ArticleEuropean journal of neurology2025
A Comparative Study of 141 Glial Fibrillary Acidic Protein Immunoglobulin G Positive Cases.
Article in European journal of neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Glial Fibrillary Acidic Protein Astrocytopathy Mimicking Wernicke's Encephalopathy.Internal medicine (Tokyo, Japan) · 2026Article
- Autoimmune glial fibrillary acidic protein astrocytopathy with full-length spinal cord lesions: a case report and literature review.BMC neurology · 2026Review
- MELAS syndrome complicated by anti-GFAP autoantibody positivity: a case report and literature review.BMC neurology · 2026Review
- Investigation of Prognostic Factors in Patients With Autoimmune Glial Fibrillary Acidic Protein Astrocytopathy.European journal of neurology · 2026Article
- MOG-Ab-associated optic neuritis with concurrent GFAP-Ab positivity following tislelizumab-based treatment: a case report.Frontiers in pharmacology · 2026Article
- Implications of coexisting neural antibodies with glial fibrillary acidic protein autoimmunity: a single center retrospective cohort study.BMC neurology · 2025Article
- Relevance of Kappa and Lambda Free Light Chains in Autoimmune Astrocytopathy Associated With Anti-GFAP Antibodies.Annals of clinical and translational neurology · 2025Article
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Authors and funding
26 authors.
Funding
Abstract
backgroundGlial fibrillary acidic protein-immunoglobulin G (GFAP-IgG) positivity is associated with autoimmune GFAP astrocytopathy (GFAP-A), but also with other autoimmune encephalitides and viral infections. We attempted to elucidate the characteristics of GFAP-A in relation to other GFAP-IgG-positive encephalitides and constructed a differential diagnosis model.
methods141 GFAP-IgG-positive cases were identified, including 52 astrocytopathy (GFAP-A group), 48 autoimmune encephalitis (AE-G), and 41 viral encephalitis (VE-G). Multivariate logistic regression was employed to create a diagnostic model, with validation using an external cohort.
resultCompared to the AE-G group, the GFAP-A patients showed more onset age ≥ 50 years, headache, fever, consciousness disturbance, MRI radial vascular enhancement, cerebrospinal fluid (CSF) antibody titer grade ≥ 4, and CSF proteins ≥ 700 mg/L, but less female sex, limb numbness, visual disturbances, and CSF chloride ≤ 120 mmol/L. Among these, CSF antibody titer grade ≥ 4, CSF protein ≥ 700 mg/L, and absence of visual disturbances were independent risk factors for GFAP-A diagnosis. Compared to the VE-G group, the GFAP-A patients showed more course ≥ 14 days, onset age ≥ 50 years, limb weakness, serum potassium ≤ 3.9 mmol/L, CSF antibody titer grade ≥ 4, CSF leukocytes ≤ 46*10, MRI radial vascular enhancement, MRI involvement of brainstem, and MRI involvement of spinal cord, but less headache, fever, nausea, and vomiting. Among these, serum potassium ≤ 3.9 mmol/L, MRI spinal cord involvement, and absence of nausea and vomiting were independent risk factors for GFAP-A diagnosis.
conclusionsBased on critical clinical indicators identified, we constructed a differential diagnosis model for GFAP-A.
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