The role of obstructive sleep apnea syndrome and obesity in determining leptin in the exhaled breath condensate.

Leptin plays a key role in obstructive sleep apnea syndrome (OSAS). Leptin production in human airways has been previously evaluated by measuring leptin concentration in the exhaled breath condensate and in the induced sputum. The aim was to study leptin expression in the cells of induced sputum and in exhaled breath condensate of subjects with OSAS. Moreover, leptin concentrations in the blood were measured in the same groups of subjects. We enrolled four groups of patients: (1) obese patients with OSAS (OO); (2) non-obese patients with OSAS (NOO); (3) obese patients without OSAS (ONO); and (4) non-obese subjects without OSAS (C). Leptin expression was evaluated by immunocytochemistry in the sputum cells of the enrolled subjects. The concentrations of leptin in the exhaled breath condensate and plasma were measured by using a specific enzyme immunoassay. Leptin protein expression and the percentage of macrophages and neutrophils expressing leptin were higher in the induced sputum of OO, NOO and ONO patients than in C. Leptin concentrations in the exhaled breath condensate were significantly higher in OO patients (5.12 (3.8-6.6) ng ml(-1)) than in NOO (4.1 (3.9-5.2) ng ml(-1)) and ONO (4.2 (3.6-5.0) ng ml(-1)) patients. The concentration of leptin in plasma was significantly more elevated in OO (36 (24-65.9) ng ml(-1)) than in NOO (30.2 (12.4-51.4) ng ml(-1)), whereas it was not significantly different in ONO patients. This study showed that leptin in sputum and in the exhaled breath condensate is higher in obese patients with OSAS than in obese subjects without OSAS. Moreover, different mechanisms for determining leptin concentrations in the exhaled breath condensate and the blood are suggested.

Diurnal PaCO2 tension in obese women: relationship with sleep disordered breathing.

OBJECTIVE: Several obese subjects show a wide array of respiratory disturbances during sleep due to an increased upper-airway resistance. The aim of the present study was to evaluate diurnal PaCO(2) tension in nonsmoking obese women and the possible relationship of this parameter with the presence of sleep disordered breathing (SDB). DESIGN: Cross-sectional study of PaCO(2) tension in obese women. PATIENTS AND METHODS: A total of 91 nonsmoking obese women (BMI > or =30 kg/m(2), aged 42.8+/-15.7 y) were recruited and evaluated for general and anthropometric parameters, respiratory function, sleep-related symptoms, and sleep disorders of breathing. RESULTS: A total of 10 subjects (10.9%) had diurnal hypercapnia (PaCO(2)> or =43 mmHg). Age, BMI, neck circumference, apnoea/hypopnoea index, and nocturnal desaturation (expressed as TST(SaO(2<90%)); TST(SaO(2<90%))=percentage of total sleep time with oxyhaemoglobin saturation <90%) were significantly higher in obese patients with diurnal hypercapnia, compared to normocapnic women. Moreover, hypercapnic patients had reduced forced expiratory volume in 1 s compared to normocapnic individuals. By using multiple regression analysis, the best fitting model (r=0.62, P<0.001) for predicting diurnal PaCO(2) tension in the study population showed that 24.23% of the variance may be explained by TST(SaO(2<90%)), according to the equation: PaCO(2)=0.09 age+0.07 TST(SaO(2<90%))+33.00. CONCLUSIONS: This study suggests that severity of SDB is the most important factor in determining diurnal PaCO(2) tension in apparently healthy nonsmoking obese women.