Risk Of COPD Research Articles

Relationships between oxidative balance score and asthma, COPD, with asthma-COPD overlap in American adults: Findings from NHANES 2013-2018

Background Oxidative stress plays a crucial role in the development of multiple chronic respiratory diseases. Oxidative Balance Score (OBS) composing of 16 dietary factors and 4 lifestyle factors has been developed to evaluate the effect of oxidants/antioxidants produced by dietary intake and lifestyle habits on the overall oxidative balance. However, the relationships between OBS with asthma, COPD, and asthma-COPD overlap (ACO) are still unclear. Methods A total of 10,942 adults aged 20 years and older from the 2013-2018 National Health and Nutrition Examination Survey were included in the analyses. ANOVA and chi-square tests were used to compare characteristics between different OBS subgroups.Multiple multivariate logistic regression was used to analyze the associations between OBS and asthma, COPD, and ACO.RCS curves were used to describe the dose-response effect of the associations. Subgroup analyses and interaction effects were employed to reflect the stability of the associations. Results In the fully adjusted models, OBS was found to be negatively associated with asthma, COPD, and ACO. OBS at Q2, Q3, and Q4 (OR: 0.66, 95% CI: 0.46-0.97) were negatively associated with the risk of asthma. OBS at Q2 and Q4 were negatively associated with the risk of COPD. OBS at Q2 and Q4 were negatively associated with the risk of ACO. The RCS curves reflected the negative dose-response trend of association. Moreover, the associations were stable in various subgroups. Conclusion The negative associations between OBS and asthma, COPD, and ACO were found in American adults, providing evidence for dietary and lifestyle prevention.

The association between non-high-density lipoprotein cholesterol to high-density lipoprotein cholesterol ratio and chronic obstructive pulmonary disease: the mediating role of dietary inflammatory index.

Numerous studies have indicated a potential correlation between COPD, lipid metabolism, and dietary inflammation. However, the exact mechanisms by which dietary inflammation regulates the pathological processes of COPD related to lipid metabolism remain unclear. NHHR is a novel composite index of atherosclerotic lipid profiles, while the Dietary Inflammatory Index (DII) measures diet-induced inflammation. This study explores the relationship between NHHR and COPD and evaluates whether DII mediates this association. We employed multivariable logistic regression, smooth curve fitting, threshold effect analysis, and subgroup analysis to explore the relationship between NHHR and the incidence of COPD. Additionally, we conducted a mediation analysis to explore the potential relationship between dietary inflammatory index (DII) levels and the relationship between NHHR and COPD. This analysis encompassed 13,452 participants, with 2,332 reporting incidents of COPD. Following adjustment for all covariates using multivariable logistic regression, each unit increase in NHHR level and DII level was associated with a 10% (OR = 1.10, 95% CI: 1.05, 1.16) and 8% (OR = 1.08, 95% CI: 1.04, 1.13) increase, respectively, in the incidence rate of COPD. Furthermore, compared to the lowest quartile, the highest quartile of NHHR level and DII level was associated with a 47% (p < 0.001) and 50% (p < 0.001) increase, respectively, in the incidence rate of COPD. Smooth curve fitting and threshold effect analysis revealed a nonlinear relationship between NHHR and the risk of COPD, with a breakpoint at 2.60. Mediation analysis indicated that DII mediated 7.24% of the association between NHHR and COPD (p = 0.004). Higher NHHR levels are associated with an increased prevalence of COPD. Moreover, this association is mediated by DII, suggesting that an anti-inflammatory diet may be beneficial.

Low smoking exposure and development and prognosis of COPD over four decades: a population-based cohort study.

