Background: Chronic obstructive pulmonary disease (COPD) is a respiratory disorder with a complex etiology involving genetic and environmental factors. The dysbiosis of gut microbiota has been implicated in COPD. Mendelian Randomization (MR) provides a tool to investigate causal links using genetic variants as instrumental variables. This study aims to employ MR analysis to explore the causal relationship between gut microbiota, lung function, and COPD. Methods: We utilized genome-wide association study (GWAS) data from MiBioGen, UK Biobank and FinnGen, which were related to gut microbial taxa, lung function parameters including forced vital capacity in one second (FEV1), forced vital capacity (FVC), and percentage of predicted FEV1 (FEV1%pred), as well as GWAS data for COPD. MR analysis was conducted to assess the causal effects of gut microbiota on lung function and the risk of COPD. Sensitivity analysis was utilized to examine the stability of the causal relationships. Multiple testing and reverse analysis were employed to evaluate the robustness of these relationships. Results: Using the IVW method, 64 causal correlations were identified. Through conducting sensitivity analysis, multiple testing, and reverse analysis, we identified 14 robust and stable causal relationships. The bacterial taxa that showed a positive association with lung function included Desulfovibrionaceae, Erysipelotrichales, Desulfovibrionales, Clostridiales, Clostridia, Deltaproteobacteria and Erysipelotrichia, while Selenomonadales and Negativicutes showed a negative association with lung function. The abundance of Holdemanella were positively correlated with the risk of COPD, while FamilyXIII exhibited a negative correlation with the risk of COPD. Conclusion: Several microbial taxa were discovered to have a positive causal correlation with lung function, offering potential insights into the development of probiotics. The presence of microbial taxa negatively correlated with lung function and positively correlated with COPD emphasized the potential impact of gut microbiota dysbiosis on respiratory health.
{"title":"Genetic Insights into the Gut-Lung Axis: Mendelian Randomization Analysis on Gut Microbiota, Lung Function, and COPD","authors":"Zi-Xuan Cheng, Jian-Lan Hua, Zhi-Jun Jie, Xing-Jing Li, Jing Zhang","doi":"10.2147/copd.s441242","DOIUrl":"https://doi.org/10.2147/copd.s441242","url":null,"abstract":"<strong>Background:</strong> Chronic obstructive pulmonary disease (COPD) is a respiratory disorder with a complex etiology involving genetic and environmental factors. The dysbiosis of gut microbiota has been implicated in COPD. Mendelian Randomization (MR) provides a tool to investigate causal links using genetic variants as instrumental variables. This study aims to employ MR analysis to explore the causal relationship between gut microbiota, lung function, and COPD.<br/><strong>Methods:</strong> We utilized genome-wide association study (GWAS) data from MiBioGen, UK Biobank and FinnGen, which were related to gut microbial taxa, lung function parameters including forced vital capacity in one second (FEV<sub>1</sub>), forced vital capacity (FVC), and percentage of predicted FEV<sub>1</sub> (FEV<sub>1</sub>%pred), as well as GWAS data for COPD. MR analysis was conducted to assess the causal effects of gut microbiota on lung function and the risk of COPD. Sensitivity analysis was utilized to examine the stability of the causal relationships. Multiple testing and reverse analysis were employed to evaluate the robustness of these relationships.<br/><strong>Results:</strong> Using the IVW method, 64 causal correlations were identified. Through conducting sensitivity analysis, multiple testing, and reverse analysis, we identified 14 robust and stable causal relationships. The bacterial taxa that showed a positive association with lung function included <em>Desulfovibrionaceae</em>, Erysipelotrichales, Desulfovibrionales, Clostridiales, <em>Clostridia, Deltaproteobacteria</em> and <em>Erysipelotrichia</em>, while Selenomonadales and <em>Negativicutes</em> showed a negative association with lung function. The abundance of <em>Holdemanella</em> were positively correlated with the risk of COPD, while <em>FamilyXIII</em> exhibited a negative correlation with the risk of COPD.<br/><strong>Conclusion:</strong> Several microbial taxa were discovered to have a positive causal correlation with lung function, offering potential insights into the development of probiotics. The presence of microbial taxa negatively correlated with lung function and positively correlated with COPD emphasized the potential impact of gut microbiota dysbiosis on respiratory health.<br/><br/>","PeriodicalId":13792,"journal":{"name":"International Journal of Chronic Obstructive Pulmonary Disease","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140026062","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Purpose: Acute kidney injury (AKI) is a common complication of acute exacerbation of chronic obstructive pulmonary disease (AECOPD), and inflammation is the potential link between AKI and AECOPD. However, little is known about the incidence and risk stratification of AKI in critically ill AECOPD patients. In this study, we aimed to establish risk model based on white blood cell (WBC)-related indicators to predict AKI in critically ill AECOPD patients. Material and Methods: For the training cohort, data were taken from the Medical Information Mart for eICU Collaborative Research Database (eICU-CRD) database, and for the validation cohort, data were taken from the Medical Information Mart for Intensive Care-IV (MIMIC-IV) database. The study employed logistic regression analysis to identify the major predictors of WBC-related biomarkers on AKI prediction. Subsequently, a risk model was developed by multivariate logistic regression, utilizing the identified significant indicators. Results: Finally, 3551 patients were enrolled in training cohort, 926 patients were enrolled in validation cohort. AKI occurred in 1206 (33.4%) patients in training cohort and 521 (56.3%) patients in validation cohort. According to the multivariate logistic regression analysis, four WBC-related indicators were finally included in the novel risk model, and the risk model had a relatively good accuracy for AKI in the training set (C-index, 0.764, 95% CI 0.749– 0.780) as well as in the validation set (C-index, 0.738, 95% CI: 0.706– 0.770). Even after accounting for other models, the critically ill AECOPD patients in the high-risk group (risk score > 3.44) still showed an increased risk of AKI (odds ratio: 4.74, 95% CI: 4.07– 5.54) compared to those in low-risk group (risk score ≤ 3.44). Moreover, the risk model showed outstanding calibration capability as well as therapeutic usefulness in both groups for AKI and ICU mortality and in-hospital mortality of critical ill AECOPD patients. Conclusion: The novel risk model showed good AKI prediction performance. This risk model has certain reference value for the risk stratification of AECOPD complicated with AKI in clinically.
