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Background: Chronic obstructive pulmonary disease (COPD) is characterized by progressive airflow obstruction and destruction of lung tissue, primarily attributed to tobacco smoking. However, other factors like biomass-burning smoke (BS) exposure are also implicated. COPD has been described as an accelerated aging disease, and telomere length is a biomarker of aging. Methods: This study examined telomere length in 189 Mexican individuals, from which 93 developed COPD secondary to BS exposure (BE-COPD); the rest of the participants were exposed to BS but did not develop the disease. Lung function parameters were measured by spirometry, and relative telomere length (rTL) from peripheral blood DNA was determined using multiplex qPCR. Results: Results showed rTL to inversely correlate with age (R2=-0.207, p = 0.006) and with the hours-a-day of BS exposure (R2=-0.297, p < 0.001). Within BE-COPD cases, rTL was associated with daily BS exposure, and BE-COPD individuals exhibited a reduced rTL compared to controls (1.39 ± 0.45 vs. 0.89 ± 0.50; p < 0.001). When compared by rTL length in BE-COPD cases, longer telomeres were associated with decreased COPD risk (β = 0.134, 95% CI = 0.053–0.339; p < 0.001). However, no significant relationship was found between rTL and clinical or lung function parameters in the BE-COPD group. Conclusions: This is the first study to document that individuals with COPD secondary to biomass smoke exposure present shorter telomeres than BS-exposed subjects who did not develop the disease. [ABSTRACT FROM AUTHOR]

Background: Chronic obstructive pulmonary disease (COPD) is a chronic respiratory condition characterized by high morbidity and mortality rates. This study aims to assess the clinical outcomes of COPD patients after implementing an algorithm within the MyTatva app. Methods: The study involved a sample of 10 COPD patients, evaluating key parameters such as Forced Expiratory Volume in 1 s (FEV1), Forced Vital Capacity, Weight, Body Mass Index (BMI), Fat-Free Mass Index, and Distance Covered during the 6-Minute Walk Test (6MWT) before and after the algorithm's implementation in the MyTatva app. Patient satisfaction was assessed through a CSAT survey. Results: Following the implementation of the MyTatva care plan, significant improvements were observed in several key clinical outcomes for COPD patients. FEV1 increased from a median of 3.24–2.0 L (p = 0.0379), while weight and BMI decreased significantly, with a reduction in weight from a median of 86–70 kg (p = 0.0007) and a corresponding decrease in BMI from 28.43 to 24 kg/m2 (p = 0.0031). The distance covered during the 6MWT also improved from 420 to 568 m (p = 0.0019). The participation of 10 COPD patients in surveys yielded an overall CSAT score of 85%, indicating a high level of satisfaction with the MyTatva app. Conclusion: The comprehensive features and functionalities of the MyTatva app, combined with the personalized care plan and real-time feedback mechanisms, have led to substantial clinical improvements in COPD management. These findings highlight the promise of this innovative digital therapeutic approach in addressing chronic respiratory conditions. [ABSTRACT FROM AUTHOR]

Coughing is a symptom of many respiratory diseases. An increased amount of coughs may signal an (upcoming) health issue, while a decreasing amount of coughs may indicate an improved health status. The presence of a cough can be identified by a cough classifier. The cough density fluctuates considerably over the course of a day with a pattern that is highly subject-dependent. This paper provides a case study of cough patterns from Chronic Obstructive Pulmonary Disease (COPD) patients as determined by a stationary semi-automated cough monitor. It clearly demonstrates the variability of cough density over the observation time, its patient specificity and dependence on health status. Furthermore, an earlier established empirical finding of a linear relation between mean and standard deviation of a session's cough count is validated. An alert mechanism incorporating these findings is described. [ABSTRACT FROM AUTHOR]

