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Stroke. 2000;31:2670-2677

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(Stroke. 2000;31:2670.)
© 2000 American Heart Association, Inc.


Original Contribution

Release of Glial Tissue–Specific Proteins After Acute Stroke

A Comparative Analysis of Serum Concentrations of Protein S-100B and Glial Fibrillary Acidic Protein

Manfred Herrmann, MD, PhD; Pieter Vos, MD, PhD; Michael T. Wunderlich, MD; Chris H. M. M. de Bruijn, PhD Karl J. B. Lamers, PhD

From the Division of Neuropsychology and Behavioral Neurology (M.H.) and Department of Neurology (M.T.W.), Otto von Guericke University, Magdeburg, Germany; Department of Neurology, University Hospital Nijmegen, Nijmegen, the Netherlands (P.V., K.J.B.L.); Department of Cellular Neuroscience, Faculty of Medicine, Maastricht University, Maastricht, the Netherlands (C.H.M.M. de B.); and Hanse Institute for Advanced Study, Delmenhorst/Bremen, Germany (M.H.).

Correspondence to Manfred Herrmann, MD, PhD, Division of Neuropsychology and Behavioral Neurology, Otto-von-Guericke University, Leipziger Str. 44, D-39120 Magdeburg, Germany. E-mail manfred.herrmann{at}medizin.uni-magdeburg.de

Background and Purpose—This study was aimed at the comparative analysis of serum concentrations of glial fibrillary acidic protein (GFAP) and protein S-100B in patients with acute stroke.

Methods—We investigated 32 patients with stroke symptoms consistent with cerebral ischemia in the anterior territory of vascular supply. Serial venous blood samples were taken after admission to the hospital and during the first 4 days after onset of stroke. Evaluation of lesion topography and volume of infarcted brain area was based on cranial CT data. The patients’ clinical status was consecutively evaluated by the National Institutes of Health Stroke Scale (NIHSS) and the Barthel Index score at discharge from the hospital.

Results—Protein S-100B and GFAP release was found to be significantly correlated (r=0.96; P<0.001). The release of both biochemical markers was associated with the volume of brain lesions (S-100B: r=0.957, P<0.0001; GFAP: r=0.955, P<0.0001) and the neurological status at discharge from the hospital (S-100B: r=0.821, P=0.0002; GFAP: r=0.717, P=0.0003). The highest correlation between both S-100B and GFAP serum concentration and Barthel score was calculated at the last time of blood sampling, 4 days after stroke onset (S-100B: r=0.621, P<0.001; GFAP: r=0.655, P<0.001). The release of both astroglia derived proteins differed between different subtypes of stroke. GFAP was found to be a more sensitive marker of brain damage in patients with smaller lacunar lesions or minor strokes.

Conclusions—Our results indicate that postischemic release patterns of GFAP and S-100B protein may allow insight into the underlying pathophysiology of acute cerebral infarcts and may be used as a valuable tool of clinical stroke treatment.


Key Words: glial fibrillary acidic protein • nerve tissue protein S-100 • outcome • stroke




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