A diagnosis of COPD is mainly considered in individuals with >10 pack-years of smoking. We tested the hypothesis that low smoking exposure, below the critical threshold of 10 pack-years, increases risk of COPD and leads to poor prognosis. We followed non-obstructed adult smokers from the Copenhagen City Heart Study for COPD, defined as a forced expiratory volume in 1 s (FEV1)/forced vital capacity <0.70 and FEV1 <80% predicted, and for related clinical outcomes. First, we followed individuals for 5 years according to baseline smoking for risk of developing COPD, and thereafter for up to four decades for severe exacerbations and death. In 6098 non-obstructed smokers, 1781 (29%) developed COPD after 5 years of follow-up: 23% of individuals with <10 pack-years of smoking at baseline, 26% of those with 10-19.9 pack-years, 30% of those with 20-39.9 pack-years and 39% of those with ≥40 pack-years. During four decades of follow-up, we recorded 620 exacerbations and 5573 deaths. Compared to individuals without COPD with <10 pack‑years of smoking, multivariable adjusted hazard ratios (HRs) for exacerbations were 1.94 (95% CI 1.36-2.76) in those without COPD and ≥10 pack-years, 2.83 (95% CI 1.72-4.66) in those with COPD and <10 pack-years, 4.34 (95% CI 2.93-6.43) in those with COPD and 10-19.9 pack-years, 4.39 (95% CI 2.98-6.46) in those with COPD and 20-39.9 pack-years and 4.98 (95% CI 3.11-7.97) in those with COPD and ≥40 pack-years. Corresponding HRs for all-cause mortality were 1.20 (95% CI 1.10-1.32), 1.31 (95% CI 1.13-1.53), 1.59 (95% CI 1.40-1.79), 1.81 (95% CI 1.62-2.03) and 1.81 (95% CI 1.55-2.10). Low smoking exposure below the critical threshold of 10 pack-years increases risk of COPD in middle-aged adults within 5 years, and these individuals have increased risk of severe exacerbation and early death over four decades.

Associations of dietary inflammation index and composite dietary antioxidant index with preserved ratio impaired spirometry in US adults and the mediating roles of triglyceride-glucose index: NHANES 2007–2012

BackgroundPrevious studies have shown that inflammatory and antioxidant dietary patterns can modify the risk of COPD, yet few studies have examined the association of these diets with its early signs (PRISm), and the potential role of metabolic disorders remains to be elucidated. MethodsData from 9529 individuals who participated in the 2007–2012 National Health and Nutrition Examination Survey (NHANES) were analyzed. The Dietary Inflammation Index (DII) and the Dietary Antioxidant Composite Index (CDAI) were assessed using 24-h dietary recall, multiple metabolic indicators were calculated according to biochemical markers, and lung function parameters defined PRISm cases. Individual and joint effects of DII and CDAI were evaluated by generalized linear models and binary logistic regression models, and mediation effects of metabolic indicators were further explored by causal mediation analysis. ResultsIncreased DII was associated with decreased lung function (FEV1: β = −18.82, FVC: β = −29.2; OR = 1.04) and increased metabolic indicators (β = 0.316, 0.036, 0.916, 0.033, and 0.145 on MAP, UA, TC, TyG, and MS, respectively). Contrary to this, CDAI were positively and negatively associated with lung function (FEV1: β = 3.42; FVC: β = 4.91; PRISm: OR = 0.99) and metabolic indicators (β < 0), respectively. Joint effects of DII and CDAI indicated the minimal hazard effects of DII on TyG (β = −0.11), FEV1 (β = 72.62), FVC (β = 122.27), and PRISm (OR = 0.79) in subjects with high CDAI when compared with those with low CDAI (low DII + high CDAI vs. high DII + low CDAI). Furthermore, TyG mediated 13.74 %, 8.29 %, and 21.70 % of DII- and 37.30 %, 20.90 %, and 12.32 % of CDAI-FEV1, -FVC, and -PRISm associations, respectively. ConclusionsThese findings indicated that CDAI can attenuate the adverse effects of DII on metabolic disorders and lung function decline, which provides new insight for diet modification in preventing early lung dysfunction.

Genetic variations in the antioxidant genes and their role in modulating susceptibility towards chronic obstructive pulmonary disease in the North Indian population

