COPD: Journal of Chronic Obstructive Pulmonary Disease最新文献

Exacerbations of chronic obstructive pulmonary disease (COPD) are associated with loss of lung function, poor quality of life, loss of exercise capacity, risk of serious cardiovascular events, hospitalization, and death. However, patients underreport exacerbations, and evidence suggests that unreported exacerbations have similar negative health implications for patients as those that are reported. Whilst there is guidance for physicians to identify patients who are at risk of exacerbations, they do not help patients recognise and report them. Newly developed tools, such as the COPD Exacerbation Recognition Tool (CERT) have been designed to achieve this objective. This review focuses on the underreporting of COPD exacerbations by patients, the factors associated with this, the consequences of underreporting, and potential solutions.

Type 2 diabetes is a frequent comorbidity in chronic obstructive pulmonary disease (COPD) patients, with the GOLD treatment recommendations asserting that the presence of diabetes be disregarded in the choice of treatment.

In a cohort of COPD patients with frequent exacerbations, initiators of single-inhaler triple therapy or dual bronchodilators were compared on the incidence of COPD exacerbation and pneumonia over one year, adjusted by propensity score weighting and stratified by type 2 diabetes.

The COPD cohort included 1,114 initiators of triple inhalers and 4,233 of dual bronchodilators (28% with type 2 diabetes). The adjusted hazard ratio (HR) of exacerbation with triple therapy was 1.04 (95% CI: 0.86-1.25) among COPD patients with type 2 diabetes and 0.74 (0.65-0.85) in those without. The incidence of severe pneumonia was elevated with triple therapy among patients with type 2 diabetes (HR 1.77; 1.14-2.75).

Triple therapy in COPD is effective among those without, but not those with, type 2 diabetes. Future therapeutic trials in COPD should consider diabetes comorbidity.

Chest CT provides a way to quantify pulmonary airway and vascular tree measurements. In patients with COPD, CT airway measurement differences in females are concomitant with worse quality-of-life and other outcomes. CT total airway count (TAC), airway lumen area (LA), and wall thickness (WT) also differ in females with long-COVID. Our objective was to evaluate CT airway and pulmonary vascular and quality-of-life measurements in females with COPD as compared to ex-smokers and patients with long-COVID. Chest CT was acquired 3-months post-COVID-19 infection in females with long-COVID for comparison with the same inspiratory CT in female ex-smokers and COPD patients. TAC, LA, WT, and pulmonary vascular measurements were quantified. Linear regression models were adjusted for confounders including age, height, body-mass-index, lung volume, pack-years and asthma diagnosis. Twenty-one females (53 ± 14 years) with long-COVID, 17 female ex-smokers (69 ± 9 years) and 13 female COPD (67 ± 6 years) patients were evaluated. In the absence of differences in quality-of-life scores, females with long-COVID reported significantly different LA (p = 0.006) compared to ex-smokers but not COPD (p = 0.7); WT% was also different compared to COPD (p = 0.009) but not ex-smokers (p = 0.5). In addition, there was significantly greater pulmonary small vessel volume (BV₅) in long-COVID as compared to female ex-smokers (p = 0.045) and COPD (p = 0.003) patients and different large (BV₁₀) vessel volume as compared to COPD (p = 0.03). In females with long-COVID and highly abnormal quality-of-life scores, there was CT evidence of airway remodelling, similar to ex-smokers and patients with COPD, but there was no evidence of pulmonary vascular remodelling.Clinical Trial Registration: www.clinicaltrials.gov NCT05014516 and NCT02279329.

This study aimed to explore the self-management strategies of Danish patients living with advanced Chronic Obstructive Pulmonary Disease (COPD), with a particular focus on their daily life and their interactions with the respiratory outpatient clinic. Data were collected through semi-structured interviews with 11 patients with COPD affiliated with a Danish respiratory outpatient clinic. The data were thematically analyzed as suggested by Braun & Clarke. The analysis revealed one overarching theme, three main themes, and six subthemes. The overarching theme 'In a strained healthcare system patients with COPD struggle to access needed support to be able to self-manage their disease' revolved around the challenges that patients face in an overburdened healthcare system as they seek support to effectively self-manage their condition. The three main themes were: (1) Only physical symptoms provide legal access to the respiratory outpatient clinic, (2) For patients, the measurements serve as indicators of their health status and overall well-being, (3) Healthcare professionals' skills and not the mode of contact matters to the patients. Healthcare professionals should be aware that the rhetoric surrounding a busy healthcare system with a stressed-out staff also affects patients. Patients with COPD may be particularly sensitive to this message and try to avoid burdening the healthcare system further by setting aside their own needs. However, this approach can lead to neglecting symptoms of deterioration and mental symptoms, which increase the risk of disease progression and subsequent risk of hospital admission.

