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Journal of Immunology Research
Volume 2015, Article ID 450391, 9 pages
http://dx.doi.org/10.1155/2015/450391
Research Article

Heterogeneity of Polyneuropathy Associated with Anti-MAG Antibodies

1Department of Neurology, Centre de Référence “Neuropathies Périphériques Rares”, CHU Limoges, 2 Avenue Martin Luther-King, 87042 Limoges, France
2Department of Neurology, CHU Poitiers, University of Poitiers, 2 Rue de la Milétrie, 86021 Poitiers, France
3Centre de Biologie et de Pathologie Est, Hospices Civils de Lyon, 69000 Lyon, France

Received 4 November 2014; Accepted 7 April 2015

Academic Editor: Douglas C. Hooper

Copyright © 2015 Laurent Magy et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Polyneuropathy associated with IgM monoclonal gammopathy and anti-myelin associated glycoprotein (MAG) antibodies is an immune-mediated demyelinating neuropathy. The pathophysiology of this condition is likely to involve anti-MAG antibody deposition on myelin sheaths of the peripheral nerves and it is supposed to be distinct from chronic inflammatory demyelinating neuropathy (CIDP), another immune-mediated demyelinating peripheral neuropathy. In this series, we have retrospectively reviewed clinical and laboratory findings from 60 patients with polyneuropathy, IgM gammopathy, and anti-MAG antibodies. We found that the clinical picture in these patients is highly variable suggesting a direct link between the monoclonal gammopathy and the neuropathy. Conversely, one-third of patients had a CIDP-like phenotype on electrodiagnostic testing and this was correlated with a low titer of anti-MAG antibodies and the absence of widening of myelin lamellae. Our data suggest that polyneuropathy associated with anti-MAG antibodies is less homogeneous than previously said and that the pathophysiology of the condition is likely to be heterogeneous as well with the self-antigen being MAG in most of the patients but possibly being another component of myelin in the others.