Heterogeneity of Polyneuropathy Associated with Anti-MAG Antibodies

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...

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Bibliographic Details
Published in:Journal of immunology research 2015-01, Vol.2015 (2015), p.1-9
Main Authors: Vallat, Jean-Michel, Ghorab, Karima, Lebeau, Prisca, Mathis, Stéphane, Kaboré, Raphaël, Magy, Laurent, Caudie, Christiane
Format: Article
Language:English
Subjects:
Aged
Aged, 80 and over
Antibodies, Monoclonal - immunology
Autoantibodies - immunology
Female
Humans
Immunoglobulin M - immunology
Immunology
Male
Middle Aged
Myelin Sheath - immunology
Myelin-Associated Glycoprotein - immunology
Peripheral Nerves - immunology
Polyneuropathies - immunology
Polyradiculoneuropathy, Chronic Inflammatory Demyelinating - immunology
Retrospective Studies
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Summary: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.
ISSN:2314-8861
2314-7156
DOI:10.1155/2015/450391