TY - JOUR
T1 - Early signaling of inflammation in acute ischemic stroke
T2 - Clinical and rheological implications
AU - Shenhar-Tsarfaty, Shani
AU - Assayag, Einor Ben
AU - Bova, Irena
AU - Shopin, Ludmila
AU - Berliner, Shlomo
AU - Shapira, Itzhak
AU - Bornstein, Natan M.
PY - 2008
Y1 - 2008
N2 - Introduction: Several studies have highlighted the role of interleukin-6 (IL-6) as an early signal of the inflammatory response following acute ischemic stroke. This study examines the potential advantage of employing high-sensitivity (hs)-IL-6 as a possible biomarker at the early stages of acute stroke for identifying an acute phase response and its potential rheological and clinical implications. Methods: Venous blood was obtained from 186 stroke patients within 24 h of hospital admission and 3-5 days thereafter in order to characterize an inflammatory and hemorheological profile (including erythrocyte aggregation). Neurological state was assessed by the National Institutes of Health Stroke Scale (NIHSS) and the modified Rankin scale (mRs). Results: While most biomarkers displayed elevated concentrations with time, serum concentrations of hs-IL-6 declined 3-5 days following acute stroke. Initially elevated levels of hs-IL-6 at presentation further correlated with unfavorable clinical outcomes (by NIHSS and mRs) at both time points. Analysis of variance in the different quartiles identified an hs-IL-6 gradient-dependent correlation at both time points, such that the higher the initial hs-IL-6 concentration, the higher the elevation in inflammatory biomarkers and the poorer the neurological state at both time points (p < 0.001 for NIHSS and p = 0.001 for mRs, for trend across quartiles). Conclusions: This study demonstrates the potential of employing hs-IL-6 as an early stage biomarker for the prognosis of acute ischemic stroke. Such an advance would provide the means to identify at an early stage the patients who would require closer clinical surveillance and/or administration of therapeutic interventions.
AB - Introduction: Several studies have highlighted the role of interleukin-6 (IL-6) as an early signal of the inflammatory response following acute ischemic stroke. This study examines the potential advantage of employing high-sensitivity (hs)-IL-6 as a possible biomarker at the early stages of acute stroke for identifying an acute phase response and its potential rheological and clinical implications. Methods: Venous blood was obtained from 186 stroke patients within 24 h of hospital admission and 3-5 days thereafter in order to characterize an inflammatory and hemorheological profile (including erythrocyte aggregation). Neurological state was assessed by the National Institutes of Health Stroke Scale (NIHSS) and the modified Rankin scale (mRs). Results: While most biomarkers displayed elevated concentrations with time, serum concentrations of hs-IL-6 declined 3-5 days following acute stroke. Initially elevated levels of hs-IL-6 at presentation further correlated with unfavorable clinical outcomes (by NIHSS and mRs) at both time points. Analysis of variance in the different quartiles identified an hs-IL-6 gradient-dependent correlation at both time points, such that the higher the initial hs-IL-6 concentration, the higher the elevation in inflammatory biomarkers and the poorer the neurological state at both time points (p < 0.001 for NIHSS and p = 0.001 for mRs, for trend across quartiles). Conclusions: This study demonstrates the potential of employing hs-IL-6 as an early stage biomarker for the prognosis of acute ischemic stroke. Such an advance would provide the means to identify at an early stage the patients who would require closer clinical surveillance and/or administration of therapeutic interventions.
KW - Erythrocyte aggregation
KW - High-sensitivity interleukin-6
KW - Inflammation
KW - Stroke
UR - http://www.scopus.com/inward/record.url?scp=44449149285&partnerID=8YFLogxK
U2 - 10.1016/j.thromres.2007.10.019
DO - 10.1016/j.thromres.2007.10.019
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AN - SCOPUS:44449149285
VL - 122
SP - 167
EP - 173
JO - Thrombosis Research
JF - Thrombosis Research
SN - 0049-3848
IS - 2
ER -