Gloria Mak , David Bennett , Cecile Phan , Michael Chu , Douglas W. Zochodne
{"title":"Reversible rituximab demyelination in anti-MAG polyneuropathy: A role for IVIG?","authors":"Gloria Mak , David Bennett , Cecile Phan , Michael Chu , Douglas W. Zochodne","doi":"10.1016/j.jns.2025.123626","DOIUrl":null,"url":null,"abstract":"<div><h3>Background and aims</h3><div>Anti-myelin-associated glycoprotein (MAG) demyelinating neuropathy is a clinically heterogeneous slowly progressive large fiber sensorimotor polyneuropathy. Management of anti-MAG neuropathy is challenging, and a small subset of anti-MAG neuropathy patients have been previously reported to deteriorate after rituximab therapy, perhaps triggered by an upsurge in autoantibody release secondary to B lymphocyte lysis. We report a patient with this complication that responded to IVIg therapy.</div></div><div><h3>Method</h3><div>Case description and serial electrophysiological studies.</div></div><div><h3>Results</h3><div>Serial electrophysiological studies confirmed subacute demyelination in our patient with anti-MAG neuropathy treated with rituximab followed by improvement following IVIg.</div></div><div><h3>Interpretation</h3><div>The use of IVIG therapy can be considered in cases where rituximab leads to clinical and electrophysiological worsening of anti-MAG neuropathy.</div></div>","PeriodicalId":17417,"journal":{"name":"Journal of the Neurological Sciences","volume":"476 ","pages":"Article 123626"},"PeriodicalIF":3.2000,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of the Neurological Sciences","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0022510X25002436","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CLINICAL NEUROLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Background and aims
Anti-myelin-associated glycoprotein (MAG) demyelinating neuropathy is a clinically heterogeneous slowly progressive large fiber sensorimotor polyneuropathy. Management of anti-MAG neuropathy is challenging, and a small subset of anti-MAG neuropathy patients have been previously reported to deteriorate after rituximab therapy, perhaps triggered by an upsurge in autoantibody release secondary to B lymphocyte lysis. We report a patient with this complication that responded to IVIg therapy.
Method
Case description and serial electrophysiological studies.
Results
Serial electrophysiological studies confirmed subacute demyelination in our patient with anti-MAG neuropathy treated with rituximab followed by improvement following IVIg.
Interpretation
The use of IVIG therapy can be considered in cases where rituximab leads to clinical and electrophysiological worsening of anti-MAG neuropathy.
期刊介绍:
The Journal of the Neurological Sciences provides a medium for the prompt publication of original articles in neurology and neuroscience from around the world. JNS places special emphasis on articles that: 1) provide guidance to clinicians around the world (Best Practices, Global Neurology); 2) report cutting-edge science related to neurology (Basic and Translational Sciences); 3) educate readers about relevant and practical clinical outcomes in neurology (Outcomes Research); and 4) summarize or editorialize the current state of the literature (Reviews, Commentaries, and Editorials).
JNS accepts most types of manuscripts for consideration including original research papers, short communications, reviews, book reviews, letters to the Editor, opinions and editorials. Topics considered will be from neurology-related fields that are of interest to practicing physicians around the world. Examples include neuromuscular diseases, demyelination, atrophies, dementia, neoplasms, infections, epilepsies, disturbances of consciousness, stroke and cerebral circulation, growth and development, plasticity and intermediary metabolism.