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标题: 治疗结束 HBsAg、HBcrAg 和 HBV RNA 可预测慢性乙型肝炎患者治疗 [打印本页]

作者: StephenW    时间: 2022-8-9 21:30     标题: 治疗结束 HBsAg、HBcrAg 和 HBV RNA 可预测慢性乙型肝炎患者治疗

治疗结束 HBsAg、HBcrAg 和 HBV RNA 可预测慢性乙型肝炎患者治疗后 ALT 突然发作的风险
西尔维娅·M·布雷肯霍夫 1、罗伯特·J·德克奈特 2、玛戈·J·H·范·坎彭豪特 2、安妮米克·阿·范·德·艾克 3、威廉·P·布劳威尔 2、弗洛里安·范·博梅尔 4、安德烈·布恩斯特拉 2、贝蒂娜·E·汉森 5、托马斯·伯格 4、哈里·L·A·詹森6、罗伯特·德曼 2、米兰·J·索内维尔德 2
隶属关系
隶属关系

    1
    荷兰鹿特丹大学医学中心 Erasmus MC 胃肠病学和肝病学系。电子地址:[email protected]
    2
    荷兰鹿特丹大学医学中心 Erasmus MC 胃肠病学和肝病学系。
    3
    荷兰鹿特丹大学医学中心 Erasmus MC 病毒科学系。
    4
    德国莱比锡莱比锡大学医学中心第二医学系肝病科。
    5
    多伦多肝病中心,多伦多总医院,大学健康网络,多伦多,加拿大;加拿大多伦多大学卫生政策、管理和评估研究所。
    6
    多伦多肝病中心,多伦多总医院,大学健康网络,多伦多,加拿大。

    PMID:35941076 DOI:10.1016/j.jmii.2022.06.002

抽象的

背景/目的:由于停药后 ALT 突然发作与不良结局相关,因此风险分层非常重要。我们的目的是研究非治疗性发作是否与病毒学结果相关,以及治疗结束 (EOT) 时新型生物标志物的血清水平是否可以预测发作。

方法:研究了参与三项基于聚乙二醇干扰素治疗的全球随机试验(99-01,PARC,ARES)的慢性乙型肝炎患者。 HBV RNA、HBsAg 和 HBcrAg 在 EOT 进行量化。 EOT 生物标志物水平和耀斑之间的关联被评估为连续数据和分类后。发作定义为治疗停止后六个月内 ALT ≥5xULN。

结果:我们纳入了 344 名患者; 230 HBeAg 阳性和 114 HBeAg 阴性。患者主要是白种人(77.0%),基因型 A/B/C/D 占 23.3/7.3/13.4/52.3%。在 122 名患者 (35.5%) 中观察到发作。发作与较低的持续反应率相关(在有和没有发作的患者中分别为 3.5% 和 26.8%;p < 0.001)。较高的 HBsAg (OR 1.586, 95%CI 1.231-2.043)、HBV RNA (OR 1.695, 95%CI 1.371-2.094) 和 HBcrAg (OR 1.518, 95%CI 1.324-1.740) 水平与较高的发作风险相关 (p < 0.001)。生物标志物的组合进一步改善了风险分层,尤其是 HBsAg + HBV RNA。在针对包括 HBeAg 状态和 EOT 反应(HBV DNA <200 IU/mL)在内的潜在预测因素进行调整的多变量分析中,结果是一致的。

结论:未治疗的 ALT 耀斑与有利的病毒学结果无关。较高的 EOT 血清 HBsAg、HBcrAg 和 HBV RNA 与停药后发作的较高风险相关。这些发现可用于指导有关停止治疗和治疗后随访的决策。

试验注册:ClinicalTrials.gov:NCT00114361、NCT00146705、NCT00877760。

关键词:耀斑;乙肝病毒;乙型肝炎病毒;肝病学;肝;血清生物标志物。

版权所有 © 2022。Elsevier B.V. 出版
利益冲突声明

竞争利益声明 SB 从 Gilead 获得了不受限制的研究资助。 AB 已获得罗氏、吉利德科学、富士瑞生物和杨森的研究资助。 RdK 获得了来自 Gilead、Janssen、AbbVie 和 Norgine 的咨询/演讲酬金,并获得了 Gilead 和 Janssen 的研究资助。 FvB 已获得研究支持并为罗氏提供咨询服务。 TB 已获得研究支持、咨询和/或演讲费用 Gilead、Roche、Merck、AbbVie、Bristol-Myers Squibb 和 Janssen。 BH 已从 Intercept、Cymbay、Genfit、Mirum、Albireo、Calliditas 和 Cheomab 获得研究支持和咨询费用。 HJ 收到了来自 Gilead、Roche、Merck、AbbVie、Bristol-Myers Squibb、Arbutus、Janssen 和 MedImmune 的研究支持、咨询和/或演讲费用。 MS 已获得罗氏、Innogenetics、BMS、吉利德和 Fujirebio 的演讲者费用和研究支持。其他作者报告没有披露。
作者: StephenW    时间: 2022-8-9 21:30

