Abstract
BackgroundVascular invasion, including microvascular invasion (MVI) and portal vein tumor thrombus (PVTT), is associated with the postoperative recurrence of hepatocellular carcinoma (HCC). We aimed to investigate the potential impact of hepatitis B virus (HBV) activity on the development of vascular invasion.MethodsPatients with HBV and tumor-related factors of HCC who had undergone hepatectomy were retrospectively enrolled and analyzed to identify the risk factors for developing vascular invasion.ResultsA total of 486 patients were included in this study. The overall proportion of patients with vascular invasion, including MVI and PVTT, was 60.3% (293/486). The incidence of MVI was 58.2% (283/486) whereas PVTT was 22.2% (108/486). Univariate analysis revealed that positive Hepatitis B virus surface Antigen (HBsAg) was significantly associated with the presence of vascular invasion. In a multivariate regression analysis carried out in patients with HBV-related HCC, positive Hepatitis B virus e Antigen (HBeAg)(OR = 1.83, P = 0.019) and a detectable seral HBV DNA load (OR = 1.68, P = 0.027) were independent risk factors of vascular invasion. The patients in the severe MVI group had a significantly higher rate of positive seral HBsAg (P = 0.005), positive seral HBeAg (P = 0.016), a detectable seral HBV DNA load (> 50 IU/ml) (P < 0.001) and a lower rate of anti-viral treatment (P = 0.002) compared with those in the mild MVI group and MVI-negative group. Whereas, HCC with PVTT invading the main trunk showed a significantly higher rate of positive HBsAg (P = 0.007), positive HBeAg (P = 0.04), cirrhosis (P = 0.005) and a lower rate of receiving antiviral treatment (P = 0.009) compared with patients with no PVTT or PVTT invading the ipsilateral portal vein. Patients with vascular invasion also had a significantly higher level of seral HBV DNA load than patients without vascular invasion (P = 0.008).ConclusionsIn HCC patients, HBV infection and active HBV replication were associated with the development of vascular invasion.
Highlights
Vascular invasion, including microvascular invasion (MVI) and portal vein tumor thrombus (PVTT), is associated with the postoperative recurrence of hepatocellular carcinoma (HCC)
Macrovascular invasion mostly occurs in the portal vein system and is known as a portal vein tumor thrombus (PVTT); a PVTT can be identified during imaging examination or intraoperative exploration
A large tumor size, multinodular lesion, elevated level of desc-carboxy prothrombin (DCP) and certain imaging characteristics were reported to be factors predicting the presence of MVI, whereas the tumor size, Edmondson-Steiner histological grading, number of nodules and α-fetoprotein (AFP) level were associated with PVTT [2, 5, 7, 8]
Summary
Vascular invasion, including microvascular invasion (MVI) and portal vein tumor thrombus (PVTT), is associated with the postoperative recurrence of hepatocellular carcinoma (HCC). Surgical resection and liver transplantation could offer a promising prognosis for selected patients with HCC, the high postoperative recurrence rate has impaired long-time survival. Vascular invasion, including microvascular and macrovascular invasion, has been proven to be an independent factor predicting high recurrence and poor survival rate [2,3,4]. A large tumor size, multinodular lesion, elevated level of desc-carboxy prothrombin (DCP) and certain imaging characteristics were reported to be factors predicting the presence of MVI, whereas the tumor size, Edmondson-Steiner histological grading, number of nodules and α-fetoprotein (AFP) level were associated with PVTT [2, 5, 7, 8]
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