Chronic obstructive pulmonary disease (COPD) exacerbations are major contributors to morbidity and mortality, highlighting the need to better understand their molecular mechanisms to improve prevention, diagnosis, and treatment. This study investigated differential gene expression profiles and key biological processes in COPD exacerbations categorized based on sputum microbiome profiling. An observational study was performed on a cohort of 16 COPD patients, who provided blood and sputum samples during exacerbations, along with five stable-state samples as controls. Exacerbations were classified using 16S rRNA sequencing to analyze the sputum microbiota and multiplex PCR to detect respiratory viruses. Blood transcriptomic profiling was conducted using Oxford Nanopore technology, followed by differential gene expression and pathway enrichment analyses. A total of 768 regulated genes were identified across the exacerbation groups, with 35 shared genes associated with neutrophil activation. Bacterial exacerbations activated pathways related to phagocytosis and toll-like receptor signaling, while viral exacerbations were linked to pro-inflammatory responses and mitochondrial damage. Exacerbations of unknown origin showed activation of pathways involved in protozoan defense and neutrophilic asthma. Biomarkers such as IFITM3 and ISG15 for bacterial exacerbations, DEFA3 for viral, and CD47 for unknown-origin exacerbations were identified. These findings highlight distinct transcriptomic profiles and biological pathways in COPD exacerbations, emphasizing the central role of neutrophil-driven inflammation and identifying potential biomarkers for improved differential diagnosis and personalized management. [ABSTRACT FROM AUTHOR]

Introduction: In response to the SARS-CoV-2 pandemic in March 2020 and required adherence to infection control measures and patient and staff safety, an integrated respiratory team (IRT) developed guideline-based templates to support the team in teleconsultation reviews of their patients. Patients had been diagnosed with sleep disordered breathing, chronic obstructive pulmonary disease, asthma, interstitial lung disease or had oxygen assessment needs. Methods: Nine IRT members collaboratively developed content for the templates to assist in clinical reviews. In February 2023 semi-structured interviews were conducted and recorded with eight of the IRT members using Microsoft Teams, then thematically analysed. Results: Qualitative analysis revealed 13 themes. The templates were considered time-saving and advantageous in teleconsultation reviews. They supported evidence-based, structured, and consistent reviews. They were felt to uphold patient safety, supporting knowledge and skills. IRT members reported the templates had no adverse effects on autonomy, patient-professional relationships or person-centred care. They facilitated good multidisciplinary team working and communication. One interviewee reported that the templates supported the Nursing and Midwifery Council Code. Conclusion: The templates continue to be used across the regional service by the IRT. Their benefit has been realised beyond the pandemic. Refinements will be made as guidelines are updated. The development of these innovative templates may be of interest and value to other respiratory teams. [ABSTRACT FROM AUTHOR]

Background: Chronic obstructive pulmonary disease (COPD) and asthma are the two most prevalent chronic respiratory diseases, significantly impacting public health. Utilizing clinical questionnaires to identify and differentiate patients with COPD and asthma for further diagnostic procedures has emerged as an effective strategy to address this issue. We developed a new diagnostic tool, the COPD-Asthma Differentiation Questionnaire (CAD-Q), to differentiate between COPD and asthma in adults. Methods: A cross-sectional study with diagnostic test analysis was done. Relevant clinical variables for diagnosing COPD and asthma were identified through crude Odds Ratios (OR) and a logistic regression model provided adjusted ORs. The CAD-Q, including sensitivity, specificity, predictive values, likelihood ratios, and ROC-curve, was compared to the LFQ, CDQ, PUMA, "Could it be COPD," and COPD-PS questionnaires. Results: 235 (52.9%) patients had COPD and 209 (47.1%) had asthma. A score ≥ 20 on the CAD-Q questionnaire showed a ROC-curve of 70% (95% CI: 65–75; p < 0.001) with a sensitivity of 83.8% (95% CI: 81.1–86.6), specificity of 47.8% (95% CI: 44.1–51.6), positive predictive value of 37.8% (95% CI: 34.2–41.5), negative predictive value of 88.7% (95% CI: 86.3–91), LR + of 1.61 (95% CI: 1.447–1.786), LR − of 0.34 (95% CI: 0.304–0.376) for diagnosing COPD. When comparing CAD-Q with other questionnaires for differentiating COPD and asthma, CAD-Q and CDQ had the highest sensitivity (83.8% and 77.9%). PUMA and "Could it be COPD" had the highest specificity (62.7% and 62.6%). CAD-Q and COPD-PS showed the highest negative predictive values (88.7% and 62.1%). CAD-Q, LFQ, and CDQ had the highest a ROC-curve (70%, 66%, and 66%). Conclusion: The CAD-Q questionnaire effectively discriminated between COPD and asthma, outperforming previous tools. These findings support further research and refinement of diagnostic tools and call for validation in diverse clinical settings. [ABSTRACT FROM AUTHOR]