Keywords: risk model, acute kidney injury, prediction, white blood cell, acute exacerbation of chronic obstructive pulmonary disease
目的：急性肾损伤（AKI）是慢性阻塞性肺疾病（AECOPD）急性加重的常见并发症，而炎症是 AKI 和 AECOPD 之间的潜在联系。然而，人们对 AECOPD 重症患者 AKI 的发生率和风险分层知之甚少。本研究旨在建立基于白细胞相关指标的风险模型，以预测重症 AECOPD 患者的 AKI：训练队列的数据来自 eICU 合作研究数据库（eICU-CRD）的医学信息市场，验证队列的数据来自重症监护医学信息市场-IV（MIMIC-IV）数据库。研究采用逻辑回归分析确定了白细胞相关生物标志物对 AKI 预测的主要预测因素。随后，利用确定的重要指标，通过多变量逻辑回归建立了风险模型：最后，3551 名患者被纳入训练队列，926 名患者被纳入验证队列。训练队列中有1206名（33.4%）患者发生了AKI，验证队列中有521名（56.3%）患者发生了AKI。根据多变量逻辑回归分析，四个白细胞相关指标最终被纳入新的风险模型，该风险模型在训练组（C 指数为 0.764，95% CI 为 0.749-0.780）和验证组（C 指数为 0.738，95% CI 为 0.706-0.770）中对 AKI 的准确性相对较好。即使考虑了其他模型，与低风险组（风险评分≤3.44）相比，高风险组（风险评分≥3.44）的 AECOPD 重症患者发生 AKI 的风险仍然增加（几率比：4.74，95% CI：4.07- 5.54）。此外，该风险模型在两组 AECOPD 危重症患者的 AKI、ICU 死亡率和院内死亡率方面均显示出卓越的校准能力和治疗作用：结论：新型风险模型具有良好的AKI预测性能。关键词：风险模型；急性肾损伤；预测；白细胞；慢性阻塞性肺疾病急性加重期
{"title":"Prognostic Value of Leukocyte-Based Risk Model for Acute Kidney Injury Prediction in Critically Ill Acute Exacerbation of Chronic Obstructive Pulmonary Disease Patients","authors":"Min Cai, Yue Deng, Tianyang Hu","doi":"10.2147/copd.s444888","DOIUrl":"https://doi.org/10.2147/copd.s444888","url":null,"abstract":"<strong>Purpose:</strong> Acute kidney injury (AKI) is a common complication of acute exacerbation of chronic obstructive pulmonary disease (AECOPD), and inflammation is the potential link between AKI and AECOPD. However, little is known about the incidence and risk stratification of AKI in critically ill AECOPD patients. In this study, we aimed to establish risk model based on white blood cell (WBC)-related indicators to predict AKI in critically ill AECOPD patients.<br/><strong>Material and Methods:</strong> For the training cohort, data were taken from the Medical Information Mart for eICU Collaborative Research Database (eICU-CRD) database, and for the validation cohort, data were taken from the Medical Information Mart for Intensive Care-IV (MIMIC-IV) database. The study employed logistic regression analysis to identify the major predictors of WBC-related biomarkers on AKI prediction. Subsequently, a risk model was developed by multivariate logistic regression, utilizing the identified significant indicators.<br/><strong>Results:</strong> Finally, 3551 patients were enrolled in training cohort, 926 patients were enrolled in validation cohort. AKI occurred in 1206 (33.4%) patients in training cohort and 521 (56.3%) patients in validation cohort. According to the multivariate logistic regression analysis, four WBC-related indicators were finally included in the novel risk model, and the risk model had a relatively good accuracy for AKI in the training set (C-index, 0.764, 95% CI 0.749– 0.780) as well as in the validation set (C-index, 0.738, 95% CI: 0.706– 0.770). Even after accounting for other models, the critically ill AECOPD patients in the high-risk group (risk score > 3.44) still showed an increased risk of AKI (odds ratio: 4.74, 95% CI: 4.07– 5.54) compared to those in low-risk group (risk score ≤ 3.44). Moreover, the risk model showed outstanding calibration capability as well as therapeutic usefulness in both groups for AKI and ICU mortality and in-hospital mortality of critical ill AECOPD patients.<br/><strong>Conclusion:</strong> The novel risk model showed good AKI prediction performance. This risk model has certain reference value for the risk stratification of AECOPD complicated with AKI in clinically.<br/><br/><strong>Keywords:</strong> risk model, acute kidney injury, prediction, white blood cell, acute exacerbation of chronic obstructive pulmonary disease<br/>","PeriodicalId":13792,"journal":{"name":"International Journal of Chronic Obstructive Pulmonary Disease","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140026063","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Abstract: Neither asthma nor chronic obstructive pulmonary disease (COPD) is a single disease consisting of a uniform pathogenesis; rather, they are both syndromes that result from a variety of basic distinct pathogeneses. Many of the basic pathogeneses overlap between the two diseases, and multiple basic pathogeneses are simultaneously involved at varying proportions in individual patients. The specific combination of different basic pathogeneses in each patient determines the phenotype of the patient, and it varies widely from patient to patient. For example, type 2 airway inflammation and neutrophilic airway inflammation may coexist in the same patient, and quite a few patients have clinical characteristics of both asthma and COPD. Even in the same patient, the contribution of each pathogenesis is expected to differ at different life stages (eg, childhood, adolescence, middle age, and older), during different seasons (eg, high seasons for hay fever and rhinovirus infection), and depending on the nature of treatments. This review describes several basic pathogeneses commonly involved in both asthma and COPD, including chronic non-type 2 inflammation, type 2 inflammation, viral infections, and lung development. Understanding of the basic molecular pathogeneses in individual patients, rather than the use of clinical diagnosis, such as asthma, COPD, or even asthma COPD overlap, will enable us to better deal with the diversity seen in disease states, and lead to optimal treatment practices tailored for each patient with less disease burden, such as drug-induced side effects, and improved prognosis. Furthermore, we can expect to focus on these molecular pathways as new drug discovery targets.
