COPD: Journal of Chronic Obstructive Pulmonary Disease最新文献

{"title":"FBXL19 Targeted STK11 Degradation Enhances Cigarette Smoke-Induced Airway Epithelial Cell Cytotoxicity.","authors":"Xiuying Li, Sowmya P Lakshmi, Kiyoshi Uemasu, Zachary Lane, Rajan T Reddy, Divay Chandra, Chunbin Zou, Yu Jiang, Toru Nyunoya","doi":"10.1080/15412555.2024.2342797","DOIUrl":"10.1080/15412555.2024.2342797","url":null,"abstract":"<p><p><b>Objective:</b> To investigate the effects of cigarette smoke (CS) on Serine/Threonine Kinase 11 (STK11) and to determine STK11's role in CS-induced airway epithelial cell cytotoxicity.<b>Methods:</b> STK11 expression levels in the lung tissues of smokers with or without COPD and mice exposed to CS or room air (RA) were determined by immunoblotting and RT-PCR. BEAS-2Bs-human bronchial airway epithelial cells were exposed to CS extract (CSE), and the changes in STK11 expression levels were determined by immunoblotting and RT-PCR. BEAS-2B cells were transfected with STK11-specific siRNA or STK11 expression plasmid, and the effects of CSE on airway epithelial cell cytotoxicity were measured. To determine the specific STK11 degradation-proteolytic pathway, BEAS-2Bs were treated with cycloheximide alone or combined with MG132 or leupeptin. Finally, to identify the F-box protein mediating the STK11 degradation, a screening assay was performed using transfection with a panel of FBXL E3 ligase subunits.<b>Results:</b> STK11 protein levels were significantly decreased in the lung tissues of smokers with COPD relative to smokers without COPD. STK11 protein levels were also significantly decreased in mouse lung tissues exposed to CS compared to RA. Exposure to CSE shortened the STK11 mRNA and protein half-life to 4 h in BEAS-2B cells. STK11 protein overexpression attenuated the CSE-induced cytotoxicity; in contrast, its knockdown augmented CSE-induced cytotoxicity. FBXL19 mediates CSE-induced STK11 protein degradation <i>via</i> the ubiquitin-proteasome pathway in cultured BEAS-2B cells. FBXL19 overexpression led to accelerated STK11 ubiquitination and degradation in a dose-dependent manner.<b>Conclusions:</b> Our results suggest that CSE enhances the degradation of STK11 protein in airway epithelial cells <i>via</i> the FBXL19-mediated ubiquitin-proteasomal pathway, leading to augmented cell death.HIGHLIGHTSLung tissues of COPD-smokers exhibited a decreased STK11 RNA and protein expression.STK11 overexpression attenuates CS-induced airway epithelial cell cytotoxicity.STK11 depletion augments CS-induced airway epithelial cell cytotoxicity.CS diminishes STK11 via FBXL19-mediated ubiquitin-proteasome degradation.</p>","PeriodicalId":10704,"journal":{"name":"COPD: Journal of Chronic Obstructive Pulmonary Disease","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11186665/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140847688","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Relationship Between Chronic Obstructive Pulmonary Disease and Osteoporosis: A Scoping Review.","authors":"Ana Penedones, Diogo Mendes, Carlos Alves, Augusto Filipe, Tânia Oliveira, Francisco Batel-Marques","doi":"10.1080/15412555.2024.2356510","DOIUrl":"https://doi.org/10.1080/15412555.2024.2356510","url":null,"abstract":"<p><strong>Introduction: </strong>Potential associations between Chronic Obstructive Pulmonary Disease (COPD) and osteoporosis have been studied, but areas of uncertainty remain.</p><p><strong>Objective: </strong>This scoping review aimed to identify the published evidence on the epidemiological relationships between COPD and osteoporosis.</p><p><strong>Methods: </strong>Experimental and observational evidence evaluating relationships between COPD and osteoporosis on epidemiology, clinical manifestations, risk factors (RFs), therapeutic management and quality of life (QoL) was searched on PubMed and Embase (until May 2023). The studies were categorized according to their objectives and characteristics. Data were analyzed using descriptive statistics.</p><p><strong>Results: </strong>Ninety-nine studies were selected, namely 33 (33%) reporting epidemiologic measures, 11 (11%) clinical manifestations, 74 (75%) RFs (45 ones, of which body mass index [BMI; <i>n</i> = 22 studies], corticosteroids' use [<i>n</i> = 20], and COPD severity [<i>n</i> = 15] were the most studied), 7 (7%) therapeutic management, and 3 (3%) QoL. Twenty-seven (27.6%) studies evaluated ≥2 domains. Most studies followed a cross-sectional design (<i>n</i> = 37; 37.4%). Eighty-nine studies (90%) assessed patients with COPD at baseline and studied its relationship with osteoporosis.