Dyspnea perception in asthma: role of airways inflammation, age and emotional status.

OBJECTIVES: Dyspnea perception in asthmatics differs between subjects. Poor perception is usually associated with increased risk of asthma attack/exacerbation. The advanced stage of the disease and the presence of eosinophilic airways inflammation have been recently recognized as being responsible for poor dyspnea perception. However, few studies are available on this topic. DESIGN: The aim of this study was to analyse the influence of inflammatory pattern, age and affective status on dyspnea perception in asthmatic subjects. SUBJECTS AND INTERVENTIONS: Seventy-one consecutive asthmatic patients were recruited and underwent induced sputum, exhaled NO measurement and breath condensate collection. Perception of dyspnea was evaluated as a BORG-VAS/FEV(1) slope before and after the broncho-reversibility test and correlated with the stage of asthma, inflammatory markers, age and depression scale. RESULTS: Dyspnea perception decreases with the worsening of asthma, with the advance of age and of depression status. Furthermore, airways inflammation plays a key role in the decline of dyspnea perception as proved by the negative correlation observed between inflammatory cells in sputum, exhaled pH and NO and BORG-VAS/FEV(1) slope. CONCLUSIONS: The results of our study suggested that airways inflammation, depression status, advance age and severity of asthma influence dyspnea perception and suggest a straight control to identify and better manage poor preceptor asthmatics.

Systemic and airway inflammation in sleep apnea and obesity: the role of ICAM-1 and IL-8.

The recurrent hypoxic stress that characterizes obstructive sleep apnea (OSA) seems to play a role in the increased adherence of neutrophils to endothelial cells as well as in the resulting migration of the former to the inflamed area. Intercellular adhesion molecule 1 (ICAM-1) and interleukin (IL)-8 are markers widely used in OSA studies to investigate inflammation. The aim of this study was to measure ICAM-1 and IL-8 levels in the breath condensate and in the plasma and inflammatory cells in the induced sputum of 12 obese OSA (OO) patients, 10 nonobese OSA (NOO) patients, 10 obese non-OSA (ONO) subjects, and 8 healthy subjects (HS) using a specific enzyme immunoassay (EIA) kit. A significant increase in both plasma and exhaled IL-8 and ICAM concentrations and percentage neutrophils was observed in the induced sputum of obese OSA patients, non-obese OSA patients, and obese non-OSA subjects compared with healthy subjects. However, although these inflammatory markers were found to follow an upward trend in obese OSA patients no difference was observed in both either non-obese OSA patients and obese non-OSA subjects. Finally, a significant positive correlation was found to occur among IL-8, ICAM-1, and sputum neutrophils, as well as across the apnea-hypopnoea index (AHI), TST 90%, body mass index (BMI), and neck circumference. The data obtained confirm the occurrence of an ICAM- and IL-8-mediated neutrophilic airway inflammation in both OSA and obese patients. The degree of inflammation, which seems to worsen in cases of comorbidity (OSA and obesity), is likely to be responsible for the increased risk of developing cardiovascular events observed in these subjects, and therefore, it deserves to be elucidated even more.