PurposeChronic obstructive pulmonary disease (COPD) is one of the most widespread diseases. Previous research has found that immune cells and telomeres may affect COPD’s pathogenesis, but their combined mechanism in COPD remains unclear. This study aims to investigate the diagnostic value of telomere-associated genes and immune cells in COPD, as well as their synergistic mechanisms, thereby providing novel insights for the clinical management of COPD.Patients and MethodsData comprising 19 COPD cases, 24 control samples, and 2086 telomere-related genes (TRGs) were obtained from public databases. The differentially expressed genes (DEGs) between COPD and control were obtained by differential expression analysis. The key module genes related to different immune cells (DICs) were obtained via weighted gene co-expression network analysis (WGCNA). Subsequently, biomarkers were further identified by intersecting all genes, utilizing machine learning algorithm, and verifying the expression level.Furthermore, the nomogram was constructed, and gene set enrichment analysis (GSEA) of biomarkers was adopted. The transcription factors (TFs), microRNAs (miRNAs) and drugs linked to biomarkers were obtained from the databases. The expression of biomarkers in 10 clinical samples was validated via reverse transcription quantitative polymerase chain reaction (RT-qPCR).ResultsIn this study, ALDH2 and HNMT were identified as biomarkers. The nomogram results demonstrated that the model had an outstanding predictive ability for COPD (area under curve (AUC) = 0.88). Besides, ALDH2 and HNMT were enriched in junction, starch, and sucrose metabolism. In addition, a total of 6 TFs such as ELF3, and 2 miRNAs, such as miR-206, were linked to ALDH2 and HNMT, and clozapine was the drug that had been found to be associated with both ALDH2 and HNMT. Finally, the RT-qPCR results were consistent with bioinformatics analysis.ConclusionThis study identified 2 biomarkers (ALDH2 and HNMT), which might serve as potential targets for COPD. A nomogram model constructed based on biomarkers was employed for the clinical auxiliary diagnosis of COPD. This study provided new scientific evidence for improving the diagnostic process and individualized treatment strategies for COPD.

BackgroundInhalation therapy is the mainstay of pharmacological treatment for patients with chronic obstructive pulmonary disease (COPD). Elderly individuals with COPD often face greater challenges in using inhalers, and their experiences with inhaler use significantly influence treatment adherence and outcomes. Therefore, it is imperative to understand barriers and facilitators influencing inhaler adherence among elderly COPD patients, based on their perceptions and experiences with inhaled medications.MethodsA descriptive qualitative study was conducted using semi-structured interviews with elderly COPD patients recruited from a tertiary hospital in China. Data were analyzed through conventional content analysis with NVivo 11.ResultsA total of 20 participants (mean age: 75.9 years; 35% female) completed the interviews. Two themes with six subthemes were identified. The two themes were facilitators for inhaler adherence and barriers to inhaler adherence. Facilitators included perceived manageability of inhaler devices and perceived benefits of inhalation therapy. Barriers involved physical limitations, communication challenges between patients and health providers, forgetfulness, and inconvenient refill policies.ConclusionAdapting and optimizing inhaler devices to patient needs, increasing patient awareness of the benefits of inhalation therapy, and establishing continuous, effective pathways of patient-provider communication may represent promising approaches to improve inhaler adherence in elderly individuals with COPD.

Background and ObjectiveBronchoscopic Thermal Vapor Ablation (BTVA) is a novel endoscopic lung volume reduction (ELVR) technique designed to target emphysematous segments and reduce lung hyperinflation, especially in patients with heterogeneous emphysema. Although previous studies have demonstrated its efficacy in Western populations, data regarding BTVA outcomes in Asian cohorts remain limited. This study aimed to evaluate the short-term efficacy and safety of BTVA in patients with severe COPD in a real-world clinical setting.MethodsThis single-center, retrospective, observational study included 8 patients with advanced COPD who underwent BTVA at the Eighth Affiliated Hospital of Sun Yat-sen University between May 2023 and December 2024. Pulmonary function (FEV1, FVC, FEV1/FVC), 6-minute walk distance (6MWD), dyspnea scores (mMRC, CAT), and CT-based lung volume changes were assessed at baseline and at 1, 3, and 6 months post-treatment. Procedure-related adverse events were monitored for 1 month, and all patients were followed up for 6 months.ResultsAll patients completed the 6-month follow-up. Significant improvements in FEV1, FVC, 6MWD, and clinical symptoms (CAT and mMRC) were observed as early as 1 month post-BTVA and were sustained through 6 months. Although FEV1/FVC showed no statistically significant change at 1 and 3 months, a significant increase was detected by month 6. CT imaging at 6 months revealed a marked reduction in the targeted lung volume from 707.5 ± 115.74 mL to 335.5 ± 129.59 mL. No severe adverse events were reported.ConclusionBTVA appears to be a safe and effective minimally invasive intervention for selected patients with advanced COPD, leading to significant short-term improvements in lung function, exercise capacity, and hyperinflation. These findings support the clinical utility of BTVA in Asian populations, although larger prospective studies are needed to confirm long-term benefits and assess repeatability.

