吉兰 - 巴雷综合征是什么?
Richard A C Hughes1, David R Cornblath
1Department of Clinical Neuroscience, King's College London School of Medicine, Guy's Hospital, UK. richard.a.hughes@kcl.ac.uk
Lancet (London, England)
|November 8, 2005
概括
吉兰-巴雷综合征的亚型包括对外围神经的免疫攻击. 轴突形式与Campylobacter jejuni感染和对化体的抗体有关,而IVIg和血交换等治疗方法有助于恢复.
科学领域:
- 神经科学是一个神经科学.
- 免疫学 免疫学 免疫学
- 传染性疾病 传染性疾病
背景情况:
- 吉兰-巴雷综合征 (GBS) 是一组具有多种机制的急性外周神经病变.
- 急性炎症性脱髓化多基原蛋白神经病变 (AIDP) 亚型涉及T细胞和髓蛋白,但也建议抗体和补充作用.
- 轴突子类型,急性运动轴突神经病变 (AMAN) 和急性运动和感觉轴突神经病变 (AMSAN),越来越多地被理解.
研究的目的:
- 阐明基因巴雷综合征亚型背后的免疫机制.
- 研究Campylobacter jejuni感染和化体抗体在轴突GBS中的作用.
- 审查目前针对吉-巴雷综合征的治疗疗效.
主要方法:
- 审查关于GBS病原和临床研究的现有文献.
- 针对特定GBS亚型的抗体标 (类) 的分析.
- 检查GBS治疗的国际随机试验的发现.
主要成果:
- 轴突性GBS (AMAN,AMSAN) 强烈与对axolemmal团结体的抗体有关,通常是在Campylobacter jejuni感染之后.
- 坎比洛巴克特 (Campylobacter jejuni) 的脂糖体模仿类糖体,触发交叉反应性抗体 (例如,抗GM1,抗GQ1b).
- 血交换和静脉注射免疫球蛋白在加速GBS恢复方面表现出同等的有效性,而皮质类固醇效果较差.
结论:
- 抗体介导的攻击兰维尔节点的氏体是轴突GBS的一个关键机制.
- 坎比洛巴克特 (Campylobacter jejuni) 是通过分子模仿对轴突GBS的一个重要触发因素.
- 对GBS的有效治疗包括血交换和IVIg,但需要进一步的研究来解决持续的残疾.
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