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The aim of this study was to evaluate the predictive ability of multiple social, and clinical factors for readmission after a severe acute exacerbation of COPD (AECOPD) during various time periods. We performed a prospective cohort study in which recruited patients with AECOPD. We systematically collected numerous clinical (symptoms, pulmonary function, comorbidities, and treatment) and social (financial situation, housing situation, family support, caregiver overload, ability to perform activities, and risk of social exclusion) variables using several questionnaires and indices. The patients were followed closely for one year and readmissions at 30, 60, and 365 days were analysed. 253 patients were included, aged 68.9±9.8years, FEV1 = 42.1%±14.2%, and a Charlson's index = 1.8±0.9. Of these patients, 20.2%, 39.6%, and 63.7% were readmitted within the first 30, 90, and 365 days after discharge, respectively. In the multivariate model applied, the variables that were independently associated with readmission over all three periods of the analysis were dependence to perform basic activities of daily living (BADLs) (odds ratio [OR] = 2.10-4.10) and a history of two or more admissions within the previous year (OR = 2.78-3.78). At 90 days, a history of bacterial isolates in a previous sputum culture (OR = 2.39) and at 365 days, a high grade of dyspnoea (OR = 2.51) and obesity (OR = 2.38) were also identified as predictors of hospital readmission. The patients' limitation to perform BADLs and their history of admissions for AECOPD were the best predictive variables for the likelihood of readmission when adjusted for many other social and clinical variables, regardless of the time period considered for such prediction.

Serum cotinine has become the most widely used biomarker of secondhand smoke exposure (SHS) over time in all ages. The aim of this study was to review the serum cotinine cut-points used to classify children under 5 years as exposed to SHS. A systematic review performed in the Pubmed (MEDLINE) and EMBASE databases up to April 2021 was conducted using as key words \"serum cotinine\", \"tobacco smoke pollution\" (MeSH), \"secondhand smoke\", \"environmental tobacco smoke\" and \"tobacco smoke exposure\". Papers which assessed SHS exposure among children younger than 5 years old were included. The PRISMA 2020 guidelines were followed. Analysis was pre-registered in PROSPERO (registration number: CRD42021251263). 247 articles were identified and 51 fulfilled inclusion criteria. The selected studies were published between 1985-2020. Most of them included adolescents and adults. Only three assessed postnatal exposure exclusively among children under 5 years. None of the selected studies proposed age-specific cut-points for children < 5 years old. Cut-point values to assess SHS exposure ranged from 0.015 to 100 ng/ml. The most commonly used cut-point was 0.05 ng/ml, derived from the assay limit of detection used by the National Health and Nutrition Examination Survey (NHANES). No studies have calculated serum cotinine age-specific cut-points to ascertained SHS exposure among children under 5 years old. Children's age-specific cut-points are warranted for health research and public health purposes aimed at accurately estimating the prevalence of SHS exposure and attributable burden of disease to such exposure, and at reinforcing 100% smoke-free policies worldwide, both in homes, private vehicles and public places.

Introduction There are no published studies assessing the evolution of combined determination of the lung diffusing capacity for both nitric oxide and carbon monoxide (DL NO and DL CO ) 12 months after the discharge of patients with COVID-19 pneumonia. Methods Prospective cohort study which included patients who were assessed both 3 and 12 months after an episode of SARS-CoV-2 pneumonia. Their clinical status, health condition, lung function testings (LFTs) results (spirometry, DL NO -DL CO analysis, and six-minute walk test), and chest X-ray/computed tomography scan images were compared. Results 194 patients, age 62 years (P 25–75 , 51.5–71), 59% men, completed the study. 17% required admission to the intensive care unit. An improvement in the patients’ exercise tolerance, the extent of the areas of ground-glass opacity, and the LFTs between 3 and 12 months following their hospital discharge were found, but without a decrease in their degree of dyspnea or their self-perceived health condition. DL NO was the most significantly altered parameter at 12 months (19.3%). The improvement in DL NO -DL CO mainly occurred at the expense of the recovery of alveolar units and their vascular component, with the membrane factor only improving in patients with more severe infections. Conclusions The combined measurement of DL NO -DL CO is the most sensitive LFT for the detection of the long-term sequelae of COVID-19 pneumonia and it explain better their pathophysiology.

