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

被引:47
|
作者
Press, R [1 ]
Matá, S
Lolli, F
Zhu, J
Andersson, T
Link, H
机构
[1] Huddinge Univ Hosp, Karolinska Inst, Neuroimmunol Unit, Div Neurol, Stockholm, Sweden
[2] Univ Florence, Dipartimento Sci Neurol & Psichiatr, Serv Neurofisiopatol, I-50134 Florence, Italy
[3] Huddinge Univ Hosp, Dept Clin Neurophysiol, Stockholm, Sweden
关键词
Guillain-Barre syndrome; gangliosides; antibodies; axonal; IvIg;
D O I
10.1016/S0022-510X(01)00580-9
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Elevated anti-ganglioside antibody levels mainly of anti-GM1 and anti-GD1a specificities have been reported in THE serum of patients with Guillain-Barre syndrome (GBS). The relevance of anti-ganglio side 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 Ig, I-G and IgA classes over the course of GBS in patients who were untreated or treated with highdose 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 decreased 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 antibody peaks) and axonal damage (anti-GD1a I-M antibody peaks), compared to patients without peak antibody titers. Anti-GM1 IgG and anti-GD1a I.-M 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. (C) 2001 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:41 / 47
页数:7
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