Increased GFAP and S100beta but not NSE serum levels after subarachnoid haemorrhage are associated with clinical severity.
until further notice
SourceEuropean Journal of Neurology, 13, 6, (2006), pp. 632-638
Article / Letter to editor
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European Journal of Neurology
SubjectDCN 1: Perception and Action; DCN 3: Neuroinformatics; NCEBP 11: Alzheimer Centre; UMCN 3.2: Cognitive neurosciences; UMCN 3.3: Neurosensory disorders; UMCN 4.1: Microbial pathogenesis and host defense; UMCN 5.1: Genetic defects of metabolism
Assessment of initial disease severity after subarachnoid haemorrhage (SAH) remains difficult. The objective of the study is to identify biochemical markers of brain damage in peripheral blood after SAH. Hospital admission S100beta, glial fibrillary acidic protein (GFAP) and neuron-specific enolase (NSE) serum levels were analysed in 67 patients with SAH. Disease severity was determined by using the World Federation of Neurological Surgeons (WFNS) scale and the Fisher CT (computerized tomography) grading scale. Mean astroglial serum concentrations taken at hospital admission were increased (S100beta 2.8-fold and GFAP 1.8-fold) compared with the upper limit of normal laboratory reference values (P95). The mean NSE concentration was within normal limits. S100beta (P < 0.001) and GFAP (P =0.011) but not NSE levels were higher in patients who were in coma at the time of hospital admission compared with patients who were not. Similarly S100beta and GFAP but not NSE serum levels increased with higher WFNS scores, raised intracranial pressure and higher CT Fisher grade scores. Concerning the location of the aneurysm, S100beta and GFAP serum levels were within normal limits after a perimesencephalic type of haemorrhage and significantly increased after aneurysmal type SAH. Increased glial (S100beta and GFAP) but not neuronal (NSE) protein serum concentrations are found after SAH, associated to the clinical severity of the initial injury.
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