ArticleJournal of clinical neurology (Seoul, Korea)2025
Elevated Serum Amyloid A2 and A4 in Patients With Guillain-Barré Syndrome.
Article in Journal of clinical neurology (Seoul, Korea), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- SAA4: An Underdog Within the Serum Amyloid a Superfamily?International journal of molecular sciences · 2026Review
- Re: Comments on "Elevated Serum Amyloid A2 and A4 in Patients With Guillain-Barré Syndrome".Journal of clinical neurology (Seoul, Korea) · 2025Article
- Comments on: "Elevated Serum Amyloid A2 and A4 in Patients With Guillain-Barré Syndrome".Journal of clinical neurology (Seoul, Korea) · 2025Article
- Serum Amyloid A in Guillain-Barré Syndrome: A New Frontier in Biomarker Research.Journal of clinical neurology (Seoul, Korea) · 2025Article
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Authors and funding
7 authors.
Funding
Abstract
background and purposeGuillain-Barré syndrome (GBS) is an autoimmune-mediated disorder characterized by demyelinating or axonal injury of the peripheral nerve. Our aim is to determine whether serum amyloid A (SAA) is a biomarker of demyelinating injury and disease severity in patients with GBS.
methodsThis study retrospectively enrolled 40 patients with either the demyelinating or axonal GBS and sex- and age-matched controls with other neurological diseases as well as healthy subjects. The demographic and clinical features at entry were collected. The serum levels of the SAA isoforms SAA1, SAA2, and SAA4 were determined in the patients with GBS and the controls using the enzyme-linked immunosorbent assay and analyzed for the associations between levels of different SAA isoforms and the clinical features of the patients.
resultsThe levels of SAA2 and SAA4 were significantly higher in patients with GBS than in both the other neurological disease controls and the healthy subjects (
conclusionsIncreased levels of SAA2 and SAA4 may only represent the acute inflammatory status and so cannot be utilized as biomarkers of the disease severity or demyelinating injury in patients with GBS.
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