抑制致瘤性2 (ST2)比浊免疫法与酶联免疫吸附法在预测射血分数降低的心力衰竭患者生存中的比较

Lindsey Aurora, Edward Peterson, Hongsheng Gui, Nicole Zeld, James McCord, Yigal Pinto, Bernard Cook, Hani N Sabbah, L Keoki Williams, James Snider, David E Lanfear
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引用次数: 6

摘要

背景:抑瘤性2 (Suppressor of tumorigicity 2, ST2)是心衰(HF)患者预后和治疗反应的重要指标,然而,它是一种酶联免疫吸附试验(ELISA),可能比较繁琐和昂贵。可以在普通化学分析仪上运行的浊度免疫测定(TIA)可以克服这一问题。我们研究了一种新的ST2 TIA,并将其与商用ST2 (ELISA)进行了比较。方法:年龄≥18岁符合Framingham HF定义的患者在Henry Ford医院(2007年10月- 2015年3月)进行前瞻性登记并捐献血液样本。结果:试验间Spearman相关系数为0.77。非参数回归无显著比例差异(斜率= 0.97),系统差异很小(3.2 ng/mL)。在单变量分析中,TIA和ELISA ST2均与生存率显著相关,效应大小相似(HR分别为4.46和3.50)。结论:一种用于ST2定量的新型TIA方法与ELISA高度相关,并提供同样强大的风险分层。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Suppression tumorigenicity 2 (ST2) turbidimetric immunoassay compared to enzyme-linked immunosorbent assay in predicting survival in heart failure patients with reduced ejection fraction.

Background: Suppressor of tumorigenicity 2 (ST2) is a powerful marker of prognosis and treatment response in heart failure (HF), however, it is an enzyme-linked immunosorbent assay (ELISA) which may be cumbersome and costly. A turbidimetric immunoassay (TIA) that can run on common chemistry analyzers could overcome this. We studied a novel TIA for ST2, comparing it to commercial ST2 (ELISA).

Methods: Patients age ≥ 18 years meeting Framingham definition for HF were enrolled in a prospective registry (Oct 2007 - March 2015) at Henry Ford Hospital and donated blood samples. Participants with reduced ejection fraction (<50%) and available plasma samples were included and valid ST2 measurements were obtained on the same sample using both TIA and ELISA (N = 721). The primary endpoint was all cause death. Correlation between the methods was quantified. The association with survival was tested using unadjusted and adjusted (for MAGGIC score and NTproBNP) Cox models and comparing the Area Under the Curve (AUC).

Results: The inter-assay Spearman correlation coefficient was 0.77. Nonparametric regression showed no significant proportional difference (slope = 0.97) and a very small systematic difference (3.2 ng/mL). In univariate analyses, both TIA and ELISA ST2 were significant associates of survival with similar effect sizes (HR 4.46 and 3.50, respectively, both p < 0.001). In models adjusted for MAGGIC score, both ST2 remained significant in Cox models and incrementally improved AUC vs. MAGGIC alone (MAGGIC AUC = 0.757; TIA + MAGGIC AUC = 0.786, p = 0.025; ELISA + MAGGIC AUC = 0.793, p = 0.033). In models with both MAGGIC and NTproBNP included, both ST2 still remained significant but did not improve AUC.

Conclusions: A novel TIA method for ST2 quantification correlates highly with ELISA and offers similarly powerful risk-stratification.

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