</p><p><strong>Conclusion: </strong>There are well-established features linking COPD and osteoporosis, including shared RFs, such as smoking, elderly, physical inactivity, or low BMI. Others deserve clarification, including the impact of COPD severity, or the use of inhaled corticosteroids on the incidence of osteoporosis and fractures, as well as the value of performing routine imaging tests, or prescribing anti-resorptive medications in COPD to prevent osteoporotic-related outcomes. QoL studies are also lacking. Investigating such issues is needed to propose clinical guidelines for managing osteoporosis in patients with COPD.</p>","PeriodicalId":10704,"journal":{"name":"COPD: Journal of Chronic Obstructive Pulmonary Disease","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141854968","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beyond Spirometry: Linking Wasted Ventilation to Exertional Dyspnea in the Initial Stages of COPD.","authors":"J Alberto Neder, Giles Santyr, Brandon Zanette, Miranda Kirby, Marina Pourafkari, Matthew D James, Sandra G Vincent, Carrie Ferguson, Chu-Yi Wang, Nicolle J Domnik, Devin B Phillips, Janos Porszasz, William W Stringer, Denis E O'Donnell","doi":"10.1080/15412555.2023.2301549","DOIUrl":"10.1080/15412555.2023.2301549","url":null,"abstract":"<p><p>Exertional dyspnea, a key complaint of patients with chronic obstructive pulmonary disease (COPD), ultimately reflects an increased inspiratory neural drive to breathe. In non-hypoxemic patients with largely preserved lung mechanics - as those in the initial stages of the disease - the heightened inspiratory neural drive is strongly associated with an exaggerated ventilatory response to metabolic demand. Several lines of evidence indicate that the so-called excess ventilation (high ventilation-CO₂ output relationship) primarily reflects poor gas exchange efficiency, namely increased physiological dead space. Pulmonary function tests estimating the extension of the wasted ventilation and selected cardiopulmonary exercise testing variables can, therefore, shed unique light on the genesis of patients' out-of-proportion dyspnea. After a succinct overview of the basis of gas exchange efficiency in health and inefficiency in COPD, we discuss how wasted ventilation translates into exertional dyspnea in individual patients. We then outline what is currently known about the structural basis of wasted ventilation in \"minor/trivial\" COPD vis-à-vis the contribution of emphysema versus a potential impairment in lung perfusion across non-emphysematous lung. After summarizing some unanswered questions on the field, we propose that functional imaging be amalgamated with pulmonary function tests beyond spirometry to improve our understanding of this deeply neglected cause of exertional dyspnea. Advances in the field will depend on our ability to develop robust platforms for deeply phenotyping (structurally and functionally), the dyspneic patients showing unordinary high wasted ventilation despite relatively preserved FEV₁.</p>","PeriodicalId":10704,"journal":{"name":"COPD: Journal of Chronic Obstructive Pulmonary Disease","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139721974","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recognizing the Shades of Grey in the Diagnosis of COPD.","authors":"J Alberto Neder","doi":"10.1080/15412555.2024.2402706","DOIUrl":"https://doi.org/10.1080/15412555.2024.2402706","url":null,"abstract":"","PeriodicalId":10704,"journal":{"name":"COPD: Journal of Chronic Obstructive Pulmonary Disease","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142364683","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impressions and Perceptions of a Smartphone and Smartwatch Self-Management Tool for Patients With COPD: A Qualitative Study.","authors":"Robert Wu, Maryann Calligan, Tanya Son, Harshmeet Rakhra, Eyal de Lara, Alex Mariakakis, Andrea S Gershon","doi":"10.1080/15412555.2023.2277158","DOIUrl":"10.1080/15412555.2023.2277158","url":null,"abstract":"<p><strong>Background: </strong>Patients with chronic obstructive pulmonary disease (COPD) often do not seek care until they experience an exacerbation. Improving self-management for these patients may increase health-related quality of life and reduce hospitalizations. Patients are willing to use wearable technology for real-time data reporting and perceive mobile technology as potentially helpful in COPD management, but there are many barriers to the uptake of these technologies.