尽管成功进行了抗乙型肝炎病毒治疗和肿瘤消融，但新的，

StephenW

World J Hepatol. 2019 Jan 27;11(1):65-73. doi: 10.4254/wjh.v11.i1.65.
Persistent risk for new, subsequent new and recurrent hepatocellular carcinoma despite successful anti-hepatitis B virus therapy and tumor ablation: The need for hepatitis B virus cure.
Shinn BJ1, Martin A1, Coben RM1, Conn MI1, Prieto J1, Kroop H1, DiMarino AJ1, Hann HW2.
Author information

1
    Division of Gastroenterology and Hepatology, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PA 19107, United States.
2
    Division of Gastroenterology and Hepatology, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PA 19107, United States. [email protected].

Abstract

Hepatitis B virus (HBV) is one of the most significant hepatocarcinogens. The ultimate goal of anti-HBV treatment is to prevent the development of hepatocellular carcinoma (HCC). During the last two decades, with the use of currently available anti-HBV therapies (lamivudine, entecavir and tenofovir disoproxil fumatate), there has been a decrease in the incidence of HBV-associated HCC (HBV-HCC). Furthermore, several studies have demonstrated a reduction in recurrent or new HCC development after initial HCC tumor ablation. However, during an observation period spanning 10 to 20 years, several case reports have demonstrated the development of new, subsequent new and recurrent HCC even in patients with undetectable serum HBV DNA. The persistent risk for HCC is attributed to the presence of covalently closed circular DNA (cccDNA) in the hepatocyte nucleus which continues to work as a template for HBV replication. While a functional cure (loss of hepatitis B surface antigen and undetectable viral DNA) can be attained with nucleos(t)ide analogues, these therapies do not eliminate cccDNA. Of utmost importance is successful eradication of the transcriptionally active HBV cccDNA from hepatocyte nuclei which would be considered a complete cure. The unpredictable nature of HCC development in patients with chronic HBV infection shows the need for a complete cure. Continued support and encouragement for research efforts aimed at developing curative therapies is imperative. The aims of this minireview are to highlight these observations and emphasize the need for a cure for HBV.
KEYWORDS:

Antiviral therapy; Hepatitis B; Hepatocellular carcinoma; Persistent Risk for hepatocellular carcinoma; Tumor ablation

PMID:
    30705719
PMCID:
    PMC6354125
DOI:
    10.4254/wjh.v11.i1.65

StephenW

世界J Hepatol。 2019年1月27日; 11（1）：65-73。 doi：10.4254 / wjh.v11.i1.65。
尽管成功进行了抗乙型肝炎病毒治疗和肿瘤消融，但新的，随后的新发和复发性肝细胞癌仍然存在风险：需要乙型肝炎病毒治愈。
Shinn BJ1，Martin A1，Coben RM1，Conn MI1，Prieto J1，Kroop H1，DiMarino AJ1，Hann HW2。
作者信息

1
    美国宾夕法尼亚州费城托马斯杰斐逊大学医院医学系消化内科和肝脏病科，19107，美国。
2
    美国宾夕法尼亚州费城托马斯杰斐逊大学医院医学系消化内科和肝脏病科，19107，美国。 [email protected]。

抽象

乙型肝炎病毒（HBV）是最重要的肝癌之一。抗HBV治疗的最终目标是预防肝细胞癌（HCC）的发展。在过去二十年中，通过使用目前可用的抗HBV疗法（拉米夫定，恩替卡韦和替诺福韦地索普西酯富马酸盐），HBV相关HCC（HBV-HCC）的发病率降低。此外，一些研究已经证明在初始HCC肿瘤消融后复发或新的HCC发展减少。然而，在一个跨越10到20年的观察期间，一些病例报告证明了新的，随后的新的和复发的HCC的发展，即使在血清HBV DNA检测不到的患者中也是如此。 HCC的持续风险归因于肝细胞核中存在共价闭合环状DNA（cccDNA），其继续作为HBV复制的模板。虽然可以用核苷（t）ide类似物实现功能性治愈（乙型肝炎表面抗原和不可检测的病毒DNA的丧失），但这些疗法不能消除cccDNA。最重要的是成功地从肝细胞核中根除转录活性的HBV cccDNA，这被认为是完全治愈的。慢性HBV感染患者HCC发展的不可预测性表明需要彻底治愈。必须继续支持和鼓励旨在开发治疗疗法的研究工作。这种观点的目的是强调这些观察结果，并强调治疗HBV的必要性。
关键词：

抗病毒治疗;乙型肝炎;肝细胞癌;肝细胞癌的持续风险;肿瘤消融

结论：
    30705719
PMCID：
    PMC6354125
DOI：
    10.4254 / wjh.v11.i1.65