C. Robalo-Cordeiro

Operational definitions of asthma in recent epidemiological studies are inconsistent

ObjectiveThe best combination of questions to define asthma in epidemiological asthma studies is not known. We summarized the operational definitions of asthma used in prevalence studies and empirically assess how asthma prevalence estimates vary depending on the definition used.MethodsWe searched the Thomson Reuters ISI Web of knowledge and included (1) cross-sectional studies (2) on asthma prevalence (3) conducted in the general population and (4) containing an explicit definition of asthma. The search was limited to the 100 most-cited papers or published since January 2010. For each paper, we recorded the asthma definition used and other variables. Then we applied the definitions to the data of the Portuguese National Asthma survey (INAsma) and of the 2005–2006 National Health and Nutrition Examination Survey (NHANES) computing asthma prevalence estimates for the different definitions.ResultsOf 1738 papers retrieved, 117 were included for analysis. Lifetime asthma, diagnosed asthma and current asthma were defined in 8, 12 and 29 different ways, respectively. By applying definitions of current asthma on INAsma and NHANES data, the prevalence ranged between 5.3%-24.4% and 1.1%-17.2%, respectively.ConclusionsThere is considerable heterogeneity in the definitions of asthma used in epidemiological studies leading to highly variable estimates of asthma prevalence. Studies to inform a standardized operational definition are needed. Meanwhile, we propose a set of questions to be reported when defining asthma in epidemiological studies.

Should we use gait speed in COPD, FEV1 in frailty and dyspnoea in both?

Frailty is a progressive physiological decline in multiple organ systems marked by loss of function, loss of physiological reserve and increased vulnerability to disease [1]. Biological (inflammation and loss of hormones), clinical (e.g. sarcopenia and osteoporosis) and social factors are involved in frailty onset, evolution and prognosis [2, 3]. Links between frailty, dyspnoea and chronic respiratory diseases represent a novel and practical approach http://ow.ly/10zIvj

Idiopathic pulmonary fibrosis in the era of antifibrotic therapy: Searching for new opportunities grounded in evidence

Idiopathic pulmonary fibrosis (IPF) is a progressive and fatal lung disease that up to now has been associated with a poor prognosis. However, the results of the INPULSIS and ASCEND trials and the approval of nintedanib and pirfenidone have marked the beginning of a new era for IPF patients. Questions remain, however. Should these drugs be used earlier? What effect will they have on more severe disease? Will their effects last beyond the trial period? This manuscript is the outcome of a multidisciplinary meeting between pulmonology, radiology, and pathology clinicians on the use of antifibrotic agents in IPF. In our opinion, the existing data show that pirfenidone and nintedanib slow functional decline in early stages of disease. These drugs also appear to result in therapeutic benefits when administered to patients with advanced disease at diagnosis and maintain effective over time. The data also suggest that continuing antifibrotic therapy after disease progression may confer benefits, but more evidence is needed. Early diagnosis and treatment are crucial for reducing functional decline, slowing disease progression, and improving quality of life.

Obstructive sleep apnoea syndrome is an under-recognized cause of uncontrolled asthma across the life cycle

Obstructive sleep apnoea syndrome (OSA) is a clinical syndrome marked by recurring episodes of upper airway obstruction that lead to markedly reduced (hypopnoea) or absent (apnoea) airflow at the nose/mouth. These episodes of impaired ventilation are usually accompanied by loud snoring and hypoxemia, and are typically terminated by brief arousals.1 However, despite having significant breathing problems during sleep, most patients have no readily detectable respiratory abnormality while awake. OSA is a very common yet underdiagnosed disorder often occurring in a context of multimorbidity.2 The pathophysiological mechanisms involved in OSA are complex and not fully understood. Critical upper airway narrowing/collapse usually occurs in the oropharynx, between the nasal choanae and epiglottis, an area lacking rigid structural support. Patency of this vulnerable segment is dependent on the action of pharyngeal dilator and abductor muscles that are normally activated in a rhythmic fashion during each inspiration. Collapse of the upper airway occurs if the negative upper airway pressure generated by inspiratory pump muscles exceeds the dilating force of these upper airway muscles.3 A variety of factors contribute to upper airway narrowing in patients with OSA. Obesity contributes to OSA pathogenesis in multiple ways including altering upper airway anatomy and collapsibility, ventilatory control and increasing respiratory work load. OSA itself contributes to the development of obesity. Moreover, both OSA and obesity promote the activation of inflammatory pathways, which is likely a key mechanism in cardiovascular and metabolic disease processes.4 Anatomical factors that predispose to upper airway narrowing should be sought in the physical examination of a patient suspected of having OSA, which, in addition to tonsillar hypertrophy, include retrognathia, micrognathia, and macroglossia.5 However, the most common physical finding is a non-specific narrowing of the pharyngeal airway with reduced visualization of the posterior pharyngeal wall. The etiology of OSA in children differs