COPD: Journal of Chronic Obstructive Pulmonary Disease最新文献

Aim: Identifying patients at risk for acute exacerbations of COPD (AECOPDs) is crucial to improve outcomes. We aimed to evaluate the ability of three health status instruments to predict AECOPDs in subjects with and without previous AECOPDs.

Methods: A prospective cohort study of COPD patients from primary and outpatient care in three Swedish regions. AECOPDs were retrieved from medical records. The modified Medical Research Council Dyspnoea scale (mMRC), the COPD Assessment Test (CAT), and the Clinical COPD Questionnaire (CCQ) were evaluated. Thresholds for AECOPD prediction were estimated using receiver operator characteristic (ROC) curves. Predictive values were assessed using crude and multivariable Cox regression models.

Results: We included 572 patients (59% women, age 69 ± 8 years, FEV₁ 57 ± 18% of predicted) in 2014-2016. All three instruments independently predicted future AECOPDs within three years (adjusted hazard ratio [aHR] 1.5-1.8) using thresholds mMRC ≥ 2, CAT ≥13, and CCQ ≥ 1.6. Patients without prior-year AECOPDs but high scores on all instruments had a similar AECOPD risk as those with prior AECOPDs but scores below threshold (aHR 2.4-2.5). Among patients with ≥1 AECOPD the year before inclusion and at least one of the three health status instruments above threshold, the aHR for future AECOPD during the study period ranged from 4.6 to 5.7.

Conclusions: mMRC, CAT, and CCQ were independently associated with AECOPDs over the following three-year period. The health status instruments provided additional predictive value for future AECOPDS in patients both with and without previous AECOPDs.

Abbreviations:  aHR: Adjusted Hazard Ratio; AECOPD: Acute Exacerbations of Chronic Obstructive Pulmonary Disease; AUC: Area Under Curve; BMI: Body Mass Index; CAT: COPD Assessment Test; CCQ: Clinical COPD Questionnaire; COPD: Chronic Obstructive Pulmonary Disease; DAG: Directed Acyclic Graphs; FEV1: Forced Expiratory Volume in 1 Second; FVC: Forced Vital Capacity; GOLD: Global Initiative for Obstructive Lung Disease; HR: Hazard Ratio; IHD: Ischaemic Heart Disease; ICS: Inhaled Corticosteroids; IQR: Interquartile Range; mMRC: Modified Medical Research Council Dyspnoea Scale; ROC: Receiver Operator Characteristic; SD: Standard Deviation; TIE: Tools for Identifying Exacerbations.

The present study included the first patients with COPD on long-term oxygen therapy who experienced second-by-second oxygen adjustments in their homes based on oxygen saturation. A device capable of automatically titrating the patient's oxygen was installed in the patients' home aiming at increasing the time spent within target saturation. We explored patients' experiences with this automated home oxygen titration, focusing on how maintaining target saturation affected daily life. Semi-structured interviews were conducted with eight men and four women after installation. Systematic text condensation was used in the analysis. Three main themes emerged from patient narratives: (1) "This is my life" - Patients preferred maintaining stable oxygen saturation, associating hypoxemia with dyspnea, discomfort, and difficulties with daily tasks. (2) "Getting the oxygen, I need" - Many patients reported improved ability to perform daily activities when oxygen was automatically adjusted. (3) "New technology gives hope for my life" - Patients expressed optimism about the potential of home-based technology, offering suggestions to improve usability, mainly by reducing concentrator noise. Our findings suggested high acceptability of the automated oxygen in the patients' home, as they believed it to increase the time spend with sufficient oxygen, especially during daily activities. Integrating patient insights is essential for implementation and acceptance of automated home oxygen therapy.

Background: Individuals with chronic obstructive pulmonary disease (COPD) often lead sedentary lives, which is linked to negative health outcomes. Understanding the causes of this behaviour is essential for designing effective interventions. In the time following a hospital discharge, people with COPD may be especially sedentary and develop habits that contribute to this behaviour. Therefore, this is an important point at which to evaluate the reasons behind sedentary behaviour.

Methods: From one acute hospital in England, 12 participants with a recent COPD exacerbation were recruited. Following discharge, semi-structured interviews were conducted to identify perceptions of and barriers and facilitators to reducing sedentary behaviour. Reflexive thematic analysis was employed.

Findings: Two themes developed: "Focusing on survival" and "Loneliness, social isolation and lack of purpose". Factors contributing to sedentary behaviour include the need for rest, social isolation, symptom management, fear of dying or being readmitted to hospital from over-exertion, adherence to health professional advice, and lack of motivation and purpose. Concerns about socioeconomic disparities were noted. Participants were ready to embrace positive lifestyle changes.

