Association of Changed Serum Brain Biomarkers With Perihematomal Edema and Early Clinical Outcome in Primary ICH Patients.
Biomarkers
Brain
/ pathology
Brain Edema
/ diagnostic imaging
Cerebral Hemorrhage
/ complications
Cross-Sectional Studies
Edema
/ complications
Hematoma
/ complications
Humans
Intracranial Hemorrhages
/ complications
Matrix Metalloproteinase 9
/ metabolism
Vascular Endothelial Growth Factor A
/ metabolism
Journal
The neurologist
ISSN: 2331-2637
Titre abrégé: Neurologist
Pays: United States
ID NLM: 9503763
Informations de publication
Date de publication:
01 Jul 2022
01 Jul 2022
Historique:
pubmed:
3
12
2021
medline:
12
7
2022
entrez:
2
12
2021
Statut:
epublish
Résumé
Perihematomal edema (PHE) following primary intracranial hemorrhages (ICHs) affects the patient outcome. Also, serum biomarkers such as S100 calcium-binding protein B (S100B) and glial fibrillary acidic protein (GFAP) have been associated with ICHs outcome. We aimed to investigate the association between these biomarkers and PHE in ICH patients. In this cross-sectional study, patients with primary ICH between January 2020 and August 2020 were evaluated. All participants underwent spiral brain computed tomography scans upon admission, and 48 to 72 hours later and quantification of initial hematoma volume was performed. Serum level of matrix metalloproteinase-9 (MMP-9), vascular endothelial growth factor (VEGF), GFAP, and S100B on admission were measured by enzyme-linked immunosorbent assays. Acute clinical outcome was assessed by the modified-Rankin scale, National Institute of Health Stroke Scale (NIHSS), and ICH score. Thirty-seven ICH patients (21 patients with a favorable outcome and 16 unfavorable) were studied. Compared with survival patients, nonsurvivor patients showed a higher serum level of MMP-9, VEGF, GFAP, and S100B ( P <0.05). Scores of absolute PHE, edema expansion distance, and PHE growth rate in the nonsurvivor group were higher than the survivors ( P <0.001). The regression model revealed that MMP-9, VEGF, ICH score, and hematoma volume were associated with the PHE growth rate. S100B and ICH score were associated with edema expansion distance. Our data showed that the serum level of molecular biomarkers was associated with higher PHE volume and PHE scores were higher in nonsurvival patients, suggesting it may have a pathogenic role in developing PHE after ICH.
Sections du résumé
BACKGROUND
BACKGROUND
Perihematomal edema (PHE) following primary intracranial hemorrhages (ICHs) affects the patient outcome. Also, serum biomarkers such as S100 calcium-binding protein B (S100B) and glial fibrillary acidic protein (GFAP) have been associated with ICHs outcome. We aimed to investigate the association between these biomarkers and PHE in ICH patients.
METHODS
METHODS
In this cross-sectional study, patients with primary ICH between January 2020 and August 2020 were evaluated. All participants underwent spiral brain computed tomography scans upon admission, and 48 to 72 hours later and quantification of initial hematoma volume was performed. Serum level of matrix metalloproteinase-9 (MMP-9), vascular endothelial growth factor (VEGF), GFAP, and S100B on admission were measured by enzyme-linked immunosorbent assays. Acute clinical outcome was assessed by the modified-Rankin scale, National Institute of Health Stroke Scale (NIHSS), and ICH score.
RESULTS
RESULTS
Thirty-seven ICH patients (21 patients with a favorable outcome and 16 unfavorable) were studied. Compared with survival patients, nonsurvivor patients showed a higher serum level of MMP-9, VEGF, GFAP, and S100B ( P <0.05). Scores of absolute PHE, edema expansion distance, and PHE growth rate in the nonsurvivor group were higher than the survivors ( P <0.001). The regression model revealed that MMP-9, VEGF, ICH score, and hematoma volume were associated with the PHE growth rate. S100B and ICH score were associated with edema expansion distance.
CONCLUSIONS
CONCLUSIONS
Our data showed that the serum level of molecular biomarkers was associated with higher PHE volume and PHE scores were higher in nonsurvival patients, suggesting it may have a pathogenic role in developing PHE after ICH.
Identifiants
pubmed: 34855658
doi: 10.1097/NRL.0000000000000400
pii: 00127893-202207000-00003
doi:
Substances chimiques
Biomarkers
0
Vascular Endothelial Growth Factor A
0
Matrix Metalloproteinase 9
EC 3.4.24.35
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
168-172Informations de copyright
Copyright © 2021 Wolters Kluwer Health, Inc. All rights reserved.
Déclaration de conflit d'intérêts
The authors declare no conflict of interest.
Références
Brunswick AS, Hwang BY, Appelboom G, et al. Serum biomarkers of spontaneous intracerebral hemorrhage induced secondary brain injury. J Neurol Sci. 2012;321:1–10.
Li N, Liu YF, Ma Li, et al. Association of molecular markers with perihematomal edema and clinical outcome in intracerebral hemorrhage. Stroke. 2013;44:658–663.
