Early predictors of new-onset immune-related seizures: a preliminary study.

BACKGROUND: Approximately 60% of patients with autoimmune encephalitis (AE) exhibit secondary acute symptomatic seizures and showed highly sensitive to immunotherapy. However, it is difficult for many patients to receive early immunotherapy since the early identification of the cause in AE is more complex. This study aimed to investigate the early predictors of initial immune-related seizures and to guide the evaluation of treatment and prognosis. METHODS: One hundred and fifty-four patients with new-onset "unknown etiology" seizures with a course of disease less than 6 months were included. Serum and/or cerebrospinal fluid neuron-specific autoantibodies (NSAbs), including N-methyl-D-aspartate receptor (NMDAR), α-amino-3-hydroxy-5- Methyl-4-isoxazole propionic acid receptor 1 (AMPAR1), AMPAR2, anti-leucine rich glioma inactivated 1 antibody (LGI1), anti-gamma-aminobutyric acid type B receptor (GABABR), anti-contact protein-related protein-2 (CASPR2) were used to screen for immune etiology of the seizures. In addition, patients with epilepsy and encephalopathy were also examined via brain MRI, long-term video EEG, antibody prevalence in epilepsy and encephalopathy (APE2) score, and modified Rankin Scale (mRS). A logistic regression model was used to analyze the early predictors of immune etiology. RESULTS: Thirty-four cases (22.1%) were positive for NSAbs. Among all 154 patients, 23 cases of autoimmune encephalitis (AE) (21 cases of NSAbs positive), 1 case of ganglionic glioma (NSAbs positive), 130 cases of epilepsy or seizures (12 cases of NSAbs positive) were recorded. Also, there were 17 patients (11.0%) with APE2 ≥ 4 points, and all of them met the clinical diagnosis of AE. The sensitivity and specificity of APE2 ≥ 4 points for predicting AE were 73.9% and 100%. The results of multivariate analysis showed that the NSAbs and APE2 scores independently influenced the early prediction of initial immune-related seizures (P < 0.05). CONCLUSION: NSAbs and APE2 scores could act as early predictors of initial immune-related seizures.

Correlation between inflammatory markers over time and disease severity in status epilepticus: a preliminary study.

Objectives: Convulsive status epilepticus (CSE) is a major subtype of status epilepticus that is known to be closely associated with systemic inflammation. Some important inflammatory biomarkers of this disorder include the neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), monocyte-to-lymphocyte ratio (MLR), systemic immune inflammation index (SII), and pan-immune inflammation value (PIV). This study aimed to determine the NLR, PLR, MLR, SII, and PIV levels before and after treatment in adult patients with CSE and investigated the relationship of these parameters with disease severity. Methods: This retrospective study analyzed data from 103 adult patients with CSE and 103 healthy controls. The neutrophil, monocyte, platelet, and lymphocyte counts, as well as the NLR, PLR, MLR, SII, and PIV, were compared in adult patients with CSE during acute seizures (within 2 h of admission) and after treatment relief (1-2 weeks of complete seizure control). Furthermore, multivariate linear regression analysis investigated the relationship between NLR, PLR, MLR, SII, and PIV with the Status Epilepticus Severity Score (STESS). Results: The data revealed significant differences (p < 0.05) in neutrophils, monocytes, lymphocytes, NLR, PLR, MLR, SII, and PIV between adult patients with CSE during acute seizures and after treatment relief. The average neutrophil count was high during acute seizures in the patient group and decreased after remission. In contrast, the average lymphocyte count was lower after remission (p < 0.05). Furthermore, significant differences (p < 0.05) were observed in monocytes, lymphocytes, platelets, NLR, PLR, MLR, and PIV levels between adult patients with CSE after remission and the healthy control group. Multivariate linear regression analysis showed no significant correlation between NLR, PLR, MLR, SII, and PIV with STESS. Conclusion: The results of this study indicated that adult patients with CSE experienced a transient systemic inflammatory response during acute seizures, which gradually returned to baseline levels after remission. However, there was a lack of robust clinical evidence correlating the severity of adult CSE and systemic inflammatory response.

High STK40 Expression as an Independent Prognostic Biomarker and Correlated with Immune Infiltrates in Low-Grade Gliomas.

BACKGROUND: Expression of STK40 is observed in some cancer types, while its role in low-grade gliomas (LGG) is unclear. The present study aimed to demonstrate the relationship between STK40 and LGG based on The Cancer Genome Atlas (TCGA) database and bioinformatics analysis. METHODS: Kruskal-Wallis test, Wilcoxon sign-rank test, and logistic regression were used to evaluate the relationship between clinicopathological features and STK40 expression. Kaplan-Meier method and Cox regression analysis were used to evaluate prognostic factors. Gene set enrichment analysis (GSEA) and immuno-infiltration analysis were used to determine the significant involvement of STK40 in function. RESULTS: High STK40 expression in LGG was associated with WHO grade (P<0.001), IDH status (P<0.001), primary therapy outcome (P=0.027), 1p/19q codeletion (P<0.001) and histological type (P<0.001). High STK40 expression predicted a poorer overall survival (OS) (HR: 3.07; 95% CI: 2.09-4.51; P<0.001), progression-free survival (PFS) (HR:2.11; 95% CI: 1.59-2.81; P<0.001) and disease specific survival (DSS) (HR: 3.27; 95% CI: 2.17-4.92; P<0.001). STK40 expression (HR: 2.284; 95% CI: 1.125-4.637; P=0.022) was independently correlated with OS in LGG patients. GSEA demonstrated that pathways including cell cycle mitotic, neutrophil degranulation, signaling by Rho GTPases, signaling by interleukins, M phase, PI3K-Akt signaling pathway and naba secreted factors were differentially enriched in STK40 high expression phenotype. Immune infiltration analysis showed that STK40 expression was correlated with some types of immune infiltrating cells. CONCLUSION: STK40 expression was significantly correlated with poor survival and immune infiltration in LGG, and it may be a promising prognostic biomarker in LGG.