Uetz-von Allmen E, Sturzenegger M, Rieben R, Rihs F, Frauenfelder A, Nydegger U E
Regional Red Cross Blood Transfusion Center, Bern, Switzerland.
Eur Neurol. 1998;39(2):103-10. doi: 10.1159/000007916.
So far, the pathogenic significance and use for diagnosis of antiganglioside GM1 antibodies (anti-GM1) are unclear. We therefore compared serum IgM and IgG antimonosialo ganglioside GM1 levels of 33 patients with presumed immune-mediated neuropathies, 100 patients with various other central or peripheral neurological disorders, and 110 controls by ELISA. We also measured the complement-activating capacity of anti-GM1 by C5b-9-GM1-ELISA to evaluate its value to distinguish between pathogenic and nonpathogenic autoantibodies. Low levels of anti-GM1 were observed in all disease categories and in controls (healthy blood donors). Twenty-four of the controls including the 10 with the highest serum IgM or IgG anti-GM1 were examined for neurological disorders in a double-blind checkup study. In the patients, elevated IgM anti-GM1 levels were predominantly found in those with neuropathies (NP), but barely in patients with central nervous system disease (CNSD). We found elevated IgG anti-GM1 levels predominantly in patients with NP of inflammatory origin (multifocal motor neuropathy, chronic inflammatory demyelinating polyneuropathy or Guillain-Barré syndrome), rarely in patients with NP of noninflammatory origin or CNSD, but not in the control disease group myasthenia gravis (MG). Median levels of IgM-, IgG-, (IgM+IgG)-, and C5b-9-binding anti-GM1 were significantly higher in patients with inflammatory NP as compared to the controls (p < 0.025). In addition, median levels of IgG- and (IgM+IgG)-anti-GM1 were significantly higher in inflammatory NP versus CNSD. Elevated complement-binding activity was associated with low or elevated IgM and/or IgG anti-GM1. Nevertheless, there was a significant correlation between anti-GM1 level (IgM+IgG) and the respective complement-activating capacity (r = 0.758; n = 243). Estimation of anti-GM1 and their respective complement-activating capacity may be helpful in the diagnosis of inflammatory neuropathies. However, neither an elevated anti-GM1 level nor an increased C5b-9 binding seems specific for a given disease category (e.g. peripheral nerve disease) nor a disease process (e.g. demyelination or inflammation).
迄今为止，抗神经节苷脂GM1抗体（抗GM1）的致病意义及诊断用途尚不清楚。因此，我们通过酶联免疫吸附测定法（ELISA）比较了33例疑似免疫介导性神经病患者、100例患有各种其他中枢或周围神经系统疾病的患者以及110名对照者的血清IgM和IgG抗单唾液酸神经节苷脂GM1水平。我们还通过C5b - 9 - GM1 - ELISA检测了抗GM1的补体激活能力，以评估其区分致病性和非致病性自身抗体的价值。在所有疾病类别以及对照者（健康献血者）中均观察到低水平的抗GM1。对包括10名血清IgM或IgG抗GM1水平最高的对照者在内的24名对照者进行了双盲检查研究，以排查神经系统疾病。在患者中，IgM抗GM1水平升高主要见于患有神经病（NP）的患者，而在患有中枢神经系统疾病（CNSD）的患者中则很少见。我们发现IgG抗GM1水平升高主要见于炎症性起源的NP患者（多灶性运动神经病、慢性炎症性脱髓鞘性多发性神经病或吉兰 - 巴雷综合征），在非炎症性起源的NP患者或CNSD患者中很少见，但在对照疾病组重症肌无力（MG）患者中未发现升高。与对照者相比，炎症性NP患者的IgM -、IgG -、（IgM + IgG） - 和C5b - 9结合抗GM1的中位数水平显著更高（p < 0.025）。此外，炎症性NP患者的IgG - 和（IgM + IgG） - 抗GM1中位数水平显著高于CNSD患者。补体结合活性升高与低或高的IgM和/或IgG抗GM1相关。然而，抗GM1水平（IgM + IgG）与各自的补体激活能力之间存在显著相关性（r = 0.758；n = 243）。抗GM1及其各自补体激活能力的评估可能有助于炎症性神经病的诊断。然而，抗GM1水平升高或C5b - 9结合增加似乎都对特定疾病类别（如周围神经疾病）或疾病过程（如脱髓鞘或炎症）不具有特异性。