BackgroundChronic obstructive pulmonary disease (COPD) is a common respiratory disease; however, measures for preventing COPD and delaying disease progression are limited. Therefore, identifying genetic variations and novel biomarkers related to COPD incidence and progression is crucial for improving clinical outcomes. Here, we investigated the potential of the endoplasmic reticulum stress-related gene DNAJB1 as a risk gene in COPD and its clinical value via bioinformatics and Mendelian randomization.MethodsWe first performed differential gene analysis on single-cell sequencing datasets then identified candidate genes and genetic loci using Mendelian randomization analysis and co-localization analysis, respectively. Machine-learning analysis of microarray data was used to identify potential biomarkers. Subsequently, we explored the biological role of DNAJB1 through cellular communication, functional enrichment, and correlation analyses with inflammatory factors.ResultsDNAJB1 was identified as a risk gene for COPD that shares genetic variants with COPD. Nine key biological genes, including DNAJB1, were identified as potential diagnostic biomarkers. High DNAJB1 expression and high scores for the endoplasmic reticulum stress gene set were validated using the microarray dataset.ConclusionOur finding reveals DNAJB1 as a COPD risk gene and identifies a diagnostic genetic marker panel, providing useful perspectives for early diagnosis and the development of potential therapeutic targets.

PurposeThis study aimed to evaluate the association between the forced expiratory volume in 3 s (FEV3) to forced vital capacity (FVC) and computed tomography (CT)-defined abnormalities, and to assess its potential value in predicting incident chronic obstructive pulmonary disease (COPD) over a 3-year period.Participants and MethodsThis 3-year community-based cohort study enrolled participants with normal lung function (post-bronchodilator FEV1/FVC ≥ 0.70 and FEV1 ≥ 80% predicted). Baseline assessments included questionnaires, spirometry, CT scans, and impulse oscillometry. Participants were stratified by post-bronchodilator FEV3/FVC tertiles. Outcomes included acute respiratory events, annual lung function decline, and COPD incidence. Data were analyzed using mixed-effects models, log-binomial regression, and zero-inflated negative binomial models.ResultsOf the 981 participants with normal baseline lung function stratified by post-bronchodilator FEV3/FVC tertiles (high: ≥95.5%, medium: 91.9–95.4%, low: ≤91.8%), 807 completed the 3-year follow-up. Compared to the high-FEV3/FVC group, participants in the low-FEV3/FVC group tended to be older (60.5 vs 55.7 years) and included more males (80.4% vs 38.8%) and smokers. The low-FEV3/FVC group also demonstrated a lower baseline post-bronchodilator FEV1/FVC (74.0% vs 85.1%) and higher prevalence of emphysema (53.5% vs 18.3%). Longitudinal analysis revealed a greater annual post-bronchodilator FEV1 decline in the low-FEV3/FVC group (adjusted mean difference: 10 mL, 95% confidence interval [CI]: 0 to 21mL; p = 0.043) and an increased risk of developing COPD (19.4% versus 1.9%; adjusted relative risk: 4.96, 95% CI: 1.96–12.51; p = 0.001) than the high-FEV3/FVC group, with no difference in acute respiratory events.ConclusionA reduced FEV3/FVC ratio was associated with an increased risk of accelerated lung function decline and progression to COPD in individuals with normal spirometry. As a readily accessible measure derived from routine spirometry, FEV3/FVC may have a role in early COPD detection.

IntroductionSputum biomarker measurements are used to measure airway inflammation in COPD patients. We have previously validated a Luminex assay able to quantify 15 analytes in COPD sputum supernatant. This assay demonstrated sputum protein expression profiles associated with neutrophilia, airway bacterial colonisation and current smoking in COPD.MethodsWe report repeat sputum supernatant analysis at 6 months from a sub-group of COPD patients who participated in the original study. 48 COPD patients provided a repeat sputum sample at 6 months. 15 panel analytes were detectable.ResultsRepeated sputum cytokine measurements showed a significant positive correlation between baseline and 6 months for all analytes except IL-1RA with intraclass correlation coefficient (ICC) indicating good to excellent repeatability. IL-1β, IL-2, IL-8, IL-17A, G-CSF, MIP-1α, MIP-1β and TNF-α were significantly correlated with sputum neutrophil percentage at 6 months. IL-1β, IL-4, IL-8 and G-CSF were significantly increased in Haemophilus influenzae colonised patients and IL-1β, IL-4, IL-8, G-CSF, IFN-γ, IP-10, MCP-1, MIP-1α, MIP-1β and TNF-α were significantly higher in ex-smoking COPD patients.DiscussionA multiplex immunoassay used at repeated visits in COPD patients showed a high degree of reproducibility for the majority of analytes. There were reproducible inflammatory signatures in sputum associated with clinical characteristics in COPD patients.