Background: Changes in the original protocol of clinical trials should be clearly declared to the readers of journal publications. Otherwise, they can lead to selective outcome reporting bias or distort the appropriate judgement of the study’s external validity and statistical power, among other problems. Objectives: To identify silent protocol modifications in phase III and IV clinical trials examining multiple sclerosis (MS) drugs that have been carried out between 2010 and mid-2023. Design: Comparative analysis of ClinicalTrials.gov and associated peer-reviewed journal publications. Methods: An advanced search in ClinicalTrials.gov was performed and consecutive searches in PubMed, EMBASE and Google Scholar were conducted looking for the main journal publication derived from each trial. Information regarding trial design, eligibility criteria, primary outcomes and sample size estimation was simultaneously collected from ClinicalTrials.gov and publications, and subsequently compared. Results: In total, 112 trials were appraised. Most studies matched between data sources in terms of study arms (96.4%), assignment (99.1%) and randomization (100.0%). Concordance was also high but comparatively lower for masking (82.1%). A total of 3051 eligibility criteria were extracted, 45.5% of which matched, 25.1% were omitted in publications, 2.8% were modified and 26.6% were added. Fifty-eight trials (51.8%) completely matched regarding their published primary outcomes, whereas 20 had major inconsistencies (17.9%) and 34 (30.4%) minor inconsistencies. Fourteen trials were inconsistent in their estimated sample size; among these, the median difference between registry and publications was 36.5 individuals (interquartile range 17–161). The proportion of trials exhibiting silent protocol changes was similar regardless of study phase, industry involvement or type of registration. Conclusion: Silent protocol changes are common in MS clinical trials and potentially hinder the interpretation and applicability of results. Efforts must be made to promote more transparency in the field of MS clinical research.

The underdiagnosis of chronic obstructive pulmonary disease (COPD) could be improved through screening using portable devices simpler than conventional spirometers in specific healthcare settings to reach a higher percentage of the at-risk population. This study was designed to assess the validity and reliability of the COPD-6 portable device to screen for COPD in non-specialized healthcare settings. Prospective cohort study to validate a diagnostic test. Three cohorts were recruited: primary care (PC), emergency services (ES) and community pharmacies (CPh). individuals with risk factors for COPD (>40 years, smoking >10 pack-years, with respiratory symptoms). The values measured using the COPD-6 were FEV1, FEV6 and the FEV1/FEV6 ratio. Subsequently, participants underwent conventional spirometry at hospital, using a post-bronchodilator FEV1/FVC value <0.7 as the gold standard criterion for the COPD diagnosis. 437 participants were included, 362 were valid for the analysis. COPD was diagnosed in 114 patients (31.5%). The area under the ROC curve for the COPD-6 for COPD screening was 0.8.The best cut-off point for the FEV1/FEV6 ratio was 0.8 (sensitivity, 92.1%) using spirometry with the bronchodilator test as the gold standard. There were practically no differences in the COPD-6 performance in the different settings and also regarding age, gender and smoking status. The COPD-6 device is a valid tool for COPD screening in non-specialized healthcare settings. In this context, the best cut-off point for the FEV1/FEV6 ratio is 0.8.

Background: Inflammatory bowel disease (IBD) develops from a dysregulated immune response influenced by environmental exposures. Radon, a radioactive gas, has known biological effects, but its role in IBD remains unexplored. Objectives: To examine the association between residential radon exposure and the risk and clinical course of IBD. Design: A case–control study with 1-year prospective follow-up of cases. Methods: We included 178 newly diagnosed IBD patients and 178 age- and sex-matched controls in Santiago de Compostela, Spain, from June 2020 to September 2023. Residential radon levels were measured using passive detectors for 3 months. Outcomes included IBD diagnosis, disease extent, hospitalizations, and flares. Logistic regression was used to estimate odds ratios adjusted for age and sex. Results: Median residential radon was 144.5 Bq/m3 in IBD cases and 189.5 Bq/m3 in controls. Higher radon levels were associated with reduced odds of IBD (OR 0.5 for 100–299 and >299 Bq/m3 vs 0–99 Bq/m3). No significant association was found between radon levels and hospitalizations or flares. Among ulcerative colitis patients, higher radon was linked to more extensive disease. Conclusion: Higher residential radon exposure might be inversely associated with IBD risk. However, it does not appear to influence disease progression. Further studies are needed to confirm these findings, since this is the first study on this topic, and chance or selection bias might be present. Plain language summary Does radon in homes affect the risk and severity of inflammatory bowel disease? This study looked at whether home radon levels affect inflammatory bowel disease (IBD). People with IBD had lower radon exposure than those without. Higher radon levels were linked to less IBD, but didn’t affect how the disease progressed. Radon might play a protective role, especially in ulcerative colitis cases.

Background Lung cancer (LC) is the most commonly diagnosed cancer and the leading cause of cancer-related death in both sexes worldwide. Although the principal risk factor in the western world is tobacco smoking, genetic factors, including alpha-1 antitrypsin deficiency (AATD), have been associated with increased risk. This study is the continuation of an earlier one published by the same group in 2015, aimed at analysing risk of LC in never-smokers, associated with carriers of the AATD genotype. Methods A multicentre case–control study was conducted in Spain across the period January 2011 to August 2019. Cases were non-smokers diagnosed with LC, and controls were composed of never-smoking individuals undergoing major non-cancer-related surgery. Data were collected on epidemiological characteristics, exposure to environmental tobacco smoke (ETS), residential radon levels, and alpha-1 antitrypsin (AAT) genotype. Results The study included 457 cases (42%) and 631 controls (58%), with a predominance of women (72,8%). The most frequent histological type was adenocarcinoma (77.5%), followed by squamous cell carcinoma (7.7%). No association of risk of LC was found with the status of AATD genotype carrier, both overall and broken down by age, sex, or exposure to ETS. Conclusions No risk association was found between being a carrier of an AAT deficiency genotype and LC among never-smokers. In order to establish the existence of an association, we consider it important to expand the studies in never smokers in different geographical areas as well as to include patients with previous chronic lung diseases to assess if it influences the risk.