BackgroundChronic Obstructive Pulmonary Disease (COPD) is a persistent inflammatory lung condition characterized by an obstruction in removing oxygen from the lungs. Oxidant and antioxidant imbalance have long been hallmarks of COPD development, where the amount of antioxidants produced is less than that of oxidants. Here, polymorphism in the antioxidant enzymes like Catalase, Superoxide dismutase and Glutathione peroxidase plays an essential role in regulating the levels of oxidants. Methods1000 subjects, including 500 COPD cases and 500 controls, have been recruited and genotyped to assess the correlation between COPD and the particular SNPS of antioxidant genes. Logistic regression was used to compute odds ratios (ORs) and 95 % confidence intervals (CIs) to assess the association between SNPs and COPD risk. The relationship between spirometry value and COPD for all SNPs has been analyzed using Kruskal Wallis's. Haplotype analysis has also been performed. The effect of SNP interactions on COPD risk was assessed through the Multifactor Dimensionality Reduction (MDR) approach, a nonparametric test for overcoming some of the limitations of the logistic regression for detecting and characterizing SNP interactions. ResultsOur findings indicated a strong association between COPD and the variations in the CAT rs7943316 (OR = 0.61, Pc = 0.0001), SOD2 rs4880 (OR = 2.07, Pc = 0.0006), and GPx rs1050450 (OR = 0.60, Pc = 0.0018). Furthermore, SOD2 rs4880 was associated with forced vital capacity (FVC) and forced expiratory volume in 1 s (FEV1) of COPD patients. Our study found that the triple combination of SOD1 (rs2234694), SOD1 (rs36232792) and SOD2 (rs4880) was found to be elevating the risk of COPD (OR = 2.83, Pc = 0.006). SOD2 rs4880 and GPx rs1050450 are also linked to cough and mucus production. The Haplotype study reveals a substantial relationship between CAT (rs7943316 and rs1001179) and SOD (rs2234694 and rs4880), which increases the risk of COPD. The three-locus model (CAT rs794331, CAT rs1101179, and GPx rs1050450) was the most effective for COPD risk assessment based on the MDR findings, which were statistically significant (p < 0.0001). ConclusionThis study shows that rs7943316, rs4880, and rs1050450 are associated with the risk of COPD in the north Indian population and have the potential to enhance our knowledge of COPD at the molecular level, which in turn might pave the way for earlier detection, treatment, and preventive efforts.

Association between nutrition-related indicators with the risk of chronic obstructive pulmonary disease and all-cause mortality in the elderly population: evidence from NHANES.

This study aims to use six nutrition-related indicators to assess the relationship between nutritional status and the risk of COPD as well as the all-cause mortality rate, and to determine the most reliable predictive indicators. Data from the National Health and Nutrition Examination Survey (NHANES) spanning the years 2013 to 2018 were extracted. Nutritional status was evaluated using Controlling nutritional status (CONUT) score, Geriatric Nutritional Risk Index (GNRI), Advanced Lung Cancer Inflammation Index (ALI), Prognostic Nutritional Index (PNI), Triglycerides (TG) × Total Cholesterol (TC) × Body Weight (BW) Index (TCBI), and Albumin-to-Globulin Ratio (AGR) nutritional-related indicators. Multivariate weighted logistic and Cox regression models were employed to assess the correlation between the six nutritional-related indicators and the risk of COPD and as all-cause mortality. The restricted cubic spline tests were applied to explore potential nonlinear relationships, and ROC curves and C-index analyses were conducted to compare the predictive capabilities of different indicators. Stratified analysis and propensity score matching (PSM) to assess the robustness of the results. In this study, Lower ALI, lower GNRI, and higher CONUT scores were positively correlated with an increased risk of COPD (OR: 1.77, 95% CI: 1.10-2.84) (OR: 8.66, 95% CI: 2.95-25.5), and (OR: 5.11, 95% CI: 1.72-15.2), respectively. It was found that ALI and GNRI had a non-linear relationship with the risk of COPD. After propensity score matching (PSM), the associations between ALI, GNRI, CONUT scores, and COPD remained consistent. Lower ALI, PNI, and GNRI scores were positively associated with all-cause mortality in COPD patients (HR: 2.41, 95% CI: 1.10-5.27), (HR: 3.76, 95% CI: 1.89-7.48), and (HR: 4.55, 95% CI: 1.30-15.9), respectively, with GNRI displaying a non-linear relationship with all-cause mortality. ROC curve and C-index analyses indicated that ALI had the best predictive ability for both COPD risk and all-cause mortality. ALI, GNRI, and CONUT scores are correlated with the risk of COPD, while ALI, PNI, and GNRI scores are associated with all-cause mortality in COPD patients. Compared to other nutritional scores, ALI may provide more effective predictive value for both risk and all-cause mortality.

Dissecting causal relationships between immune cells, plasma metabolites, and COPD: a mediating Mendelian randomization study.

