Virological response to entecavir is associated with a lower probability of dise

StephenW

AASLD Liver Meeting. Abstract 240. Virological response to entecavir is
associated with a lower probability of disease progression: results from
377 chronic hepatitis B patients R. Zoutendijk1; J. G. Reijnders1; F.
Zoulim2; . S. Brown3; D. J. Mutimer4; K. Deterding5; W. P. Hofmann6; J.
Petersen7; M. Fasano8; M. Buti9; T. Berg10; M. J. Sonneveld1; B. E.
Hansen1; H. Wedemeyer 5; H. L. Janssen1 1. Department of Gastroenterology
and Hepatology, Erasmus MC, Rotterdam, Netherlands. 2. Department of
Hepatology, Hospices Civils de Lyon, Lyon, France. 3. Department of
Hepatology and Gastroenterology, Imperial College , London, United Kingdom.
4. NIHR Biomedical Research Unit and Centre for Liver Research, Queen
Elizabeth Hospital, Birmingham, United Kingdom. 5. Department of
Gastroenterology, Hepatology, and Endocrinology, Medical School Hannover,
Hannover, Germany. 6. Medizinische Klinik 1, Klinikum der Johan Wolfgang
Goethe-Universitat, Frankfurt am Main, Germany. 7. Liver Unit, IFI
institute, Asklepios Klinik St. Georg, Hamburg, Germany. 8. Clinic of
Infectious Diseases, University of Bari, Bari, Italy. 9. Department of
Hepatology, Hospital Vall de Hebron, Barcelona, Spain. 10. Department of
Hepatology, University Clinic Leipzig, Leipzig, Germany.

Background The ultimate goal of hepatitis B virus (HBV) treatment is to
reduce disease progression to (decompensated) cirrhosis, hepatocellular
carcinoma (HCC) and premature death. Entecavir (ETV) inhibits HBV
replication, but whether ETV induced viral suppression is associated with
an improved clinical outcome is not well known. The aim of this study was
to investigate the effect of ETV therapy on event-free survival in chronic
HBV patients. Methods: In this investigator-initiated project we studied
all HBV monoinfected patients treated with ETV monotherapy from 10 large
European referral centers within the Virgil Network. Virological response
(VR) was defined as serum HBV DNA <80 IU/mL. Clinical endpoints considered
were hepatic decompensation, occurrence of HCC and death. Probability of
event-free survival was estimated by Kaplan Meier and Cox analysis. Results
A total of 377 patients (mean age 43±14 years; 75% male; 41% HBeAg+; HBV
DNA 5.7±2.1 log IU/ml, 30% nucleos(t)ide analogue (NA) and 22%
(peg)interferon experienced) treated with ETV monotherapy were included. A
total of 133 patients had advanced liver disease (by ultrasound or
histology) of whom 30 (23%) patients had advanced fibrosis (F3), 93 (70%)
patients had compensated cirrhosis and 10 (8%) patients had decompensated
cirrhosis at baseline. Cumulative probability of achieving VR was
comparable between these groups (p=0.49). Six patients developed
decompensation, four were diagnosed with HCC and eight patients died during
a median follow up of 19 [IQR 11-32] months. Median time to event was 36
(IQR 22-85) weeks. Patients with an event were older (p=0.08) and had a
higher MELD score at baseline (p=0.02). Occurrence of events was not
influenced by sex (p=0.37), HBeAg status (p=0.32), previous NA-therapy
(p=0.16), baseline ALT (p=0.95), HBV DNA (p=0.46) and follow up duration
(p=0.31). Cumulative probability of an event was higher in cirrhotic
patients, also when excluding decompensated patients (both p<0.001).
Importantly, patients with a VR during ETV therapy had a higher probability
of disease-free survival in a Cox model (HR 0.20, 95% CI 0.06-0.67,
p=0.009) with VR as time dependent covariate after adjusting for age, both
in the overall cohort and among patients with advanced liver disease (HR
0.18, 95% CI 0.05-0.73, p=0.02). When excluding events during the first
three months of ETV therapy this association remained significant.
Conclusion: This study shows that suppression of HBV by ETV improves the
probability of an event free survival in CHB. Importantly, the improved
clinical outcome is still apparent in patients with advanced liver disease.




