From the Faculty of Medicine (N.S.), University of Malaya, Kuala Lumpur, Malaysia; Dokkyo Medical University (N.K., K.H.), Tochigi, Japan; Graduate School of Medicine (S.S., S.K.), Chiba University, Japan; National Neurosciences Institute (T.U.), Singapore; and National University Singapore (Y.-C.C., N.Y.), Singapore.
Neurology. 2014 Jul 8;83(2):118-24. doi: 10.1212/WNL.0000000000000577. Epub 2014 Jun 11.
To comprehensively investigate the relationship between antibodies to single glycolipids and their complexes and Guillain-Barré syndrome subtypes and clinical features.
In acute sera from 199 patients with Guillain-Barré syndrome, immunoglobulin G (IgG) antibodies to glycolipids and ganglioside complexes were tested using ELISA against individual antigens from single glycolipids including gangliosides (LM1, GM1, GM1b, GD1a, GalNAc-GD1a, GD1b, GT1a, GT1b, GQ1b) and a neutral glycolipid, asialo-GM1 (GA1), and antigens from the combination of 2 different glycolipids. Based on serial nerve conduction studies, the electrodiagnoses were as follows: 69 demyelinating subtype, 85 axonal subtypes, and 45 unclassified.
Significant associations were detected between acute motor axonal neuropathy subtype and IgG antibodies to GM1, GalNAc-GD1a, GA1, or LM1/GA1 complex. Reversible conduction failure was significantly associated with IgG antibodies to GM1, GalNAc-GD1a, GD1b, or complex of LM1/GA1. No significant association was demonstrated between acute inflammatory demyelinating polyneuropathy and any of the glycolipids or ganglioside complexes. Anti-ganglioside complex antibodies alone were detected in 7 patients (5 axonal subtype).
The current study demonstrates that antibodies to single glycolipids and ganglioside complexes are associated with acute motor axonal neuropathy or acute motor conduction block neuropathy but not acute inflammatory demyelinating polyneuropathy.
This study provides Class II evidence that antibodies to glycolipids are increased in patients with acute motor axonal neuropathy and acute motor conduction block neuropathy but not acute inflammatory demyelinating polyneuropathy.
全面研究单糖脂抗体及其复合物与吉兰-巴雷综合征亚型和临床特征的关系。
采用 ELISA 法检测 199 例吉兰-巴雷综合征患者急性血清中针对单个糖脂的 IgG 抗体,包括神经节苷脂(LM1、GM1、GM1b、GD1a、GalNAc-GD1a、GD1b、GT1a、GT1b、GQ1b)和中性糖脂神经节苷脂(GA1),以及 2 种不同糖脂组合的抗原。根据连续的神经传导研究,电诊断如下:69 例脱髓鞘亚型,85 例轴索亚型,45 例未分类。
急性运动轴索性神经病亚型与 GM1、GalNAc-GD1a、GA1 或 LM1/GA1 复合物 IgG 抗体之间存在显著相关性。可逆性传导失败与 GM1、GalNAc-GD1a、GD1b 或 LM1/GA1 复合物 IgG 抗体显著相关。急性炎症性脱髓鞘性多发性神经病与任何糖脂或神经节苷脂复合物均无显著相关性。7 例患者(5 例轴索亚型)单独检测到抗神经节苷脂复合物抗体。
本研究表明,针对单个糖脂和神经节苷脂复合物的抗体与急性运动轴索性神经病或急性运动传导阻滞神经病有关,但与急性炎症性脱髓鞘性多发性神经病无关。
本研究提供了 II 级证据,表明急性运动轴索性神经病和急性运动传导阻滞神经病患者的糖脂抗体增加,但急性炎症性脱髓鞘性多发性神经病患者的糖脂抗体没有增加。