J 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.

Základní údaje

Originální název

Serum and cerebrospinal fluid phosphorylated neurofilament heavy subunit as a marker of neuroaxonal damage in tick-borne encephalitis.

Autoři

FOŘTOVÁ, Andrea (203 Česká republika), Václav HÖNIG (203 Česká republika), Martin PALUS (203 Česká republika), Jiří SALÁT (203 Česká republika), Martina PÝCHOVÁ (203 Česká republika, domácí), Lenka KRBKOVÁ (203 Česká republika, domácí), Tereza VYHLÍDALOVÁ, Michal F. KŘÍHA, Aleš CHRDLE a Daniel RŮŽEK (203 Česká republika, garant, domácí)

Vydání

Journal of General Virology, Microbiology Society, 2022, 0022-1317

Další údaje

Jazyk

angličtina

Typ výsledku

Článek v odborném periodiku

Obor

10607 Virology

Stát vydavatele

Velká Británie a Severní Irsko

Utajení

není předmětem státního či obchodního tajemství

Odkazy

Impakt faktor

Impact factor: 3.800

Kód RIV

RIV/00216224:14310/22:00125775

Organizační jednotka

Přírodovědecká fakulta

DOI

UT WoS

000798232700001

Klíčová slova anglicky

biomarker; brain injury; flavivirus; neurofilament; tick-borne encephalitis

Štítky

Příznaky

Mezinárodní význam, Recenzováno
Změněno: 2. 6. 2022 10:36, Mgr. Marie Šípková, DiS.

Anotace

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.