Abstract
Background and Objectives: Obstructive sleep apnoea (OSA) is associated with heightened systemic inflammation and a hypercoagulation state. Soluble urokinase-type plasminogen activator receptor (suPAR) plays a role in fibrinolysis and systemic inflammation. However, suPAR has not been investigated in OSA. Materials and Methods: A total of 53 patients with OSA and 15 control volunteers participated in the study. Medical history was taken and in-hospital sleep studies were performed. Plasma suPAR levels were determined by ELISA. Results: There was no difference in plasma suPAR values between patients with OSA (2.198 ± 0.675 ng/mL) and control subjects (2.088 ± 0.976 ng/mL, p = 0.62). Neither was there any difference when patients with OSA were divided into mild (2.134 ± 0.799 ng/mL), moderate (2.274 ± 0.597 ng/mL) and severe groups (2.128 ± 0.744 ng/mL, p = 0.84). There was no significant correlation between plasma suPAR and indices of OSA severity, blood results or comorbidities, such as hypertension, diabetes, dyslipidaemia or cardiovascular disease. Plasma suPAR levels were higher in women when all subjects were analysed together (2.487 ± 0.683 vs. 1.895 ± 0.692 ng/mL, p < 0.01), and also separately in controls (2.539 ± 0.956 vs. 1.411 ± 0.534 ng/mL, p = 0.02) and patients (2.467 ± 0.568 vs. 1.991 ± 0.686 ng/mL, p < 0.01). Conclusions: Our results suggest that suPAR does not play a significant role in the pathophysiology of OSA. The significant gender difference needs to be considered when conducting studies on circulating suPAR.
Highlights
Obstructive sleep apnoea (OSA) is a common disease which is characterised by repetitive collapse of the upper airways during sleep which results in intermittent hypoxia and frequent microarousals.These processes lead to the development of cardiometabolic comorbidities, such as hypertension, cardiovascular disease, diabetes and dyslipidaemia, which frequently accompany OSA.Chronic intermittent hypoxia and increased sympathetic tone induce production of pro-inflammatory molecules, such as interleukin (IL)-6, IL-1β, tumour necrosis factor-α [1] or complement elements [2] and suppresses the release of anti-inflammatory [3,4] molecules
Our results suggest that Soluble urokinase-type plasminogen activator receptor (suPAR) does not play a significant role in the pathophysiology of OSA
AHI—apnoea–hypopnoea index, BMI—body mass index, DBP—diastolic blood pressure, CRP—C-reactive protein, ESS—Epworth Sleepiness Scale, Glomerular filtration rate (GFR)—glomerular filtration rate, HDL-C—high density lipoprotein cholesterol, LDL-C—low density lipoprotein cholesterol, ODI—oxygen desaturation index, SBP—systolic blood pressure, SPT—sleep period time, Total sleep time (TST)—total sleep time, TST90%—total sleep time spent with oxygen saturation below 90%
Summary
Obstructive sleep apnoea (OSA) is a common disease which is characterised by repetitive collapse of the upper airways during sleep which results in intermittent hypoxia and frequent microarousals.These processes lead to the development of cardiometabolic comorbidities, such as hypertension, cardiovascular disease, diabetes and dyslipidaemia, which frequently accompany OSA.Chronic intermittent hypoxia and increased sympathetic tone induce production of pro-inflammatory molecules, such as interleukin (IL)-6, IL-1β, tumour necrosis factor-α [1] or complement elements [2] and suppresses the release of anti-inflammatory [3,4] molecules. Obstructive sleep apnoea (OSA) is a common disease which is characterised by repetitive collapse of the upper airways during sleep which results in intermittent hypoxia and frequent microarousals. These processes lead to the development of cardiometabolic comorbidities, such as hypertension, cardiovascular disease, diabetes and dyslipidaemia, which frequently accompany OSA. Obstructive sleep apnoea (OSA) is associated with heightened systemic inflammation and a hypercoagulation state. Results: There was no difference in plasma suPAR values between patients with OSA (2.198 ± 0.675 ng/mL) and control subjects (2.088 ± 0.976 ng/mL, p = 0.62). Neither was there any difference when patients with OSA were divided into mild
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