341 research outputs found
Access to social and health services as a health opportunity. Effects of pandemic on older people
No full textThe contribution of small-Airway abnormalities in chronic obstructive pulmonary disease clinical manifestations: More than a functional issue
No full textThe contribution of small airways abnormalities - i.e. those occurring in the peripheral membranous bronchioles with internal diameter < 2 mm [1,2] - in driving the clinical manifestations of Chronic Obstructive Pulmonary Disease (COPD) is well recognised and already encapsulated in the definition of the disease [3]. Several studies have already demonstrated the relative contribution of small airway and lung parenchyma abnormalities to the severity of airflow limitation, mainly related to peripheral airway collapse and/or emphysema [1,4]. Furthermore, a milestone study on this topic by Hogg and colleagues [5] showed strong correlations between the severity of lung function impairment and the degree of luminal occlusion and the inflammatory infiltrate of the small airways in COPD patients. Notably, small airways abnormalities seem to antedate the development of spirometrically detectable airflow obstructionm as shown in asymptomatic smokers [6]. Taken together, these observations strongly suggest that small airway inflammatory and structural abnormalities may represent the incipit towards the development and progression of COPD in smokers.
In the current issue, Crisafulli et al. aimed at establishing the prevalence of small airway impairment in COPD patients, evaluated by impulse oscillometry system (IOS). Interestingly, the prevalence of small airway impairment was assessed across COPD severity by means of “A to D grade classification” according to the recent GOLD guidelines [1]. This classification, beside lung function, takes into account the assessment of symptoms/quality of life and the risk of exacerbations as determinants of COPD severity. The authors found a similar higher impairment in small airway function in GOLD stage B (symptomatic patients, with mild airflow obstruction) and C (pauci-symptomatic patients, but with more severe airflow obstruction) compared to GOLD stage A (pauci-symptomatic patients, and mild airflow obstruction); of note, the percentage of patients with small airway impairment [defined as peripheral airway resistance (R5-R20) value >0.07 kPa·s·L-1 at IOS] was significantly lower in GOLD C than in GOLD B. This latter group of patients (individuals who are highly symptomatic despite mild airflow obstruction), has been shown to experience worse long-term survival rates when compared to patients with more severe airflow obstruction but milder symptomatology [7]. Thus the symptomatic and/or COPD patients with poor quality of life can be those characterised by predominant small airway abnormalities which, in turn, contribute to the severity of the clinical manifestation of the disease.
The current paper has also the merit of having identified a proportion of subjects with an established diagnosis of COPD who do not show functional features of small airway abnormalities. These findings confirm that the population of COPD patients is heterogeneous not only in terms of symptoms and lung function, but also with regard to the prevalent component of the disease (i.e. small airway disease vs. emphysema). The current findings, together with previous publications [5,8] showing that small airway abnormalities affect the severity of the clinical manifestation of COPD, call for a more comprehensive lung functional evaluation that should include measurements of the peripheral portion of the airways in a routine manner.
We support the concept that not only small airway impairment contributes to airflow obstruction in COPD but also, and even more importantly, to the clinical manifestations of the disease hampering the symptom-related quality of life and possibly the long term prognosis
Interactions of airway pathogens and inflammatory processes
No full textThe clinical history of chronic obstructive pulmonary disease (COPD) is punctuated by recurrent episodes of increases in dyspnea, cough, or sputum production named exacerbations. In addition to increasing COPD-associated morbidity and mortality, exacerbations contribute to loss of lung function and impaired health status in COPD patients (1)
Interactions of airway pathogens and inflammatory processes
No full textThe clinical history of chronic obstructive pulmonary disease (COPD) is punctuated by recurrent episodes of increases in dyspnea, cough, or sputum production named exacer- bations. In addition to increasing COPD-associated morbidity and mortality, exacerbations contribute to loss of lung function and impaired health status in COPD patients (1).
Although it is often assumed that exacerbations are associated with increased airway inflammation, there is little information on the nature of the acute-on-chronic inflammation that characterizes these episodes. Most of the data currently available refer to soluble indirect markers of airway inflammation rather than inflammatory cell infiltration per se (2).
Infections of the tracheobronchial tree, together with air pollution, are considered the most common causes of COPD exacerbations (1). Whether different patterns of airway inflammation correspond to different etiologies is largely unknown. Better understanding of these relationships and of the underlying pathophysiological mechanisms would give the opportunity to identify relevant targets (pathogens and inflammation) for the treatment and prevention of COPD exacerbations.