This study employed Mendelian Randomization (MR) to investigate the causal relationships among immune cells, COPD, and potential metabolic mediators. Utilizing summary data from genome-wide association studies, we analyzed 731 immune cell phenotypes, 1,400 plasma metabolites, and COPD. Bidirectional MR analysis was conducted to explore the causal links between immune cells and COPD, complemented by two-step mediation analysis and multivariable MR to identify potential mediating metabolites. Causal relationships were identified between 41 immune cell phenotypes and COPD, with 6 exhibiting reverse causality. Additionally, 21 metabolites were causally related to COPD. Through two-step MR and multivariable MR analyses, 8 cell phenotypes were found to have causal relationships with COPD mediated by 8 plasma metabolites (including one unidentified), with 1-methylnicotinamide levels showing the highest mediation proportion at 26.4%. We have identified causal relationships between 8 immune cell phenotypes and COPD, mediated by 8 metabolites. These findings contribute to the screening of individuals at high risk for COPD and offer insights into early prevention and the precocious diagnosis of Pre-COPD.

Clinical guideline highlights for the hospitalist: GOLD COPD update 2024.

Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease (2024 Report) RELEASE DATE: December 4, 2023 PRIOR VERSIONS: Initial report was released in 2001 with major revisions in 2006, 2011, 2017, and 2023. This 2024 release is an update to the 2023 major revision DEVELOPER: Global Initiative for Chronic Obstructive Lung Disease (GOLD) FUNDING SOURCE: GOLD TARGET POPULATION: Adults with a diagnosis of or at risk for COPD.

The Impact of Malnutrition on the Developing Lung and Long-Term Lung Health: A Narrative Review of Global Literature.

Worldwide, over 2 billion children under the age of 5 experience stunting, wasting, or are underweight. Malnutrition contributes to 45% of all deaths in this age group (approximately 3.1 million deaths) [1]. Poverty, food insecurity, suboptimal feeding practices, climate change, and conflict are all contributing factors. Malnutrition causes significant respiratory problems, including increased risk of respiratory infections, impaired lung function, and increased risk of subsequent adult respiratory disease, including asthma, COPD, and lung cancer. Childhood malnutrition not only has serious consequences for children's health but it also has numerous consequences on wellbeing and educational attainment. Childhood malnutrition is a complex and multifaceted problem. However, by understanding and addressing the underlying causes, and investing in prevention and treatment programs, it is possible to maximize children's health and wellbeing on a global scale. This narrative review will focus on the impact of childhood malnutrition on lung development, the consequent respiratory disease, and what actions can be taken to reduce the burden of malnutrition on lung health.

Statins did not reduce the frequency of exacerbations in individuals with COPD and cardiovascular comorbidities in the COSYCONET cohort

BackgroundThe evidence regarding effects of statins on exacerbation risk in COPD remains controversial. Previous studies often excluded patients with cardiovascular comorbidities despite their high prevalence in COPD and role for exacerbations. Based on the cardioprotective properties of statins, we hypothesised that statins may reduce the risk of exacerbations especially in patients with cardiovascular comorbidities.MethodsOne thousand eight hundred eighty seven patients of the German COPD cohort COSYCONET (COPD and Systemic Consequences Comorbidities Network) of GOLD grades 1–4 (37.8% female, mean age 64.78 ± 8.3) were examined at baseline and over a period of 4.5 years for the occurrence of at least one exacerbation or severe exacerbation per year in cross-sectional and longitudinal analyses adjusted for age, gender, BMI, GOLD grade and pack-years. Due to their collinearity, various cardiovascular diseases were tested in separate analyses, whereby the potential effect of statins in the presence of a specific comorbidity was tested as interaction between statins and comorbidity. We also identified patients who never took statins, always took statins, or initiated statin intake during the follow-up.ResultsOne thousand three hundred six patients never took statins, 31.6% were statin user, and 12.9% initiated statins during the follow-up. Most cardiovascular diseases were significantly (p < 0.05)may associated with an increased risk of COPD exacerbations, but in none of them the intake of statins was a significant attenuating factor, neither overall nor in modulating the increased risk linked to the specific comorbidities. The results of the cross-sectional and longitudinal analyses were consistent with each other, also those regarding at least 1 exacerbation or at least 1 severe exacerbation per year.ConclusionThese findings complement the existing literature and may suggest that even in patients with COPD, cardiovascular comorbidities and a statin therapy that targets these comorbidities, the effects of statins on exacerbation risk are either negligible or more subtle than a reduction in exacerbation frequency.Trial registrationTrial registration ClinicalTrials.gov, Identifier: NCT01245933.Other Study ID (BMBF grant): 01GI0881, registered 18 November 2010, study start 2010–11, primary completion 2013–12, study completion 2023–09.https://clinicaltrials.gov/study/NCT01245933?cond=COPD&term=COSYCONET&rank=3

