Wei Xubiao, Li Nan, Li Shanshan, Shi Jie, Guo Weixing, Zheng Yaxin, Cheng Shuqun
Department of Hepatic Surgery VI, Eastern Hepatobiliary Surgery Hospital, Second Military Medical University, 225 Changhai Road, Yangpu District, Shanghai, 200438, China.
BMC Cancer. 2017 May 2;17(1):304. doi: 10.1186/s12885-017-3293-6.
Vascular 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.
Patients 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.
A 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).
In HCC patients, HBV infection and active HBV replication were associated with the development of vascular invasion.
血管侵犯，包括微血管侵犯（MVI）和门静脉癌栓（PVTT），与肝细胞癌（HCC）术后复发相关。我们旨在研究乙型肝炎病毒（HBV）活性对血管侵犯发生的潜在影响。
回顾性纳入并分析接受肝切除术的HBV及HCC肿瘤相关因素患者，以确定发生血管侵犯的危险因素。
本研究共纳入486例患者。包括MVI和PVTT在内的血管侵犯患者总体比例为60.3%（293/486）。MVI发生率为58.2%（283/486），而PVTT为22.2%（108/486）。单因素分析显示，乙型肝炎病毒表面抗原（HBsAg）阳性与血管侵犯显著相关。在对HBV相关HCC患者进行的多因素回归分析中，乙型肝炎病毒e抗原（HBeAg）阳性（OR = 1.83，P = 0.019）和可检测到的血清HBV DNA载量（OR = 1.68，P = 0.027）是血管侵犯的独立危险因素。重度MVI组患者血清HBsAg阳性率（P = 0.005）、血清HBeAg阳性率（P = 0.016）、可检测到的血清HBV DNA载量（>50 IU/ml）（P < 0.001）显著高于轻度MVI组和MVI阴性组，抗病毒治疗率（P = 0.002）低于轻度MVI组和MVI阴性组。而与无PVTT或PVTT侵犯同侧门静脉的患者相比，PVTT侵犯主干的HCC患者HBsAg阳性率（P = 0.007）、HBeAg阳性率（P = 0.04）、肝硬化发生率（P = 0.005）显著更高，接受抗病毒治疗率（P = 0.009）更低。血管侵犯患者的血清HBV DNA载量水平也显著高于无血管侵犯患者（P = 0.008）。
在HCC患者中，HBV感染和活跃的HBV复制与血管侵犯的发生相关。
