Abstract
Uric acid has been shown to be related to the severity of obstructive sleep apnoea syndrome (OSAS) in adults. We assessed the role of uric acid in OSAS in a cohort of older patients. A total of 164 patients aged >65 years, admitted to our sleep laboratory between January 1st, 2016 and July 1st, 2018 with a complaint of snoring, underwent overnight polysomnography and were retrospectively evaluated. A total of 126 patients who fulfilled the inclusion criteria (mean age 69.16±3.68 years, 56% men) were included. The control group was comprised of 14 patients, while the OSAS group consisted of 112 patients (31 mild, 44 moderate and 37 severe cases). No differences were observed in age, sex, hip circumference, waist/hip ratio or comorbidities between the groups. The Epworth Sleepiness Scale score, body mass index (BMI), and waist circumference were significantly higher in OSAS patients than in controls (p=0.001, p=0.02, and p=0.36, respectively). Uric acid was not correlated with any of the sleep parameters, and no significant differences were detected between the groups. Hyperuricemic patients were similar in terms of sleep parameters and comorbidities in comparison with the other patients. No relationship was observed between uric acid level and OSAS severity, as defined by the apnoea-hypopnea index. Further studies are needed to determine the value of uric acid as a marker of OSAS, after controlling for cardiovascular comorbidities, in older patients with this syndrome.
Highlights
Obstructive sleep apnoea syndrome (OSAS) is defined as recurrent partial or complete pharyngeal closure during sleep resulting in apnoea or hypopnea
No differences were observed in age, sex, hip circumference, waist/hip ratio, comorbidities between the control and OSAS subgroups
When the patients with OSAS were grouped by their apnoea-hypopnea index (AHI) value, no significant difference in uric acid level was detected among groups (Figure 1)
Summary
Obstructive sleep apnoea syndrome (OSAS) is defined as recurrent partial or complete pharyngeal closure during sleep resulting in apnoea or hypopnea. These recurrent episodes result in a cycle of intermittent hypoxia and subsequent reoxygenation[1]. The recurrent hypoxia observed in OSAS increases xanthine degradation of adenosine triphosphate, which causes increased serum uric acid levels. Uric acid is an end-product of purine metabolism, and an increase in its concentration may reflect heightened activity of the xanthine oxidase pathway, which is in turn related to increased free radical and cytokine production, cell apoptosis and endothelial dysfunction[4,5,6]. Previous studies in patients with OSAS have shown that their serum uric acid levels are elevated compared to controls[7,8]
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