Detailed Information on Publication Record
2022
Serum and cerebrospinal fluid phosphorylated neurofilament heavy subunit as a marker of neuroaxonal damage in tick-borne encephalitis.
FOŘTOVÁ, Andrea, Václav HÖNIG, Martin PALUS, Jiří SALÁT, Martina PÝCHOVÁ et. al.Basic information
Original name
Serum and cerebrospinal fluid phosphorylated neurofilament heavy subunit as a marker of neuroaxonal damage in tick-borne encephalitis.
Authors
FOŘTOVÁ, Andrea (203 Czech Republic), Václav HÖNIG (203 Czech Republic), Martin PALUS (203 Czech Republic), Jiří SALÁT (203 Czech Republic), Martina PÝCHOVÁ (203 Czech Republic, belonging to the institution), Lenka KRBKOVÁ (203 Czech Republic, belonging to the institution), Tereza VYHLÍDALOVÁ, Michal F. KŘÍHA, Aleš CHRDLE and Daniel RŮŽEK (203 Czech Republic, guarantor, belonging to the institution)
Edition
Journal of General Virology, Microbiology Society, 2022, 0022-1317
Other information
Language
English
Type of outcome
Článek v odborném periodiku
Field of Study
10607 Virology
Country of publisher
United Kingdom of Great Britain and Northern Ireland
Confidentiality degree
není předmětem státního či obchodního tajemství
References:
Impact factor
Impact factor: 3.800
RIV identification code
RIV/00216224:14310/22:00125775
Organization unit
Faculty of Science
UT WoS
000798232700001
Keywords in English
biomarker; brain injury; flavivirus; neurofilament; tick-borne encephalitis
Tags
International impact, Reviewed
Změněno: 2/6/2022 10:36, Mgr. Marie Šípková, DiS.
Abstract
V originále
Extensive axonal and neuronal loss is the main cause of severe manifestations and poor outcomes in tick-borne encephalitis (TBE). Phosphorylated neurofilament heavy subunit (pNF-H) is an essential component of axons, and its detection in cerebrospinal fluid (CSF) or serum can indicate the degree of neuroaxonal damage. We examined the use of pNF-H as a biomarker of neuroaxonal injury in TBE. In 89 patients with acute TBE, we measured CSF levels of pNF-H and 3 other markers of brain injury (glial fibrillary acidic protein, S100B and ubiquitin C-terminal hydrolase L1) and compared the results to those for patients with meningitis of other aetiology and controls. Serum pNF-H levels were measured in 80 patients and compared with findings for 90 healthy blood donors. TBE patients had significantly (P<0.001) higher CSF pNF-H levels than controls as early as hospital admission. Serum pNF-H concentrations were significantly higher in samples from TBE patients collected at hospital discharge (P<0.0001) than in controls. TBE patients with the highest peak values of serum pNF-H, exceeding 10 000 pg ml−1, had a very severe disease course, with coma or tetraplegia. Patients requiring intensive care had significantly higher serum pNF-H levels than other TBE patients (P<0.01). Elevated serum pNF-H values were also observed in patients with incomplete recovery (P<0.05). Peak serum pNF-H levels correlated positively with the duration of hospitalization (P=0.005). Measurement of pNF-H levels in TBE patients might be useful for assessing disease severity and determining prognosis.