Serum regenerative islet-derived protein 1α: a novel and sensitive biomarker for endoscopic disease activity in ulcerative colitis

血清再生胰岛衍生蛋白1α:溃疡性结肠炎内镜疾病活动性的新型敏感生物标志物

阅读:1

Abstract

INTRODUCTION: Mucosal healing (MH) has established as a long-term therapeutic goal for inflammatory bowel disease (IBD). Regenerative Islet-derived Protein 1α (reg1α) was reported to be closely related to gastrointestinal mucosal injury; however, its potential in monitoring MH remains unexplored. METHODS: Serum reg1α levels were quantified in 156 consecutive IBD patients (January 2021-December 2023) and stratified by endoscopic findings into MH (n = 136) and non-mucosal healing (NMH) groups. Diagnostic performance of reg1α was evaluated and compared to C-reactive protein (CRP) using receiver operating characteristic analysis. RESULTS: A total of 136 patients (85 with CD and 51 with UC) were finally included. Serum reg1α levels were significantly correlated with endoscopic activity. Patients in NMH group demonstrating markedly higher reg1α levels than those in MH group (92.6 vs. 55.5 ng/ml, p < 0.001). In UC, reg1α outperformed CRP in sensitivity (82.4% vs. 55.9%, p = 0.012) and accuracy (80.4% vs. 70.6%, p = 0.001) for monitoring MH. This superiority persisted in UC subgroups with non-or mild clinical symptoms. Combined index (reg1α + CRP) and multivariate model (incorporating clinical indices, reg1α and CRP) also enhanced sensitivity and accuracy over CRP alone in UC (all p < 0.05). However, reg1α showed no significantly higher efficacy in monitoring NMH compared to CRP in CD. In CRP-normal patients, patients with NMH had higher reg1α levels than those with MH in UC (77.6 vs. 49.8 ng/ml, p = 0.018), but not in CD. CONCLUSION: Reg1α represents as a novel and sensitive biomarker of endoscopic disease activity in patients with UC, even in patients with non- or mild clinical symptoms or normal CRP levels.

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。