Frequency and clinical correlates of anti–neural IgM antibodies in neuropathy associated with IgM monoclonal gammopathy

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Abstract
We studied the frequency and clinical correlates of different IgM specificities in 75 patients with neuropathy associated with IgM monoclonal gammopathy. Patients were tested for IgM reactivity with the myelin‐associated glycoprotein, PO, neurofilaments, and tubulin by immunoblot; with GM1, asialo‐GM1, GM2, GD1a, GD1b, sulfatide, and chondroitin sulfate C by enzyme‐linked immunosorbent assay; and with brain and nerve glycolipids by overlay highperformance thin‐layer chromatography. Forty‐two patients (56%) had high titers of IgM antibodies to MAG; 4 (5%), to sulfatide (1 also to myelin‐associated glycoprotein); 4 (5%), to the 200‐kd neurofilament (2 also to myelin‐associated protein); and 1 each, to GD1b and chondroitin sulfate C. No reactivity was found in 26 patients (35%). More patients with anti–myelin‐associated glycoprotein IgM (62%) than with unknown IgM reactivity (31%) had a predominantly sensory neuropathy (p < 0.025). Nerve conduction findings were consistent with a demyelinating neuropathy in 77% of patients reactive to myelin‐associated glycoprotein and 24% with unknown reactivity (p < 0.0001) and the mean conduction velocity of peroneal nerve was lower in the former group (22.9 m/sec) than in the latter group (39.6 m/sec) (p < 0.000001). Patients with anti–sulfatide IgM had a sensorimotor neuropathy with morphological evidence of demyelination while anti–neurofilament IgM was not associated with homogeneous findings. Patients with anti–GD1b or anti–chondroitin sulfate C IgM had a predominantly motor impairment. The frequent occurrence of anti–neural IgM antibodies in neuropathy associated with IgM gammopathy, and their frequent, though not constant association with similar neuropathy features, support their possible pathogenetic role in the neuropathy.