Pathogenesis of chronic inflammatory demyelinating polyradiculoneuropathy

被引：111

作者：

Hughes, RAC ^{[1
]}

Allen, D ^{[1
]}

Makowska, A ^{[1
]}

Gregson, NA ^{[1
]}

机构：

[1] Kings Coll London, Sch Med, Guys Hosp, Dept Clin Neurosci, London SE1 1UL, England

来源：

JOURNAL OF THE PERIPHERAL NERVOUS SYSTEM | 2006年 / 11卷 / 01期

关键词：

pathogenesis; chronic inflammatory demyelinating polyradiculoneuropathy;

D O I：

10.1111/j.1085-9489.2006.00061.x

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

The acute lesions of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) consist of endoneurial foci of chemokine and chemokine receptor expression and T cell and macrophage activation. The myelin protein antigens, P2, P0, and PMP22, each induce experimental autoimmune neuritis in rodent models and might be autoantigens in CIDP. The strongest evidence incriminates P0, to which antibodies have been found in 20% of cases. Failure of regulatory T-cell mechanism is thought to underlie persistent or recurrent disease, differentiating CIDP from the acute inflammatory demyelinating polyradiculoneuropathy form of Guillain-Barre syndrome. Corticosteroids, intravenous immunoglobulin and plasma exchange each provide short term benefit but the possible long-term benefits of immunosuppressive drugs have yet to be confirmed in randomised, controlled trials.

引用

页码：30 / 46

页数：17

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