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|Authors:||Yuki, N. |
|Citation:||Yuki, N., Hartung, H.-P. (2012-06-14). Guillain-Barré syndrome. New England Journal of Medicine 366 (24) : 2294-2304. ScholarBank@NUS Repository. https://doi.org/10.1056/NEJMra1114525|
|Abstract:||The Guillain-Barré syndrome, an acute immune-mediated neuropathy, still carries a grave prognosis. The syndrome is manifested as a spectrum of peripheral-nerve disorders with several clinical variants that are characterized by the distribution of weakness of the limbs or cranialnerve- innervated muscles, underlying pathological abnormalities, and associated autoantibodies. 5-7,34,35,37,85 The most frequent antecedent infection is C. jejuni infection, which is associated with 30% of cases of the Guillain-Barré syndrome and 20% of cases of the Miller Fisher syndrome.9,40 Molecular mimicry between the bacterial and peripheral-nerve components appears to elicit autoantibodies and induce the development of the axonal subtype of the Guillain-Barré syndrome or the Miller Fisher syndrome after enteritis with C. jejuni. 40,50,53,54 Eculizumab, erythropoietin, and fasudil, which have been used in the treatment of other, unrelated medical conditions, have shown promise in animal models of the Guillain- Barré syndrome, 57,58,60 but clinical studies are lacking. Copyright © 2012 Massachusetts Medical Society.|
|Source Title:||New England Journal of Medicine|
|Appears in Collections:||Staff Publications|
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