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The Neuropathies of Waldenström's Macroglobulinemia (WM) and IgM-MGUS

Published online by Cambridge University Press:  02 December 2014

Christopher J. Klein ,
Joon-Shik Moon ,
Michelle L. Mauermann ,
Steven R. Zeldenrust ,
Yanhong Wu ,
Angela Dispenzieri  and
Peter J. Dyck
Christopher J. Klein*
Affiliation:
Peripheral Nerve Research Laboratory, Mayo Clinic, Rochester, Minnesota, U.S.A
Joon-Shik Moon
Affiliation:
Peripheral Nerve Research Laboratory, Mayo Clinic, Rochester, Minnesota, U.S.A
Michelle L. Mauermann
Affiliation:
Peripheral Nerve Research Laboratory, Mayo Clinic, Rochester, Minnesota, U.S.A
Steven R. Zeldenrust
Affiliation:
Department of Hematology, Mayo Clinic, Rochester, Minnesota, U.S.A
Yanhong Wu
Affiliation:
Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota, U.S.A
Angela Dispenzieri
Affiliation:
Department of Hematology, Mayo Clinic, Rochester, Minnesota, U.S.A
Peter J. Dyck
Affiliation:
Peripheral Nerve Research Laboratory, Mayo Clinic, Rochester, Minnesota, U.S.A
*
Department of Neurology, Mayo Clinic, 200 First Street SW, Rochester, Minnesota, 55905, U.S.A.
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Abstract

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Background:

Neuropathy is common in Waldenström's macroglobulinemia (WM, an IgM-associated lymphoplasmacytic lymphoma) and in IgM-monoclonal gammopathy of undetermined significance (IgM-MGUS). Paraneoplastic or paraimmune mechanisms are thought to be involved in the pathogenesis of these neuropathies. Attempts at distinguishing WM and IgM-MGUS neuropathies are lacking especially among bone marrow (BM) confirmed patients.

Methods:

Retrospective analyses were performed on BM confirmed WM (N=30) and IgM-MGUS (N=73) neuropathy patients with neurologic assessments and hematologic features.

Results:

The presence of anemia and quantity of IgM monoclonal protein were significantly greater in WM. Based on multiple neurologic assessments differences were not found for: 1) length of time from neurologic symptom onset to evaluation; 2) chief complaint of painless loss of feeling in the feet, Romberg's sign and tremor; and 3) clinical motor, sensory and reflex abnormalities. Autonomic testing was normal in both diseases. Using nerve conduction (NCS) criteria for demyelination, 62% of IgM-MGUS and 27% of WM met this criteria (p=0.013). IgM MGUS patients had greater terminal conduction slowing by ulnar residual latency calculation (<0.01). The degree of axonal loss as measured by summated compound muscle action potentials and available nerve biopsy was not significantly different between diseases.

Conclusion:

Although WM and IgM-MGUS must be distinguished for hematologic prognosis and treatment, clinical neuropathy presentations of WM and IgM-MGUS are similar and likely related to comparable axonal loss in both conditions. Despite these similarities, evidence of demyelination was found by electrophysiologic studies much more commonly in IgM-MGUS. This difference may reflect varied immune mechanism(s) in the two disorders.

Type
Original Article
Information
Canadian Journal of Neurological Sciences , Volume 38 , Issue 2 , March 2011 , pp. 289 - 295
Copyright
Copyright © The Canadian Journal of Neurological 2011

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