Background: Despite the increasing body of evidence that mitochondrial activities implicate in chronic obstructive pulmonary disease (COPD), we are still far from a causal-logical and mechanistic understanding of the mitochondrial malfunctions in COPD pathogenesis. Results: Differential expression genes (DEGs) from six publicly available bulk human lung tissue transcriptomic datasets of COPD patients were intersected with the known mitochondria-related genes from MitoCarta3.0 to obtain mitochondria-related DEGs associated with COPD (MitoDEGs). The 32 hub MitoDEGs identified from protein-protein interaction (PPI) networks demonstrated superior overall diagnostic efficacy to non-hub MitoDEGs. Random forest (RF) analysis, least absolute shrinkage and selection operator (LASSO) regression, and Mendelian Randomization (MR) analysis of hub MitoDEGs further nominated NDUFS2, CAT, and MRPL2 as causal MitoDEGs for COPD, whose predominate expressions in pulmonary macrophages were revealed by an independent single-cell transcriptomic dataset of COPD human lungs. Finally, NDUFS2 was evaluated as the top-ranked contributor to COPD in the nomogram model and its downregulation in pulmonary macrophages could result in pro-inflammatory secretion, enhanced intercellular communications, whereas depressed phagocytosis of macrophages as revealed by gene set variation analysis (GSVA) and cell-cell interaction (CCI) analysis of single-cell transcriptomic dataset of COPD human lungs, which was later confirmed in COPD mouse model and macrophage cell lines. Conclusions: Our study established the causal linkage between mitochondrial malfunctions and COPD, providing a potential therapeutic avenue to alleviate pulmonary inflammation accounting for COPD by targeting mitochondria-related genes. NDUFS2, a canonical component of mitochondrial electron respiratory chain, was highlighted instrumental for the susceptibility of risk-exposed individuals to COPD. [ABSTRACT FROM AUTHOR]

Background: The personalized, free-breathing, heart rate-dependent computed tomography angiography (CTA) protocol can significantly reduce the utilization of contrast medium (CM). This proves especially beneficial for patients with chronic obstructive pulmonary disease (COPD) undergoing coronary artery CTA examinations. Objective: The aim of this study was to evaluate the feasibility of a personalized CT scanning protocol that was tailored to patients' heart rate and free-breathing for coronary CTA of patients with COPD. Methods: A total of 400 patients with COPD who need to undergo the coronary CTA were prospectively randomized into two groups (patients with vascular occlusion were excluded). Group A (n = 200) underwent CTA following a traditional protocol (70mL). The timing of the scans in Group B (n = 200) was determined according to the patient's HR and free-breathing (30mL). Results: No difference was found between the two groups in the CT values of RCA, LA, or LCX; (p = 0.131, 0.195 and 0.116). Subjective ratings of image quality (Table 2) were not statistically different between the two groups (p = 0.825). Conclusion: By adopting a heart-rate dependent and free-breathing protocol, the contrast medium volume were reduced in coronary CTA for patients with COPD, while the image quality was remained comparable to those acquired with routine CTA protocol. [ABSTRACT FROM AUTHOR]

Background: Pathobiology of asthma and chronic obstructive pulmonary disease (COPD) is associated with changes among respiratory epithelium structure and function. Increased levels of PM2.5 from urban particulate matter (UPM) are correlated with enlarged rate of asthma and COPD morbidity as well as acute disease exacerbation. It has been suggested that pre-existing pulmonary obstructive diseases predispose epithelium for different biological response than in healthy airways. The aim of this study was to assess the impact of PM2.5 on the biological response of healthy as well as asthma and COPD respiratory epithelium using 3D/spheroid culture model. Methods: The spheroids from 5 healthy controls, 8 asthma patients, and 8 COPD patients were exposed to 100 µg/ml of PM2.5 for 24 h. Results: The common pattern for healthy asthma and COPD epithelium inflammatory response to PM2.5 stimulation include the increase in IL-1β, IL-6, IL-8 mRNA expression, and secretion of IL-6. Asthmatic spheroids produced higher amount of TNF-α and IL-8, whereas COPD spheroids expressed increased mRNA level of MUC5AC and decreased level of MMP7. PM2.5 treatment induced changes in AHR and TLR4 expression on secretory epithelium in COPD. Conclusion: The response of airway epithelium to air pollution is different in healthy people than in obstructive lung disease patients. The impairment of airway epithelium in asthma and COPD changes their response to toxic environmental stimuli. This physiological dysfunction might be associated with diseases exacerbation of obstructive lung diseases. [ABSTRACT FROM AUTHOR]

