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

ArticleinEuropean Respiratory Journal 32(4):1009-15 · June 2008with5 Reads
Impact Factor: 7.64 · DOI: 10.1183/09031936.00007008 · Source: PubMed

    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-alpha 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 x 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)-alpha, 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 x mL(-1)) were significantly higher in OSA patients. There were no significant differences in plasma levels of IL-6, LTB(4), or TNF-alpha between the two study groups. There were no significant differences in blood pressure, urinary catecholamine levels, or plasma IL-6, LTB(4) and TNF-alpha 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 x mL(-1)). Obstructive sleep apnoea patients have higher levels of soluble tumour necrosis factor-alpha receptor 1 than individuals without OSA; soluble tumour necrosis factor-alpha 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.