Cross-sectional analysis finds intermittent hypoxia independently links to hyperuricemia in non-obese adults with obstructive sleep apnea, indicating oxygen desaturation disrupts uric acid balance.
This study investigated the association between serum uric acid (SUA) and obstructive sleep apnea syndrome (OSAS) and identified risk factors for elevated SUA in non-obese patients. Consecutive non-obese patients referred to the sleep center for suspected OSAS were included. Correlation, multiple linear regression, multivariable logistic regression, and ROC analyses were performed. A total of 291 participants were included. SUA levels differed significantly among groups stratified by OSAS severity (p = 0.008). The prevalence of hyperuricemia also differed significantly across OSAS severity categories (χ²=8.079, p = 0.044). Neck circumference, male sex, BMI, triglycerides, AHI, TS90%, ODI, mean SpO₂, and LaSO₂ correlated with SUA (all p < 0.05). ODI (β = 0.192, p < 0.001), and urea (β = 0.172, p = 0.002) were positively associated with SUA, whereas eGFR (β =-0.264, p = 0.001) was inversely associated with SUA. ODI remained independently associated with hyperuricemia in logistic regression analysis (OR = 1.027, 95% CI 1.008–1.046, p = 0.006). In ROC analysis, the area under the curve increased from 0.695 for the base model to 0.722 after ODI was included. Non-obese patients with OSAS had elevated SUA levels, and ODI was independently associated with both continuous SUA levels and hyperuricemia. These findings suggest that intermittent hypoxia is associated with impaired uric acid regulation in non-obese individuals with OSAS. Prospective studies are needed to establish a causal relationship.
No takes yet. Share an insight, caveat, or question.
Lin et al. (2026) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: