可溶性程序性细胞死亡-1 是长期核苷（酸）类似物治疗停止

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可溶性程序性细胞死亡-1 是长期核苷（酸）类似物治疗停止时慢性乙型肝炎患者 HBsAg 丢失的新预测因子
      

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作者 廖 G, Liu Z, Xia M, Chen H, Wu H, Li B, Yu T, Cai S , Zhang X, Peng J

2022 年 2 月 5 日收到

2022 年 4 月 23 日接受出版

2022 年 4 月 29 日出版第 2022 卷：15 页 2347-2357

DOI https://doi.org/10.2147/IDR.S360202

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批准出版的编辑：Héctor M Mora-Montes 教授
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Guichan Liao, Ziying Liu, Muye Xia, Hongjie Chen, Houji Wu, Bing Li, Tao Yu, Shaohang Cai, 张晓勇, 彭杰

器官衰竭研究国家重点实验室，广东省病毒性肝炎研究重点实验室，南方医科大学南方医院传染病科，中华人民共和国广州

通讯作者：中国广州南方医科大学南方医院传染病科，器官衰竭研究国家重点实验室，广东省病毒性肝炎研究重点实验室，彭杰，电话+86 20 6278 7428，传真+ 86 20 8771 9653, 邮箱 [email protected]

目的：免疫抑制受体，程序性死亡 1 (PD-1)，在慢性病毒感染期间的免疫抑制中起关键作用。对于停止长期核苷（酸）类似物（NA）治疗的慢性乙型肝炎患者，循环可溶性 PD-1（sPD-1）的意义仍然未知。
患者和方法：使用来自停止长期 NA 治疗的慢性乙型肝炎患者的系列血液样本进行了一项前瞻性队列研究。目前的分析包括 115 名在停用 NA 时 HBV DNA 阴性和 HBsAg 阳性的非肝硬化患者。使用夹心酶联免疫测定法测量所有可用样品中的 sPD-1 水平。
结果：62 例患者出现临床复发，14 例 HBsAg 消失，8 年累积率分别为 56.6% 和 23.4%。 sPD-1 的时间依赖性接受者操作特征曲线分析得出 156 pg/mL，相当于可检测阈值，作为预测 8 年临床复发的最佳截止值。治疗结束时 (EOT) 可检测到 sPD-1 的患者的临床复发率显着降低（48% vs 67%，风险比 [HR] 0.454，​​p = 0.006），但 HBsAg 消失的可能性显着更高（33.7 % vs 2.4%，HR 9.17，p = 0.038），分别与那些无法检测到 sPD-1 的人相比。
结论：EOT sPD-1 水平可预测治疗停止后的临床复发和 HBsAg 消失，并可能有助于指导慢性乙型肝炎病毒感染患者的有限 NA 治疗计划。

关键词：慢性乙型肝炎，停药，程序性细胞死亡1蛋白，核苷（酸）类似物

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Soluble Programmed Cell Death-1 is a Novel Predictor of HBsAg Loss in Chronic Hepatitis B Patients When Long-Term Nucleos(t)ide Analog Treatment is Discontinued
      

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Authors Liao G, Liu Z, Xia M, Chen H, Wu H, Li B, Yu T, Cai S , Zhang X, Peng J

Received 5 February 2022

Accepted for publication 23 April 2022

Published 29 April 2022 Volume 2022:15 Pages 2347—2357

DOI https://doi.org/10.2147/IDR.S360202

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Professor Héctor M Mora-Montes
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Guichan Liao, Ziying Liu, Muye Xia, Hongjie Chen, Houji Wu, Bing Li, Tao Yu, Shaohang Cai, Xiaoyong Zhang, Jie Peng

State Key Laboratory of Organ Failure Research, Guangdong Provincial Key Laboratory of Viral Hepatitis Research, Department of Infectious Diseases, Nanfang Hospital, Southern Medical University, Guangzhou, People’s Republic of China

Correspondence: Jie Peng, State Key Laboratory of Organ Failure Research, Guangdong Provincial Key Laboratory of Viral Hepatitis Research, Department of Infectious Diseases, Nanfang Hospital, Southern Medical University, Guangzhou, People’s Republic of China, Tel +86 20 6278 7428, Fax +86 20 8771 9653, Email [email protected]

Purpose: The immunoinhibitory receptor, programmed death 1 (PD-1), plays a critical role in immune suppression during chronic viral infection. The significance of circulating soluble PD-1 (sPD-1) in patients with chronic hepatitis B who have discontinued long-term nucleos(t)ide analog (NA) treatment remains unknown.
Patients and Methods: A prospective cohort study was conducted using serial blood samples from chronic hepatitis B patients who discontinued long-term NA treatment. The current analysis included 115 non-cirrhotic patients with HBV DNA negative and HBsAg positive at the moment of NA discontinuation. Levels of sPD-1 were measured in all available samples using sandwich enzyme-linked immunoassay.
Results: Sixty-two patients experienced a clinical relapse and 14 occurred HBsAg loss, with 8-year cumulative rates of 56.6% and 23.4%, respectively. Time-dependent receiver operating characteristic curve analysis for sPD-1 derived 156 pg/mL, which is equivalent to the detectable threshold, as an optimal cut-off value for predicting 8-year clinical relapse. Patients with detectable sPD-1 at end of treatment (EOT) had a significant lower incidence of clinical relapse (48% vs 67%, hazard ratio [HR] 0.454, p = 0.006), but a remarkable higher probability of HBsAg loss (33.7% vs 2.4%, HR 9.17, p = 0.038), compared to those who with undetectable sPD-1, respectively.
Conclusion: EOT sPD-1 levels predicted clinical relapse and HBsAg loss after treatment discontinuation and may help to guide a finite NA treatment plan for patients with chronic hepatitis B virus infection.

Keywords: chronic hepatitis B, discontinuation, programmed cell death 1 protein, nucleos(t)ide analogs

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