Apolipoprotein A-I: a non-negligible marker in hypertriglyceridemia-induced acute pancreatitis

载脂蛋白AI:高甘油三酯血症诱发急性胰腺炎中不可忽视的标志物

阅读:1

Abstract

BACKGROUND: Hypertriglyceridemia-induced acute pancreatitis (HTG-AP) is a severe subtype of pancreatitis with rapid progression and high mortality. Apolipoprotein A-I (ApoA-I), a key component of high-density lipoprotein (HDL), has anti-inflammatory and immunomodulatory properties, but its prognostic role in HTG-AP remains unclear. This study aimed to evaluate the correlation between ApoA-I levels and disease severity, progression, and clinical outcomes in HTG-AP patients. METHODS: A retrospective analysis was conducted on 154 HTG-AP patients admitted to the Second Affiliated Hospital of Nanchang University. Clinical, laboratory, and imaging data were collected, including ApoA-I levels, modified computed tomography severity index (MCTSI), Ranson and Acute Physiology and Chronic Health Evaluation II (APACHE II) score, hospitalization costs, and disease severity (mild acute pancreatitis (MAP)/moderately severe acute pancreatitis (MSAP)/severe acute pancreatitis (SAP)). Statistical analyses assessed correlations between ApoA-I and these parameters. RESULTS: ApoA-I in HTG-AP patients was significantly lower than the normal reference range (0.83 vs.1.20-1.60 g/L, p < 0.05). Lower ApoA-I correlated with higher MCTSI score (OR = 0.093, p = 0.001), Ranson score (r = - 0.36, p < 0.001), and APACHE II score (r = - 0.35, p < 0.001). Patients with severe disease (MSAP/SAP) had lower ApoA-I than MAP patients (0.755 ± 0.377 vs.1.033 ± 0.319 g/L, p = 0.001). ApoA-I also negatively correlated with hospitalization costs (r = - 0.25, p = 0.002). Receiver operating characteristic (ROC) curve analysis identified ApoA-I < 0.815 g/L as predictive of severe progression (sensitivity 80%, specificity 63.4%). CONCLUSIONS: ApoA-I was a promising early biomarker for HTG-AP severity and prognosis.

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。