Rationale: The impact of extracorporeal carbon dioxide removal (ECCO₂R) on work of breathing and aeration in exacerbations of chronic obstructive pulmonary disease (AECOPD) is poorly understood.

Objectives: The study explores the impact of non-invasive ventilation (NIV) and ECCO₂R on respiratory drive, effort and distribution of ventilation in AECOPD.

Methods: Patients enrolled in a randomised controlled study of the addition of ECCO₂R to NIV compared with NIV underwent oesophageal pressure measurement, electrical impedance tomography and parasternal electromyography.

Measurements and main results: 18 patients were enrolled, nine in each arm. Of these, eight in the NIV arm and seven in the ECCO₂R arm underwent physiological assessment. Patients randomised to ECCO₂R, had a period of NIV combined with ECCO₂R and, after removal of NIV, a period of ECCO₂R alone. The removal of NIV whilst remaining on ECCO₂R resulted in a respiratory acidosis (pH 7.34 (7.31-7.34) vs. 7.31 (7.31-7.34), p < 0.0001), increased work of breathing (7.43 (6.08-10.19) vs. 11.1 (8.11-15.15) J/min, p < 0.0001) and increased neural drive (884.4 (684.7-967.3) vs. 1321.1 (903.3-1575.3) AU, p = 0.0005). On day 1, the work of breathing was lower in the NIV than the ECCO₂R group (4.38 (2.76-7.27) vs. 8.03 (4.8-15.94) J/min, p < 0.0001), minute ventilation was higher (15.54 (13.14-18.48) vs. 12.24 (8.51-13.9) L/min, p < 0.0001) and neural drive was the same (1,163.8 (1,085.5-1,325.5) vs. 1,093.8 (885.7-1,258.7) AU, p = 0.5556).

Conclusions: The combination of NIV and ECCO₂R results in lower work of breathing and improved neuro-ventilatory coupling. NIV fully supports ventilation early whilst ECCO₂R improves neuro-ventilatory coupling and work of breathing over time.

Trial registration: Clinicaltrials.gov; NCT02086084; registered 1 December 2015; https://clinicaltrials.gov/study/NCT02086084?cond=copd&term=ecco2r&rank=4.

Chronic obstructive pulmonary disease (COPD) is caused by smoking, but only a small proportion of smokers have disease severe enough to develop COPD. COPD is not always progressive. The question then arises as to what explains the different trajectories of COPD. The role of autoimmunity and regulatory T (Treg) cells in the pathogenesis of COPD is increasingly being recognized. Nine published studies on Treg cells in the lung tissue or bronchoalveolar lavage fluid have shown that smokers with COPD have fewer Treg cells than smokers without COPD or nonsmokers. Three studies showed a positive correlation between Treg cell count and FEV₁%, suggesting an important role for Treg cells in COPD progression. Treg cells can regulate immunological responses via the granzyme B (GzmB) pathway. Immunohistochemical staining for GzmB in surgically resected lungs with centrilobular emphysema showed that the relationship between the amount of GzmB+ cells and FEV₁% was comparable to that between Treg cell count and FEV₁% in the COPD lung, suggesting that GzmB could be a functional marker for Treg cells. The volume fraction of GzmB+  cells in the small airways, the number of alveolar GzmB+ cells, and GzmB expression measured by enzyme-linked immunosorbent assay in the lung tissue of smokers were significantly correlated with FEV₁%. These results suggest that the GzmB content in lung tissue may determine the progression of COPD by acting as an effector molecule to control inflammatory process. Interventions to augment GzmB-producing immunosuppressive cells in the early stages of COPD could help prevent or delay COPD progression.

Chronic obstructive pulmonary disease (COPD) is recognized as a predominant contributor to mortality worldwide, which causes significant burdens to both society and individuals. Given the limited treatment options for COPD, there lies a critical realization: the imperative for expeditious development of novel therapeutic modalities that can effectively alleviate disease progression and enhance the quality of life experienced by COPD patients. Within the intricate field of COPD pathogenesis, an assortment of biologically active small molecules, encompassing small protein molecules and their derivatives, assumes crucial roles through diverse mechanisms. These mechanisms relate to the regulation of redox balance, the inhibition of the release of inflammatory mediators, and the modulation of cellular functions. Therefore, the present article aims to explore and elucidate the distinct roles played by different categories of biologically active small molecules in contributing to the pathogenesis of COPD.