Background There is a relationship between Chronic Obstructive Pulmonary Disease (COPD) and the development of lung cancer (LC). The aim of this study is to analyse several blood markers and compare their concentrations in patients with only COPD and LC + COPD. Methods Case-control study with cases presenting combined LC and COPD and two control groups (patients presenting only COPD and patients presenting only LC). We also included LC patients with descriptive purposes. In both groups, peripheral blood analyses of TNF-α, IL-6, IL-8, total leukocyte, lymphocyte and neutrophil counts, neutrophil-to-lymphocyte ratio, total platelet count, mean platelet volume, platelet-to-lymphocyte ratio, alpha 1-antitripsin (A1AT), IgE, C-reactive protein, fibrinogen, cholesterol and bilirubin were performed. We developed univariate and multivariate analyses of these markers, as well as a risk score variable, and we evaluated its performance through ROC curves. Results We included 280 patients, 109 cases (LC + COPD), 83 controls (COPD) and 88 LC without COPD. No differences were observed in the distribution by sex, age, BMI, smoking, occupational exposure, lung function, GOLD stage or comorbidity. Patients with LC + COPD had significantly higher levels of neutrophils [OR 1.00 (95%CI 1.00–1.00), p  = 0.03] and A1AT [OR 1.02 (95%CI 1.01–1.03), p  = 0.003] and lower cholesterol levels [OR 0.98 (95%CI 0.97–0.99), p  = 0.009] than COPD controls. We developed a risk score variable combining neutrophils, A1AT and cholesterol, achieving a sensitivity of 80%, a negative predictive value of 90.7% and an area under the curve of 0.78 (95%CI 0.71–0.86). Conclusions COPD patients who also have LC have higher levels of neutrophils and A1AT and lower of cholesterol. These parameters could be potentially predicting biomarkers of LC in COPD patients.

There is little information on chronic obstructive pulmonary disease (COPD) mortality trends, age of death, or male:female ratio. This study therefore sought to analyze time trends in mortality with COPD recorded as the underlying cause of death from 1980 through 2017, and with COPD recorded other than as the underlying cause of death. We conducted an analysis of COPD deaths in Galicia (Spain) from 1980 through 2017, including those in which COPD was recorded other than as the underlying cause of death from 2015 through 2017. We calculated the crude and standardized rates, and analyzed mortality trends using joinpoint regression models. There were 43,234 COPD deaths, with a male:female ratio of 2.4. Median age of death was 82 years. A change point in the mortality trend was detected in 1996 with a significant decrease across the sexes, reflected by an annual percentage change of −3.8%. Taking deaths into account in which COPD participated or contributed without being the underlying cause led to an overall 42% increase in the mortality burden. The most frequent causes of death when COPD was not considered to be the underlying cause were bronchopulmonary neoplasms and cardiovascular diseases. COPD mortality has decreased steadily across the sexes in Galicia since 1996, and age of death has also gradually increased. Multiple-cause death analysis may help prevent the underestimation of COPD mortality.

•Pooled analysis of alcohol consumption and lung cancer risk from 21 case-control studies and 1 cohort study.•Largest investigation subgroup analyses by histology and smoking groups to date.•Observed a non-linear association between total alcohol intake and risk.•This J-shaped association was most prominent for squamous cell carcinoma.•Sensitivity analyses showed no confounding by occupational exposures or lung diseases. There is inadequate evidence to determine whether there is an effect of alcohol consumption on lung cancer risk. We conducted a pooled analysis of data from the International Lung Cancer Consortium and the SYNERGY study to investigate this possible association by type of beverage with adjustment for other potential confounders. Twenty one case-control studies and one cohort study with alcohol-intake data obtained from questionnaires were included in this pooled analysis (19,149 cases and 362,340 controls). Adjusted odds ratios (OR) or hazard ratios (HR) with corresponding 95% confidence intervals (CI) were estimated for each measure of alcohol consumption. Effect estimates were combined using random or fixed-effects models where appropriate. Associations were examined for overall lung cancer and by histological type. We observed an inverse association between overall risk of lung cancer and consumption of alcoholic beverages compared to non-drinkers, but the association was not monotonic. The lowest risk was observed for persons who consumed 10–19.9 g/day ethanol (OR vs. non-drinkers = 0.78; 95% CI: 0.67, 0.91), where 1 drink is approximately 12–15 g. This J-shaped association was most prominent for squamous cell carcinoma (SCC). The association with all lung cancer varied little by type of alcoholic beverage, but there were notable differences for SCC. We observed an association with beer intake (OR for ≥20 g/day vs nondrinker = 1.42; 95% CI: 1.06, 1.90). Whether the non-monotonic associations we observed or the positive association between beer drinking and squamous cell carcinoma reflect real effects await future analyses and insights about possible biological mechanisms.