CONTINUOUS POSTIVE AIRWAY PRESSURE DECREASES ELEVATED PLASMA LEVELS OF SOLUBLE tumour NECROSIS FACTOR-A RECEPTOR 1 IN OBSTRUCTIVE SLEEP apnoea

¹ Dept of Cardiology. Hospital Virgen de la Salud. Toledo. Spain
² Dept of Pneumology. Hospital Universitario La Paz. Madrid. Spain
³ Dept of Pneumology. Hospital Universitario Son Dureta. Palma de Mallorca. Spain
⁴ Dept of Biochemistry and Molecular Biology. Hospital Universitario La Paz. Madrid. Spain
⁵ Dept of Pneumology. Hospital Virgen de la Salud. Toledo. Spain

^* To whom correspondence should be addressed. E-mail: fgr01m{at}gmail.com.

	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- receptor 1 (sTNFR-1) in patients with OSA. The aims of this 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, randomized, placebo-controlled crossover study was performed. Thirty consecutive newly diagnosed OSA patients (AHI 43.8±27.0 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-), interleukin-6 (IL-6) and leukotriene-B4 (LTB4) levels were obtained at baseline and after three months of CPAP or sham CPAP.

Nocturnal urinary levels of norepinephrine, epinephrine, and sTNFR-1 (1053±269 vs. 820±166, pg·ml^-1, P=0.032) were higher in OSA patients. There were no significant differences in plasma levels of IL-6, LTB4, or TNF- between the two study groups. There were no significant differences in blood pressure, urinary catecholamine levels, or plasma IL-6, LTB4 and TNF- levels after both treatment modalities. However, after three months of effective CPAP usage, sTNFR-1 levels were significantly reduced (1053±269 vs. 899±254, pg·ml^-1, P<0.05).

OSA patients have higher levels of sTNFR-1 than individuals without OSA, which are lowered by CPAP therapy. These findings further corroborate a potential role of inflammation in the natural history of OSA.