کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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1966629 | 1538726 | 2009 | 5 صفحه PDF | دانلود رایگان |

BackgroundGuillain-Barré syndrome (GBS) is an autoimmune inflammatory polyradiculoneuropathy that causes acute areflexic paralysis with a high risk of respiratory failure. Previously, using two-dimensional gel electrophoresis and mass spectrometry, we found that the transthyretin level was altered in the cerebrospinal fluid (CSF) of GBS patients when compared to that in CSF of control patients.MethodsWe used enzyme-linked immunosorbent assay (ELISA) to measure the transthyretin levels in the CSF and serum from 22 GBS, 4 Miller-Fisher syndrome (MFS), 9 chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), 22 multiple sclerosis (MS), 10 Alzheimer's disease (AD), and 6 viral meningitis (VM) patients, and 18 controls.ResultsThe results show that CSF transthyretin concentration of the GBS patients is significantly higher than that of the control, MS, AD and VM patients (p < 0.05), although not significantly different from that of MFS and CIDP patients.ConclusionThe increased CSF transthyretin level may be explained by barrier dysfunction or decreased CSF flow in the GBS patients along with increased intrathecal synthesis of transthyretin that might be a protective response to nerve damage.
Journal: Clinica Chimica Acta - Volume 405, Issues 1–2, July 2009, Pages 143–147