Natalia Ruiz-Nieto, Antonio Belenguer-Benavides, Anabel Zahonero-Ferriz, Helena Benetó-Andrés, Ana Monclús-Blecua
{"title":"Early prognostic factors in acute inflammatory demyelinating polyneuropathy: Role of neurofilaments","authors":"Natalia Ruiz-Nieto, Antonio Belenguer-Benavides, Anabel Zahonero-Ferriz, Helena Benetó-Andrés, Ana Monclús-Blecua","doi":"10.1016/j.neurop.2024.100173","DOIUrl":null,"url":null,"abstract":"<div><h3>Introduction</h3><div>Guillain-Barré syndrome (GBS) is an autoimmune disease that results in demyelination and axonal damage. Although the recovery is good in most patients, 20% remain significantly disabled.</div><div>Neurofilament light chain (NfL) has been established as a biomarker of axonal damage in many diseases.</div></div><div><h3>Methods</h3><div>We measured NfL, S100B, and glial fibrillary acidic protein (GFAP) concentrations from blood and cerebrospinal fluid (CSF) taken upon admission from 19 patients with a history of GBS between January 2009 and December 2019 and investigated a correlation between them and clinical outcomes.</div></div><div><h3>Results</h3><div>All patients fulfilled levels 1 or 2 of the Brighton diagnostic.</div><div>Preceding infection was reported in 11 cases (58%).</div><div>We classified 15 patients as acute inflammatory demyelinating polyneuropathy, 2 as AMAN, 1 as AMSAN, and 2 cases as Miller–Fisher syndrome.</div><div>Five patients were transferred to an ICU, with a mean stay of 13 days. Functional outcome at 6 months after discharge was good in 12 patients (70.6%).</div><div>We evaluated disease prognosis using the modified Erasmus GBS outcome score. The correlation was significant (<em>p</em> <!--><<!--> <!-->.05) in the case of NfL in serum and CSF and GFAP in CSF (<em>r</em> <!-->=<!--> <!-->0.472 for serum NfL, 0.576 for CSF NfL, and 0.544 for CSF GFAP).</div></div><div><h3>Conclusions</h3><div>We confirm the finding of elevated levels of NfL, GFAP, and S100B in CSF and plasma in the acute phase of GBS.</div><div>We can point out that their value has a certain relationship with the severity of the disease and prognosis, and that in some way, they have an influence, but we would lack more information to make good predictions.</div></div>","PeriodicalId":74283,"journal":{"name":"Neurology perspectives","volume":"4 4","pages":"Article 100173"},"PeriodicalIF":0.0000,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neurology perspectives","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2667049624000309","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Introduction
Guillain-Barré syndrome (GBS) is an autoimmune disease that results in demyelination and axonal damage. Although the recovery is good in most patients, 20% remain significantly disabled.
Neurofilament light chain (NfL) has been established as a biomarker of axonal damage in many diseases.
Methods
We measured NfL, S100B, and glial fibrillary acidic protein (GFAP) concentrations from blood and cerebrospinal fluid (CSF) taken upon admission from 19 patients with a history of GBS between January 2009 and December 2019 and investigated a correlation between them and clinical outcomes.
Results
All patients fulfilled levels 1 or 2 of the Brighton diagnostic.
Preceding infection was reported in 11 cases (58%).
We classified 15 patients as acute inflammatory demyelinating polyneuropathy, 2 as AMAN, 1 as AMSAN, and 2 cases as Miller–Fisher syndrome.
Five patients were transferred to an ICU, with a mean stay of 13 days. Functional outcome at 6 months after discharge was good in 12 patients (70.6%).
We evaluated disease prognosis using the modified Erasmus GBS outcome score. The correlation was significant (p < .05) in the case of NfL in serum and CSF and GFAP in CSF (r = 0.472 for serum NfL, 0.576 for CSF NfL, and 0.544 for CSF GFAP).
Conclusions
We confirm the finding of elevated levels of NfL, GFAP, and S100B in CSF and plasma in the acute phase of GBS.
We can point out that their value has a certain relationship with the severity of the disease and prognosis, and that in some way, they have an influence, but we would lack more information to make good predictions.