Conclusion: Our study found some people with COPD, recently discharged from hospital, may adopt a sedentary lifestyle to manage symptoms and daily activities. Interviews highlight the need to tackle socioeconomic disparities, social support, and feelings of social disconnection. Misconceptions about sedentary behaviour being part of recovery underline the need for education for individuals with COPD and health professionals. The findings suggest strategies to reduce sedentary time, such as enjoyable activities, community involvement, and incorporating sedentary behaviour reduction into pulmonary rehabilitation.

Purpose: Chronic pulmonary conditions require complex treatment strategies involving long-term antibiotic treatment, which carries the highest risk of antimicrobial resistance and adverse drug events (ADE). Specific guidance on prescribing and deprescribing can help reduce these risks and improve therapy effectiveness. The aim of the study was to determine prescribing and deprescribing practices for long-term antibiotic treatment (≥30 days) in preventing exacerbations of stable chronic pulmonary conditions in adult patients across all healthcare settings.

Patients and methods: This umbrella review was part of a larger registered study (PROSPERO, CRD42022381268) including systematic reviews and meta-analyses retrieved from PubMed, Cochrane Library, and PsycInfo. Outcomes of interest included condition, antibiotic, dose, duration, (de-) prescribing advice. Standardized methodological tools were used to assess methodological quality of the selected publications (ROBIS), facilitate data extraction (EPOC), and guide narrative summary of findings (PRIOR).

Results: In total, n = 14 publications were analyzed. (De-)prescribing advice is summarized for treatment (≥30 days) of chronic obstructive pulmonary disease, asthma, non-cystic fibrosis bronchiectasis, cystic fibrosis, and bronchiolitis obliterans syndrome. Macrolides are the most commonly recommended antibiotic for stable chronic pulmonary conditions. ADEs are the main reason for antibiotic discontinuation. Little consideration is given to emergence of antibiotic resistance.

Conclusion: There is a significant paucity of literature providing specific (de-)prescribing advice for clinical practice. More precise recommendations are required in view of patient safety.

Background and objectives: Bacterial colonization or chronic infection occurs in the lower respiratory tract of patients with chronic obstructive pulmonary disease (COPD). Previous studies on Pseudomonas aeruginosa (PA) colonization in patients with stable COPD mainly focused on its impact on prognosis, such as leading to acute exacerbations and increased mortality. However, the prevalence of PA colonization remains unknown. Evidence-based medicine is lacking regarding the association of prior antibiotics and inhaled corticosteroids (ICSs) exposure with PA colonization, intervention with antibiotic therapy for acute exacerbations, and the effect of PA eradication. We conducted this systematic review and meta-analysis to investigate these issues and inform precise treatment and prevention.

Methods: We searched PubMed, Embase, Google Scholar, Cochrane, China National Knowledge Infrastructure (CNKI), and ClinicalTrials.gov for randomized controlled trials (RCTs) and observational studies. The primary outcome was prevalence. Secondary outcomes included previous antibiotic and ICS exposure, exacerbations after antibiotic therapy, and the eradication rate of PA with inhaled antibiotics (IAs).

Results: A total of 39 studies were included, comprising 32,753 cases. The pooled prevalence was 5.6% (95% CI 0.04-0.07). Previous exposure to antibiotics and ICSs was associated with increased PA colonization, with odds ratio (OR) values of (OR = 2.85, 95% CI 1.62-5.01) and (OR = 1.89, 95% CI 1.12-3.19), respectively. Exacerbations decreased within the next year after azithromycin treatment (standardized mean difference [SMD] = -0.43, 95% CI -0.77 to -0.10). The eradication rate of PA with IAs was 0.52 (95% CI 0.46-0.57), and IAs reduced exacerbations in the following year (SMD = -0.87, 95% CI -1.38 to -0.35).

Conclusion: The prevalence of PA colonization in stable COPD was approximately 5.6%. Prior exposure to antibiotics and ICSs increased the risk of PA colonization. Azithromycin therapy reduced exacerbations in PA colonized COPD patients. The eradication rate of PA within one year after IA therapy was about 52%, and exacerbations decreased.

Chronic obstructive pulmonary disease (COPD) is one of the common chronic respiratory diseases, which causes a heavy burden to patients and society. Increasing studies suggest that ABCA1 plays an important role in COPD. ABCA1 belongs to a large class of ATP-binding (ABC) transporters. It is not only involved in the reverse transport of cholesterol, but also in the regulation of apoptosis, pyroptosis, cellular inflammation and cellular immunity. Meanwhile, ABCA1 is involved in several signaling pathways, such as SREBP pathway, LXR pathway, MAPK pathway, p62/mTOR pathway, CTRP1 pathway and so on. In addition, the ABCA1 participates in the disorder of lipid metabolism in COPD by regulating the formation of RCT and HDL, regulates the inflammation of COPD by removing excess cholesterol in macrophages, and promotes the differentiation of COPD phenotype into emphysema type. Accordingly, the ABCA1 may be a therapeutic target for COPD.

