Exhaled breath condensate cytokine level as a diagnostic tool for obstructive sleep apnea syndrome

Exhaled Breath Analysis and Sleep

“…Tumor necrosis factor (TNF) α; is a cytokine produced by different cells which plays a fundamental role in the development of inflammatory status. Two recent articles, both by Li and co-workers, 23,24 investigated TNF-α; in the EBC of OSAS patients; in both cases not only was TNF-α; values higher than in the control group, but it was also correlated with the severity of the disease. The treatment of sleep apnea with CPAP, surgery or oral appliances always found a significant decrease of different cytokines in EBC, including TNF-α;.…”

Association of Interleukin-10 gene promoter polymorphisms with obstructive sleep apnea

“…Recent studies have reported that it is a potential useful biomarker to identify presence and severity of OSAS [6][7][8]. The gene encoding for IL-10 is located on chromosome 1q32.2.…”

Effect of Continuous Positive Airway Pressure and Upper Airway Surgery on Exhaled Breath Condensate and Serum Biomarkers in Patients With Sleep Apnea

“…Obesity can be a confounding factor in EBC biomarker determination; airway inflammation has been observed in obese patients with and without OSA compared to normal weight controls, 7 while another study showed high inflammatory biomarker levels in the airways of obese patients compared to non-obese OSA patients. 8 Several studies have reported high levels of IL-6, a marker of neutrophilic inflammation, in the EBC of patients with OSA, 4,5,8,22 but only one group 8 of the presence of local inflammation. Agustí et al 23 showed that exhaled NO in patients with OSA (albeit using a different method) was not significantly different from that of the healthy population.…”

“…2,3 Some studies have focused on the usefulness of EBC in evaluating the presence of inflammation and oxidative stress in OSA patients. [4][5][6][7][8][9][10] These factors are important since the mechanical trauma caused by snoring and repeated upper airway collapse leads to local inflammation that can spread to the respiratory system and the systemic circulation, thereby contributing to the pathogenesis and continuance of OSA. Patients with severe OAS present increased proinflammatory cytokine expression in the mucosal or muscle compartments of the upper airways, accompanied by increased connective tissue deposition.…”