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; Václav HÖNIG; Martin PALUS; Jiří SALÁT; Martina PÝCHOVÁ; Lenka KRBKOVÁ; Tereza VYHLÍDALOVÁ; Michal F. KŘÍHA; Aleš CHRDLE a Daniel RŮŽEK

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

UT WoS

000798232700001

EID Scopus

2-s2.0-85129429737

Klíčová slova anglicky

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

Příznaky

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