持续低水平的乙肝病毒会在治疗过程中促进纤维化进程。

StephenW

Clin Gastroenterol Hepatol. 2020 Mar 5. pii: S1542-3565(20)30272-X. doi: 10.1016/j.cgh.2020.03.001. [Epub ahead of print]
Persistent Low Level of Hepatitis B Virus Promotes Fibrosis Progression During Therapy.
Sun Y1, Wu X1, Zhou J1, Meng T1, Wang B1, Chen S1, Liu H2, Wang T3, Zhao X1, Wu S1, Kong Y1, Ou X1, Wee A4, Theise ND5, Qiu C6, Zhang W6, Lu F7, Jia J8, You H9.
Author information

1
    Liver Research Center, Beijing Friendship Hospital, Capital Medical University, Beijing Key Laboratory of Translational Medicine on Liver Cirrhosis, National Clinical Research Center of Digestive Diseases, Beijing, China.
2
    Department of Pathology, Beijing You-an Hospital, Capital Medical University, Beijing, China.
3
    Department of Pathology, China-Japan Friendship Hospital, Beijing, China.
4
    Department of Pathology, Yong Loo Lin School of Medicine, National University of Singapore, National University Hospital, Singapore.
5
    Department of Pathology, New York University School of Medicine, New York, NY, USA.
6
    Department of Infectious Diseases, Huashan Hospital, Fudan University, Shanghai, China.
7
    State Key Laboratory of Natural and Biomimetic Drugs, Department of Microbiology & Infectious Disease Center, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China.
8
    Liver Research Center, Beijing Friendship Hospital, Capital Medical University, Beijing Key Laboratory of Translational Medicine on Liver Cirrhosis, National Clinical Research Center of Digestive Diseases, Beijing, China;. Electronic address: [email protected].
9
    Liver Research Center, Beijing Friendship Hospital, Capital Medical University, Beijing Key Laboratory of Translational Medicine on Liver Cirrhosis, National Clinical Research Center of Digestive Diseases, Beijing, China;. Electronic address: [email protected].

Abstract
BACKGROUND & AIMS:

Progression of liver fibrosis still occurs in some patients with chronic hepatitis B virus (HBV) infection despite antiviral therapy. We aimed to identify risk factors for fibrosis progression in patients who received antiviral therapy.
METHODS:

We conducted a longitudinal study of patients with chronic HBV infection and liver biopsies collected before and after 78 weeks of anti-HBV therapy. Fibrosis progression was defined as Ishak stage increase ≥ 1 or as predominantly progressive classified by P-I-R system (Beijing Classification). Levels of HBV DNA and HBV RNA in blood samples were measured by real-time quantitative PCR. HBV RNA in liver tissue was detected by in situ hybridization.
RESULTS:

A total of 239 patients with chronic HBV infection with paired liver biopsies were included. Among the 163 patients with significant fibrosis at baseline (Ishak ≥ stage 3), fibrosis progressed in 22 patients (13%), was indeterminate in 24 patients (15%), and regressed in 117 patients (72%). Univariate and multivariate analyses revealed that independent risk factors for fibrosis progression were higher rate of detected HBV DNA at week 78 (odds ratio, 4.84; 95% CI, 1.30-17.98; P=.019) and alcohol intake (odds ratio, 23.84; 95% CI, 2.68-212.50; P=.004). HBV DNA was detected in blood samples from a significantly higher proportion of patients with fibrosis progression (50%) at week 78 than patients with fibrosis regression (19%) or indeterminate fibrosis (26%) (P=.015), despite low viremia (20-200 IU/mL) in all groups. The decrease of serum HBV RNA from baseline in the fibrosis regression group was larger than that in the fibrosis progression group.
CONCLUSIONS:

In a longitudinal study of patients with chronic HBV infection, we associated liver fibrosis progression at week 78 of treatment with higher rates of detected HBV DNA. We propose that a low level of residual HBV may still promote fibrosis progression, and that patients' levels of HBV DNA should be carefully monitored.

