Background: Lung ultrasound (LUS) has proven to be useful in the evaluation of lung involvement in COVID-19. However, its effectiveness for predicting the risk of severe disease is still up for debate. The aim of the study was to establish the prognostic accuracy of serial LUS examinations in the prediction of clinical deterioration in hospitalised patients with COVID-19.Methods: Prospective single-centre cohort study of patients hospitalised for COVID-19. The study protocol consisted of a LUS examination within 24 h from admission and a follow-up examination on day 3 of hospitalisation. Lung involvement was evaluated by a 14-area LUS score. The primary end-point was the ability of LUS to predict clinical deterioration defined as need for intensive respiratory support with high-flow oxygen or invasive mechanical ventilation.Results: 200 patients were included and 35 (17.5%) of them reached the primary end-point and were transferred to the intensive care unit (ICU). The LUS score at admission had been significantly higher in the ICU group than in the non-ICU group (22 (interquartile range (IQR) 20–26)versus12 (IQR 8–15)). A LUS score at admission ≥17 was shown to be the best cut-off point to discriminate patients at risk of deterioration (area under the curve (AUC) 0.95). The absence of progression in LUS score on day 3 significantly increased the prediction accuracy by ruling out deterioration with a negative predictive value of 99.29%.Conclusion: Serial LUS is a reliable tool in predicting the risk of respiratory deterioration in patients hospitalised due to COVID-19 pneumonia. LUS could be further implemented in the future for risk stratification of viral pneumonia.

Introduction: The seven-item QEAS-7 questionnaire (exposure to asbestos questionnaire) has been designed as a useful and simple tool to establish the probability of exposure to asbestos. The objective of the present study is to validate the QEAS-7 following the recommended methodology. Methods: The QEAS-7 was prospectively administered to 90 subjects with and without asbestos-related disease (ARD), on two consecutive occasions by two independent researchers. Logical and content validity was evaluated by a committee of experts and construct validity through hypothesis testing. Intra- and interobserver reliability was assessed by calculating Cohen’s Kappa index (κ), which was estimated as weak if below 0.40, moderate if between 0.41 and 0.60 and good/very good if above 0.60. The comparison between proportions was examined using Pearson’s Chi-square test. Results: The majority of participants (88.9%) were male. Mean age was 70.8 years (SD = 8.4) and most of the sample had completed primary education but had not progressed further (62.2%). Forty-three had ARD. The logical, content and construct validity of the QEAS-7 was considered adequate both by a committee of experts and by the users interviewed. The mean administration time was 9 min and 25 s (SD = 3 min and 49 s). The verification of the five hypotheses confirmed the construct validity and the intra- and interobserver reliability to be κ = 0.93 and κ = 0.50 respectively. The concordance in the estimation of asbestos exposure was κ = 0.65. Conclusions: The QEAS-7 is a simple, valid and reliable tool for estimating the probability of exposure to asbestos. Its application in clinical practice appears justified. What is already known about this subject? No studies have been published to date on the validation of specific questionnaires designed to determine asbestos exposure for routine use by healthcare staff in the clinical setting. What are the new findings? This questionnaire can be considered a comprehensible, viable, valid and reliable instrument for identifying exposure to asbestos. Its brevity and simplicity of administration make it ideally suited for use in daily clinical practice. How might this impact on policy or clinical practice in the foreseeable future? This questionnaire can be of help for physicians attending to patients with suspected asbestos-related diseases both in the hospital and in the primary care setting.

Pulmonary emphysema, a component of chronic obstructive pulmonary disease (COPD) is characterised by irreversible alveolar tissue destruction and is produced by an imbalance between proteolytic enzymes, mostly neutrophil elastase (NE), and its inhibitors, mainly alpha-1 antitrypsin (AAT). We measured elastase-inhibitory activity (EIA) in serum samples and determined whether there is an association between EIA and COPD severity. This cross-sectional study recruited COPD patients with and without severe alpha-1 antitrypsin deficiency (AATD) and healthy controls. A semi-automated method assessed EIA using a porcine elastase inhibition assay. EIA levels and the EIA/AAT ratio were compared across groups and the correlation with clinical variables was analysed. A total of 86 individuals were recruited: 36 COPD patients, 20 individuals with COPD associated with AATD (Pi*ZZ mutation), of whom 11 were on augmentation therapy, and 30 healthy controls. Positive, linear and significant relationships were observed between EIA and AAT levels. The EIA/AAT ratio was higher in non AATD-related COPD patients compared to untreated Pi*ZZ patients and controls. Further analysis in non-AATD-related COPD patients revealed a higher EIA/AAT ratio associated with older age, higher comorbidity burden and a trend towards higher severity of lung disease. The strong correlation between AAT levels and EIA suggests that the assay technique employed is robust and effective for assessing EIA. The EIA assay may serve as a potential biomarker for the assessment of the severity and prognosis of emphysema.

