Neuropathy and IgM M-proteins
Prognostic value of antibodies to MAG, SGPG, and sulfatide
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Abstract
Background: In polyneuropathy associated with immunoglobulin M (IgM) monoclonal gammopathy, antibodies to myelin-associated glycoprotein (MAG), sulfoglucuronyl paragloboside (SGPG), and sulfatide have been associated with specific clinical and electrophysiologic features. However, it is not known whether the results of antibody tests provide additional information for the individual patient (and the neurologist) in terms of future neurologic deficit or outcome.
Objective: To study the independent contribution of potential prognostic factors to the prediction of outcome of neuropathy associated with IgM monoclonal gammopathy.
Methods: In accordance with the chronology in which prognostic factors are available in clinical practice, the association between prognostic factors and outcome was evaluated by univariate and multivariate logistic regression analysis in 65 patients with polyneuropathy and IgM monoclonal gammopathy.
Results: In univariate analysis, the initial symptoms, the IgM light chain type, electrophysiologic and pathologic studies, the presence of sural nerve IgM deposition, and anti-MAG or anti-SGPG antibodies were significantly associated with outcome. However, multivariate analysis showed that only initial symptoms and electrophysiologic studies are independent prognostic factors: initial sensory symptoms of the feet are prognostic for a slowly progressive disease course and less disability at 4 years, and evidence for demyelination on electrophysiologic examination is prognostic for development of weakness and symptoms of the upper extremities at 4 years. Addition of anti-MAG or anti-SGPG antibody tests did not yield any additional prediction of outcome.
Conclusion: These results indicate that in clinical practice, antibody tests in polyneuropathy associated with IgM monoclonal gammopathy do not have a prognostic value in terms of future neurologic deficit or outcome.
- Received April 7, 2000.
- Accepted October 4, 2000.
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