Polyneuropathy in nonmalignant IgM plasma cell dyscrasia: a morphological study.
Six patients had peripheral neuropathy and nonmalignant IgM plasma cell dyscrasia. In two of them, immunological studies indicated that the monoclonal immunoglobulin reacted with myelin-associated glycoprotein, a constituent of peripheral nerve myelin. Sural nerve biopsy specimens from both patients showed morphological signs of primary damage to the myelin sheath. In the other four patients, two of whom had a monoclonal IgMK reactive with chondroitin sulfate C, the axon rather than the myelin sheath was considered the chief site of nerve injury. The morphological findings suggest that the pathogenesis of peripheral neuropathies in IgM plasma cell dyscrasia is heterogeneous. Moreover, the observations are consistent with a pathogenic interaction of the IgM paraprotein with autoantigens in peripheral nerve in some instances.
D000368:Aged; D001369:Axons / Q000648:ultrastructure; D001706:Biopsy; D004576:Electromyography; D005260:Female; D006801:Humans; D007075:Immunoglobulin M / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D009186:Myelin Sheath / Q000648:ultrastructure; D009413:Nerve Fibers, Myelinated / Q000648:ultrastructure; D010265:Paraproteinemias / Q000473:pathology*; D011115:Polyneuropathies / Q000473:pathology*; D012583:Schwann Cells / Q000648:ultrastructure; D012677:Sensation / Q000502:physiology; D013497:Sural Nerve / Q000473:pathology; D009435:Synaptic Transmission
D007075:Immunoglobulin M