Release of glial fibrillary acidic protein is related to the neurovascular status in acute ischemic stroke

Abstract

This study aimed at an analysis of glial fibrillary acidic protein (GFAP) in acute ischemic stroke, its association with the neurovascular status and its potential value as monitoring parameter. In 53 consecutive patients, serial venous blood samples were taken on admission, 6, 12, 18, 24, 48, 72, 96, and 120 h after stroke onset. The neurovascular status was assessed by repetitive extracranial and transcranial duplex sonography. Neurologic deficits were quantified by the National Institutes of Health stroke scale, and functional outcome was assessed with the modified Rankin Scale. Mean GFAP values were elevated from admission on with highest levels 48 h after stroke onset. GFAP release was highly correlated with severity of neurologic deficits and infarct volume. In patients with persistent middle cerebral artery occlusion, GFAP increased significantly compared with patients with normal sonographic findings (P = 0.019) and recanalization after thrombolysis resulted in a significant reduced increase (P = 0.038). GFAP concentrations were associated with the functional outcome after 3 months. Release kinetics of GFAP are associated with patients clinical deficits and infarct volume, depend on the neurovascular status on admission and on early recanalization after thrombolysis, and may be used as an additional predictor of the early course and functional outcome.

Diagnostic Accuracy of Plasma Glial Fibrillary Acidic Protein for Differentiating Intracerebral Hemorrhage and Cerebral Ischemia in Patients with Symptoms of Acute Stroke

“…Necrotic cell death and cell lysis typically do not occur within the first 6 -12 h after vessel occlusion (17,18 ). This histopathological observation correlates well with the finding that astroglial proteins (S100B, GFAP) are released into plasma with delay, not reaching peak concentrations before 48 -72 h after ischemic stroke onset (23)(24)(25)(26). A detailed analysis of the release kinetics of GFAP in ischemic stroke revealed that 75% of all values were still Ͻ0.04 g/L 12 h after the onset of symptoms, whereas the median GFAP concentration for ICH patients was 0.56 g/L at that time point.…”

“…However, the number of cells that will die has not yet been determined in the very early phase of ischemic stroke (17 ). It is known that a transient perfusion deficit alone leading to functional but not structural damage on the cellular level does not cause GFAP release into the bloodstream (26 ). For example, a patient with an occluded middle cerebral artery who undergoes successful thrombolytic treatment with rapid vessel recanalization will not show any detectable GFAP release as long as the resulting infarction is very small or nonexistent (31 ).…”

Glial and Axonal Body Fluid Biomarkers Are Related to Infarct Volume, Severity, and Outcome

“…This is considerably longer than that achieved in studies on serum S100B levels with 3 hours, 32 5 hours, 19 6 hours, 20 8 hours 21 or 24 hours 22 in some of the more recent studies. Given the previously-described wash-out pattern of S100B from the CSF into the blood 14 , one would expect to find higher CSF S100B levels during the first hours following the ischaemic stroke.…”

Serum glial fibrillary acidic protein as a marker of brain damage in patients after carotid endarterectomy

“…GFAP correlated with stroke severity and outcome. The study conducted by Wunderlich et al [25] on serum of patients with ischaemic stroke revealed that GFAP levels are increased from admission onward with the highest levels 48 hours after stroke onset. GFAP release was highly correlated with severity of neurologic deficits and infarct volume.…”