{"title":"Common Pathogeneses Underlying Asthma and Chronic Obstructive Pulmonary Disease -Insights from Genetic Studies","authors":"Nobuyuki Hizawa","doi":"10.2147/copd.s441992","DOIUrl":"https://doi.org/10.2147/copd.s441992","url":null,"abstract":"<strong>Abstract:</strong> Neither asthma nor chronic obstructive pulmonary disease (COPD) is a single disease consisting of a uniform pathogenesis; rather, they are both syndromes that result from a variety of basic distinct pathogeneses. Many of the basic pathogeneses overlap between the two diseases, and multiple basic pathogeneses are simultaneously involved at varying proportions in individual patients. The specific combination of different basic pathogeneses in each patient determines the phenotype of the patient, and it varies widely from patient to patient. For example, type 2 airway inflammation and neutrophilic airway inflammation may coexist in the same patient, and quite a few patients have clinical characteristics of both asthma and COPD. Even in the same patient, the contribution of each pathogenesis is expected to differ at different life stages (eg, childhood, adolescence, middle age, and older), during different seasons (eg, high seasons for hay fever and rhinovirus infection), and depending on the nature of treatments. This review describes several basic pathogeneses commonly involved in both asthma and COPD, including chronic non-type 2 inflammation, type 2 inflammation, viral infections, and lung development. Understanding of the basic molecular pathogeneses in individual patients, rather than the use of clinical diagnosis, such as asthma, COPD, or even asthma COPD overlap, will enable us to better deal with the diversity seen in disease states, and lead to optimal treatment practices tailored for each patient with less disease burden, such as drug-induced side effects, and improved prognosis. Furthermore, we can expect to focus on these molecular pathways as new drug discovery targets.<br/><br/><strong>Keywords:</strong> Asthma, chronic obstructive pulmonary disease (COPD), endotype, precision medicine, treatable traits approach<br/>","PeriodicalId":13792,"journal":{"name":"International Journal of Chronic Obstructive Pulmonary Disease","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140025970","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pierachille Santus, Fabiano Di Marco, Fulvio Braido, Marco Contoli, Angelo Guido Corsico, Claudio Micheletto, Girolamo Pelaia, Dejan Radovanovic, Paola Rogliani, Laura Saderi, Nicola Scichilone, Silvia Tanzi, Manlio Vella, Silvia Boarino, Giovanni Sotgiu, Paolo Solidoro
Objective: To describe the burden of moderate to severe exacerbations and all-cause mortality; the secondary objectives were to analyze treatment patterns and changes over follow-up. Design: Observational, multicenter, retrospective, cohort study with a three year follow-up period. Setting: Ten Italian academic secondary- and tertiary-care centers. Participants: Patients with a confirmed diagnosis of COPD referring to the outpatient clinics of the participating centers were retrospectively recruited. Primary and Secondary Outcome Measures: Annualized frequency of moderate and severe exacerbations stratified by exacerbation history prior to study enrollment. Patients were classified according to airflow obstruction, GOLD risk categories, and divided in 4 groups: A = no exacerbations; B = 1 moderate exacerbation; C = 1 severe exacerbation; D = ≥ 2 moderate and/or severe exacerbations. Overall all-cause mortality stratified by age, COPD category, and COPD therapy. A logistic regression model assessed the association of clinical characteristics with mortality. Results: 1111 patients were included (73% males), of which 41.5% had a history of exacerbations. As expected, the proportion of patients experiencing ≥ 1 exacerbation during follow-up increased according to pre-defined study risk categories (B: 79%, C: 84%, D: 97.4%). Overall, by the end of follow-up, 45.5% of patients without a history of exacerbation experienced an exacerbation (31% of which severe), and 13% died. Deceased patients were significantly older, more obstructed and hyperinflated, and more frequently active smokers compared with survivors. Severe exacerbations were more frequent in patients that died (23.5%, vs 10.2%; p-value: 0.002). Chronic heart failure and ischemic heart disease were the only comorbidities associated with a higher odds ratio (OR) for death (OR: 2.2, p-value: 0.001; and OR: 1.9, p-value: 0.007). Treatment patterns were similar in patients that died and survivors. Conclusion: Patients with a low exacerbation risk are exposed to a significant future risk of moderate/severe exacerbations. Real life data confirm the strong association between mortality and cardiovascular comorbidities in COPD.
