title: Antiganglioside GM1 antibodies and their complement activating capacity in central and peripheral nervous system disorders and in controls.
abstract: So far, the pathogenic significance and use for diagnosis of antiganglioside GM1 antibodies (anti-GM1) are unclear. We therefore compared serum IgM and IgG antimonosialo ganglioside GM1 levels of 33 patients with presumed immune-mediated neuropathies, 100 patients with various other central or peripheral neurological disorders, and 110 controls by ELISA. We also measured the complement-activating capacity of anti-GM1 by C5b-9-GM1-ELISA to evaluate its value to distinguish between pathogenic and nonpathogenic autoantibodies. Low levels of anti-GM1 were observed in all disease categories and in controls (healthy blood donors). Twenty-four of the controls including the 10 with the highest serum IgM or IgG anti-GM1 were examined for neurological disorders in a double-blind checkup study. In the patients, elevated IgM anti-GM1 levels were predominantly found in those with neuropathies (NP), but barely in patients with central nervous system disease (CNSD). We found elevated IgG anti-GM1 levels predominantly in patients with NP of inflammatory origin (multifocal motor neuropathy, chronic inflammatory demyelinating polyneuropathy or Guillain-Barré syndrome), rarely in patients with NP of noninflammatory origin or CNSD, but not in the control disease group myasthenia gravis (MG). Median levels of IgM-, IgG-, (IgM+IgG)-, and C5b-9-binding anti-GM1 were significantly higher in patients with inflammatory NP as compared to the controls (p < 0.025). In addition, median levels of IgG- and (IgM+IgG)-anti-GM1 were significantly higher in inflammatory NP versus CNSD. Elevated complement-binding activity was associated with low or elevated IgM and/or IgG anti-GM1. Nevertheless, there was a significant correlation between anti-GM1 level (IgM+IgG) and the respective complement-activating capacity (r = 0.758; n = 243). Estimation of anti-GM1 and their respective complement-activating capacity may be helpful in the diagnosis of inflammatory neuropathies. However, neither an elevated anti-GM1 level nor an increased C5b-9 binding seems specific for a given disease category (e.g. peripheral nerve disease) nor a disease process (e.g. demyelination or inflammation).
authors.affiliation: Regional Red Cross Blood Transfusion Center, Bern, Switzerland.
authors.forename: E
authors.initials: E
authors.lastname: Uetz-von Allmen
authors.forename: M
authors.initials: M
authors.lastname: Sturzenegger
authors.forename: R
authors.initials: R
authors.lastname: Rieben
authors.forename: F
authors.initials: F
authors.lastname: Rihs
authors.forename: A
authors.initials: A
authors.lastname: Frauenfelder
authors.forename: U E
authors.initials: UE
authors.lastname: Nydegger
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001782:Blood Donors; D016022:Case-Control Studies; D002493:Central Nervous System Diseases / Q000276:immunology*; D003167:Complement Activation / Q000276:immunology*; D015938:Complement Membrane Attack Complex / Q000096:biosynthesis; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005677:G(M1) Ganglioside / Q000276:immunology*; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood*; D007075:Immunoglobulin M / Q000097:blood*; D008297:Male; D008875:Middle Aged; D010523:Peripheral Nervous System Diseases / Q000276:immunology*
chemical_list: D015938:Complement Membrane Attack Complex; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D005677:G(M1) Ganglioside