Soluble Programmed Cell Death-1: A Potential Predictor of HBsAg Loss in Pediatric Patients with Chronic Hepatitis B Undergoing Peginterferon Therapy

可溶性程序性细胞死亡蛋白-1:接受聚乙二醇干扰素治疗的慢性乙型肝炎患儿乙肝表面抗原消失的潜在预测因子

阅读:2

Abstract

PURPOSE: Soluble programmed cell death-1 (sPD-1) level can predict hepatitis B surface antigen (HBsAg) loss in adult chronic hepatitis B (CHB) patients. However, whether sPD-1 level can serve as a potential seromarker for predicting HBsAg loss in pediatric patients remained to determine. PATIENTS AND METHODS: Ninety-two pediatric HBeAg-positive CHB patients who received peginterferon (PegIFN) therapy with available serum samples were studied retrospectively. The average follow-up time was 45.0 months. Virological biomarkers and sPD-1 were serially measured. RESULTS: A total of 45 (48.9%) children achieved HBsAg loss at the end of treatment (EOT), and 84.4% (38/45) of them remained HBsAg-negative at the end of follow-up. At baseline, sPD-1 levels were comparable between patients who subsequently achieved HBsAg loss and those who did not (P = 0.217). However, a significantly more pronounced increase in sPD-1 levels was observed during PegIFN treatment in the HBsAg loss group (P(trend) < 0.001). Consequently, at weeks 12, 24, and EOT, sPD-1 levels were significantly higher in children with HBsAg loss compared to those without (P < 0.001 at all time-points). In ROC curve analysis, sPD-1 had strong discriminatory ability for HBsAg loss at weeks 12 and 24, with area under ROC scores of 0.842 (95% CI, 0.744-0.946) and 0.863 (95% CI, 0.758-0.969), respectively, slightly lower than HBsAg but higher than HBV DNA. CONCLUSION: Early on-treatment serum sPD-1 level has a potential predictive value for HBsAg loss in pediatric patients with HBeAg-positive CHB, which might provide a clue to optimize the management of PegIFN therapy. However, a prospective, multi-center study is warranted for further validation.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。