Immunoglobulin improves a model of acute motor axonal neuropathy by preventing axonal degeneration

Immunoglobulin improves a model of acute motor axonal neuropathy by preventing axonal degeneration
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DOI:
10.1212/01.wnl.0000129917.28461.0c
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发表时间:
2004-06
期刊:
影响因子:
9.9
通讯作者:
Y. Nishimoto;M. Koga;M. Kamijo;K. Hirata;N. Yuki
Y. Nishimoto;M. Koga;M. Kamijo;K. Hirata;N. Yuki
中科院分区:
医学1区
文献类型:
--
作者:
Y. Nishimoto;M. Koga;M. Kamijo;K. Hirata;N. Yuki

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背景:静脉注射免疫球蛋白治疗格林-巴利́综合征的作用机制尚不清楚。目的:评价静脉注射免疫球蛋白(IVIg)治疗急性运动性轴索神经病(AMAN)的临床、组织学和免疫学效果。方法:用神经节苷脂包括GM1致敏兔,发病时随机分为两组。对照组15只,静脉注射同种γ球蛋白(400 mg/kg/d),共5天。每天对病情严重程度进行评分(0~13分)。发病60d后,用酶联免疫吸附试验检测抗GM1抗体,计数脊髓前根内退行性轴突数目。结果:两组患者发病时在临床评分等方面均无差异。IVIg组较生理盐水组恢复快(p=0.03)。发病60天后,静脉注射免疫球蛋白组的兔≤评分改善4分的比例(53%)高于生理盐水组(13%)(p=0.03)。发病60天后抗GM1抗体滴度在两组间无差异。发病60d后存活的兔前根轴突变性发生率IVIg组(n=11,平均4.5%)低于生理盐水组(n=8,平均11.1%)(p=0.01)。结论:静脉注射免疫球蛋白对AMAN模型的治疗效果是肯定的。IVIG可能不影响抗GM1-Ig G的产生或分解代谢,但可防止运动神经轴突变性。
Background: The action mechanism of IV immunoglobulin (IVIg) for Guillain-Barré syndrome has yet to be clarified. Objective: To evaluate clinical, histologic, and immunologic effects in a disease model of acute motor axonal neuropathy (AMAN) treated by IVIg. Methods: Rabbits were sensitized with gangliosides including GM1 and divided randomly into two groups at disease onset. One group received IV homologous γ-globulin (400 mg/kg/day) for 5 days (n = 15), and the other received saline (n = 15). Disease severity was scored (0 to 13 points) daily. Sixty days after onset, anti-GM1 antibodies were tested by ELISA, and the number of degenerative axons was counted in spinal anterior roots. Results: Between both groups at onset, there was no difference in any characteristics including clinical score. The IVIg group had faster recovery than the saline group (p = 0.03). The percentage of rabbits that improved by a score of ≤4 was higher in the IVIg (53%) than in the saline (13%) group 60 days after onset (p = 0.03). Anti-GM1 IgG titers 60 days after onset did not differ between the groups. The anterior roots of rabbits surviving 60 days after onset showed lower frequency of axonal degeneration in the IVIg-treated (n = 11; mean 4.5%) than in the saline-treated (n = 8; mean 11.1%) rabbits (p = 0.01). Conclusions: The therapeutic efficacy of IVIg in an AMAN model was confirmed. IVIg may not affect the production or catabolism of anti-GM1 IgG, but it may prevent axonal degeneration of motor nerves.