Background: Fibrosing interstitial lung diseases can evolve into acute exacerbations, which significantly impact morbidity and mortality. Currently, no routinely used clinical biomarkers can discern the potential progression in these patients. This study aims to analyze different biological markers used in routine clinical practice as possible predictive biomarkers for patients with acute fibrosing interstitial lung disease exacerbation. Methods: We conducted a retrospective, single-center study including patients diagnosed with acute exacerbation of fibrosing interstitial lung disease who required hospitalization between 2018 and 2019 at Vall d’Hebron Hospital, Spain. Patient demographics, clinical data, respiratory function, and comorbidities were collected at baseline. The primary outcome was survival at 30 days, 90 days, and 365 days, using Kaplan–Meier survival analysis and Cox regression. Results: Twenty-nine patients were included (mean age 70.4 years). At the 3-month follow-up, patients with ischemic heart disease showed higher survival rates (p = 0.02). Identifying an infection as the etiology of the exacerbation was associated with worse one-year survival rates compared to idiopathic cases (p = 0.03). Elevated levels of leukocytes (p < 0.01), neutrophils (p < 0.01), and fibrinogen (p = 0.03) were predictors of mortality. Additionally, patients who received a cumulative dose of corticosteroids between 501 and 1000 mg during the exacerbation showed higher one-year survival (p < 0.01). Conclusions: Routine clinical markers can help predict outcomes in AE-f-ILD. Further multicenter studies should validate these findings and assess the role of therapies in its management.

Early, mild and young COPD concepts are not clearly defined and are often used interchangeably to refer to the onset of the disease. Objective: To describe and compare the characteristics of mild, young and early COPD in a large sample of COPD from primary and secondary care. Methods: Pooled analysis of individual data from four multicenter observational studies of patients with stable COPD (≥40 years, FEV₁/FVC < 0.7, smoking ≥ 10 pack-years). Mild COPD was defined as FEV₁% ≥ 65%; young COPD as <55 years; and early COPD as <55 years and smoking ≤ 20 pack-years. The relationship between FEV₁(%), age and pack-years was analyzed with linear regression equations. Results: We included 5468 patients. Their mean age was 67 (SD: 9.6) years, and 85% were male. A total of 1158 (21.2%) patients had mild COPD; 636 (11.6%) had young COPD and 191 (3.5%) early COPD. The three groups shared common characteristics: they were more frequently female, younger and with less tobacco exposure compared with the remaining patients. Early COPD had fewer comorbidities and fewer COPD admissions, but no significant differences were found in ambulatory exacerbations. In linear regression analysis, the decline in FEV₁(%) was more pronounced for the first 20 pack-years for all age groups and was even more important in younger patients. Conclusions: Mild, young and early COPD patients were more frequently women. The steepest decline in FEV₁(%) was observed in individuals <55 years and smoking between 10 and 20 pack-years (early COPD), which highlights the importance of an early detection and implementation of preventive and therapeutic measures.

Background: Although the role of smoking as a risk factor for emphysema in α ₁ -antitrypsin deficiency (AATD) is well known, never-smokers with severe AATD may also develop lung disease, ranging from mild asymptomatic disease to severe emphysema. Methods: We performed a cross-sectional and observational study to analyse the characteristics of the population of never-smoker severe AATD (genotype) individuals of the international EARCO Registry. Results: 914 PI*ZZ individuals were analysed, of whom 472 (51.7%) were active or former smokers and 442 (48.3%) were never-smokers. Never-smokers were older (p<0.001), more frequently females (58.8% versus 43.9%; p<0.001) and had better forced expiratory volume in 1 s (FEV ₁ ) (81.3±26.5% versus 48.4±23% predicted; p<0.001). Lung disease was more frequent in smokers compared to never-smokers (98.5% versus 75%; p<0.001), but bronchiectasis was more frequent in never-smokers (28.6% versus 17.7%; p<0.001). A total of 319 (34.9%) patients were receiving augmentation therapy, of whom 235 (49.9%) were former smokers and 84 (19.2%) never-smokers. Among never-smokers, 320 (72.7%) were index cases, were older (61.8±11.2 versus 55.3±10.9 years; p<0.001) and had lower FEV ₁ (77.2±27.5% versus 92.7±19.3% predicted; p<0.001) compared to non-index cases, but there were no differences in sex distribution. Of the 84 never-smokers on augmentation, 11 (9.4%) were non-index cases. Conclusions: Among PI*ZZ never-smokers lung disease remains prevalent, even if milder. Nonetheless, some never-smokers develop severe lung impairment requiring augmentation therapy. Non-index cases are healthier with a higher quality of life. Among never-smokers, lower body mass index, male sex, comorbidities and pulmonary exacerbations are associated with fixed airflow obstruction.