Keywords: pulmonary disease chronic obstructive, heart failure, ischaemic heart disease, respiratory medicine, public health
{"title":"Exacerbation Burden in COPD and Occurrence of Mortality in a Cohort of Italian Patients: Results of the Gulp Study","authors":"Pierachille Santus, Fabiano Di Marco, Fulvio Braido, Marco Contoli, Angelo Guido Corsico, Claudio Micheletto, Girolamo Pelaia, Dejan Radovanovic, Paola Rogliani, Laura Saderi, Nicola Scichilone, Silvia Tanzi, Manlio Vella, Silvia Boarino, Giovanni Sotgiu, Paolo Solidoro","doi":"10.2147/copd.s446636","DOIUrl":"https://doi.org/10.2147/copd.s446636","url":null,"abstract":"<strong>Objective:</strong> To describe the burden of moderate to severe exacerbations and all-cause mortality; the secondary objectives were to analyze treatment patterns and changes over follow-up.<br/><strong>Design:</strong> Observational, multicenter, retrospective, cohort study with a three year follow-up period.<br/><strong>Setting:</strong> Ten Italian academic secondary- and tertiary-care centers.<br/><strong>Participants:</strong> Patients with a confirmed diagnosis of COPD referring to the outpatient clinics of the participating centers were retrospectively recruited.<br/><strong>Primary and Secondary Outcome Measures:</strong> Annualized frequency of moderate and severe exacerbations stratified by exacerbation history prior to study enrollment. Patients were classified according to airflow obstruction, GOLD risk categories, and divided in 4 groups: A = no exacerbations; B = 1 moderate exacerbation; C = 1 severe exacerbation; D = ≥ 2 moderate and/or severe exacerbations. Overall all-cause mortality stratified by age, COPD category, and COPD therapy. A logistic regression model assessed the association of clinical characteristics with mortality.<br/><strong>Results:</strong> 1111 patients were included (73% males), of which 41.5% had a history of exacerbations. As expected, the proportion of patients experiencing ≥ 1 exacerbation during follow-up increased according to pre-defined study risk categories (B: 79%, C: 84%, D: 97.4%). Overall, by the end of follow-up, 45.5% of patients without a history of exacerbation experienced an exacerbation (31% of which severe), and 13% died. Deceased patients were significantly older, more obstructed and hyperinflated, and more frequently active smokers compared with survivors. Severe exacerbations were more frequent in patients that died (23.5%, vs 10.2%; p-value: 0.002). Chronic heart failure and ischemic heart disease were the only comorbidities associated with a higher odds ratio (OR) for death (OR: 2.2, p-value: 0.001; and OR: 1.9, p-value: 0.007). Treatment patterns were similar in patients that died and survivors.<br/><strong>Conclusion:</strong> Patients with a low exacerbation risk are exposed to a significant future risk of moderate/severe exacerbations. Real life data confirm the strong association between mortality and cardiovascular comorbidities in COPD.<br/><br/><strong>Keywords:</strong> pulmonary disease chronic obstructive, heart failure, ischaemic heart disease, respiratory medicine, public health<br/>","PeriodicalId":13792,"journal":{"name":"International Journal of Chronic Obstructive Pulmonary Disease","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140006650","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Abstract: Most patients with chronic obstructive pulmonary disease (COPD) suffer from at least one additional, clinically relevant chronic disease. To a degree, the high global prevalence and mortality rate of COPD is closely related to its extrapulmonary effects. Moreover, the various of comorbidities of COPD and itself interact with each other, resulting in diverse clinical manifestations and individual differences, and thus further influencing the prognosis as well as healthcare burden of COPD patients. This is closely related to the common risk factors of chronic diseases (aging, smoking, inactivity, etc.). Additionally, some pathophysiological mechanisms caused by COPD, including the systemic inflammatory response, hypoxia, oxidative stress, and others, also have an impact on other systems. But comprehensive management and medical interventions have not yet been established. The clinicians should improve their knowledge and skills in diagnosing as well as treating the comorbidities of COPD, and then aim to develop more individualized, efficient diagnostic and therapeutic strategies for different patients to achieve greater clinical benefits. In this article, we will review the risk factors, mechanisms, and treatment strategies for extrapulmonary comorbidities in chronic obstructive pulmonary disease, including cardiovascular diseases, diabetes, anemia, osteoporosis, emotional disorders, and gastroesophageal reflux disease.
{"title":"Extrapulmonary Comorbidities Associated with Chronic Obstructive Pulmonary Disease: A Review","authors":"Yurong Xiang, Xiaobin Luo","doi":"10.2147/copd.s447739","DOIUrl":"https://doi.org/10.2147/copd.s447739","url":null,"abstract":"<strong>Abstract:</strong> Most patients with chronic obstructive pulmonary disease (COPD) suffer from at least one additional, clinically relevant chronic disease. To a degree, the high global prevalence and mortality rate of COPD is closely related to its extrapulmonary effects. Moreover, the various of comorbidities of COPD and itself interact with each other, resulting in diverse clinical manifestations and individual differences, and thus further influencing the prognosis as well as healthcare burden of COPD patients. This is closely related to the common risk factors of chronic diseases (aging, smoking, inactivity, etc.). Additionally, some pathophysiological mechanisms caused by COPD, including the systemic inflammatory response, hypoxia, oxidative stress, and others, also have an impact on other systems. But comprehensive management and medical interventions have not yet been established. The clinicians should improve their knowledge and skills in diagnosing as well as treating the comorbidities of COPD, and then aim to develop more individualized, efficient diagnostic and therapeutic strategies for different patients to achieve greater clinical benefits. In this article, we will review the risk factors, mechanisms, and treatment strategies for extrapulmonary comorbidities in chronic obstructive pulmonary disease, including cardiovascular diseases, diabetes, anemia, osteoporosis, emotional disorders, and gastroesophageal reflux disease.<br/><br/><strong>Keywords:</strong> chronic obstructive pulmonary disease, comorbidity, risk factors, therapeutics<br/>","PeriodicalId":13792,"journal":{"name":"International Journal of Chronic Obstructive Pulmonary Disease","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-02-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140006716","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Xiaojing Chen, Qilin Yang, Li Gao, Weinan Chen, Xiaoyu Gao, Yameng Li, Liying Ao, Dejun Sun
Background: Serum anion gap (AG) has been proven to be associated with prognosis in critically ill patients. However, few studies have investigated the association between AG and all-cause mortality in critically ill patients with chronic obstructive pulmonary disease (COPD). Objective: We hypothesized that the initial AG level would predict the mortality risk in critically ill patients with COPD. Methods: This retrospective cohort study was based on the Medical Information Mart for Intensive Care (MIMIC) IV database. We extracted demographics, vital signs, laboratory tests, comorbidity, and scoring systems from the first 24 hours after patient ICU admission. Multivariable logistic regression analysis models were used to explore the association between serum AG levels and mortality. Interaction and stratified analyses were conducted including age, gender and comorbidity. Results: A total of 5531 critically ill patients with COPD were enrolled, composed of 53.6% male and 46.4% female with a median age of 73 years. The all-cause mortality of these patients during ICU hospitalization was 13.7%. The risk of all-cause mortality increased as the AG level increased in the univariate logistic regression analysis (OR=1.13, 95% CI: 1.11– 1.15, p< 0.01). After adjusting for all the covariates in multivariate logistic regression analysis, the odds ratio was 1.06 (95% CI: 1.04– 1.09, p< 0.01). Compared with the lowest AG group Q1 (≤ 11mmol/L), the adjusted OR value for AG and mortality in Q2 (12– 13mmol/L) was 0.89 (95% CI: 0.63– 1.25, p=0.502), Q3 (14– 15mmol/L) was 0.95 (95% CI: 0.68– 1.34, p=0.788), and Q4 (≥ 16mmol/L) was 1.49 (95% CI: 1.10– 2.02, p=0.009) respectively. In addition, the results of the subgroup and stratified analyses were robust. Conclusion: AG is positively related to all-cause mortality in critically ill patients with COPD.