</p><p><strong>Objective: </strong>We aimed to understand patients' experiences using a wearable and mobile app and identify areas for improvement.</p><p><strong>Methods: </strong>We conducted semi-structured interviews as part of a larger prospective cohort study wherein patients used a wearable and app for 6 months. We asked which features patients found accessible, acceptable and useful.</p><p><strong>Results: </strong>We completed 26 interviews. We summarized our research findings into four main themes: (1) information, support and reassurance, (2) barriers to adoption, (3) impact on communication with health care providers, and (4) opportunities for improvement. Most patients found the feedback received through the app to be reassuring and useful. Some patients experienced technical difficulties with the app and found the wearable to be uncomfortable.</p><p><strong>Conclusions: </strong>Patients found a wearable device and mobile application to be acceptable and useful for the management of COPD. We identified barriers to adoption and opportunities for improvement to the design of our app. Further research is needed to understand what people with COPD and their healthcare providers want and will use in a mobile app and wearable for COPD management.</p>","PeriodicalId":10704,"journal":{"name":"COPD: Journal of Chronic Obstructive Pulmonary Disease","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139721975","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effectiveness of Aspirin on Major COPD Outcomes: A Prevalent New-User Design Observational Study.","authors":"Charles Khouri, Sophie Dell'Aniello, Pierre Ernst, Samy Suissa","doi":"10.1080/15412555.2024.2317380","DOIUrl":"10.1080/15412555.2024.2317380","url":null,"abstract":"<p><p>Observational studies that have reported an association between aspirin use in chronic obstructive pulmonary disease (COPD) with reductions in mortality and COPD exacerbations were shown to be affected by time-related biases. We assessed this association using a prevalent new-user study design that avoids these biases. We used the United Kingdom's Clinical Practice Research Datalink (CPRD) to form a cohort of patients with COPD. Aspirin initiators were matched on time and propensity score with nonusers during 2002-2018. The outcomes were all-cause mortality and COPD exacerbation within a one-year follow-up. Hazard ratios (HR) and 95% confidence interval (CI) of each outcome associated with aspirin use compared to nonuse were estimated using an as-treated approach. The study cohort included 10,287 initiators of aspirin and 10,287 matched nonusers. The cumulative incidence of all-cause mortality at one year was 11.5% for aspirin users and 9.2% for nonusers. The HR of all-cause mortality associated with aspirin initiation was 1.22 (95% CI: 1.08-1.37), while for severe exacerbation it was 1.21 (95% CI 1.08-1.37), compared with nonuse. The HR of a first moderate or severe exacerbation with aspirin use was 0.90 (95% CI 0.85-0.95). These estimates did not vary by platelet count. This large population-based study, designed to emulate a trial, found aspirin use in patients with COPD associated with a higher risk of all-cause mortality and severe exacerbation, but a lower risk of moderate or severe exacerbation. Further research is warranted to assess this reduction in moderate or severe exacerbations, particularly in patients with cardiovascular risk factors.