Atmosphere particulate matter and respiratory diseases during COVID-19 in Korea

We aimed to examine the impact of COVID-19 non-pharmaceutical interventions (NPIs) on the relationship between air pollutants and hospital admissions for respiratory and non-respiratory diseases in six metropolitan cities in South Korea. This study compared the associations between particulate matter (PM10 and PM2.5) and hospital admission for respiratory and non-respiratory diseases before (2016–2019) and during (2020) the implementation of COVID-19 NPIs by using distributed lag non-linear models. In the Pre-COVID-19 period, the association between PM10 and admission risk for asthma and COPD showed an inverted U-shaped pattern. For PM2.5, S-shaped and inverted U-shaped changes were observed in asthma and COPD, respectively. Extremely high and low levels of PM10 and extremely low levels of PM2.5 significantly decreased the risk of admission for asthma and COPD. In the Post-COVID-19 outbreak period, the overall cumulative relationship between PM10 and PM2.5 and respiratory diseases and the effects of extreme levels of PM10 and PM2.5 on respiratory diseases were completely changed. For non-respiratory diseases, PM10 and PM2.5 were statistically insignificant for admission risk during both periods. Our study may provide evidence that implementing NPIs and reducing PM10 and PM2.5 exposure during the COVID-19 pandemic has contributed to reducing hospital admissions for environment-based respiratory diseases.

Breathing new life into the study of COPD with genes identified from genome-wide association studies.

COPD is a major cause of morbidity and mortality globally. While the significance of environmental exposures in disease pathogenesis is well established, the functional contribution of genetic factors has only in recent years drawn attention. Notably, many genes associated with COPD risk are also linked with lung function. Because reduced lung function precedes COPD onset, this association is consistent with the possibility that derangements leading to COPD could arise during lung development. In this review, we summarise the role of leading genes (HHIP, FAM13A, DSP, AGER and TGFB2) identified by genome-wide association studies in lung development and COPD. Because many COPD genome-wide association study genes are enriched in lung epithelial cells, we focus on the role of these genes in the lung epithelium in development, homeostasis and injury.

Risk of chronic obstructive pulmonary disease in a large cohort of Ontario, Canada workers

Although several occupational exposures have been linked to the risk of COPD; limited data exists on sex-specific differences. This study aimed to identify at-risk occupations and sex differences for COPD risk. Cases were identified in a large surveillance system established through the linkage of former compensation claimants’ data (non-COPD claims) to physician visits, ambulatory care data, and hospital inpatient data (1983–2020). Cox proportional hazard models were used to estimate hazard ratios (HRs) and corresponding 95% confidence intervals (CI) for occupation groups (occupation at time of claim), stratified by sex. HRs were indirectly adjusted for cigarette smoking using another population dataset. A total of 29,445 male and 14,693 female incident cases of COPD were identified. Increased risks were observed in both sexes for construction (HRmale 1.15, 95% CI 1.12–1.19; HRfemale 1.54, 95% CI 1.29–1.83) transport/equipment operating (HRmale 1.32, 95% CI 1.28–1.37; HRfemale 1.53, 95% CI 1.40–1.68) farming (HRmale 1.23, 95% CI 1.15–1.32; HRfemale 1.19, 95% CI 1.04–1.37) and janitors/cleaners (HRmale 1.31, 95% CI 1.24–1.37; HRfemale 1.40, 95% CI 1.31–1.49). Increased risks were observed for females employed as chefs and cooks (HR 1.44, 95% CI 1.31–1.58), bartenders (HR 1.38, 95% CI 1.05–1.81), and those working in food/beverage preparation (HR 1.34, 95% CI 1.24–1.45) among other occupations. This study demonstrates elevated risk of COPD among both male and female workers potentially exposed to vapours, gases, dusts, and fumes, highlighting the need for occupational surveillance of COPD.

Robust positive association between serum urate and the risk of chronic obstructive pulmonary disease: hospital-based cohort and Mendelian randomisation study

BackgroundChronic obstructive pulmonary disease (COPD) and hyperuricaemia are both characterised by systemic inflammation. Preventing chronic diseases among the population with common metabolic abnormality is an effective strategy. However, the association...