背景：血清阴离子间隙（AG）已被证实与重症患者的预后有关。然而，很少有研究调查 AG 与慢性阻塞性肺病（COPD）重症患者全因死亡率之间的关系：我们假设最初的 AG 水平可预测 COPD 重症患者的死亡风险：这项回顾性队列研究基于重症监护医学信息市场（MIMIC）IV 数据库。我们提取了患者入住重症监护病房后 24 小时内的人口统计学特征、生命体征、实验室检查、合并症和评分系统。我们使用多变量逻辑回归分析模型来探讨血清 AG 水平与死亡率之间的关系。进行了包括年龄、性别和合并症在内的交互和分层分析：共纳入 5531 名慢性阻塞性肺病重症患者，其中男性占 53.6%，女性占 46.4%，中位年龄为 73 岁。这些患者在重症监护室住院期间的全因死亡率为 13.7%。在单变量逻辑回归分析中，全因死亡风险随着 AG 水平的增加而增加（OR=1.13，95% CI：1.11- 1.15，p< 0.01）。在多变量逻辑回归分析中对所有协变量进行调整后，几率比为 1.06（95% CI：1.04- 1.09，p< 0.01）。与最低 AG 组 Q1（≤ 11mmol/L）相比，Q2（12- 13mmol/L）、Q3（14- 15mmol/L）和 Q4（≥ 16mmol/L）的 AG 与死亡率的调整 OR 值分别为 0.89（95% CI：0.63- 1.25，p=0.502）、0.95（95% CI：0.68- 1.34，p=0.788）和 1.49（95% CI：1.10- 2.02，p=0.009）。此外，亚组和分层分析的结果也很可靠：AG与慢性阻塞性肺病重症患者的全因死亡率呈正相关。
{"title":"Association Between Serum Anion Gap and Mortality in Critically Ill Patients with COPD in ICU: Data from the MIMIC IV Database","authors":"Xiaojing Chen, Qilin Yang, Li Gao, Weinan Chen, Xiaoyu Gao, Yameng Li, Liying Ao, Dejun Sun","doi":"10.2147/copd.s433619","DOIUrl":"https://doi.org/10.2147/copd.s433619","url":null,"abstract":"<strong>Background:</strong> Serum anion gap (AG) has been proven to be associated with prognosis in critically ill patients. However, few studies have investigated the association between AG and all-cause mortality in critically ill patients with chronic obstructive pulmonary disease (COPD).<br/><strong>Objective:</strong> We hypothesized that the initial AG level would predict the mortality risk in critically ill patients with COPD.<br/><strong>Methods:</strong> This retrospective cohort study was based on the Medical Information Mart for Intensive Care (MIMIC) IV database. We extracted demographics, vital signs, laboratory tests, comorbidity, and scoring systems from the first 24 hours after patient ICU admission. Multivariable logistic regression analysis models were used to explore the association between serum AG levels and mortality. Interaction and stratified analyses were conducted including age, gender and comorbidity.<br/><strong>Results:</strong> A total of 5531 critically ill patients with COPD were enrolled, composed of 53.6% male and 46.4% female with a median age of 73 years. The all-cause mortality of these patients during ICU hospitalization was 13.7%. The risk of all-cause mortality increased as the AG level increased in the univariate logistic regression analysis (OR=1.13, 95% CI: 1.11– 1.15, p< 0.01). After adjusting for all the covariates in multivariate logistic regression analysis, the odds ratio was 1.06 (95% CI: 1.04– 1.09, p< 0.01). Compared with the lowest AG group Q1 (≤ 11mmol/L), the adjusted OR value for AG and mortality in Q2 (12– 13mmol/L) was 0.89 (95% CI: 0.63– 1.25, p=0.502), Q3 (14– 15mmol/L) was 0.95 (95% CI: 0.68– 1.34, p=0.788), and Q4 (≥ 16mmol/L) was 1.49 (95% CI: 1.10– 2.02, p=0.009) respectively. In addition, the results of the subgroup and stratified analyses were robust.<br/><strong>Conclusion:</strong> AG is positively related to all-cause mortality in critically ill patients with COPD.<br/><br/>","PeriodicalId":13792,"journal":{"name":"International Journal of Chronic Obstructive Pulmonary Disease","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-02-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140006913","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jian-Jun Wu, Ping-An Zhang, Ming-Zhe Chen, Yi Zhang, Wei-Sha Du, Xiao-Ning Li, Guo-Chao Ji, Liang-Duo Jiang, Yang Jiao, Xin Li
Background: Some patients with chronic obstructive pulmonary disease (COPD) benefit from glucocorticoid (GC) treatment, but its mechanism is unclear. Objective: With the help of the Gene Expression Omnibus (GEO) database, the key genes and miRNA-mRNA related to the treatment of COPD by GCs were discussed, and the potential mechanism was explained. Methods: The miRNA microarray dataset (GSE76774) and mRNA microarray dataset (GSE36221) were downloaded, and differential expression analysis were performed. Gene Ontology (GO) function and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed on the differentially expressed genes (DEGs). The protein interaction network of the DEGs in the regulatory network was constructed with the STRING database, and the key genes were screened through Cytoscape. Potential downstream target genes regulated by differentially expressed miRNAs (DEMs) were predicted by the miRWalk3.0 database, and miRNA-mRNA regulatory networks were constructed. Finally, some research results were validated. Results: ① Four DEMs and 83 DEGs were screened; ② GO and KEGG enrichment analysis mainly focused on the PI3K/Akt signalling pathway, ECM receptor interaction, etc.; ③ CD2, SLAMF7, etc. may be the key targets of GC in the treatment of COPD; ④ 18 intersection genes were predicted by the mirwalk 3.0 database, and 9 pairs of miRNA-mRNA regulatory networks were identified; ⑤ The expression of miR-320d-2 and TFCP2L1 were upregulated by dexamethasone in the COPD cell model, while the expression of miR-181a-2-3p and SLAMF7 were downregulated. Conclusion: In COPD, GC may mediate the expression of the PI3K/Akt signalling pathway through miR-181a-2-3p, miR-320d-2, miR-650, and miR-155-5p, targeting its downstream signal factors. The research results provide new ideas for RNA therapy strategies of COPD, and also lay a foundation for further research.
