Association between lipopolysaccharide-binding protein levels and disease severity in pediatric narcolepsy: A cross-sectional study.
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BACKGROUND: Narcolepsy type 1 (NT1) is a chronic neurological disorder characterized by excessive daytime sleepiness and cataplexy, with increasing evidence suggesting an immune-mediated etiology. Lipopolysaccharide-binding protein (LBP), a key marker of gut-derived immune activation, may play a role in NT1-related systemic inflammation, yet its relationship with disease risk and severity in pediatric NT1 remains unclear. METHODS: In this cross-sectional study, 96 treatment-naïve pediatric NT1 patients and 90 age- and sex-matched healthy controls were recruited. Serum levels of LBP, C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and lipopolysaccharide (LPS) were measured. Neuropsychiatric assessments included the Epworth Sleepiness Scale (ESS), Pittsburgh Sleep Quality Index (PSQI), Hamilton Anxiety Scale (HAMA-14), and Hamilton Depression Scale (HAMD-24). Logistic and linear regression analyses were used to evaluate associations between LBP and clinical characteristics. Receiver operating characteristic (ROC) curve analysis was conducted to assess the diagnostic performance of LBP. RESULTS: Pediatric NT1 patients exhibited significantly higher serum levels of LBP, CRP, IL-6, TNF-α, and LPS compared to healthy controls (all p < 0.001). Multivariate logistic regression revealed that LBP (OR = 1.663, 95 % CI: 1.522-1.813, p = 0.016) and IL-6 (OR = 1.912, 95 % CI: 1.702-2.074, p = 0.010) were independent predictors of NT1. LBP levels were negatively associated with hypocretin-1 concentrations and anxiety scores. ROC analysis showed excellent predictive performance of LBP for NT1 (AUC = 0.938, 95 % CI: 0.86-0.99). CONCLUSION: Elevated serum LBP is significantly associated with increased disease risk and greater symptom burden in pediatric NT1. LBP may serve as a promising inflammatory biomarker reflecting neuroimmune dysregulation and disease severity. Further longitudinal and mechanistic studies are warranted to explore its clinical utility and underlying pathophysiological role.