Sex-Specific Association Between the Neutrophil-to-HDL Cholesterol Ratio and Hyperuricemia in Obstructive Sleep Apnea

Background: Obstructive sleep apnea (OSA) has been associated with hyperuricemia, with systemic inflammation as a potential contributing pathway. The neutrophil-to-high-density lipoprotein cholesterol ratio (NHR) reflects both inflammatory and metabolic status, but sex-specific evidence on its association with hyperuricemia in OSA remains limited. This study aimed to investigate the relationship between NHR and hyperuricemia in OSA patients, focusing on sex differences. Methods: In this cross-sectional study, 808 OSA patients underwent polysomnography and laboratory assessments. Receiver operating characteristic curves were used to evaluate the diagnostic performance of NHR. Multivariable logistic regression, restricted cubic spline analyses, and subgroup analyses were used to assess the independent association and dose–response relationship between NHR and hyperuricemia. Results: Hyperuricemia was present in 396 (49.0%) patients. Among hyperuricemic patients, females displayed significantly milder OSA severity (lower AHI, ODI, and T90%) but higher systemic inflammatory markers, including higher NHRs, compared with males. NHR showed a relatively better diagnostic accuracy for hyperuricemia in females (AUC = 0.683). Higher NHR quartiles were independently associated with hyperuricemia, with stronger effects in females (Q4 vs. Q1: adjusted OR = 2.68, 95% CI: 1.10–6.51, p < 0.001). Restricted cubic spline analyses indicated a linear association in females (p for nonlinearity = 0.175) but it was nonlinear in males (p = 0.010). Subgroup analyses indicated consistent associations in females across age, BMI, AHI, and hyperlipidemia status. Conclusions: NHR was associated with hyperuricemia in OSA, with a stronger and linear association in females. As a simple and accessible biomarker, NHR may be valuable for hyperuricemia risk stratification in female OSA patients and may also provide insights into sex-specific inflammatory mechanisms underlying OSA-related metabolic dysfunction.