AASLD2018[411]乙型肝炎病毒的差异效应 抑制肝细胞癌 根据初始

StephenW

411
Differential Effect of Hepatitis B Viral
Suppression on Hepatocellular Carcinoma
Development According to the Phase of Initial
Antiviral Treatment: A Multicenter Study
Young Chang, Jeong-Hoon Lee, Sung Won Chung, Minseok
Albert Kim, Sun Woong Kim, Hyo Young Lee, Jun Sik Yoon,
Yun Bin Lee, Eun Ju Cho, Su Jong Yu, Yoon Jun Kim and
Jung-Hwan Yoon Sr., Department of Internal Medicine and
Liver Research Institute, Seoul National University Hospital
Background: Although antiviral therapy for chronic hepatitis B
virus (HBV) infection reduces risk of hepatocellular carcinoma
(HCC), the risk is reportedly higher in the antiviral-induced
viral suppression than inactive carriers. In this study, we
aimed to compare the effect of the phases when the antiviral
treatment started on the HCC development Methods: This
retrospective study included chronic hepatitis B patients with
suppressed HBV DNA (<2,000 IU/mL) and normal alanine
aminotransferase levels and without evidence of cirrhosis
from eight referral hospitals in Korea. Study subjects were
categorized into four groups: patients underwent antiviral
treatment from immune-tolerant phase (IT group), HBeAgpositive
hepatitis phase (HBeAg+ group), or HBeAg-negative
hepatitis phase (HBeAg- group); or inactive carriers without
any antiviral treatment (IC group). Primary endpoint was an
HCC development. Kaplan-Meier survival analysis and Cox
proportional hazard model were used for statistical analysis.
Results: A total of 887 patients were included: 63 in IT
group, 151 in HBeAg+ group, 365 in HBeAg- group, and 308
in IC group. In univariate analyses, there was no significant
difference in the risk of HCC development between IT group
and IC group (hazard ratio [HR]=0.85, 95% confidence interval
[CI]=0.10–7.15, P=0.98). However, both HBeAg+ (HR=4.01,
95% CI=1.57–10.28, P=0.001) and HBeAg- (HR=3.04, 95%
CI=1.29–7.07, P=0.007) groups showed significantly higher
risk of HCC occurrence. The 5-year risk of HCC occurrence
was 5.6% in IT group, 10.9% in HBeAg+ group, 8.3% in
HBeAg- group, and 1.9% in IC group (Figure 1). In multivariate
analyses, IT group consistently showed similar risk of HCC
development compared to IC group (adjusted HR [aHR]=0.85,
95% CI=0.10–7.15, P=0.88). Both HBeAg+ (aHR=2.91,
95% CI=1.13–7.42, P=0.03) and HBeAg- (aHR=2.48, 95%
CI=1.05–5.85, P=0.04) groups showed significantly higher
risk of HCC development than IC group. Conclusion: Even if
HBV DNA suppression has equally achieved, the risk of HCC
development varies depending on the phase of initial antiviral
therapy. Early antiviral therapy from immune-tolerant phase
is associated with low risk of HCC similar to that of natural
inactive carriers which is significantly lower than the risk of
patients treated from immune-active phases.

StephenW

411
乙型肝炎病毒的差异效应
抑制肝细胞癌
根据初始阶段的发展
抗病毒治疗：多中心研究
Young Chang，Jeong-Hoon Lee，Sung Won Chung，Minseok
Albert Kim，Sun Woong Kim，Hyo Young Lee，Jun Sik Yoon，
李云斌，Eun Ju Cho，苏咏玉，尹俊金和
Jung-Hwan Yoon，内科和内科
首尔国立大学医院肝脏研究所
背景：虽然抗病毒治疗慢性乙型肝炎
病毒（HBV）感染可降低肝细胞癌的风险
（HCC），据报道，抗病毒诱导的风险更高
病毒抑制比非活动载体。在这项研究中，我们
旨在比较抗病毒药物阶段的效果
治疗开始于HCC的发展方法：这个
回顾性研究包括慢性乙型肝炎患者
抑制HBV DNA（<2,000 IU / mL）和正常丙氨酸
氨基转移酶水平，没有肝硬化的证据
来自韩国的八家转诊医院。研究对象是
分为四组：患者接受抗病毒治疗
免疫耐受期治疗（IT组），HBeAg阳性
肝炎阶段（HBeAg +组），或HBeAg阴性
肝炎阶段（HBeAg-组）;或没有的非活动运营商
任何抗病毒治疗（IC组）。主要终点是
HCC发展。 Kaplan-Meier生存分析和Cox
比例风险模型用于统计分析。
结果：共纳入887名患者：IT患者63名
组，HBeAg +组151例，HBeAg组365例，308例
在IC集团。在单变量分析中，没有显着性
IT组之间HCC发展风险的差异
和IC组（风险比[HR] = 0.85,95％置信区间
[CI] = 0.10-7.15，P = 0.98）。但是，HBeAg +均为+（HR = 4.01，
95％CI = 1.57-10.28，P = 0.001）和HBeAg-（HR = 3.04,95％
CI = 1.29-7.07，P = 0.007）组显示显着更高
发生HCC的风险。 HCC发生的5年风险
IT组为5.6％，HBeAg +组为10.9％，组为8.3％
HBeAg-组，IC组为1.9％（图1）。在多变量
分析显示，IT组始终表现出类似的HCC风险
与IC组相比的发展（调整后的HR [aHR] = 0.85，
95％CI = 0.10-7.15，P = 0.88）。 HBeAg +（aHR = 2.91，
95％CI = 1.13-7.42，P = 0.03）和HBeAg-（aHR = 2.48,95％
CI = 1.05-5.85，P = 0.04）组显示显着更高
HCC发展的风险高于IC组。结论：即使
HBV DNA抑制同样实现了HCC的风险
发育程度取决于最初的抗病毒药物的阶段
治疗。免疫耐受期的早期抗病毒治疗
与HCC相似的低风险与自然相关
不活跃的运营商，其风险显着低于
从免疫活性期治疗的患者。