{"title":"Analysis of Key Genes and miRNA-mRNA Networks Associated with Glucocorticoids Treatment in Chronic Obstructive Pulmonary Disease","authors":"Jian-Jun Wu, Ping-An Zhang, Ming-Zhe Chen, Yi Zhang, Wei-Sha Du, Xiao-Ning Li, Guo-Chao Ji, Liang-Duo Jiang, Yang Jiao, Xin Li","doi":"10.2147/copd.s441716","DOIUrl":"https://doi.org/10.2147/copd.s441716","url":null,"abstract":"<strong>Background:</strong> Some patients with chronic obstructive pulmonary disease (COPD) benefit from glucocorticoid (GC) treatment, but its mechanism is unclear.<br/><strong>Objective:</strong> With the help of the Gene Expression Omnibus (GEO) database, the key genes and miRNA-mRNA related to the treatment of COPD by GCs were discussed, and the potential mechanism was explained.<br/><strong>Methods:</strong> The miRNA microarray dataset (GSE76774) and mRNA microarray dataset (GSE36221) were downloaded, and differential expression analysis were performed. Gene Ontology (GO) function and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed on the differentially expressed genes (DEGs). The protein interaction network of the DEGs in the regulatory network was constructed with the STRING database, and the key genes were screened through Cytoscape. Potential downstream target genes regulated by differentially expressed miRNAs (DEMs) were predicted by the miRWalk3.0 database, and miRNA-mRNA regulatory networks were constructed. Finally, some research results were validated.<br/><strong>Results:</strong> ① Four DEMs and 83 DEGs were screened; ② GO and KEGG enrichment analysis mainly focused on the PI3K/Akt signalling pathway, ECM receptor interaction, etc.; ③ CD2, SLAMF7, etc. may be the key targets of GC in the treatment of COPD; ④ 18 intersection genes were predicted by the mirwalk 3.0 database, and 9 pairs of miRNA-mRNA regulatory networks were identified; ⑤ The expression of miR-320d-2 and TFCP2L1 were upregulated by dexamethasone in the COPD cell model, while the expression of miR-181a-2-3p and SLAMF7 were downregulated.<br/><strong>Conclusion:</strong> In COPD, GC may mediate the expression of the PI3K/Akt signalling pathway through miR-181a-2-3p, miR-320d-2, miR-650, and miR-155-5p, targeting its downstream signal factors. The research results provide new ideas for RNA therapy strategies of COPD, and also lay a foundation for further research.<br/><br/>","PeriodicalId":13792,"journal":{"name":"International Journal of Chronic Obstructive Pulmonary Disease","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140006767","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Georges Abi Abdallah, Sylvain Diop, Matthieu Jamme, Stéphane Legriel, Alexis Ferré
Background: Data are scarce on respiratory infections during severe acute exacerbation of chronic obstructive pulmonary disease (COPD). This study aimed to investigate respiratory infection patterns in the intensive care unit (ICU) and identify variables associated with infection type and patient outcome. Methods: A retrospective, single-centre cohort study. All patients admitted (2015– 2021) to our ICU for severe acute exacerbation of COPD were included. Logistic multivariable regression analysis was performed to predict factors associated with infection and assess the association between infection and outcome. Results: We included 473 patients: 288 (60.9%) had respiratory infection and 139 (29.4%) required invasive mechanical ventilation. Eighty-nine (30.9%) had viral, 81 (28.1%) bacterial, 34 (11.8%) mixed, and 84 (29.2%) undocumented infections. Forty-seven (9.9%) patients died in the ICU and 67 (14.2%) in hospital. Factors associated with respiratory infection were temperature (odds ratio [+1°C]=1.43, P= 0.008) and blood neutrophils (1.07, P= 0.002). Male sex (2.21, P= 0.02) and blood neutrophils were associated with bacterial infection (1.06, P= 0.04). In a multivariable analysis, pneumonia (cause-specific hazard=1.75, P= 0.005), respiratory rate (1.17, P=0.04), arterial partial pressure of carbon-dioxide (1.08, P= 0.04), and lactate (1.14, P= 0.02) were associated with the need for invasive MV. Age (1.03, P= 0.03), immunodeficiency (1.96, P= 0.02), and altered performance status (1.78, P= 0.002) were associated with hospital mortality. Conclusions: Respiratory infections, 39.9% of which were bacterial, were the main cause of severe acute exacerbation of COPD. Body temperature and blood neutrophils were single markers of infection. Pneumonia was associated with the need for invasive mechanical ventilation but not with hospital mortality, as opposed to age, immunodeficiency, and altered performance status.
Plain Language Summary: - This study investigates the prevalence, characteristics, and impact on outcomes of different types of respiratory infections triggering severe acute exacerbations of COPD.- Our retrospective cohort study of 473 critically ill patients found that respiratory infections, of which 39.9% were bacterial, were the main cause of severe exacerbation.- The type of infection (viral, bacterial, or mixt) was not associated with the need for invasive mechanical ventilation or mortality.- Early identification of the infectious agent is crucial for implementing effective therapy; however, the type of infection was not associated with the main outcomes.
