Serum oxidative stress influences neurological recovery after surgery to treat acutely worsening symptoms of compression myelopathy: a cross-sectional human study.
Adult
Aged
Aged, 80 and over
Biomarkers
/ blood
Cervical Vertebrae
/ physiopathology
Cross-Sectional Studies
Female
Humans
Male
Middle Aged
Ossification of Posterior Longitudinal Ligament
/ blood
Oxidative Stress
/ physiology
Preoperative Period
Reactive Oxygen Species
/ blood
Recovery of Function
/ physiology
Severity of Illness Index
Spinal Cord Compression
/ blood
Treatment Outcome
Compression myelopathy
Reactive oxygen metabolites
Serum oxidative stress
Surgical outcome
Journal
BMC musculoskeletal disorders
ISSN: 1471-2474
Titre abrégé: BMC Musculoskelet Disord
Pays: England
ID NLM: 100968565
Informations de publication
Date de publication:
07 Dec 2019
07 Dec 2019
Historique:
received:
29
07
2019
accepted:
22
11
2019
entrez:
8
12
2019
pubmed:
8
12
2019
medline:
28
4
2020
Statut:
epublish
Résumé
Recent reports indicate that oxidative stress induced by reactive oxygen species is associated with the pathobiology of neurodegenerative disorders that involve neuronal cell apoptosis. Here we conducted a cross-sectional study to evaluate serum levels of oxidative stress in cervical compression myelopathy. Thirty-six serum samples were collected preoperatively from patients treated for acutely worsening compression myelopathy (AM) and chronic compression myelopathy (CM). Serum levels of oxidative stress markers were evaluated by measuring derivatives of reactive oxygen metabolites (ROM), which reflect concentrations of hydroperoxides. ROM in healthy individuals range from 250 to 300 (U. CARR), whereas ROM >340-400 and > 400 define moderate and severe levels of oxidative stress, respectively. Difference of ROM by the cause of disorders whether cervical spondylotic myelopathy (CSM) or cervical ossification of longitudinal ligament (OPLL), correlations between ROM and patient age, body mass index (BMI), history of smoking, existence of diabetes were examined. Neurological evaluations according to Japanese Orthopaedic Association (JOA) scores were performed and correlated with ROM. ROM increased to 349.5 ± 54.8, representing a moderate oxidative stress, in CM samples. ROM increased to 409.2 ± 77.9 in AM samples, reflecting severe oxidative stress which were significantly higher than for CM samples (p < 0.05). There was no significant difference by the cause of disorders (CSM or OPLL). ROM were significantly increased in AM serum samples from female patients versus AM male and CM patients (p < 0.05). There were no correlations between ROM and age, BMI, history of smoking, and existence of diabetes. A negative correlation between ROM and recovery rate of JOA score (R Although moderate oxidative stress was present in patients with CM, levels of oxidative stress increased in severity in patients with AM. These results suggest that postsurgical neurological recovery is influenced by severe oxidative stress in AM.
Sections du résumé
BACKGROUND
BACKGROUND
Recent reports indicate that oxidative stress induced by reactive oxygen species is associated with the pathobiology of neurodegenerative disorders that involve neuronal cell apoptosis. Here we conducted a cross-sectional study to evaluate serum levels of oxidative stress in cervical compression myelopathy.
METHODS
METHODS
Thirty-six serum samples were collected preoperatively from patients treated for acutely worsening compression myelopathy (AM) and chronic compression myelopathy (CM). Serum levels of oxidative stress markers were evaluated by measuring derivatives of reactive oxygen metabolites (ROM), which reflect concentrations of hydroperoxides. ROM in healthy individuals range from 250 to 300 (U. CARR), whereas ROM >340-400 and > 400 define moderate and severe levels of oxidative stress, respectively. Difference of ROM by the cause of disorders whether cervical spondylotic myelopathy (CSM) or cervical ossification of longitudinal ligament (OPLL), correlations between ROM and patient age, body mass index (BMI), history of smoking, existence of diabetes were examined. Neurological evaluations according to Japanese Orthopaedic Association (JOA) scores were performed and correlated with ROM.
RESULTS
RESULTS
ROM increased to 349.5 ± 54.8, representing a moderate oxidative stress, in CM samples. ROM increased to 409.2 ± 77.9 in AM samples, reflecting severe oxidative stress which were significantly higher than for CM samples (p < 0.05). There was no significant difference by the cause of disorders (CSM or OPLL). ROM were significantly increased in AM serum samples from female patients versus AM male and CM patients (p < 0.05). There were no correlations between ROM and age, BMI, history of smoking, and existence of diabetes. A negative correlation between ROM and recovery rate of JOA score (R
CONCLUSIONS
CONCLUSIONS
Although moderate oxidative stress was present in patients with CM, levels of oxidative stress increased in severity in patients with AM. These results suggest that postsurgical neurological recovery is influenced by severe oxidative stress in AM.
Identifiants
pubmed: 31810443
doi: 10.1186/s12891-019-2966-5
pii: 10.1186/s12891-019-2966-5
pmc: PMC6898939
doi:
Substances chimiques
Biomarkers
0
Reactive Oxygen Species
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
589Subventions
Organisme : Japan Society for the Promotion of Science
ID : 16K20072
Références
J Neurol. 1996 Feb;243(2):109-16
pubmed: 8750545
Eur Spine J. 2014 Feb;23(2):362-72
pubmed: 24097230
Clin Chem Lab Med. 2006;44(11):1372-5
pubmed: 17087652
Oxid Med Cell Longev. 2016;2016:6094631
pubmed: 26881034
J Nutr. 2001 Dec;131(12):3208-11
pubmed: 11739867
JCI Insight. 2017 Jun 2;2(11):null
pubmed: 28570271
Horm Res Paediatr. 2012;78(3):158-64
pubmed: 23052543
Semin Neurol. 2002 Jun;22(2):143-8
pubmed: 12524559
J Clin Neurosci. 2014 Dec;21(12):2175-8
pubmed: 25065845
Int Arch Allergy Immunol. 2008;146 Suppl 1:67-72
pubmed: 18504410
Spine (Phila Pa 1976). 2000 Mar 15;25(6):670-6
pubmed: 10752097
Acta Neuropathol. 2009 Jul;118(1):151-66
pubmed: 19271225
J Neuropathol Exp Neurol. 2006 Jul;65(7):631-41
pubmed: 16825950
Mod Rheumatol. 2014 Nov;24(6):926-30
pubmed: 24670128
Mol Med Rep. 2015 Oct;12(4):5349-54
pubmed: 26151839
J Spinal Disord Tech. 2007 Feb;20(1):7-13
pubmed: 17285045
Spine (Phila Pa 1976). 2015 Jul 15;40(14):1101-7
pubmed: 25494311
Spine Surg Relat Res. 2017 Dec 20;1(1):7-13
pubmed: 31440606
Eur Spine J. 2012 Mar;21(3):482-9
pubmed: 21935680
Eur Spine J. 2016 Jul;25(7):2294-301
pubmed: 27072553
Hypertens Res. 2011 Sep;34(9):1041-5
pubmed: 21677660
Eur Spine J. 2018 Aug;27(8):1824-1830
pubmed: 29557051