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Association between serum glial fibrillary acidic protein levels and neurological deficit severity in acute ischemic stroke: A cross-sectional study

Source: PubMed Central Open Access, NCBI / U.S. National Library of Medicine

Surgical Neurology InternationalLast synced 9/5/2026Status: syncedPMID: 42695011 pmidDOI: 10.25259/SNI_645_2026

Background: Glial fibrillary acidic protein (GFAP) is an astrocytic biomarker released following blood-brain barrier disruption in acute ischemic stroke. This study aimed to evaluate the association between serum GFAP levels and the severity of neurological deficits and to assess the diagnostic performance of GFAP in identifying severe neurological deficits. st1 Methods: A cross-sectional analytic study was conducted at Prof. Dr. I.G.N.G. Ngoerah General Hospital, Denpasar, Bali, from April to May 2026. Eighty-five patients with neuroimaging-confirmed acute ischemic stroke were enrolled. Serum GFAP levels were measured using enzyme-linked immunosorbent assay approximately 72 h after symptom onset. Neurological severity was assessed using the National Institutes of Health Stroke Scale (NIHSS) by a blinded board-certified neurologist. Bivariate analysis, receiver operating characteristic (ROC) analysis, and multivariate logistic regression were performed. st2 Results: The mean age was 54.14 ± 7.77 years, and 61.2% were male. Median NIHSS score was 8 (range: 3–30), and median serum GFAP level was 2.06 ng/mL (range: 0.17–19.64). Serum GFAP levels showed a strong positive correlation with NIHSS scores (r = 0.786,< 0.001). ROC analysis demonstrated excellent diagnostic accuracy for severe neurological deficits (NIHSS ≥16), with an area under the ROC curve of 0.984 (95% confidence interval [CI]: 0.961–1.000). The optimal GFAP cutoff was 2.37 ng/mL, yielding 96.9% sensitivity and 96.

Abstract

Background: Glial fibrillary acidic protein (GFAP) is an astrocytic biomarker released following blood-brain barrier disruption in acute ischemic stroke. This study aimed to evaluate the association between serum GFAP levels and the severity of neurological deficits and to assess the diagnostic performance of GFAP in identifying severe neurological deficits. st1 Methods: A cross-sectional analytic study was conducted at Prof. Dr. I.G.N.G. Ngoerah General Hospital, Denpasar, Bali, from April to May 2026. Eighty-five patients with neuroimaging-confirmed acute ischemic stroke were enrolled. Serum GFAP levels were measured using enzyme-linked immunosorbent assay approximately 72 h after symptom onset. Neurological severity was assessed using the National Institutes of Health Stroke Scale (NIHSS) by a blinded board-certified neurologist. Bivariate analysis, receiver operating characteristic (ROC) analysis, and multivariate logistic regression were performed. st2 Results: The mean age was 54.14 ± 7.77 years, and 61.2% were male. Median NIHSS score was 8 (range: 3–30), and median serum GFAP level was 2.06 ng/mL (range: 0.17–19.64). Serum GFAP levels showed a strong positive correlation with NIHSS scores (r = 0.786,< 0.001). ROC analysis demonstrated excellent diagnostic accuracy for severe neurological deficits (NIHSS ≥16), with an area under the ROC curve of 0.984 (95% confidence interval [CI]: 0.961–1.000). The optimal GFAP cutoff was 2.37 ng/mL, yielding 96.9% sensitivity and 96.2% specificity. Multivariate analysis identified GFAP as an independent variable associated with severe neurological deficits (adjusted odds ratio = 3.675; 95% CI: 1.682–8.029;= 0.001). st3 Conclusion: Serum GFAP levels were strongly associated with neurological severity and may serve as a potential biomarker for early stroke severity stratification. st4

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