</p>","PeriodicalId":10704,"journal":{"name":"COPD: Journal of Chronic Obstructive Pulmonary Disease","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140118999","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dendritic Cells Promote the Differentiation of ILCs into NCR^-ILC3s in the Lungs of Mice Exposed to Cigarette Smoke.","authors":"Caixia Liang, Ying Shen, Yifang Xu, Yi Liang, Shilin Qiu, Haijuan Tang, Xiaoning Zhong","doi":"10.1080/15412555.2024.2389909","DOIUrl":"https://doi.org/10.1080/15412555.2024.2389909","url":null,"abstract":"<p><p>The involvement of Group 3 innate lymphoid cells (ILC3s) and dendritic cells (DCs) in chronic lung inflammation has been increasingly regarded as the key to understand the inflammatory mechanisms of smoke-related chronic obstructive pulmonary disease (COPD). However, the mechanism underlying the engagement of both remains unclear. Our study aimed to explore NCR^-ILC3 differentiation in the lungs of mice exposed to cigarette smoke (CS) and to further investigate whether DCs activated by CS exposure contribute to the differentiation of ILCs into NCR^-ILC3s. The study involved both <i>in vivo</i> and <i>in vitro</i> experiments. In the former, the frequencies of lung NCR^-ILC3s and NKp46^-IL-17A⁺ ILCs and the expression of DCs, CD40, CD86, IL-23, and IL-1β quantified by flow cytometry were compared between CS-exposed mice and air-exposed mice. In the latter, NKp46^-IL-17A⁺ ILC frequencies quantified by flow cytometry were compared after two cocultures, one involving lung CD45⁺Lin^-CD127⁺ ILCs sorted from air-exposed mice and DCs sifted by CD11c magnetic beads from CS-exposed mice and another including identical CD45⁺Lin^-CD127⁺ ILCs and DCs from air-exposed mice. The results indicated significant increases in the frequencies of NCR^-ILC3s and NKp46^-IL-17A⁺ ILCs; in the expression of DCs, CD40, CD86, IL-23, and IL-1β in CS-exposed mice; and in the frequency of NKp46^-IL-17A⁺ ILCs after the coculture with DCs from CS-exposed mice. In conclusion, CS exposure increases the frequency of lung ILCs and NCR^-ILC3s. CS-induced DC activation enhances the differentiation of ILCs into NCR^-ILC3s, which likely acts as a mediating step in the involvement of NCR-ILC3s in chronic lung inflammation.</p>","PeriodicalId":10704,"journal":{"name":"COPD: Journal of Chronic Obstructive Pulmonary Disease","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141981914","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification and Validation of Aging Related Genes Signature in Chronic Obstructive Pulmonary Disease.","authors":"Tian-Tian Li, Hong-Yan Bai, Jing-Hong Zhang, Xiu-He Kang, Yi-Qing Qu","doi":"10.1080/15412555.2024.2379811","DOIUrl":"https://doi.org/10.1080/15412555.2024.2379811","url":null,"abstract":"<p><strong>Purpose: </strong>Chronic Obstructive Pulmonary Disease (COPD) is regarded as an accelerated aging disease. Aging-related genes in COPD are still poorly understood.</p><p><strong>Method: </strong>Data set GSE76925 was obtained from the Gene Expression Omnibus (GEO) database. The \"limma\" package identified the differentially expressed genes. The weighted gene co-expression network analysis (WGCNA) constructes co-expression modules and detect COPD-related modules. The least absolute shrinkage and selection operator (LASSO) and the support vector machine recursive feature elimination (SVM-RFE) algorithms were chosen to identify the hub genes and the diagnostic ability. Three external datasets were used to identify differences in the expression of hub genes. Real-time reverse transcription polymerase chain reaction (RT-qPCR) was used to verify the expression of hub genes.</p><p><strong>Result: </strong>We identified 15 differentially expressed genes associated with aging (ARDEGs). The SVM-RFE and LASSO algorithms pinpointed four potential diagnostic biomarkers. Analysis of external datasets confirmed significant differences in PIK3R1 expression. RT-qPCR results indicated decreased expression of hub genes. The ROC curve demonstrated that PIK3R1 exhibited strong diagnostic capability for COPD.</p><p><strong>Conclusion: </strong>We identified 15 differentially expressed genes associated with aging. Among them, PIK3R1 showed differences in external data sets and RT-qPCR results. Therefore, PIK3R1 may play an essential role in regulating aging involved in COPD.</p>","PeriodicalId":10704,"journal":{"name":"COPD: Journal of Chronic Obstructive Pulmonary Disease","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141975319","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Assessment of the Relationship Between Genetic Determinants of Obesity, Unhealthy Eating Habits and Chronic Obstructive Pulmonary Disease: A Mendelian Randomisation Study.","authors":"Tongyao Sun, Jun Wang, Min Zheng, Chengsen Cai, Jianjian Yu, Lina Fu, Lei Duan","doi":"10.1080/15412555.2024.2309236","DOIUrl":"10.1080/15412555.2024.2309236","url":null,"abstract":"<p><p><b>Background:</b> Clinical studies have shown that the onset and exacerbation of chronic obstructive pulmonary disease (COPD) are related to obesity and dietary behaviours, but the genetic relationship between them is not clear.