Abstract
OBJECTIVE: Benign paroxysmal positional vertigo (BPPV) is a common vestibular disorder that responds well to canalith repositioning maneuvers but is frequently complicated by recurrence. Increasing evidence suggests that systemic inflammation may influence disease course and recurrence risk. This study aimed to investigate the association between routinely available systemic inflammatory markers and BPPV recurrence within 6 months. METHODS: In this single-center retrospective cohort study, 300 adult patients diagnosed with BPPV between January 2020 and December 2024 were included. Neutrophil-to-lymphocyte ratio (NLR), systemic immune-inflammation index (SII), and C-reactive protein (CRP) levels measured at initial presentation were analyzed. Recurrence within 6 months following successful canalith repositioning maneuvers was defined as the primary outcome. Group comparisons were performed using non-parametric tests. Independent predictors of recurrence were identified using multivariable logistic regression analysis, and receiver operating characteristic (ROC) analysis was used to evaluate discriminatory performance. RESULTS: During the six-month follow-up period, recurrence occurred in 78 patients (26.0%). Patients with recurrence had significantly higher NLR and CRP levels compared with those without recurrence (both p < 0.001). SII values were also elevated in the recurrence group, although the difference was less pronounced (p = 0.048). In multivariable analysis adjusted for age, sex, and canal involvement, both NLR (odds ratio [OR]: 1.42; 95% confidence interval [CI]: 1.18-1.71) and CRP (OR: 1.27; 95% CI: 1.10-1.46) emerged as independent predictors of BPPV recurrence. ROC analysis demonstrated moderate discriminatory ability for NLR (AUC = 0.71) and CRP (AUC = 0.69), whereas SII showed limited predictive performance (AUC = 0.62). CONCLUSION: Systemic inflammatory markers, particularly NLR and CRP, are independently associated with recurrence risk in BPPV. Given their low cost and widespread availability, these markers may provide complementary information for early risk stratification. Further prospective and multicenter studies are required to clarify causal mechanisms and confirm clinical applicability.