{"title":"Respiratory Infection Triggering Severe Acute Exacerbations of Chronic Obstructive Pulmonary Disease","authors":"Georges Abi Abdallah, Sylvain Diop, Matthieu Jamme, Stéphane Legriel, Alexis Ferré","doi":"10.2147/copd.s447162","DOIUrl":"https://doi.org/10.2147/copd.s447162","url":null,"abstract":"<strong>Background:</strong> Data are scarce on respiratory infections during severe acute exacerbation of chronic obstructive pulmonary disease (COPD). This study aimed to investigate respiratory infection patterns in the intensive care unit (ICU) and identify variables associated with infection type and patient outcome.<br/><strong>Methods:</strong> A retrospective, single-centre cohort study. All patients admitted (2015– 2021) to our ICU for severe acute exacerbation of COPD were included. Logistic multivariable regression analysis was performed to predict factors associated with infection and assess the association between infection and outcome.<br/><strong>Results:</strong> We included 473 patients: 288 (60.9%) had respiratory infection and 139 (29.4%) required invasive mechanical ventilation. Eighty-nine (30.9%) had viral, 81 (28.1%) bacterial, 34 (11.8%) mixed, and 84 (29.2%) undocumented infections. Forty-seven (9.9%) patients died in the ICU and 67 (14.2%) in hospital. Factors associated with respiratory infection were temperature (odds ratio [+1°C]=1.43, <em>P=</em> 0.008) and blood neutrophils (1.07, <em>P=</em> 0.002). Male sex (2.21, <em>P=</em> 0.02) and blood neutrophils were associated with bacterial infection (1.06, <em>P=</em> 0.04). In a multivariable analysis, pneumonia (cause-specific hazard=1.75, <em>P=</em> 0.005), respiratory rate (1.17, <em>P</em>=0.04), arterial partial pressure of carbon-dioxide (1.08, <em>P=</em> 0.04), and lactate (1.14, <em>P=</em> 0.02) were associated with the need for invasive MV. Age (1.03, <em>P=</em> 0.03), immunodeficiency (1.96, <em>P=</em> 0.02), and altered performance status (1.78, <em>P=</em> 0.002) were associated with hospital mortality.<br/><strong>Conclusions:</strong> Respiratory infections, 39.9% of which were bacterial, were the main cause of severe acute exacerbation of COPD. Body temperature and blood neutrophils were single markers of infection. Pneumonia was associated with the need for invasive mechanical ventilation but not with hospital mortality, as opposed to age, immunodeficiency, and altered performance status.<br/><br/><strong>Plain Language Summary:</strong> - This study investigates the prevalence, characteristics, and impact on outcomes of different types of respiratory infections triggering severe acute exacerbations of COPD.- Our retrospective cohort study of 473 critically ill patients found that respiratory infections, of which 39.9% were bacterial, were the main cause of severe exacerbation.- The type of infection (viral, bacterial, or mixt) was not associated with the need for invasive mechanical ventilation or mortality.- Early identification of the infectious agent is crucial for implementing effective therapy; however, the type of infection was not associated with the main outcomes.<br/><br/>","PeriodicalId":13792,"journal":{"name":"International Journal of Chronic Obstructive Pulmonary Disease","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139978529","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Purpose: This study sought to examine the potential association between serum Klotho levels and the prevalence of COPD in the United States. Patients and Methods: This study was a cross-sectional analysis involving 4361 adults aged 40– 79 years participating in the US National Health and Nutrition Examination Survey (NHANES) conducted between 2013 and 2016. Our investigation utilized multivariate logistic regression and restricted cubic spline (RCS) regression to explore the potential correlation between serum Klotho concentrations and the prevalence of COPD. Additionally, we conducted stratified and interaction analyses to evaluate the consistency and potential modifiers of this relationship. Results: In this study encompassing 4631 patients (with an average age of 57.6 years, 47.5% of whom were male), 445 individuals (10.2%) were identified as having COPD. In the fully adjusted model, ln-transformed serum Klotho was negatively associated with COPD (OR = 0.71; 95% CI: 0.51– 0.99; p = 0.043). Meanwhile, compared with quartile 1, serum Klotho levels in quartiles 2– 4 yielded odds ratios (ORs) (95% CI) for COPD were 0.84 (0.63~1.11), 0.76 (0.56~1.02), 0.84 (0.62~1.13), respectively. A negative relationship was observed between the ln-transformed serum Klotho and occurrence of COPD (nonlinear: p = 0.140). the association between ln-transformed serum Klotho and COPD were stable in stratified analyses. Conclusion: Serum Klotho was negatively associated with the incidence of COPD, when ln-transformed Klotho concentration increased by 1 unit, the risk of COPD was 29% lower.