The fixed-dose combination of beclometasone dipropionate/formoterol fumarate (BDP/FF) delivered via pressurised metered-dose inhaler (pMDI) has demonstrated efficacy in chronic obstructive pulmonary disease (COPD), in studies predominantly conducted in Caucasian adults. The current study evaluated the efficacy and safety of BDP/FF pMDI in Chinese patients with COPD, as part of registration for COPD in China. This double-blind, double-dummy, randomised, parallel-group study was conducted in patients with COPD of Chinese ethnicity aged ≥40 years. After a 4-week open-label budesonide/formoterol fumarate (BUD/FF) run-in period, patients were randomised to BUD/FF or BDP/FF for 24 weeks. The primary objective was to demonstrate non-inferiority of BDP/FF to BUD/FF in terms of change from baseline in pre-dose morning forced expiratory volume in 1 sec (FEV₁) at Week 24 (i.e. the lower 95% CI limit of the difference was above the pre-defined non-inferiority margin of -0.07 L). Of 750 patients randomised (377 BDP/FF; 373 BUD/FF), 87.6% completed the study. The primary endpoint was met in both the per-protocol (adjusted mean difference -0.001 L [95% CI: -0.025, 0.022], non-inferiority p < 0.001) and intention-to-treat populations (-0.001 L [-0.024, 0.022]; non-inferiority p < 0.001). There were no statistically significant BDP/FF-BUD/FF differences for the secondary endpoints, and a similar proportion of patients had adverse events (BDP/FF, 51.7%; BUD/FF, 51.2%), with most mild/moderate in severity. In conclusion, BDP/FF pMDI was non-inferior to BUD/FF in terms of pre-dose morning FEV₁, supported by a range of secondary endpoints. Both treatments were similarly tolerated. The study supports the use of BDP/FF pMDI in Chinese patients with COPD.

Study registration: China Centre for Drug Evaluation (CTR20180475).

Chronic obstructive pulmonary disease (COPD) is preventable and requires early screening. The study aimed to examine the clinical values of long non-coding RNA (lncRNA) SNHG5 in COPD diagnosis and prognosis. Out of 160 COPD patients, 80 were in the stable stage and 80 were in the acute exacerbation of COPD stage (AECOPD). SNHG5 expression was detected via qRT-PCR. The survival analysis was conducted using Cox regression analysis and K-M curve. SNHG5 levels significantly reduced in both stable COPD and AECOPD groups compared with the control group, with AECOPD group recording the lowest values. SNHG5 levels were negatively correlated with GOLD stage. Serum SNHG5 can differentiate stable COPD patients from healthy individuals (AUC = 0.805), and can screen AECOPD from stable ones (AUC = 0.910). SNHG5 negatively influenced the release of inflammatory cytokines. For AECOPD patients, those with severe cough and wheezing dyspnea symptoms exhibited the lowest values of SNUG5. Among the 80 AECOPD patients, 16 cases died in the one-year follow-up, all of whom had low levels of SNHG5. SNHG5 levels independently influenced survival outcomes, patients with low SNHG5 levels had a poor prognosis. Thus, lncRNA SNHG5, which is downregulated in patients with COPD (especially AECOPD), can potentially protect against AECOPD and serve as a novel prognostic biomarker for AECOPD.

Objective: To investigate the relationship between cough sensitivity and acute exacerbation in stable chronic obstructive pulmonary disease (COPD) patients.

Methods: Stable COPD patients who visited our department from July 2022 to June 2023 were included. They were subjected to cough sensitivity test, spirometry, induced sputum cytology examination, questionnaire assessment such as cough symptom score, etc. They were followed up for 12 months, and were divided into the acute exacerbation (AE) group and the stable group according to whether acute exacerbation occurred during the follow-up period. We compared the differences in cough sensitivity, pulmonary function, and questionnaires between the two groups, analyzed the relationship between cough sensitivity and acute exacerbation, and screened the risk factors for AECOPD.

Results: A total of 145 patients with stable COPD were included. AE group (n = 94) had lower FEV₁/FVC (50.08 ± 11.11 versus 54.28 ± 11.58, p = 0.03) and cough sensitivity lgC₅ [-0.01(0.90) versus 0.59(0.90), p < 0.01] than those in the stable group (n = 51) patients, the daytime cough symptom score [2(2) versus 1(2), p = 0.02] and VAS score [50(40) versus 30(50), p < 0.01] were higher than stable group. Multivariate logistic regression analysis showed lgC₅ (OR = 0.34, 95% CI = 0.16-0.71, p < 0.01) was an independent risk factor for AECOPD. When lgC₅ was used to predict acute exacerbation in stable COPD patients, the AUC was 0.69, the sensitivity was 59.57%, and the specificity was 72.55%.

Conclusion: Although causality is not necessarily demonstrated, baseline cough sensitivity lgC₅ in stable COPD patients is an independent risk factor for AECOPD, and it has some predictive value for future acute exacerbations.