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. 1993 Feb;114(2):193-9.
doi: 10.1016/0022-510x(93)90297-c.

Clinical, neurophysiological and immunological evidence of polyneuropathy in patients with monoclonal gammopathies

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Clinical, neurophysiological and immunological evidence of polyneuropathy in patients with monoclonal gammopathies

M Vrethem et al. J Neurol Sci. 1993 Feb.

Abstract

In this study we estimated the prevalence of polyneuropathy (PN) in patients with monoclonal gammopathies. 31 patients with monoclonal gammopathies (19 with monoclonal gammopathy of uncertain significance (MGUS), 10 with multiple myeloma (MM), and 2 with Waldenström's macroglobulinemia), were studied by clinical and neurophysiological examination, blood tests to exclude other causes of PN, ELISA assays to detect antibodies to peripheral nerve myelin (PNM), and antibodies to myelin associated glycoprotein (MAG). 11 of 31 patients (36%) had a clinical PN, 3 (10%) had a probable PN (signs but no symptoms), and 4 (13%) had a subclinical PN (only neurophysiological signs of PN). Thus, in total 18 patients (58%) had some form of PN, in contrast to an age-matched control group (n = 33) where only 2 persons (6%) had some form of PN; 1 had a probable PN and 1 had a subclinical PN. 3 patients had anti-PNM and anti-MAG antibodies of IgM isotype, all 3 patients showing a demyelinating PN. The remaining patients with PN had a mild or moderate distal PN. One patient had a myelopathy and 1 had amyotrophic lateral sclerosis (ALS). IgM isotype of the M-protein was associated with a high risk of clinical PN (5 out of 6 (83%)), in contrast to IgG (5 out of 18 (28%)) and IgA (1 out of 6 (17%)). We conclude that PN is a common finding in patients with monoclonal gammopathies, but only some of them are of the demyelinating type and associated with antibodies to PNM or MAG.

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