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J Trace Elem Med Biol. 2019 Jan;51:141-149. doi: 10.1016/j.jtemb.2018.10.006. Epub 2018 Oct 12.

Relation of selenium status to neuro-regeneration after traumatic spinal cord injury.

Author information

1
Heidelberg Trauma Research Group, Department of Trauma and Reconstructive Surgery, Center for Orthopedics, Trauma Surgery and Spinal Cord Injury, Heidelberg University Hospital, Heidelberg, Germany.
2
Institute for Experimental Endocrinology, Charité - Universitätsmedizin Berlin, Berlin, Germany.
3
BG Trauma Centre Ludwigshafen, Department of Trauma Surgery and Orthopedics, Medical Director, Ludwigshafen, Germany.
4
Institute for Experimental Endocrinology, Charité - Universitätsmedizin Berlin, Berlin, Germany. Electronic address: lutz.schomburg@charite.de.
5
BG Trauma Centre Ludwigshafen, Department of Paraplegiology, Ludwigshafen, Germany.

Abstract

INTRODUCTION:

The trace element selenium (Se) is crucial for the biosynthesis of selenoproteins. Both neurodevelopment and the survival of neurons that are subject to stress depend on a regular selenoprotein biosynthesis and sufficient Se supply by selenoprotein P (SELENOP).

HYPOTHESIS:

Neuro-regeneration after traumatic spinal cord injury (TSCI) is related to the Se status.

STUDY DESIGN:

Single-centre prospective observational study.

PATIENTS AND METHODS:

Three groups of patients with comparable injuries were studied; vertebral fractures without neurological impairment (n = 10, group C), patients with TSCI showing no remission (n = 9, group G0), and patients with remission developing positive abbreviated injury score (AIS) conversion within 3 months (n = 10, group G1). Serum samples were available from different time points (upon admission, and after 4, 9 and 12 h, 1 and 3 days, 1 and 2 weeks, and 1, 2 and 3 months). Serum trace element concentrations were determined by total reflection X-ray fluorescence, SELENOP by ELISA, and further parameters by laboratory routine.

RESULTS:

Serum Se and SELENOP concentrations were higher on admission in the remission group (G1) as compared to G0. During the first week, both parameters remained constant in C and G0, whereas they declined significantly in the remission group. Similarly, the concentration changes between admission and 24 h were most pronounced in this group of recovering patients (G1). Binary logistic regression analysis including the delta of Se and SELENOP within the first 24 h indicated an AUC of 90.0% (CI: 67.4%-100.0%) with regards to predicting the outcome after TSCI.

CONCLUSION:

A Se deficit might constitute a risk factor for poor outcome after TSCI. A dynamic decline of serum Se and SELENOP concentrations after admission may reflect ongoing repair processes that are associated with higher odds for a positive clinical outcome.

KEYWORDS:

Biomarker; Brain; ELISA; Inflammation; Injury; Neurodegeneration; Neuron; Paraplegia; Precision medicine; Prediction; Profile; Recovery; Selenoprotein P; Supplementation; Surgery; Trace element; Zinc

PMID:
30466924
DOI:
10.1016/j.jtemb.2018.10.006
[Indexed for MEDLINE]

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