Unraveling the causality between chronic obstructive pulmonary disease and its common comorbidities using bidirectional Mendelian randomization

BackgroundChronic obstructive pulmonary disease (COPD) frequently coexists with various diseases, yet the causal relationship between COPD and these comorbidities remains ambiguous. As a result, the aim of our study is to elucidate the potential causality between COPD and its common comorbidities.MethodsWe employed the Mendelian randomization (MR) method to analyze single nucleotide polymorphism (SNP) data of common comorbidities with COPD from FinnGen and Integrative Epidemiology Unit (IEU) databases. Causality was primarily assessed using the inverse variance weighting (IVW) method. Multivariable Mendelian randomization (MVMR) analysis was also conducted to eliminate the interference of smoking-related phenotypes. Sensitivity analysis was conducted to ensure the reliability of our findings.ResultsPreliminary univariable MR revealed an increased risk of lung squamous cell carcinoma (LUSC) (IVW: OR = 1.757, 95% CI = 1.162–2.657, P = 0.008), chronic kidney disease (CKD) (IVW: OR = 1.193, 95% CI = 1.072–1.326, P < 0.001), chronic periodontitis (IVW: OR = 1.213, 95% CI = 1.038–1.417, P = 0.012), and heart failure (HF) (IVW: OR = 1.127, 95% CI = 1.043–1.218, P = 0.002). Additionally, the reverse MR analysis indicated that genetic susceptibility to HF (IVW: OR = 1.272, 95% CI = 1.084–1.493, P = 0.003), obesity (IVW: OR = 1.128, 95% CI = 1.056–1.205, P < 0.001), depression (IVW: OR = 1.491, 95% CI = 1.257–1.770, P < 0.001), and sleep apnea syndrome (IVW: OR = 1.209, 95% CI = 1.087–1.345, P < 0.001) could raise the risk of COPD. The MVMR analysis showed no causal effect of COPD on susceptibility to chronic periodontitis after adjusting for smoking.ConclusionsOur study identified that COPD may elevate the risk of LUSC, HF, and CKD. Additionally, our analysis revealed that HF, sleep apnea symptoms, depression, and obesity might also increase the susceptibility to COPD. These findings revealed a potential causal relationship between COPD and several prevalent comorbidities, which may provide new insights for disease early prediction and prevention.

Estimating the health impact of nicotine exposure by dissecting the effects of nicotine versus non-nicotine constituents of tobacco smoke: A multivariable Mendelian randomisation study.

The detrimental health effects of smoking are well-known, but the impact of regular nicotine use without exposure to the other constituents of tobacco is less clear. Given the increasing daily use of alternative nicotine delivery systems, such as e-cigarettes, it is increasingly important to understand and separate the effects of nicotine use from the impact of tobacco smoke exposure. Using a multivariable Mendelian randomisation framework, we explored the direct effects of nicotine compared with the non-nicotine constituents of tobacco smoke on health outcomes (lung cancer, chronic obstructive pulmonary disease [COPD], forced expiratory volume in one second [FEV-1], forced vital capacity [FVC], coronary heart disease [CHD], and heart rate [HR]). We used Genome-Wide Association Study (GWAS) summary statistics from Buchwald and colleagues, the GWAS and Sequencing Consortium of Alcohol and Nicotine, the International Lung Cancer Consortium, and UK Biobank. Increased nicotine metabolism increased the risk of COPD, lung cancer, and lung function in the univariable analysis. However, when accounting for smoking heaviness in the multivariable analysis, we found that increased nicotine metabolite ratio (indicative of decreased nicotine exposure per cigarette smoked) decreases heart rate (b = -0.30, 95% CI -0.50 to -0.10) and lung function (b = -33.33, 95% CI -41.76 to -24.90). There was no clear evidence of an effect on the remaining outcomes. The results suggest that these smoking-related outcomes are not due to nicotine exposure but are caused by the other components of tobacco smoke; however, there are multiple potential sources of bias, and the results should be triangulated using evidence from a range of methodologies.

COPD Assessment Test and risk of readmission in patients with bronchiectasis: a prospective cohort study.

