Elevated cerebrospinal fluid neuronal injury biomarkers within 24 hours of onset in infection-triggered acute encephalopathy compared to complex febrile seizures

被引：0

作者：

Oikawa, Shizuka ^{[1
]}

Yamaguchi, Hiroshi ^{[1
]}

Nishiyama, Masahiro ^{[2
]}

Ito, Tatsuhito ^{[1
]}

Kawamura, Aoi ^{[1
]}

Sameshima, Tomohiro ^{[1
]}

Soma, Kento ^{[2
]}

Ueda, Takuya ^{[1
]}

Tokumoto, Shoichi ^{[1
]}

Ishida, Yusuke ^{[2
]}

Kurosawa, Hiroshi ^{[3
]}

Nozu, Kandai ^{[1
]}

Maruyama, Azusa ^{[2
]}

Tanaka, Ryojiro ^{[4
]}

Nagase, Hiroaki ^{[1
]}

机构：

[1] Kobe Univ, Grad Sch Med, Dept Pediat, 7-5-2 Kusunoki Cho,Chuo Ku, Kobe, Hyogo 6500017, Japan

[2] Hyogo Prefectural Kobe Childrens Hosp, Dept Neurol, Kobe, Hyogo, Japan

[3] Hyogo Prefectural Kobe Childrens Hosp, Dept Pediat Crit Care Med, Kobe, Hyogo, Japan

[4] Hyogo Prefectural Kobe Childrens Hosp, Dept Emergency & Gen Pediat, Kobe, Hyogo, Japan

来源：

JOURNAL OF THE NEUROLOGICAL SCIENCES | 2024年 / 466卷

关键词：

AESD; Emergency department; GFAP; GDF-15; NSE; Seizure; Status epilepticus; S100B; Tau; BIPHASIC SEIZURES; DIAGNOSIS; ENOLASE; PROTEIN; CSF;

D O I：

10.1016/j.jns.2024.123238

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

Objective: This study aimed to measure and compare cerebrospinal fluid neuronal injury biomarkers in the acute phase of complex febrile seizure (CFS) and infection-triggered acute encephalopathy (AE). Furthermore, we determined the pathogenesis of AE with biphasic seizures and late reduced diffusion (AESD). Methods: Pediatric patients with febrile status epilepticus who visited Hyogo Prefectural Kobe Children's Hospital from November 1, 2016, to December 31, 2022, and whose cerebrospinal fluid samples were collected within 24 h of neurological symptom onset were included. Patients were classified as having CFS or infection-triggered AE according to their definitions. Patients with AE were further categorized into AESD or unclassified AE. Cerebrospinal fluid biomarkers (neuron-specific enolase, growth differentiation factor 15 [GDF-15], S100 calcium- binding protein B [S100B], glial fibrillary acidic protein, and tau protein were measured and compared among the groups. Results: Total of 63 patients (45 with CFS and 18 with AE) were included. Among the AE patients, nine were classified as having AESD and nine as having unclassified AE. S100B levels were significantly higher in patients with AESD than in patients with CFS (485 pg/ml vs. 175.3 pg/ml) and were even higher in patients with AESD and neurological sequelae (702.4 pg/ml). GDF-15 levels were significantly elevated in patients with AE compared to patients with CFS (85.8 pg/ml vs. 23.6 pg/ml). Conclusions: The elevation of S100B suggests that activated astrocytes may be closely associated with the early pathology of AESD. Elevated GDF-15 levels in infection-triggered AE suggest the activation of defense mechanisms caused by stronger neurological injury.

引用

页数：8