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StephenW

肝病学会肝会议。摘要240。
恩替卡韦病毒学应答

降低疾病的恶化的可能性：结果从结果377慢性乙型肝炎患者
R. Zoutendijk 1，JG Reijnders1;楼
Zoulim2;布恩3; DJ Mutimer4; K. Deterding 5;可湿性粉剂Hofmann6的J.
Petersen7; M.法萨诺8 M. Buti 9 T.伯格10兆焦耳Sonneveld1;
Hansen1 H.魏德迈5; H. L.扬森1。消化内科
和肝病，荷兰鹿特丹的伊拉斯谟的MC，。 2。系
肝病，收容所Civils里昂，里昂，法国。 3。系
肝病和胃肠病学，帝国学院，伦敦，英国。
4。 NIHR生物医学研究组和肝癌的研究，皇后中心
伊利沙伯医院，伯明翰，英国。 5。系
胃肠病，肝病，内分泌，汉诺威医学院，
汉诺威，德国。 6。 1，Klinikum DER约翰沃尔夫冈Medizinische Klinik
歌德大学，德国美因河畔法兰克福。 7。肝组，国际金融机构
研究所，Asklepios Klinik圣乔治，汉堡，德国。 8。诊所
传染病，巴里，意大利巴里大学。 9。系
肝病，医院瓦尔德希伯伦，巴塞罗那，西班牙。 10。系
肝病，德国莱比锡，莱比锡大学医院。

背景B型肝炎病毒（HBV）治疗的最终目标是
减少疾病进展（失代偿期）肝硬化，肝癌
肝细胞癌（HCC）和过早死亡。恩替卡韦（ETV）抑制乙肝病毒
复制，但无论是ETV引起的病毒抑制与
改善临床结果是不为人所熟知。这项研究的目的是
ETV治疗的效果，以探讨在慢性的无事件生存
乙肝患者。方法：研究者发起的这个项目，我们研究
所有乙肝monoinfected ETV单药治疗的患者从10个大
维吉尔网络内的欧洲转介中心。病毒学应答
（VR）的定义为血清HBV DNA <80 IU /毫升。临床终点为

肝功能失代偿，肝癌的发生和死亡。概率
无事件生存率用Kaplan Meier和Cox分析估计。结果
一共有377例（平均年龄43 ± 14岁的男性75％; HBeAg的41％+;乙肝
DNA的5.7 ± 2.1logIU / ml的，30％的核苷（酸）（NA）和22％
（PEG）干扰素经历）ETV单药治疗都包括在内。一
共有133例晚期肝病（经超声或
组织学），其中30人（23％）患者有先进的纤维化（F3），93（70％）
患者肝硬化和10（8％）患者有代偿补偿
肝硬化患者在基线。实现VR的累积概率
这些群体之间具有可比性（P = 0.49）。 6个患者发展
失代偿，4个被确诊肝癌和8名患者死亡期间
中位随访19 [IQR 11-32]个月。事件的平均时间为36
（IQR 22-85）周。事件患者年龄较大（P = 0.08）和一个
较高的MELD评分在基线（P = 0.02）。事件的发生是没有
影响性（P = 0.37），HBeAg的状态（P = 0.32），以前NA治疗
（P = 0.16），基线ALT（P = 0.95），HBV - DNA（P = 0.46）和后续的持续时间
（P = 0.31）。累积概率事件是肝硬化
患者，还时不包括失代偿期患者（P <0.001）。
更重要的是，ETV治疗期间与VR的患者有较高的概率
无病生存，在Cox模型（HR 0.20，95％CI 0.06-0.67
P = 0.009）与时间依赖协变量的VR年龄调整后，无论
在整体人群中晚期肝病患者（HR
0.18，95％CI 0.05-0.73，P = 0.02）。当不包括在第一事件
这个协会ETV治疗3个月仍然显著。
结论：这项研究表明，ETV抑制HBV的提高CHB

无事件生存率
件。更重要的是，改善
在晚期肝病患者的临床结果仍是明显的。