<b>Aims:</b> To investigate the relationship between the genetic determinants of obesity, dietary habits (alcohol consumption, intake of sweets, salt intake) and COPD.<b>Methods:</b> Exposure and outcome datasets were obtained from the IEU Open GWAS project. The exposure dataset includes dietary habits (Salt added to food, Sweets intake, Alcohol consumption), obesity level (represented by body mass index (BMI) and body fat percentage (BFP) data sets.). The outcome dataset includes COPD and acute COPD admissions. The collected data were imported into the RStudio software and conducted Mendelian randomisation analysis. Additionally, heterogeneity and horizontal pleiotropy tests were conducted on the data to ensure the veracity of the results.<b>Results:</b> The results showed that BMI was positively correlated with the risk of acute COPD admission (OR = 1.74, 95% CI 1.39-2.18) and COPD (OR = 1.81, 95%CI 1.41-2.33). In addition, BFP was also a risk factor for COPD (OR = 1.98, 95% CI 1.42-2.77) and acute exacerbation of COPD admission (OR = 1.99, 95%CI 1.43-2.77). The increase of salt, sugar and alcohol consumption will not increase the risk of COPD and the risk of hospitalisation due to COPD.<b>Conclusion:</b> Therefore, we should strengthen the guidance of diet and living habits of obese patients. For patients with heavier weight and higher body fat rate, they should be instructed to lose weight and fat to prevent the occurrence of COPD. For obese patients with COPD, more attention should be paid to prevent the occurrence of acute exacerbation of COPD in advance.</p>","PeriodicalId":10704,"journal":{"name":"COPD: Journal of Chronic Obstructive Pulmonary Disease","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139721973","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"EQ-5D Based Utility Values for Adults with Chronic Obstructive Pulmonary Disease: A Systematic Review, Meta-Analysis, and Meta-Regression.","authors":"Natasha Salant, Syed Mohiuddin, Yuanyuan Zhang, Lynda Ayiku, Kusal Lokuge, Paul Jacklin, Lesley Owen","doi":"10.1080/15412555.2024.2385358","DOIUrl":"https://doi.org/10.1080/15412555.2024.2385358","url":null,"abstract":"<p><p>Chronic obstructive pulmonary disease (COPD) is a common lung disease that negatively affects health-related quality of life (QoL). Utility values, which measure QoL by weighting health states with societal preferences, are required for the cost-utility models that drive economic evaluations and policy decisions. Moayeri et al. published a systematic review and meta-analysis of utilities (EQ-5D) in COPD in June 2016. The current study investigated changes in mean utilities in more recent studies thereafter, exploring heterogeneity in utilities across diverse clinical and study characteristics. Systematic searches of databases, such as MEDLINE and Embase were undertaken from 1 July 2015 until 20 May 2024. A random-effects meta-analysis of utilities (EQ-5D) was performed which addressed inter-study heterogeneity and subgroup analyses. The pooled general mean (95% CI) utility value was 0.761 (0.726-0.795) from 43 studies, whereas Moayeri et al. reported 0.673 (0.653-0.693) from 32 studies. This improvement in mean utilities could be due to increased awareness, early detection, and better medical interventions over the past decade, but demonstrates that a general utility value should be approached with caution given significant heterogeneity. Four meta-regressions were performed on each subgroup: region, method of elicitation, reported comorbidities, and disease stage; of which, method of elicitation, disease stage, and region were found to be significant moderators of utilities. It is, therefore, important to use meta-analysed utilities for cost-utility analyses that reflect the context and patient population of the model. Moreover, these results provide additional evidence for the precision and sensitivity of EQ-5D-5L over EQ-5D-3L.</p>","PeriodicalId":10704,"journal":{"name":"COPD: Journal of Chronic Obstructive Pulmonary Disease","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141854967","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}