Submit Data |  Help |  Video Tutorials |  News |  Publications |  FTP Download |  REST API |  Citing RGD |  Contact   

Usefulness of serum S100B as a marker for the acute phase of aquaporin-4 autoimmune syndrome.

Authors: Fujii, C  Tokuda, T  Ishigami, N  Mizuno, T  Nakagawa, M 
Citation: Fujii C, etal., Neurosci Lett. 2011 Apr 20;494(1):86-8. Epub 2011 Mar 1.
Pubmed: (View Article at PubMed) PMID:21371524
DOI: Full-text: DOI:10.1016/j.neulet.2011.02.063

The aquaporin-4 (AQP4) water channel antibody is used in the diagnosis of neuromyelitis optica (NMO) due to its high sensitivity and high specificity. However, some patients are reported to have neither optic neuritis nor myelitis despite being positive for the AQP4-autoantibody (AQP4-Ab). Therefore, recent reports suggest that such patients should be diagnosed as having 'AQP4-autoimmune syndrome'. In this study, we quantified the levels of glial fibrillar acidic protein (GFAP) and S100B by enzyme-linked immunosorbent assay (ELISA) in CSF and serum samples simultaneously obtained in the acute phase of ten AQP4-autoantibody (AQP4Ab)-positive and seven AQP4Ab-negative patients. Serum levels of S100B were significantly higher in the acute phase of the AQP4Ab-positive patients (2.92+/-1.22pg/ml) than in the AQP4Ab-negative patients (0.559+/-0.180pg/ml, p=0.0250), while serum levels of GFAP were not different between the two groups (AQP4Ab-positive vs. AQP4Ab-negative: 0.120+/-0.113ng/ml vs. 0.00609+/-0.00609ng/ml, p=0.193). Furthermore, the CSF and serum levels of S100B had a significant positive correlation in AQP4Ab-positive patients (n=10, r=0.673, p=0.0390). Our results raise the possibility that serum levels of S100B, but not GFAP, examined in the acute phase of the disease might be a useful biomarker for the relapse of AQP4 autoimmune syndrome.

Annotation

Disease Annotations
Objects Annotated

Additional Information

 
CRRD Object Information
CRRD ID: 5508767
Created: 2011-10-21
Species: All species
Last Modified: 2011-10-21
Status: ACTIVE



NHLBI Logo

RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.