End-of-treatment HBsAg, HBcrAg and HBV RNA predict the risk of off-treatment ALT flares in chronic hepatitis B patients
Sylvia M Brakenhoff  1 , Robert J de Knegt  2 , Margo J H van Campenhout  2 , Annemiek A van der Eijk  3 , Willem P Brouwer  2 , Florian van Bömmel  4 , André Boonstra  2 , Bettina E Hansen  5 , Thomas Berg  4 , Harry L A Janssen  6 , Robert A de Man  2 , Milan J Sonneveld  2
Affiliations
Affiliations

    1
    Department of Gastroenterology and Hepatology, Erasmus MC, University Medical Center, Rotterdam, the Netherlands. Electronic address: [email protected].
    2
    Department of Gastroenterology and Hepatology, Erasmus MC, University Medical Center, Rotterdam, the Netherlands.
    3
    Department of Viroscience, Erasmus MC, University Medical Center, Rotterdam, the Netherlands.
    4
    Division of Hepatology, Department of Medicine II, Leipzig University Medical Center, Leipzig, Germany.
    5
    Toronto Center for Liver Disease, Toronto General Hospital, University Health Network, Toronto, Canada; Institute of Health Policy, Management and Evaluation, University of Toronto, Toronto, Canada.
    6
    Toronto Center for Liver Disease, Toronto General Hospital, University Health Network, Toronto, Canada.

    PMID: 35941076 DOI: 10.1016/j.jmii.2022.06.002

Abstract

Background/purpose(s): Since ALT flares after therapy withdrawal are associated with adverse outcomes, risk stratification is of major importance. We aimed to study whether off-treatment flares are related with virological outcomes, and if serum levels of novel biomarkers at end-of-treatment (EOT) can predict flares.

Methods: Chronic hepatitis B patients who participated in three global randomised trials of peginterferon-based therapy were studied (99-01, PARC, ARES). HBV RNA, HBsAg and HBcrAg were quantified at EOT. Associations between EOT biomarker levels and flares were assessed as continuous data and after categorisation. Flares were defined as ALT ≥5xULN during six months after therapy cessation.

Results: We included 344 patients; 230 HBeAg-positive and 114 HBeAg-negative. Patients were predominantly Caucasian (77.0%) and had genotype A/B/C/D in 23.3/7.3/13.4/52.3%. Flares were observed in 122 patients (35.5%). Flares were associated with lower rates of sustained response (3.5% vs 26.8% among patients with and without a flare; p < 0.001). Higher HBsAg (OR 1.586, 95%CI 1.231-2.043), HBV RNA (OR 1.695, 95%CI 1.371-2.094) and HBcrAg (OR 1.518, 95%CI 1.324-1.740) levels were associated with higher risk of flares (p < 0.001). Combinations of biomarkers further improved risk stratification, especially HBsAg + HBV RNA. Findings were consistent in multivariate analysis adjusted for potential predictors including HBeAg-status and EOT-response (HBV DNA <200 IU/mL).

Conclusion: Off-treatment ALT flares were not associated with favourable virological outcomes. Higher EOT serum HBsAg, HBcrAg and HBV RNA were associated with a higher risk of flares after therapy withdrawal. These findings can be used to guide decision-making regarding therapy discontinuation and off-treatment follow-up.

Trial registration: ClinicalTrials.gov: NCT00114361, NCT00146705, NCT00877760.

Keywords: Flare; HBV; Hepatitis B virus; Hepatology; Liver; Serum biomarkers.

Copyright © 2022. Published by Elsevier B.V.
Conflict of interest statement

Declaration of competing interest SB received an unrestricted research grant from Gilead. AB has been received research grants from Roche, Gilead Sciences, Fujirebio, and Janssen. RdK has received honoraria for consulting/speaking from Gilead, Janssen, AbbVie, and Norgine and received research grants form Gilead and Janssen. FvB has received research support and provided consultancy for Roche. TB has received research support, consulting and/or speaking fees Gilead, Roche, Merck, AbbVie, Bristol-Myers Squibb, and Janssen. BH has received research support and consultancy fees from Intercept, Cymabay, Genfit, Mirum, Albireo, Calliditas and Chemomab. HJ has received research support, consulting and/or speaking fees from Gilead, Roche, Merck, AbbVie, Bristol-Myers Squibb, Arbutus, Janssen and MedImmune. MS has received speaker’s fees and research support from Roche, Innogenetics, BMS, Gilead and Fujirebio. The other authors report no disclosures.

作者: StephenW    时间: 2022-8-9 21:30

https://doi.org/10.1016/j.jmii.2022.06.002




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