Marcelo de Mello Rieder1, Jean Pierre Oses2, Fernanda Machado Kutchak1, Mônia Sartor3, André Cecchini4, Marcelo Salimen Rodolphi3, Carolina David Wiener2, Afonso Kopczynski3, Alexandre Pastoris Muller5, Nathan Ryzewski Strogulski3, Randhall B Carteri3, Gisele Hansel6, Marino Muxfeldt Bianchin7, Luis Valmor Portela8. 1. Postgraduate Program in Medical Sciences, Universidade Federal do Rio Grande do Sul- UFRGS, Porto Alegre, RS, Brazil; BRAIN Center of Experimental Research, Hospital de Clinicas de Porto Alegre (HCPA), Porto Alegre, RS, Brazil; Hospital Cristo Redentor, Porto Alegre, Rio Grande do Sul, Brazil. 2. Postgraduate Program in Health and Behavior, Universidade Católica de Pelotas, Pelotas, Rio Grande do Sul, Brazil. 3. Laboratory of Neurotrauma and Biomarkers, Department of Biochemistry, Postgraduate Program in Biochemistry, ICBS, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil. 4. Hospital Cristo Redentor, Porto Alegre, Rio Grande do Sul, Brazil; Department of Legal Medicine and Neurology, Universidade Luterana do Brazil, Canoas, Rio Grande do Sul, Brazil. 5. Laboratory of Exercise, Biochemistry and Physiology, Universidade do Extremo Sul Catarinense, Criciúma, Santa Catarina, Brazil. 6. Laboratory of Exercise, Biochemistry and Physiology, Universidade do Extremo Sul Catarinense, Criciúma, Santa Catarina, Brazil; Penn Center for Brain Injury and Repair and Department of Neurosurgery, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA. 7. Postgraduate Program in Medical Sciences, Universidade Federal do Rio Grande do Sul- UFRGS, Porto Alegre, RS, Brazil; BRAIN Center of Experimental Research, Hospital de Clinicas de Porto Alegre (HCPA), Porto Alegre, RS, Brazil. 8. Laboratory of Neurotrauma and Biomarkers, Department of Biochemistry, Postgraduate Program in Biochemistry, ICBS, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil. Electronic address: roskaportela@gmail.com.
Abstract
BACKGROUND: A plethora of reactive cellular responses emerge immediately after a traumatic spinal cord injury (SCI) and may influence the patient's outcomes. We investigated whether serum concentrations of neuron-specific enolase, interleukin-6, glial-derived neurotrophic factor, and neurotrophic growth factor reflect the acute-phase responses to different etiologies of SCI and may serve as predictive biomarkers of neurologic and functional outcomes. METHODS: Fifty-two patients were admitted to the intensive care unit after SCI due to traffic accidents, falls, and firearm wounds and had blood samples collected within 48 hours and 7 days after SCI. Thirty-six healthy subjects with no history of SCI were included as controls. Neurologic and functional status was evaluated on the basis of American Spinal Injury Association and Functional Independence Measure scores over a period of 48 hours and 6 months after SCI. RESULTS: Serum NSE increased significantly 48 hours and 7 days after SCI compared with controls, while interleukin-6 increased only at 48 hours. In contrast, the neurotrophic growth factor level significantly decreased 48 hours and 7 days after SCI. Serum glial-derived neurotrophic factor level did not differ from control at any time point. Also, there was no significant difference in biomarker concentrations between the etiologies of SCI or the level of spinal injury. There were no correlations between biomarker levels at 48 hours with neurologic or functional outcomes 7 days and 6 months after SCI. CONCLUSIONS: Our results suggest expansive axonal damage coupled with an acute proinflammatory response after SCI. However, in our study biomarker concentration did not correlate with short- or long-term prognosis, such as survival rate or sensory and motor function.
BACKGROUND: A plethora of reactive cellular responses emerge immediately after a traumatic spinal cord injury (SCI) and may influence the patient's outcomes. We investigated whether serum concentrations of neuron-specific enolase, interleukin-6, glial-derived neurotrophic factor, and neurotrophic growth factor reflect the acute-phase responses to different etiologies of SCI and may serve as predictive biomarkers of neurologic and functional outcomes. METHODS: Fifty-two patients were admitted to the intensive care unit after SCI due to traffic accidents, falls, and firearm wounds and had blood samples collected within 48 hours and 7 days after SCI. Thirty-six healthy subjects with no history of SCI were included as controls. Neurologic and functional status was evaluated on the basis of American Spinal Injury Association and Functional Independence Measure scores over a period of 48 hours and 6 months after SCI. RESULTS: Serum NSE increased significantly 48 hours and 7 days after SCI compared with controls, while interleukin-6 increased only at 48 hours. In contrast, the neurotrophic growth factor level significantly decreased 48 hours and 7 days after SCI. Serum glial-derived neurotrophic factor level did not differ from control at any time point. Also, there was no significant difference in biomarker concentrations between the etiologies of SCI or the level of spinal injury. There were no correlations between biomarker levels at 48 hours with neurologic or functional outcomes 7 days and 6 months after SCI. CONCLUSIONS: Our results suggest expansive axonal damage coupled with an acute proinflammatory response after SCI. However, in our study biomarker concentration did not correlate with short- or long-term prognosis, such as survival rate or sensory and motor function.
Authors: Ralph J Marino; Michael Leff; Diana D Cardenas; Jayne Donovan; David Chen; Steve Kirshblum; Benjamin E Leiby Journal: Neurotrauma Rep Date: 2020-11-13