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Reversible rituximab demyelination in anti-MAG polyneuropathy: A role for IVIG?
Gloria Mak1, David Bennett2, Cecile Phan1
1Division of Neurology, Department of Medicine, Neuroscience and Mental Health Institute, University of Alberta, Edmonton, Canada.
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.
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