Copyright © 2020 AGA Institute. Published by Elsevier Inc. All rights reserved.
KEYWORDS:

CHB; efficacy; low viremia; regression

PMID:
    32147592
DOI:
    10.1016/j.cgh.2020.03.001

StephenW

Castro Gastroenterol Hepatol。 2020年3月5日。pii：S1542-3565（20）30272-X。 doi：10.1016 / j.cgh.2020.03.001。 [Epub提前发行]
持续低水平的乙肝病毒会在治疗过程中促进纤维化进程。
孙Y1，吴X1，周J1，孟T1，王B1，陈S1，刘H2，王T3，赵X1，吴S1，孔Y1，欧X1，Wee A4，Theise ND5，邱C6，张W6，陆F7 ，贾J8，游H9。
作者信息

1个
    首都医科大学附属北京友谊医院肝脏研究中心，国家肝病消化病临床研究中心，北京肝硬化转化医学重点实验室，北京。
2
    首都医科大学附属北京佑安医院病理科，北京
3
    中日友好医院病理科，北京。
4
    新加坡国立大学，新加坡国立大学医院，Yong Loo Lin医学院病理学系。
5
    美国纽约大学纽约大学医学院病理学系。
6
    复旦大学附属华山医院传染病科，上海。
7
    北京大学健康科学中心基础医学学院微生物与传染病中心，天然与仿生药物国家重点实验室，北京。
8
    首都医科大学附属北京友谊医院肝病研究中心，国家肝病消化病临床研究中心，北京市肝硬化转化医学重点实验室，北京；电子地址：[email protected]。
9
    首都医科大学附属北京友谊医院肝病研究中心，国家肝病消化病临床研究中心，北京市肝硬化转化医学重点实验室，北京；电子地址：[email protected]。

抽象
背景与目的：

尽管进行了抗病毒治疗，但某些慢性乙型肝炎病毒（HBV）感染患者仍会发生肝纤维化。我们旨在确定接受抗病毒治疗的患者纤维化进展的危险因素。
方法：

我们对78例抗HBV治疗前后的慢性HBV感染和肝活检患者进行了纵向研究。纤维化进展定义为Ishak阶段增加≥1或主要通过P-I-R系统进行分类（北京分类）。通过实时定量PCR测量血液样品中的HBV DNA和HBV RNA水平。通过原位杂交检测肝组织中的HBV RNA。
结果：

总共包括239例慢性HBV感染的成对肝活检患者。在基线时（Ishak≥3期）有明显纤维化的163例患者中，有22例（13％）进展为纤维化，有24例（15％）不确定为纤维化，有117例（72％）消退。单因素和多因素分析显示，纤维化进展的独立危险因素是在第78周时检出HBV DNA的比率更高（比值比为4.84； 95％CI为1.30-17.98； P = .019）和酒精摄入量（比值比为23.84； 95％CI，2.68-212.50； P = .004）。尽管有低病毒血症，但在第78周时，从纤维化进展患者（50％）的血液样本中检测到HBV DNA的比例明显高于纤维化消退（19％）或不确定的纤维化患者（26％）（P = .015） （20-200 IU / mL）在所有组中。纤维化消退组的血清HBV RNA从基线开始的下降幅度大于纤维化进展组。
结论：

在一项关于慢性HBV感染患者的纵向研究中，我们将治疗第78周时肝纤维化的进展与检测到的HBV DNA的发生率较高相关。我们建议，低水平的残留HBV可能仍会促进纤维化进程，因此应仔细监测患者的HBV DNA水平。

版权所有©2020 AGA Institute。由Elsevier Inc.出版。保留所有权利。
关键字：

CHB;功效;低病毒血症；回归

PMID：
    32147592
DOI：
    10.1016 / j.cgh.2020.03.001

StephenW

https://www.cghjournal.org/article/S1542-3565(20)30272-X/pdf

sky8989

这样的话，我们大部分人都逃不了肝纤维化了