1，李K1，谭B1，曲L1，曹J1，朱C1。
作者信息

1
    1青岛大学附属医院肝胆胰外科，山东省青岛市江苏路16号，邮政编码266003。
2
    青岛大学医学院，青岛市宁夏路308号，山东省266071
3
    2青岛大学附属医院感染科，青岛市五台山路1677号，山东省266555

抽象
背景：

慢性乙型肝炎病毒（HBV）感染是肝硬化和肝细胞癌（HCC）发生和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月青岛大学附属医院660例肝细胞癌肝切除患者的临床和病理资料回顾性分析。
结果：

该研究共涉及660名患者，MVI发生率为46.8％（309/660）。单变量分析显示，HBV阳性表面抗原（HBsAg），可检测的HBV DNA载量和抗病毒治疗的施用与MVI的形成显着相关。血清HBsAg阳性患者的多变量logistic回归分析显示，可检测的HBV DNA载量（OR = 5.33，P <0.001）是MVI的独立危险因素。抗病毒治疗超过六个月（OR = 0.37，P = 0.002）是抵抗MVI的独立保护因素。具有严重MVI的患者组具有显着更高的HBV感染率（P = 0.017），可检测的HBV DNA载量（> 100IU / ml）率（P <0.001），以及明显的低抗病毒治疗率（P = 0.021）。
结论：

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

乙型肝炎病毒DNA;肝细胞癌;微血管侵犯;术后复发

结论：
    30679943
PMCID：
    PMC6341680
DOI：
    10.1186 / s13027-019-0219-8

StephenW

https://infectagentscancer.biome ... 6/s13027-019-0219-8