Keywords: α-Klotho (Klotho), chronic obstructive pulmonary disease, cross-sectional study, National Health and Nutrition Survey, NHANES
{"title":"Association Between Serum Klotho and Chronic Obstructive Pulmonary Disease in US Middle-Aged and Older Individuals: A Cross-Sectional Study from NHANES 2013–2016","authors":"Yushan Shi, Zhangmeng Xu, Shuangshuang Pu, Kanghong Xu, Yanan Wang, Chunlai Zhang","doi":"10.2147/copd.s451859","DOIUrl":"https://doi.org/10.2147/copd.s451859","url":null,"abstract":"<strong>Purpose:</strong> This study sought to examine the potential association between serum Klotho levels and the prevalence of COPD in the United States.<br/><strong>Patients and Methods:</strong> This study was a cross-sectional analysis involving 4361 adults aged 40– 79 years participating in the US National Health and Nutrition Examination Survey (NHANES) conducted between 2013 and 2016. Our investigation utilized multivariate logistic regression and restricted cubic spline (RCS) regression to explore the potential correlation between serum Klotho concentrations and the prevalence of COPD. Additionally, we conducted stratified and interaction analyses to evaluate the consistency and potential modifiers of this relationship.<br/><strong>Results:</strong> In this study encompassing 4631 patients (with an average age of 57.6 years, 47.5% of whom were male), 445 individuals (10.2%) were identified as having COPD. In the fully adjusted model, ln-transformed serum Klotho was negatively associated with COPD (OR = 0.71; 95% CI: 0.51– 0.99; p = 0.043). Meanwhile, compared with quartile 1, serum Klotho levels in quartiles 2– 4 yielded odds ratios (ORs) (95% CI) for COPD were 0.84 (0.63~1.11), 0.76 (0.56~1.02), 0.84 (0.62~1.13), respectively. A negative relationship was observed between the ln-transformed serum Klotho and occurrence of COPD (nonlinear: p = 0.140). the association between ln-transformed serum Klotho and COPD were stable in stratified analyses.<br/><strong>Conclusion:</strong> Serum Klotho was negatively associated with the incidence of COPD, when ln-transformed Klotho concentration increased by 1 unit, the risk of COPD was 29% lower.<br/><br/><strong>Keywords:</strong> α-Klotho (Klotho), chronic obstructive pulmonary disease, cross-sectional study, National Health and Nutrition Survey, NHANES<br/>","PeriodicalId":13792,"journal":{"name":"International Journal of Chronic Obstructive Pulmonary Disease","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139968170","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Sanne HB van Dijk, Marjolein GJ Brusse-Keizer, Charlotte C Bucsán, Eline H Ploumen, Wendy JC van Beurden, Job van der Palen, Carine JM Doggen, Anke Lenferink
Background: Due to shared symptoms, acute heart failure (AHF) is difficult to differentiate from an acute exacerbation of COPD (AECOPD). This systematic review aimed to identify markers that can diagnose AHF underlying acute dyspnea in patients with COPD presenting at the hospital. Methods: All types of observational studies and clinical trials that investigated any marker’s ability to diagnose AHF in acutely dyspneic COPD patients were considered eligible for inclusion. An AI tool (ASReview) supported the title and abstract screening of the articles obtained from PubMed, Scopus, Web of Science, the Cochrane Library, Embase, and CINAHL until April 2023. Full text screening was independently performed by two reviewers. Twenty percent of the data extraction was checked by a second reviewer and the risk of bias was assessed in duplicate using the QUADAS-2 tool. Markers’ discriminative abilities were evaluated in terms of sensitivity, specificity, positive and negative predictive values, and the area under the curve when available. Results: The search identified 10,366 articles. After deduplication, title and abstract screening was performed on 5,386 articles, leaving 153 relevant, of which 82 could be screened full text. Ten distinct studies (reported in 16 articles) were included, of which 9 had a high risk of bias. Overall, these studies evaluated 12 distinct laboratory and 7 non-laboratory markers. BNP, NT-proBNP, MR-proANP, and inspiratory inferior vena cava diameter showed the highest diagnostic discrimination. Conclusion: There is not much evidence for the use of markers to diagnose AHF in acutely dyspneic COPD patients in the hospital setting. BNPs seem most promising, but should be interpreted alongside imaging and clinical signs, as this may lead to improved diagnostic accuracy. Future validation studies are urgently needed before any AHF marker can be incorporated into treatment decision-making algorithms for patients with COPD. Protocol Registration: CRD42022283952.
{"title":"Lack of Evidence Regarding Markers Identifying Acute Heart Failure in Patients with COPD: An AI-Supported Systematic Review","authors":"Sanne HB van Dijk, Marjolein GJ Brusse-Keizer, Charlotte C Bucsán, Eline H Ploumen, Wendy JC van Beurden, Job van der Palen, Carine JM Doggen, Anke Lenferink","doi":"10.2147/copd.s437899","DOIUrl":"https://doi.org/10.2147/copd.s437899","url":null,"abstract":"<strong>Background:</strong> Due to shared symptoms, acute heart failure (AHF) is difficult to differentiate from an acute exacerbation of COPD (AECOPD). This systematic review aimed to identify markers that can diagnose AHF underlying acute dyspnea in patients with COPD presenting at the hospital.<br/><strong>Methods:</strong> All types of observational studies and clinical trials that investigated any marker’s ability to diagnose AHF in acutely dyspneic COPD patients were considered eligible for inclusion. An AI tool (ASReview) supported the title and abstract screening of the articles obtained from PubMed, Scopus, Web of Science, the Cochrane Library, Embase, and CINAHL until April 2023. Full text screening was independently performed by two reviewers. Twenty percent of the data extraction was checked by a second reviewer and the risk of bias was assessed in duplicate using the QUADAS-2 tool. Markers’ discriminative abilities were evaluated in terms of sensitivity, specificity, positive and negative predictive values, and the area under the curve when available.<br/><strong>Results:</strong> The search identified 10,366 articles. After deduplication, title and abstract screening was performed on 5,386 articles, leaving 153 relevant, of which 82 could be screened full text. Ten distinct studies (reported in 16 articles) were included, of which 9 had a high risk of bias. Overall, these studies evaluated 12 distinct laboratory and 7 non-laboratory markers. BNP, NT-proBNP, MR-proANP, and inspiratory inferior vena cava diameter showed the highest diagnostic discrimination.<br/><strong>Conclusion:</strong> There is not much evidence for the use of markers to diagnose AHF in acutely dyspneic COPD patients in the hospital setting. BNPs seem most promising, but should be interpreted alongside imaging and clinical signs, as this may lead to improved diagnostic accuracy. Future validation studies are urgently needed before any AHF marker can be incorporated into treatment decision-making algorithms for patients with COPD.<br/><strong>Protocol Registration:</strong> CRD42022283952.<br/><br/>","PeriodicalId":13792,"journal":{"name":"International Journal of Chronic Obstructive Pulmonary Disease","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139948684","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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