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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
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