Temporal profile of anti-ganglioside antibodies and their relation to clinical parameters and treatment in Guillain-Barre syndrome

Citation
R. Press et al., Temporal profile of anti-ganglioside antibodies and their relation to clinical parameters and treatment in Guillain-Barre syndrome, J NEUR SCI, 190(1-2), 2001, pp. 41-47
Citations number
20
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF THE NEUROLOGICAL SCIENCES
ISSN journal
0022-510X → ACNP
Volume
190
Issue
1-2
Year of publication
2001
Pages
41 - 47
Database
ISI
SICI code
0022-510X(20010915)190:1-2<41:TPOAAA>2.0.ZU;2-L
Abstract
Elevated anti-ganglioside antibody levels mainly of anti-GM1 and anti-GD1a specificities have been reported in THE serum of patients with Guillain-Bar re syndrome (GBS). The relevance of anti-ganglio side antibodies other than anti-GM1 and anti-GD1a IgG antibodies and the temporal profile of anti-gan glioside antibodies in GBS is less clear. We studied serum antibodies to GM 1, GD1a, GD1b, GQ1b, sulfatide and cardiolipin of the Ig, I-G and IgA class es over the course of GBS in patients who were untreated or treated with hi ghdose intravenous immunoglobulin (Mg). Antibodies to GD1b, GQ1b, sulfatide and cardiolipin were not detected in the sera of the GBS patients examined in this study. Anti-GM1 I-G titers peaked around 40 days and anti-GD1a lam around 90 days after GBS onset. Titers of anti-GM1 IgG antibodies decrease d following Mg 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 a ntibody peaks) and axonal damage (anti-GD1a I-M antibody peaks), compared t o patients without peak antibody titers. Anti-GM1 IgG and anti-GD1a I.-M an tibodies are thus strongly associated with more severe- and predominantly a xonal cases of GBS. The appearance of anti-GM1 IgG and anti-GD1a antibody p eaks 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 da ta 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 patient s with GBS. (C) 2001 Elsevier Science B.V. All rights reserved.