Table_1_Selenium-Binding Protein 1 (SELENBP1) as Biomarker for Adverse Clinical Outcome After Traumatic Spinal Cord Injury.DOCX

Introduction: Traumatic spinal cord injury (TSCI) presents a diagnostic challenge as it may have dramatic consequences for the affected patient. Additional biomarkers are needed for improved care and personalized therapy.Objective: Serum selenium binding protein 1 (SELENBP1) has been detected in myocardial infarction, reflecting hypoxic tissue damage and recovery odds. As SELENBP1 is usually not detected in the serum of healthy subjects, we tested the hypothesis that it may become detectable in TSCI and indicate tissue damage and regeneration odds.Methods: In this prospective observational study, patients with comparable injuries were allocated to three groups; vertebral body fractures without neurological impairment (control “C”), TSCI without remission (“G0”), and TSCI with signs of remission (“G1”). Consecutive serum samples were available from different time points and analyzed for SELENBP1 by sandwich immunoassay, for trace elements by X-ray fluorescence and for cytokines by multiplex immunoassays.Results: Serum SELENBP1 was elevated at admission in relation to the degree of neurological impairment [graded as A, B, C, or D according to the American Spinal Injury Association (AISA) impairment scale (AIS)]. Patients with the most severe neurological impairment (classified as AIS A) exhibited the highest SELENBP1 concentrations (p = 0.011). During the first 3 days, SELENBP1 levels differed between G0 and G1 (p = 0.019), and dynamics of SELENBP1 correlated to monocyte chemoattractant protein 1, chemokine ligand 3 and zinc concentrations.Conclusion: Circulating SELENBP1 concentrations are related to the degree of neurological impairment in TSCI and provide remission odds information. The tight correlation of SELENBP1 with CCL2 levels provides a novel link between Se metabolism and immune cell activation, with potential relevance for neurological damage and regeneration processes, respectively.

引言：创伤性脊髓损伤（TSCI）在诊断上构成了挑战，因为它可能对受影响的病人产生灾难性的后果。为了提高护理质量和实现个性化治疗，需要更多的生物标志物。目标：血清硒结合蛋白1（SELENBP1）在心肌梗死中被检测到，反映了缺氧性组织损伤和恢复的可能性。由于SELENBP1通常不在健康人的血清中检测到，我们假设它在TSCI中可能变得可检测，并指示组织损伤和再生的可能性。方法：在这项前瞻性观察性研究中，具有可比损伤的患者被分配到三个组；无神经功能损害的椎体骨折（对照组“C”）、无缓解的TSCI（G0组）和有缓解迹象的TSCI（G1组）。连续的血清样本在不同时间点可用，并通过夹心免疫测定法分析SELENBP1，通过X射线荧光分析微量元素，通过多重免疫测定法分析细胞因子。结果：血清SELENBP1在入院时与神经功能损害程度（根据美国脊髓损伤协会（AISA）损害量表[AIS]分级为A、B、C或D）相关升高。神经功能损害最严重的患者（归类为AIS A）表现出最高的SELENBP1浓度（p = 0.011）。在前3天，G0组和G1组之间的SELENBP1水平存在差异（p = 0.019），SELENBP1的动态变化与单核细胞趋化蛋白1、趋化因子配体3和锌浓度相关。结论：循环中的SELENBP1浓度与TSCI的神经功能损害程度相关，并提供了缓解的可能性信息。SELENBP1与CCL2水平紧密相关，为硒代谢与免疫细胞激活之间提供了一个新的联系，这对于神经损伤和再生过程可能具有潜在的相关性。