Many exacerbations are associated with symptoms of infection of the tracheobron- chial tree, and bacteria have been considered the main infective cause of exacerbations (1). Determining the contribution of bacteria to exacerbations is difficult, as COPD patients are often colonized with bacteria even when clinically stable (3). The proportion of patients with positive bacterial cultures and a high bacterial load increases during exacerbations in most, although not in all, studies (4–6). Newer molecular techniques have recently shown that colonization is not a static condition and there is a frequent turnover of different strains of bacteria evoking specific host responses (7). Thus, it is likely that a change in the strain but not the organism may be responsible for the exacerbations. Therefore, previous studies lacking in the molecular characterization of bacterial strains may have missed evidence of a new infection. Indeed, it has been documented that the acquisition of a new strain of colonizing bacteria increases the risk of an exacerbation (8). In the last few decades, the use of highly sensitive diagnostic methods, such as polymerase chain reaction (PCR), to evaluate the association between respiratory virus infections and COPD exacerbations has shown that viruses are responsible for a much higher proportion of exacerbations than was previously realized. In a study of the East London COPD cohort, respiratory viruses were detected in 39% of exacerbations, the most common being rhinoviruses that accounted for 58% of viruses (9). A respiratory virus was detected in around 50% of patients with severe COPD exacerbation admitted to hospitals in Germany and Italy, with rhinovirus again being the most common (5,10). In patients with very severe COPD exacerbations requiring intubation and mechanical ventilation, viruses were identified in 47% of patients (11). At variance with bacterial infections, the respiratory viruses more commonly found at exacerbations were virtually absent in stable state (5,12), suggesting that they play a relevant role in the etiology of the acute episodes
Urban Health at a Glance in Italy by PASSI and PASSI d’Argento Surveillance Systems Data
No full text(1) The percentage of the world’s urban population is 56% and is expected to reach 68% by 2050. In this study, we have investigated the dimensions of individual health by relating them to the type of residing municipality. (2) We also analyzed the health status, prevention, lifestyle, and elderly conditions in illustrated from PASSI and PASSI d’Argento (PdA) surveillance systems data by estimating the prevalence rates and adjusted odds ratios (ORs) for different municipal residences. (3) Urban areas negatively influence some health outcomes, such as respiratory system diseases (OR = 1.24; 95% CI 1.18–1.30). With regards to the spontaneous participation in screening programs from female adults residing in urban areas, we observed ORs of 1.24 (1.13–1.37) and 1.30 (1.12–1.39) for breast and uterine cervix cancers, respectively. Urban contexts seem to promote healthy lifestyles, as there is a lower consumption of alcohol in both adult (0.92; 0.88–0.95) and elderly populations (0.85; 0.77–0.94), although sedentary life is more widespread. Compared to elderly residents living in rural settings, urban individuals find their neighborhood less safe and are less considered as a “resource”. (4) Urban areas promote some unhealthy conditions but can also be a valuable source of services and perspectives. According to the increasing urban population, public health policies towards implementing sustainable development should be established
Ruolo delle infezioni respiratorie nelle riacutizzazioni di BPCO [Role of respiratory infections in COPD exacerbations]
No full textLa storia naturale della broncopneumopatia cronica ostruttiva (BPCO) è caratterizzata da episodi ricorrenti di peggioramento della sintomatologia, denominati riacutizzazioni. Le riacutizzazioni contribuiscono al progressivo peggioramento di questa patologia e all'aumento della morbidità e mortalità ad essa correlate. Le infezioni, sia batteriche che virali, costituiscono la causa principale delle riacutizzazioni della malattia. La conoscenza dei meccanismi infiammatori ed immunologici ad esse correlati è fondamentale per lo sviluppo di una strategia terapeutica efficace nella prevenzione e nel trattamento delle riacutizzazioni stesse. In questa revisione viene approfondito il ruolo delle infezioni virali e batteriche nelle riacutizzazioni della BPCO, focalizzando l'attenzione soprattutto sugli approcci terapeutici volti a prevenire le riacutizzazioni della malattia
Asthma: a chronic infectious disease?
No full textThere are increasing data to support the "hygiene" and "microbiota" hypotheses of a protective role of infections in modulating the risk of subsequent development of asthma. There is less evidence that respiratory infections can actually cause the development of asthma. There is some evidence that rhinovirus respiratory infections are associated with the development of asthma, particularly in childhood, whereas these infections in later life seem to have a weaker association with the development of asthma. The role of bacterial infections in chronic asthma remains unclear. This article reviews the available evidence indicating that asthma may be considered as a chronic infectious diseas
Foregone care in the Italian elderly population: a new challenge for the National Health System
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