title: Temporal profile of anti-ganglioside antibodies and their relation to clinical parameters and treatment in Guillain-Barré syndrome.
abstract: Elevated anti-ganglioside antibody levels mainly of anti-GM1 and anti-GD1a specificities have been reported in THE serum of patients with Guillain-Barré syndrome (GBS). The relevance of anti-ganglioside antibodies other than anti-GM1 and anti-GD1a IgG antibodies and the temporal profile of anti-ganglioside antibodies in GBS is less clear. We studied serum antibodies to GM1, GD1a, GD1b, GQ1b, sulfatide and cardiolipin of the IgM, IgG and IgA classes over the course of GBS in patients who were untreated or treated with high dose intravenous immunoglobulin (IvIg). Antibodies to GD1b, GQ1b, sulfatide and cardiolipin were not detected in the sera of the GBS patients examined in this study. Anti-GM1 IgG titers peaked around 40 days and anti-GD1a IgM around 90 days after GBS onset. Titers of anti-GM1 IgG antibodies decreased following IvIg treatment. Patients with antibody peaks, defined as fivefold or higher increase in antibody titer compared to the lowest antibody titer over the course of GBS, had higher disability scores during the first two weeks of GBS and a worse clinical outcome (anti-GM1 IgG and anti-GD1a IgM antibody peaks) and axonal damage (anti-GD1a IgM antibody peaks), compared to patients without peak antibody titers. Anti-GM1 IgG and anti-GD1a IgM antibodies are thus strongly associated with more severe- and predominantly axonal cases of GBS. The appearance of anti-GM1 IgG and anti-GD1a antibody peaks in the serum after the termination of the acute phase of GBS suggests that these antibodies are produced secondary to nerve damage in GBS. The data does not exclude the possibility that secondarily secreted anti-GM1 IgG and anti-GD1a IgM antibodies may themselves be biologically active and play a role in disease propagation and/or recovery from disease in some patients with GBS.
authors.affiliation: Neuroimmunology Unit, Division of Neurology, Karolinska Institutet, Huddinge University Hospital, Stockholm, Sweden. Rayomand.Press@neurotec.ki.se
authors.forename: R
authors.initials: R
authors.lastname: Press
authors.forename: S
authors.initials: S
authors.lastname: Matá
authors.forename: F
authors.initials: F
authors.lastname: Lolli
authors.forename: J
authors.initials: J
authors.lastname: Zhu
authors.forename: T
authors.initials: T
authors.lastname: Andersson
authors.forename: H
authors.initials: H
authors.lastname: Link
mesh_terms: D000906:Antibodies / Q000097:blood* / Q000276:immunology*; D001369:Axons / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D002308:Cardiolipins / Q000276:immunology / Q000378:metabolism; D018450:Disease Progression; D005260:Female; D005677:G(M1) Ganglioside / Q000276:immunology / Q000378:metabolism; D005732:Gangliosides / Q000276:immunology* / Q000378:metabolism; D020275:Guillain-Barre Syndrome / Q000097:blood* / Q000188:drug therapy / Q000276:immunology*; D006801:Humans; D007070:Immunoglobulin A / Q000097:blood / Q000276:immunology; D007074:Immunoglobulin G / Q000097:blood / Q000276:immunology; D007075:Immunoglobulin M / Q000097:blood / Q000276:immunology; D016756:Immunoglobulins, Intravenous / Q000737:chemistry / Q000276:immunology / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D013433:Sulfoglycosphingolipids / Q000276:immunology / Q000378:metabolism; D013997:Time Factors
chemical_list: D000906:Antibodies; D002308:Cardiolipins; D005732:Gangliosides; D007070:Immunoglobulin A; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D016756:Immunoglobulins, Intravenous; D013433:Sulfoglycosphingolipids; C021298:ganglioside, GD1a; C033851:ganglioside, GD1b; D005677:G(M1) Ganglioside; C039129:GQ1b ganglioside