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Mediators of Inflammation
Volume 2014, Article ID 564091, 8 pages
http://dx.doi.org/10.1155/2014/564091
Research Article

Changes in Cerebrospinal Fluid Biomarkers in Human Herpesvirus-6-Associated Acute Encephalopathy/Febrile Seizures

1Department of Pediatrics, Tokyo Metropolitan Fuchu Medical Center for the Disabled, 2-9-2 Musashidai, Fuchu, Tokyo 183-8553, Japan
2Department of Brain Development and Neural Regeneration, Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan
3Department of Pediatrics, School of Medicine, Juntendo University, Tokyo 113-8421, Japan
4Department of Neurology, National Center for Child Health and Development, Tokyo 157-8535, Japan
5Division of Neurology, Saitama Children’s Medical Center, Saitama 339-8551, Japan

Received 20 June 2014; Revised 2 September 2014; Accepted 3 September 2014; Published 11 September 2014

Academic Editor: Yung-Hsiang Chen

Copyright © 2014 Naoyuki Tanuma et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

To determine the involvement of oxidative stress in the pathogenesis of acute encephalopathy associated with human herpesvirus-6 (HHV-6) infection, we measured the levels of oxidative stress markers 8-hydroxy-2′-deoxyguanosine (8-OHdG) and hexanoyl-lysine adduct (HEL), tau protein, and cytokines in cerebrospinal fluid (CSF) obtained from patients with HHV-6-associated acute encephalopathy (HHV-6 encephalopathy) and complex febrile seizures associated with HHV-6 (HHV-6 complex FS) . We also examined changes in CSF-8OHdG and CSF-HEL levels in patients with HHV-6 encephalopathy before and after treatment with edaravone, a free radical scavenger. CSF-8-OHdG levels in HHV-6 encephalopathy and HHV-6 complex FS were significantly higher than in control subjects. In contrast, CSF-HEL levels showed no significant difference between groups. The levels of total tau protein in HHV-6 encephalopathy were significantly higher than in control subjects. In six patients with HHV-6 infection (5 encephalopathy and 1 febrile seizure), the CSF-8-OHdG levels of five patients decreased after edaravone treatment. Our results suggest that oxidative DNA damage is involved in acute encephalopathy associated with HHV-6 infection.