AUTOANTIBODIES TO PERIPHERAL-NERVE GLYCOSPHINGOLIPIDS SPG, SLPG, AND SGPG IN GUILLAIN-BARRE-SYNDROME AND CHRONIC INFLAMMATORY DEMYELINATINGPOLYNEUROPATHY

Unlike CNS myelin, human peripheral nerve myelin has the acidic glycos phingolipids sialosyl paragloboside (SPG), sialosyl lactosaminyl parag loboside (SLPG), and sulfated glucuronyl paragloboside (SGPG). To eluc idate the pathogenesis of Guillain-Barre syndrome (GBS) and chronic in flammatory demyelinating neuropathy (CIDP), we investigated the autoan tibodies to peripheral nerve molecules in patients with these diseases and compared the frequency of the autoantibodies with that of autoant ibody to GM1 which is present in both the CNS and PNS. The report of S heikh et al. (Ann. Neurol. 1995; 38: 350) that Campylobacter jejuni be ars the SGPG epitope led us to study whether sera from patients with G BS subsequent to C. jejuni enteritis have anti-SGPG antibody; but, hig h anti-SGPG antibody titers were not found in the GBS patients from wh om C. jejuni was isolated. Although the frequency of the anti-SPG, ant i-SLPG, and anti-SGPG antibodies were lower than that of the anti-GM1 antibody in GBS, 5 patients with demyelinating GBS had high IgG anti-S PG antibody titers. IgG anti-SPG antibody may function in the developm ent of demyelinating GBS. We found that 6 CIDP patients had elevated I gM anti-SGPG antibody titers. Immunoelectrophoresis failed to detect I gM M-protein in 3 of the patients. IgM anti-SGPG antibody could be a d iagnostic marker for a subgroup of CIDP with or without paraprotein.