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During recent years there has been a growing interest in using non-invasive biomarkers to understand and monitor the airway inflammation in subjects with respiratory tract disorders and mainly asthma and chronic obstructive pulmonary disease (COPD). Sputum induction is generally a well-tolerated and safe procedure and a European Respiratory Society Task Force has published a comprehensive review on sputum methodology. Induced sputum cell count and, to a lesser extent, mediator measurements have been particularly well validated. In asthma, the sputum and the cell culture supernatant can be used for the measurement of a variety of soluble mediators, including eosinophil-derived proteins, nitric oxide (NO) derivatives, cytokines and remodelling-associated proteins. Sputum eosinophilia (> 3) is a classic feature of asthma although half of the patients seems to be non eosinophilic. Measuring the percentage of sputum eosinophils has proved to be useful in the clinical arena in helping to predict short term response to inhaled corticosteroids (ICS) and tailor the dose of ICS in the severe patients but there is scope for the application of other induced sputum markers potentially useful in clinical practice. The widespread application of induced sputum in asthma across the spectrum of disease severity has given insight into the relationship between airway function and airway inflammation, proposed new disease phenotypes and defined which of these phenotypes respond to current therapy, and perhaps most importantly provided an additional tool to guide the clinical management of asthmatic patients. To date sputum induction is the only non-invasive measure of airway inflammation that has a clearly proven role in asthma management.

Objective: Although obstructive sleep apnea syndrome (OSAS) is accompanied by increased atherosclerotic cardiovascular disease burden, its relation with arterial stiffness is not yet well determined. We investigated whether essential hypertensive subjects with OSAS are characterized by increased arterial stiffness. Methods: Our study population consisted of 46 consecutive subjects with newly diagnosed untreated stage I–II essential hypertension suffering from OSAS (35 men, aged 49±8 years) and 53 hypertensive subjects without OSAS, matched for age, sex, and smoking status. All subjects underwent polysomnography, echocardiography and aortic stiffness evaluation by means of carotid-femoral pulse wave velocity (c-f PWV) measurements. Results: Hypertensives with OSAS [apnea hypopnea index (AHI) ⩾5] compared to hypertensives without OSAS (AHI < 5), demonstrated increased levels of body mass index (31.4±4 vs 29.3±4 kg/m2, p = 0.015), office systolic/diastolic blood pressure (BP) (151/99vs145/94 mmHg respectively, p < 0.05, for both cases) and relative wall thickness (0.46±0.06 vs 0.42±0.07, p = 0.010). Hypertensives with OSAS compared to those without OSAS had significantly increased c-f PWV by 9% (8.56±0.49 vs 7.85±0.93 m/s, p = 0.001) and this difference remained significant even after adjustment for confounders (p = 0.04). In the total study population, c-f PWV was correlated with age (r = 0.35, p = 0.015), office systolic BP (r = 0.30, p = 0.007), relative wall thickness (r = 0.30, p = 0.03), logAHI (r = 0.389, p = 0.0001) and minimum oxygen saturation (minSatO2) (r = –0.418, p = 0.0001). Conclusions: OSAS has a significant incremental effect on aortic stiffening in the setting of middle-aged essential hypertensive subjects. This finding suggests that the presence of OSAS in a hypertensive patient accelerates vascular damage, increasing cardiovascular risk.