Bronchiectasis is a chronic and debilitating lung disease, characterised by irreversible dilatation of the bronchi as consequence of airway injury and remodelling due to recurrent or chronic airway inflammation and infection. The underlying aetiologies include autoimmune diseases, severe infections, genetic abnormalities and acquired disorders.The pathogenesis of bronchiectasis is poorly understood. Three distinct pathogenetic elements, namely infection, inflammation and enzymatic actions, which interact with each other, have been implicated in the pathophysiology of bronchiectasis.Some recent observations indicate that airway inflammation in bronchiectasis comes from a deregulated cytokine network independent of bacterial airway colonisation.In the present review, current knowledge about cellular and molecular inflammatory events in the dynamic process of host-pathogen interaction that are thought to play a relevant role in the pathogenic mechanisms of airway wall destruction leading to bronchiectasis are discussed.

The number and significance of airway eosinophils in stable COPD is controversial. Aims of this study were to evaluate airway inflammation in patients with stable COPD compared with other groups, and to examine the correlations between inflammatory markers and functional indices of airway obstruction. Cellular analysis and evaluation of eosinophil cationic protein (ECP) levels in induced sputum were made in 46 subjects (10 patients with clinically stable COPD, 15 patients with asthma, 11 asymptomatic smokers, and 10 healthy control subjects). As expected, eosinophils were significantly (p < 0.01) higher in patients with asthma (22.2%) than in other groups (COPD, 0.7%; smokers, 0.2%; control subjects, 0.2%), and neutrophils were significantly (p < 0.01) higher in patients with COPD (77.5%) than in the other groups (asthma, 26.7%; smokers, 33.1%; control subjects, 35.9%). However, eosinophils were also increased in patients with COPD, as compared with healthy controls (p < 0.05). Sputum ECP levels were significantly and similarly higher in both asthma and COPD groups than in the other two groups (p < 0.01). In patients with COPD and asymptomatic smokers, considered as a whole, good correlations were found between eosinophils and ECP, on the one hand, and between FEV(1) and the FEV(1)/FVC ratio, on the other. Our data suggest that eosinophils may be involved in the airway inflammation of COPD.

Patients with chronic obstructive pulmonary disease (COPD) have an increased cardiovascular morbidity and mortality. Flow-mediated (FMD) and nitrate-mediated dilatation (NMD) are considered non-invasive methods to assess endothelial function and surrogate markers of subclinical atherosclerosis. We performed a systematic review with meta-analysis and meta-regression to evaluate the impact of COPD on FMD and NMD. Studies were systematically searched in the PubMed, Web of Science, Scopus and EMBASE databases. The random-effect method was used to take into account the variability among included studies. A total of eight studies were included in the final analysis, eight with data on FMD (334 COPD patients) and two on NMD (104 COPD patients). Compared to controls, COPD patients show a significantly lower FMD (MD -3.15%; 95% CI -4.89, -1.40; P < 0.001) and NMD (MD -3.53%; 95% CI -7.04, -0.02; P = 0.049). Sensitivity analyses substantially confirms the results. Meta-regression models show that a more severe degree of airway obstruction is associated with a more severe FMD impairment in COPD patients than in controls. Regression analyses confirm that the association between COPD and endothelial dysfunction is independent of baseline smoking status and most traditional cardiovascular risk factors. In conclusion, COPD is significantly and independently associated with endothelial dysfunction. These findings may be useful to plan adequate cardiovascular prevention strategies in this clinical setting, with particular regard to patients with a more severe disease.

Our study showed that the volumetric quantification adds further informations to the routine evaluation for optimizing the selection of patients scheduled for endobronchial valve treatment.

BACKGROUND: Patients with kyphoscoliosis and severe respiratory impairment frequently experience reduction in exercise tolerance, limitation in daily life activities, and deterioration in health-related quality of life (HRQOL). Noninvasive ventilation (NIV) as an add-on treatment to long-term oxygen therapy (LTOT) was shown to improve symptoms and HRQOL in these patients. Pulmonary rehabilitation can increase exercise capacity and HRQOL in patients with COPD, but its role in patients with restrictive thoracic disease, such as kyphoscoliosis, is uncertain. The aim of this study was to analyze the effects of combining pulmonary rehabilitation with LTOT and NIV treatments on arterial blood gases and the 6-min walk test (6MWT) in a homogeneous group of subjects with kyphoscoliosis. METHODS: Twenty-three subjects with kyphoscoliosis and respiratory failure who were being treated with both LTOT and NIV and who had been referred to a pulmonary rehabilitation program were retrospectively analyzed. Eighteen subjects were included, and there was no control group. Pulmonary rehabilitation involved educational and physical training sessions and was carried out daily for 4 -6 weeks. Exercise intensity was personalized based on individual tolerance, physiologic parameters, or physiotherapist judgment. RESULTS: Upon completion of pulmonary rehabilitation, a significant improvement in 6-min walk distance was observed (P ‫؍‬ .04). The dyspnea score at the end of the 6MWT improved as well, although the improvement did not reach statistical significance (P ‫؍‬ .06). These changes were not confirmed at a 12-month follow-up visit. No significant effects of pulmonary rehabilitation on arterial blood gases were observed. CONCLUSIONS: A combined intervention including a tailored pulmonary rehabilitation program together with LTOT and NIV seems to be of short-term benefit in subjects with kyphoscoliosis and severe respiratory impairment.