Abstract

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.

Highlights

  • Traumatic spinal cord injury (TSCI) presents a diagnostic challenge as it may have dramatic consequences for the affected patient

  • A total of 44 patients were eligible for the current study, including 34 patients with neurological impairment, divided into 19 patients with remission and 15 patients without remission

  • The TSCI was caused by a fall in 59% of cases, and by accident in 32% of cases

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Summary

Introduction

Traumatic spinal cord injury (TSCI) presents a diagnostic challenge as it may have dramatic consequences for the affected patient. Traumatic spinal cord injury (TSCI) remains one of the most severe injuries and affects predominantly young patients (Furlan et al, 2013; Spinal Cord Injury [SCI], 2016). A secondary injury phase is driven by complex inflammatory responses, involving excitotoxicity, ischemia/hypoxia, inflammation, increased spinal cord intraparenchymal pressure, and oxidative stress. These processes determine the extent of neuronal loss after the mechanical insult (Kwon et al, 2004; Shadgan et al, 2019). Objective and early biomarkers for the extent of damage with potential relevance for remission and prognosis are urgently needed (Kwon et al, 2019)

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