Purpose: The purpose of this study was to conduct a meta-analysis of the effects of aerobic exercise combined with respiratory training on patients with stable chronic obstructive pulmonary disease (COPD). Methods: The data of randomized controlled trials on the effects of aerobic exercise combined with respiratory training on patients with stable COPD published up to March 2024 were retrieved from six electronic databases (PubMed, Web of Science, Cochrane Library, Embase, CNKI and China Science and Technology Journal Database). The risk of bias and quality of evidence were assessed using the Cochrane Collaboration tool, and the Physiotherapy Evidence Database (PEDro) Scale approach, respectively. Results: A total of 9 eligible trials with 449 patients with stable COPD were identified. The quality of evidence was moderate. Compared with the control group, the meta-analysis of aerobic exercise combined with respiratory training revealed a significant improvement in the St. George's Respiratory Disease Questionnaire (SGRQ) score (standardized mean difference) (SMD=-0.68, 95% CI [-0.98, -0.39], p < 0.0001), 6-minute walking distance (6MWD) (standardized mean difference) (SMD = 0.84, 95% CI [0.58, 1.11], p < 0.00001), and exercise time (mean difference) (MD = 2.45, 95% CI [0.46, 4.44], p = 0.02). Moreover, aerobic exercise combined with respiratory training improved the secondary outcome measures. These included the modified Medical Research Council dyspnea Scale (mMRC) (SMD=-0.89, 95% CI [-1.32, -0.46], p < 0.00001), Chronic Respiratory Disease Questionnaire (CRQ) (MD = 1.43, 95% CI [-0.56, 3.41], p = 0.16). Conclusion: The results showed that this combination therapy significantly improved the patient's exercise endurance, effectively alleviated the symptoms of dyspnea, and significantly improved the patient's health-related quality of life.

The role of lipid-lowering drugs in chronic obstructive pulmonary disease (COPD) is controversial in clinical studies. This study aimed to explore the causal relationship between lipid-lowering drugs and COPD from a genetic perspective, and to evaluate the potential effects of this relationship. Four hundred and thirty-one lipid-related phenotypes and two COPD datasets were obtained from Genome-Wide Association Studies (GWAS) and analysed together using Mendelian randomization (MR). Genetic variants associated with genes encoding targets of lipid-lowering drugs were extracted from the Global Lipid Genetics Consortium. Expression quantitative trait loci data in relevant tissues were adopted to validate lipid-lowering drug targets that reached significance. We found that four lipid abnormalities were associated with COPD risk. Genetically proxied inhibition of HMG-CoA reductase (HMGCR) and PCSK9 is associated with an increased risk of COPD. And there is a significant MR correlation between increased whole blood HMGCR expression and COPD. HMGCR and PCSK9 inhibitors are associated with onset of COPD, lung function, and COPD-associated infections. Mediation analyses were performed to explore potential mediators of how genetically proxied inhibition of HMGCR and PCSK9 influences the risk of COPD through different immune cell phenotypes and inflammatory factor levels. Our findings indicate a potential link between the use of HMGCR and PCSK9 inhibitors and increased risk of COPD and exacerbation of COPD phenotypes. This suggests effects beyond LDL-C modulation, potentially involving immune cell function and inflammatory factors.

Background: Chronic obstructive pulmonary disease (COPD) affects over 300 million people and is the third leading cause of death. People with COPD spend a large amount of their day sedentary, which is associated with reduced life expectancy.

Methods: A systematic search was conducted across electronic databases, including Medline, CINAHL, PsycINFO, and Cochrane Library. Due to the heterogeneity of study design and siting of the activity monitor, a narrative synthesis was conducted.

Results: 1086 studies were identified; six met inclusion criteria, and two reported a decreased sedentary time. Nordic walking reduced sedentary time by 128 minutes/day compared to baseline, significantly more than the control group (p < 0.01). Another study using a behaviour change intervention reduced sedentary behaviour by 64 minutes/day compared to baseline, significantly more than the control group (p = 0.018). Both studies were conducted for over 12 weeks, with a multi-modal approach incorporating behaviour change techniques, goal setting, education, self-monitoring and feedback. No studies focusing on reducing sedentary behaviour alone reported significant changes.

Conclusions: Few interventional studies have focused on reducing sedentary behaviour in people with COPD. Interventions that have effectively reduced sedentary time primarily focused on physical activity and adopted a multi-modal strategy. This suggests that future interventions could consider a multi-modal approach, which includes behaviour change and the incorporation of enjoyable light physical activities into daily living. We cannot conclude from the available evidence that solely targeting sedentary time will reduce sedentary behaviour. Longer interventions may reduce sedentary behaviour, but there is a lack of studies on both short- and long-term approaches.PROSPERO registration number CRD 42024510434.