BackgroundClinical trial data showed a potential, albeit conflicting, higher cardiovascular risk associated with an inhaled triple therapy of long-acting muscarinic antagonists, long-acting β2 agonists, and inhaled corticosteroids (LAMA/LABA/ICS) versus LABA/ICS in patients with chronic obstructive pulmonary disease (COPD). Evidence from routine care environments remains scant. We sought to assess cardiovascular safety profiles of LAMA/LABA/ICS versus LABA/ICS, targeting fixed-dose combination (FDC) single inhalers.MethodsThis cohort study conducted in a nationwide Taiwanese database recruited patients with COPD who received LAMA/LABA/ICS FDC or LABA/ICS FDC between 2019/1/1 and 2022/12/31. We applied Cox regression models with variable-ratio propensity score (PS) matching to compare hospitalized cardiovascular events, including acute myocardial infarction, unstable angina, ischemic stroke, heart failure, and cardiac dysrhythmia, between the treatment groups.ResultsA total of 28,851 patients (n=5,836 for LAMA/LABA/ICS FDC and n=23,015 for LABA/ICS FDC) were included in the PS-matched cohort. The hazard ratio (HR) of composite cardiovascular events comparing LAMA/LABA/ICS FDC to LABA/ICS FDC was 1.00 (95% confidence interval [CI], 0.78–1.28) and the results did not materially change for individual outcomes. There was also no increased risk associated with LAMA/LABA/ICS FDC in patients having prior hospitalized cardiovascular episodes (HR, 0.86; 95% CI, 0.62–1.20), having prior hospitalized COPD exacerbations (HR, 0.93; 95% CI, 0.62–1.39), or receiving treatment longer than one year (HR, 0.76; 95% CI, 0.38–1.54).ConclusionThis Taiwanese cohort study did not find a higher risk of various cardiovascular outcomes comparing LAMA/LABA/ICS FDC versus LABA/ICS FDC in patients with COPD, even in high-risk subpopulations.

BackgroundCOPD is the seventh-leading cause of death in France. The randomized controlled trials ETHOS (NCT02465567) and IMPACT (NCT02164513) have demonstrated a reduction in exacerbations (primary endpoint) and suggest a decrease in mortality (secondary endpoint) with single-inhaler triple therapy (SITT)—containing a long-acting beta-2 agonist, long-acting anticholinergics, and an inhaled corticosteroid—in patients with COPD. No study has evaluated the potential impact of increased SITT use in France.ObjectiveTo evaluate the impact of increased SITT use in COPD on exacerbations, mortality, and medical costs in France.MethodsA stochastic model was constructed using GOLD therapeutic recommendations and literature data on patient characteristics, prevalence, incidence, treatment distribution, COPD severity and treatment changes, mortality, and exacerbations to model the French COPD population. Two scenarios were studied: Status Quo (no increase in SITT use) and Increased SITT, using the GOLD stage and exacerbation history to initiate SITT treatment in modeled patients, considering the annual probabilities of transitioning from one GOLD stage to another over a 10-year period.ResultsIncreased SITT use compared to the Status Quo over a 10-year period could reduce severe and moderate exacerbations by 8.0% and 9.2%, respectively, all-cause mortality by 8.5%, and medical costs by 875 million euros (excluding additional SITT costs), and extend the life of patients by 0.6 years per patient with COPD.ConclusionThe model shows that increased SITT use in France, in line with recent recommendations, could be associated with a reduction in exacerbation rates, mortality, and costs in patients with COPD.

PurposeTo describe and analyze the potential profile characteristics associated with coping styles of dyspnea-related fear among patients with chronic obstructive pulmonary disease (COPD) and to explore the influencing factors of potential categories.Patients and MethodsFrom March 2023 to August 2024, a cross-sectional study survey, involving 539 COPD patients from four tertiary hospitals, was conducted in Suzhou, China, by convenience sampling. The general information questionnaire, medical coping modes questionnaire, breathlessness beliefs questionnaire, 13-Beck depression inventory, revised COPD anxiety questionnaire, breathlessness catastrophizing scale, COPD self-efficacy scale and the modified medical research council dyspnea scale were employed for data collection. Latent profile analysis was performed to analyze the characteristics on coping styles of dyspnea-related fear among COPD patients, and logistic regression analysis was performed to explore the influencing factors of potential categories.ResultsFour profiles of coping styles of dyspnea-related fear were identified, designated as “low fear–confrontation (n = 151, 28.01%)”, “moderate-high fear–acceptance-resignation (n = 126, 23.38%)”, “moderate fear–confrontation (n = 160, 29.69%)”, and “high fear–avoidance (n = 102, 18.92%)”. Logistic regression analysis showed that disease duration, lung function, frequency of acute exacerbation during the previous year, depression, degree of dyspnea, anxiety, comorbidities and disease knowledge were factors influencing the coping styles of dyspnea-related fear in the different subgroups (P <0.05).ConclusionThere are obvious characteristic profiles on coping styles of dyspnea-related fear among patients with COPD, with differences in disease duration, frequencies of acute exacerbation, lung function, knowledge of COPD, comorbidity, degree of dyspnea, anxiety and depression across subgroups, which provide insight to identify and adopt early intervention strategies.