Wêglewski A, Ryglewicz D, Mular A, et al. Changes of protein S100B serum concentration during ischemic and hemorrhagic stroke in relation to the volume of stroke lesion. Neurol Neurochir Pol. 2005;39:310–317.
Foerch C, Curdt I, Yan B, et al. Serum glial fibrillary acidic protein as a biomarker for intracerebral haemorrhage in patients with acute stroke. J Neurol Neurosurg Psychiatry. 2006;77:181–184.
Petzold A, Keir G, Kerr M, et al. Early identification of secondary brain damage in subarachnoid hemorrhage: a role for glial fibrillary acidic protein. J Neurotrauma. 2006;23:1179–1184.
Hu YY, Dong XQ, Yu WH, et al. Change in plasma S100B level after acute spontaneous basal ganglia hemorrhage. Shock. 2010;33:134–140.
Undén J, Strandberg K, Malm J, et al. Explorative investigation of biomarkers of brain damage and coagulation system activation in clinical stroke differentiation. J Neurol. 2009;256:72–77.
Rosell A, Ortega-Aznar A, Alvarez-Sabín J, et al. Increased brain expression of matrix metalloproteinase-9 after ischemic and hemorrhagic human stroke. Stroke. 2006;37:1399–1406.
Power C, Henry S, Del Bigio MR, et al. Intracerebral hemorrhage induces macrophage activation and matrix metalloproteinases. Ann Neurol. 2003;53:731–742.
Hernandez-Guillamon M, Delgado P, Penalba A, et al. MMP-2/MMP-9 plasma level and brain expression in cerebral amyloid angiopathy-associated hemorrhagic stroke. Brain Pathol. 2012;22:133–141.
Castellazzi M, Tamborino C, De Santis G, et al. Timing of serum active MMP-9 and MMP-2 levels in acute and subacute phases after spontaneous intracerebral hemorrhage. Acta Neurochir Suppl. 2010:106:137–140.
Sobrino T, Arias S, Rodríguez-González R, et al. High serum levels of growth factors are associated with good outcome in intracerebral hemorrhage. J Cereb Blood Flow Metab. 2009;29:1968–1974.
Selim M, Norton C. Perihematomal edema: Implications for intracerebral hemorrhage research and therapeutic advances. J Neurosci Res. 2020;98:212–218.
Ironside N, Chen C-J, Ding D, et al. Perihematomal edema after spontaneous intracerebral hemorrhage. Stroke. 2019;50:1626–1633.
Sansing L, Messe SR, Cucchiara BL, et al. Anti-adrenergic medications and edema development after intracerebral hemorrhage. Neurocrit Care. 2011;14:395–400.
Yang J, Arima H, Wu G, et al. Prognostic significance of perihematomal edema in acute intracerebral hemorrhage: pooled analysis from the intensive blood pressure reduction in acute cerebral hemorrhage trial studies. Stroke. 2015;46:1009–1013.
Murthy SB, Moradiya Y, Dawson J, et al. Perihematomal edema and functional outcomes in intracerebral hemorrhage: influence of hematoma volume and location. Stroke. 2015;46:3088–3092.
Appelboom G, Bruce SS, Hickman ZL, et al. Volume-dependent effect of perihaematomal oedema on outcome for spontaneous intracerebral haemorrhages. J Neurol Neurosurg Psychiatry. 2013;84:488–493.
Gebel JM Jr, Jauch EC, Brott TG, et al. Natural history of perihematomal edema in patients with hyperacute spontaneous intracerebral hemorrhage. Stroke. 2002;33:2631–2635.
Lattanzi S, Napoli MD, Ricci S, et al. Matrix metalloproteinases in acute intracerebral hemorrhage. Neurotherapeutics. 2020;17:484–496.
Senn R, Elkind MSV, Montaner J, et al. Potential role of blood biomarkers in the management of nontraumatic intracerebral hemorrhage. Cerebrovasc Dis. 2014;38:395–409.
Perry LA, Lucarelli T, Penny-Dimri JC, et al. Glial fibrillary acidic protein for the early diagnosis of intracerebral hemorrhage: systematic review and meta-analysis of diagnostic test accuracy. Int J Stroke. 2019;14:390–399.
Aydin I, Algin A, Poyraz MK, et al. Diagnostic value of serum glial fibrillary acidic protein and S100B serum levels in emergency medicine patients with traumatic versus nontraumatic intracerebral hemorrhage. Niger J Clin Pract. 2018;21:1645–1650.
Howe MD, Zhu L, Sansing LH, et al. Serum markers of blood-brain barrier remodeling and fibrosis as predictors of etiology and clinicoradiologic outcome in intracerebral hemorrhage. Front Neurol. 2018;9:746.
Shi W, Wang Z, Pu J, et al. Changes of blood–brain barrier permeability following intracerebral hemorrhage and the therapeutic effect of minocycline in rats. Acta Neurochir Suppl. 2011:61–67.
Zhang X, Li H, Hu S, et al. Brain edema after intracerebral hemorrhage in rats: the role of inflammation. Neurol India. 2006;54:402–407.
Bernstein JE, Savla P, Dong F, et al. Inflammatory markers and severity of intracerebral hemorrhage. Cureus. 2018;10:e3529.