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

Abstract

BackgroundChronic 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.MethodsA 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.ResultsThis 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).ConclusionsHBV 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.

Mechanisms of portal vein tumour thrombus formation and development in patients with hepatocellular carcinoma

“…Importantly, a lower incidence of MVI has been found in AVT patients than that in non‐AVT patients (38.7% vs. 48.6%, p = 0.001), and AVT has been demonstrated as a protective factor of MVI (OR = 0.758) and early tumour recurrence (OR = 0.732). The other two studies further showed the similar conclusions that HBV replication was an independent risk of vascular invasion and AVT had an inhibitory effect on vascular invasion formation 43,44 . In addition, in a retrospective study that included 486 patients, we reported that the serum HBV levels might be associated with the extent of vascular invasion, and AVT could suppress the development of vascular invasion in patients with HBV‐related HCC 45 …”

New Insights Into a Classification-Based Microvascular Invasion Prediction Model in Hepatocellular Carcinoma: A Multicenter Study

“…The molecular biological mechanisms of such a distinct influence remain to be clarified. Interestingly, given the previous studies which would suggest otherwise ( 16 , 32 ), we were surprised that preoperative HBV-DNA level was not found to be significantly associated with MVI in our HCC patients.…”

Preoperative antiviral therapy and microvascular invasion in hepatitis B virus-related hepatocellular carcinoma: A meta-analysis

“…Twenty-one studies were screened in the full text evaluation, and according to our inclusion criteria, 15 irrelevant records were excluded. Finally, six studies met our inclusion criteria and were, therefore, included in this meta-analysis (Huang et al, 2017;Lei et al, 2016;Li et al, 2018b;Liu et al, 2019;Qu et al, 2019;Wei et al, 2017).…”

“…Included studies were published from 2016 to 2019, and Table 1 details characteristics of all included studies. One study had a prospective design (Lei et al, 2016), and all others had a retrospective design (Huang et al, 2017;Li et al, 2018b;Liu et al, 2019;Qu et al, 2019;Wei et al, 2017). In total, of 4,988 participants, ranging from 349 to 2,362, 1,005 participants had antiviral treatment, and 2,069 participants showed MVI.…”