Abstract

Background Guillain-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. Methods We 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. Results The 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. Conclusion The 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.

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