Readmission following bronchiectasis exacerbation is a common and challenging clinical problem and few simple predictive tools exist. The COPD Assessment Test (CAT) is an easy-to-use questionnaire. This study aims to evaluate the predictive value of CAT scores in determining the risk of readmission in patients with bronchiectasis exacerbation. We conducted a prospective cohort study in 106 bronchiectasis patients admitted with exacerbation. All patients completed the CAT at admission and at discharge. Patients were followed-up for 12 months to collect data on readmission. The area under the curve was used to measure the predictive value of CAT at admission, CAT at discharge and change in CAT for readmission due to bronchiectasis exacerbation. 46 patients were readmitted for bronchiectasis exacerbation within 12 months. High CAT at admission was an independent risk factor for readmission within 12 months in patients with acute exacerbation of bronchiectasis (hazard ratio 3.201, 95% CI 1.065-9.624; p<0.038) after adjustment for confounding variables. The cut-off value of CAT at admission and CAT at discharge to predict 12-month readmission in patients with acute exacerbation of bronchiectasis was 23.5 (sensitivity 62.2%, specificity 83.6%) and 15.5 (sensitivity 52.2%, specificity 87.0%). CAT at admission is a strong predictor of readmission in patients with bronchiectasis exacerbation.

Association Between Serum Klotho and Chronic Obstructive Pulmonary Disease in US Middle-Aged and Older Individuals: A Cross-Sectional Study from NHANES 2013-2016.

This study sought to examine the potential association between serum Klotho levels and the prevalence of COPD in the United States. 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. 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. 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.

ERJ Podcast February 2024: Beetroot juice and cardiovascular risk in COPD.

ERJ Podcast February 2024: Beetroot juice and cardiovascular risk in COPD.

Effect of twice daily inhaled albuterol on cardiopulmonary exercise outcomes, dynamic hyperinflation, and symptoms in secondhand tobacco-exposed persons with preserved spirometry and air trapping: a randomized controlled trial

BackgroundIn tobacco-exposed persons with preserved spirometry (active smoking or secondhand smoke [SHS] exposure), air trapping can identify a subset with worse symptoms and exercise capacity. The physiologic nature of air trapping in the absence of spirometric airflow obstruction remains unclear. The aim of this study was to examine the underlying pathophysiology of air trapping in the context of preserved spirometry and to determine the utility of bronchodilators in SHS tobacco-exposed persons with preserved spirometry and air trapping.MethodsWe performed a double-blinded placebo-controlled crossover randomized clinical trial in nonsmoking individuals at risk for COPD due to exposure to occupational SHS who had preserved spirometry and air trapping defined as either a residual volume-to-total lung capacity ratio (RV/TLC) > 0.35 or presence of expiratory flow limitation (EFL, overlap of tidal breathing on maximum expiratory flow-volume loop) on spirometry at rest or during cardiopulmonary exercise testing (CPET). Those with asthma or obesity were excluded. Participants underwent CPET at baseline and after 4-week trials of twice daily inhalation of 180 mcg of albuterol or placebo separated by a 2-week washout period. The primary outcome was peak oxygen consumption (VO2) on CPET. Data was analyzed by both intention-to-treat and per-protocol based on adherence to treatment prescribed.ResultsOverall, 42 participants completed the entire study (66 ± 8 years old, 91% female; forced expiratory volume in 1 s [FEV1] = 103 ± 16% predicted; FEV1 to forced vital capacity [FVC] ratio = 0.75 ± 0.05; RV/TLC = 0.39 ± 0.07; 85.7% with EFL). Adherence was high with 87% and 93% of prescribed doses taken in the treatment and placebo arms of the study, respectively (P = 0.349 for comparison between the two arms). There was no significant improvement in the primary or secondary outcomes by intention-to-treat or per-protocol analysis. In per-protocol subgroup analysis of those with RV/TLC > 0.35 and ≥ 90% adherence (n = 27), albuterol caused an improvement in peak VO2 (parameter estimate [95% confidence interval] = 0.108 [0.014, 0.202]; P = 0.037), tidal volume, minute ventilation, dynamic hyperinflation, and oxygen-pulse (all P < 0.05), but no change in symptoms or physical activity.ConclusionsAlbuterol may improve exercise capacity in the subgroup of SHS tobacco-exposed persons with preserved spirometry and substantial air trapping. These findings suggest that air trapping in pre-COPD may be related to small airway disease that is not considered significant by spirometric indices of airflow obstruction.