Reversible rituximab demyelination in anti-MAG polyneuropathy: A role for IVIG?
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.
Case description and serial electrophysiological studies.
Serial electrophysiological studies confirmed subacute demyelination in our patient with anti-MAG neuropathy treated with rituximab followed by improvement following IVIg.
The use of IVIG therapy can be considered in cases where rituximab leads to clinical and electrophysiological worsening of anti-MAG neuropathy.
Case description and serial electrophysiological studies.
Serial electrophysiological studies confirmed subacute demyelination in our patient with anti-MAG neuropathy treated with rituximab followed by improvement following IVIg.
The use of IVIG therapy can be considered in cases where rituximab leads to clinical and electrophysiological worsening of anti-MAG neuropathy.