CPAP decreases plasma levels of soluble tumour necrosis factor-  receptor 1 in obstructive sleep apnoea

Abstract

There is increasing evidence that inflammation plays an important role in the development of cardiovascular complications in patients with obstructive sleep apnoea (OSA).No previous works have studied levels of soluble tumour necrosis factor-a receptor (sTNFR)-1 in patients with OSA. The aims of the present study were to examine serum levels of sTNFR-1 and the effect of nasal continuous positive airway pressure (CPAP) in patients with OSA.A prospective, randomised, placebo-controlled crossover study was performed. In total, 30 consecutive newly diagnosed OSA patients (apnoea/hypopnoea index 43.8¡27.0 events?h -1 ) and 15 healthy obese patients were selected. Urinary levels of norepinephrine and epinephrine, as well as plasma sTNFR-1, tumour necrosis factor (TNF)-a, interleukin (IL)-6 and leukotriene (LT)B 4 levels were obtained at baseline and after 3 months of CPAP or sham CPAP.Nocturnal urinary levels of norepinephrine, epinephrine and sTNFR-1 (1,053¡269 versus 820¡166 pg?mL -1 ) were significantly higher in OSA patients. There were no significant differences in plasma levels of IL-6, LTB 4 , or TNF-a between the two study groups. There were no significant differences in blood pressure, urinary catecholamine levels, or plasma IL-6, LTB 4 and TNF-a levels after both treatment modalities. However, after 3 months of effective CPAP usage, sTNFR-1 levels were significantly reduced (1,053¡269 versus 899¡254 pg?mL -1 ). Obstructive sleep apnoea patients have higher levels of soluble tumour necrosis factor-a receptor 1 than individuals without OSA; soluble tumour necrosis factor-a receptor 1 levels are lowered by continuous positive airway pressure therapy. These findings further corroborate a potential role of inflammation in the natural history of obstructive sleep apnoea.

Sleep apnoea, sleepiness, inflammation and insulin resistance in middle-aged males and females

“…This is consistent with previous literature in that most placebo-controlled studies have not reported a beneficial effect of CPAP on inflammation/metabolic profile [21][22][23][24][25][26][27][28]. One study reported an improvement in TNFR-1 values, but failed to show improvement in any other inflammatory markers [22] and two studies observed an improvement of insulin sensitivity in obese subjects [28] and in those with severe apnoea and impaired glucose tolerance [27], compared to sham-CPAP. In one of these two studies, insulin sensitivity was measured with repeated sampling of insulin and glucose (short insulin tolerance test), whereas in the other CPAP did not improve glucose tolerance compared to placebo.…”

“…Notably, only a few of these previous studies, performed almost exclusively on obese subjects, were placebo-controlled and the majority of them have shown no effect of short-term CPAP use on the inflammatory/metabolic profile [21][22][23][24][25][26][27][28].…”

Study of Insulin Resistance, Inflammatory Cytokines and Adhesive Molecules in Obese Subjects with Obstructive Sleep Apnea

“…Our findings are similar to many case-controlled researches demonstrated increased level of TNF-α in patient with OSA in comparison to controls, along with significant reduction in TNF-α value with CPAP therapy [24][25][26]. Further studies proved that TNF-α level was increased in OSA [27][28][29]. In addition, Dyugovskaya et al [30] stated that T-lymphocytes expressed isolated higher levels of TNF-α than control cells in OSA patients [30].…”

High D-dimer levels after stopping anticoagulants in pulmonary embolism with sleep apnoea

“…OSA could potentially play a role in all these three mechanistic pathways. Apnoea increase oxidative stress [17], and activate inflammatory cascade that impairs endothelial function [18]. OSA-related haemodynamic alterations may slow intravenous flow [19], and lastly, cross-sectional studies support increased coagulability, platelet activity and aggregability [20,21] and decreased fibrinolytic capacity in OSA.…”