Isabel Fragata1, Alejandro Bustamante2, Anna Penalba2, Patrícia Ferreira3, Ana Paiva Nunes3, Patrícia Canhão4,5, Joan Montaner2,6,7. 1. Neuroradiology Department, Centro Hospitalar Lisboa Central, Rua Jose Antonio Serrano, 1150-099, Lisbon, Portugal. isabelfragata@gmail.com. 2. Neurovascular Research Laboratory, Vall d'Hebron Institute of Research (VHIR), Barcelona, Spain. 3. Unidade Cérebro-Vascular, Centro Hospitalar Lisboa Central, Lisbon, Portugal. 4. Neurology Department, Centro Hospitalar Lisboa Norte, Lisbon, Portugal. 5. Faculdade de Medicina, Instituto de Medicina Molecular, Universidade de Lisboa, Lisbon, Portugal. 6. Institute de Biomedicine of Seville, IBiS/Hospital Universitario Virgen del Rocío/CSIC/University of Seville, Seville, Spain. 7. Department of Neurology, Hospital Universitario Virgen Macarena, Seville, Spain.
Abstract
BACKGROUND: There is increasing evidence for the role of inflammation in clinical outcome after subarachnoid hemorrhage (SAH). Specifically, the TNF-alfa(α) pathway seems to be relevant after SAH. Although the TNF-α main receptor, TNF-R1 is associated with aneurysm growth and rupture, its relation to prognosis is unknown. We sought to compare TNF-R1 levels in peripheral venous blood and arterial blood closer to the ruptured aneurysm to study the association of TNF-R1 blood levels with poor prognosis (modified Rankin Scale > 2 at discharge, 3 and 6 months) and complications (hydrocephalus or delayed cerebral ischemia/DCI) following SAH. METHODS: We included consecutive SAH patients admitted in the first 72 h of symptoms. Blood samples were simultaneously collected from a peripheral vein and from the main parent artery of the aneurysm. Levels of TNF-R1 were measured using enzyme-linked immunosorbent assays. RESULTS: We analyzed 58 patients. Arterial and venous levels of TNF-R1 were correlated (R = 0.706, p < 0.001). In multivariate regression analysis, venous TNF-R1 was an independent predictor of poor outcome at 6 months after adjusting by age and sex [odds ratio (OR) 11.63; 95% CI 2.09-64.7, p = 0.005] and after adjusting by Glasgow Coma Scale and Fisher scales (OR 8.74; 95% CI 1.45-52.7, p = 0.018). There was no association of TNF-R1 with DCI. A cut-off for arterial TNF-R1 of 1523.7 pg/mL had 75% sensitivity/66% specificity for the prediction of hydrocephalus. CONCLUSION: Levels of venous TNF-R1 are associated with poor outcome in SAH. A specific association was found between levels of arterial TNF-R1 and hydrocephalus. These results are consistent with the role of TNF-α pathway in SAH and need to be validated in larger cohorts.
BACKGROUND: There is increasing evidence for the role of inflammation in clinical outcome after subarachnoid hemorrhage (SAH). Specifically, the TNF-alfa(α) pathway seems to be relevant after SAH. Although the TNF-α main receptor, TNF-R1 is associated with aneurysm growth and rupture, its relation to prognosis is unknown. We sought to compare TNF-R1 levels in peripheral venous blood and arterial blood closer to the ruptured aneurysm to study the association of TNF-R1 blood levels with poor prognosis (modified Rankin Scale > 2 at discharge, 3 and 6 months) and complications (hydrocephalus or delayed cerebral ischemia/DCI) following SAH. METHODS: We included consecutive SAH patients admitted in the first 72 h of symptoms. Blood samples were simultaneously collected from a peripheral vein and from the main parent artery of the aneurysm. Levels of TNF-R1 were measured using enzyme-linked immunosorbent assays. RESULTS: We analyzed 58 patients. Arterial and venous levels of TNF-R1 were correlated (R = 0.706, p < 0.001). In multivariate regression analysis, venous TNF-R1 was an independent predictor of poor outcome at 6 months after adjusting by age and sex [odds ratio (OR) 11.63; 95% CI 2.09-64.7, p = 0.005] and after adjusting by Glasgow Coma Scale and Fisher scales (OR 8.74; 95% CI 1.45-52.7, p = 0.018). There was no association of TNF-R1 with DCI. A cut-off for arterial TNF-R1 of 1523.7 pg/mL had 75% sensitivity/66% specificity for the prediction of hydrocephalus. CONCLUSION: Levels of venous TNF-R1 are associated with poor outcome in SAH. A specific association was found between levels of arterial TNF-R1 and hydrocephalus. These results are consistent with the role of TNF-α pathway in SAH and need to be validated in larger cohorts.
Authors: Karl-Michael Schebesch; Alexander Brawanski; Sylvia Bele; Petra Schödel; Andreas Herbst; Elisabeth Bründl; Simone Maria Kagerbauer; Jan Martin; Anette Lohmeier; Eva-Maria Stoerr; Martin Proescholdt Journal: Neurol Res Date: 2013-08-02 Impact factor: 2.448
Authors: Caron M Hong; Cigdem Tosun; David B Kurland; Volodymyr Gerzanich; David Schreibman; J Marc Simard Journal: Biomarkers Date: 2014-02-05 Impact factor: 2.658
Authors: S H-Y Chou; S K Feske; S L Simmons; R G J Konigsberg; S C Orzell; A Marckmann; G Bourget; D J Bauer; P L De Jager; R Du; K Arai; E H Lo; M M Ning Journal: Transl Stroke Res Date: 2011-11-10 Impact factor: 6.829
Authors: Bettina H Clausen; Martin Wirenfeldt; Sofie S Høgedal; Lars H Frich; Helle H Nielsen; Henrik D Schrøder; Kamilla Østergaard; Bente Finsen; Bjarne W Kristensen; Kate L Lambertsen Journal: Acta Neuropathol Commun Date: 2020-06-05 Impact factor: 7.801
Authors: Reyes de Torres; Fernando Mancha; Alejandro Bustamante; Patricia Canhao; Isabel Fragata; Joan Montaner Journal: Future Sci OA Date: 2019-11-05