Xiaoying Yao, Baojun Qiao, Fangzhen Shan, Qingqing Zhang, Yan Song, Jin Song, Yuzhong Wang
{"title":"格林-巴利综合征患者血清淀粉样蛋白A2和A4升高。","authors":"Xiaoying Yao, Baojun Qiao, Fangzhen Shan, Qingqing Zhang, Yan Song, Jin Song, Yuzhong Wang","doi":"10.3988/jcn.2024.0469","DOIUrl":null,"url":null,"abstract":"<p><strong>Background and purpose: </strong>Guillain-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.</p><p><strong>Methods: </strong>This 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.</p><p><strong>Results: </strong>The levels of SAA2 and SAA4 were significantly higher in patients with GBS than in both the other neurological disease controls and the healthy subjects (<i>p</i><0.05 for all). The level of SAA1 did not differ between patients with GBS and the controls. The level of SAA2 was considerably higher in GBS patients with antecedent infection than in those without infection (<i>p</i>=0.020). The levels of different SAA isoforms were not associated with the disease severity or other clinical features of patients with GBS (<i>p</i>>0.05 for all).</p><p><strong>Conclusions: </strong>Increased 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.</p>","PeriodicalId":15432,"journal":{"name":"Journal of Clinical Neurology","volume":"21 3","pages":"213-219"},"PeriodicalIF":2.9000,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12056137/pdf/","citationCount":"0","resultStr":"{\"title\":\"Elevated Serum Amyloid A2 and A4 in Patients With Guillain-Barré Syndrome.\",\"authors\":\"Xiaoying Yao, Baojun Qiao, Fangzhen Shan, Qingqing Zhang, Yan Song, Jin Song, Yuzhong Wang\",\"doi\":\"10.3988/jcn.2024.0469\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background and purpose: </strong>Guillain-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.</p><p><strong>Methods: </strong>This 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.</p><p><strong>Results: </strong>The levels of SAA2 and SAA4 were significantly higher in patients with GBS than in both the other neurological disease controls and the healthy subjects (<i>p</i><0.05 for all). The level of SAA1 did not differ between patients with GBS and the controls. The level of SAA2 was considerably higher in GBS patients with antecedent infection than in those without infection (<i>p</i>=0.020). The levels of different SAA isoforms were not associated with the disease severity or other clinical features of patients with GBS (<i>p</i>>0.05 for all).</p><p><strong>Conclusions: </strong>Increased 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.</p>\",\"PeriodicalId\":15432,\"journal\":{\"name\":\"Journal of Clinical Neurology\",\"volume\":\"21 3\",\"pages\":\"213-219\"},\"PeriodicalIF\":2.9000,\"publicationDate\":\"2025-05-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12056137/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Clinical Neurology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.3988/jcn.2024.0469\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"CLINICAL NEUROLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Clinical Neurology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.3988/jcn.2024.0469","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"CLINICAL NEUROLOGY","Score":null,"Total":0}
Elevated Serum Amyloid A2 and A4 in Patients With Guillain-Barré Syndrome.
Background and purpose: Guillain-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.
Methods: This 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.
Results: The levels of SAA2 and SAA4 were significantly higher in patients with GBS than in both the other neurological disease controls and the healthy subjects (p<0.05 for all). The level of SAA1 did not differ between patients with GBS and the controls. The level of SAA2 was considerably higher in GBS patients with antecedent infection than in those without infection (p=0.020). The levels of different SAA isoforms were not associated with the disease severity or other clinical features of patients with GBS (p>0.05 for all).
Conclusions: Increased 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.
期刊介绍:
The JCN aims to publish the cutting-edge research from around the world. The JCN covers clinical and translational research for physicians and researchers in the field of neurology. Encompassing the entire neurological diseases, our main focus is on the common disorders including stroke, epilepsy, Parkinson''s disease, dementia, multiple sclerosis, headache, and peripheral neuropathy. Any authors affiliated with an accredited biomedical institution may submit manuscripts of original articles, review articles, and letters to the editor. The JCN will allow clinical neurologists to enrich their knowledge of patient management, education, and clinical or experimental research, and hence their professionalism.