Objectives: To explore the factors related to the progression of chronic obstructive pulmonary disease (COPD). Methods: 80 COPD patients treated between January 2020 and December 2022. The patients' pulmonary functions at their first hospital admission were categorized into four groups: Grade I, Grade II, Grade III and Grade IV. Each group was further divided into a progression group and a non-progression group based on the disease progression over one year or several years of follow-up. Patients with other respiratory diseases, malignant tumors, severe heart, kidney, liver dysfunctions, or immune deficiencies affecting the prognosis were excluded. General information, clinical data, treatment data, and statistical analysis of the patients. Results: In comparison with the non-progression group, the progression group had significantly higher age, smoking behavior, COPD history, hemoptysis history, CRP levels, IL-6 levels, and Pneumonia Severity Index (PSI) scores, exhibiting significantly lower FEV1, FEV1% predicted, PaO2, and PaCO2. More frequent use of antibiotics, corticosteroids, oxygen therapy, and mechanical ventilation were observed in the progression group than that in the non-progression group (P < 0.05). As a consequence, the progression group had a worse prognosis as indicated by higher hospitalization costs, longer hospital stay, and higher rate of acute exacerbations than the non-progression group (P < 0.05). Multifactorial logistic regression analysis showed that age ≥ 65 years, PSI score ≥ 130 points, and multidrug-resistant bacteria infection were independent risk factors for the progression of COPD (P < 0.05). Conclusions: Older COPD patients, higher PSI score, and multidrug-resistant bacteria infection have a worse prognosis and need more intensive treatment and follow-up. [ABSTRACT FROM AUTHOR]

While the impact of air pollution on acute exacerbations of chronic obstructive pulmonary disease (AECOPD) has been widely studied, its effect on hospitalization outcomes remains less explored. This study examines the influence of short-term air pollution exposure on adverse hospitalization outcomes—mortality, mechanical ventilation use, and prolonged hospitalization—in patients with non-infectious severe AECOPD in Novi Sad, Serbia. Using a five-year time-series analysis, concentrations of selected air pollutants (PM10, PM2.5, SO2, and NO2) and meteorological data were integrated with hospitalization outcomes. Distributed lag non-linear models (DLNMs) revealed significant associations between rising air pollutant levels and some unfavorable outcomes. Exposure to rising PM2.5 (urban background) and SO2 (urban traffic) concentrations were linked to higher risks of mechanical ventilation (cumulative OR 21.95 (95% CI 1.07–449.45) and 11.37 (95% CI 1.25–103.27), respectively) and prolonged non-infectious AECOPD hospitalization (cumulative RR 2.27 (95% CI 1.14–4.52) and 2.24 (95% CI 1.38–3.64), respectively). No cumulative lag effects on mortality were observed, though specific patterns emerged in individual lag models. These findings highlight the critical role of improving air quality in reducing some COPD-related hospitalization risks. [ABSTRACT FROM AUTHOR]

Background/Objectives: Hypercapnic respiratory failure (HRF) is a primary cause of admittance to the intensive care unit (ICU). This study aimed to investigate the factors that affect the length of hospital stay in HRF patients. Methods: This study was designed as a retrospective, cross-sectional analysis of patients who were admitted to the ICU because of HRF between 2022 and 2024. The demographic and clinical characteristics of the patients and laboratory results were recorded. The Charlson Comorbidity Index (CCI) was calculated. The relationship between these parameters and the length of hospital stay was assessed. Results: A total of 138 patients were included in the study. The average length of hospital stay was 11.45 days, and 37% of the patients were included in the long-term hospitalization group. The degree of hypercapnia was not associated with the length of hospital stay. It was determined that the patients' albumin levels and CCI were significant determinants of the length of hospital stay. The combined assessment of these two parameters was found to be superior compared to their separate evaluations. Conclusions: In our study, hypoalbuminemia and a higher CCI were identified as predictors of a prolonged ICU stay in HRF patients. Albumin levels of <3.25 g/dL and CCI scores of ≥5 were linked to longer stays, with this combined evaluation offering greater predictive value. These factors can guide patient management. [ABSTRACT FROM AUTHOR]

Background: Chronic obstructive pulmonary disease (COPD) is characterized by progressive and incurable airflow obstruction and chronic inflammation. Both TGF-β1 and CXCL8 have been well described as fundamental to COPD progression. DNA methylation and histone acetylation, which are well-understood epigenetic mechanisms regulating gene expression, are associated with COPD progression. However, a deeper understanding of the complex mechanisms associated with DNA methylation, histone post-translational changes and RNA methylation in the context of regulatory pathways remains to be elucidated. We here report on how DNA methylation and histone acetylation inhibition differentially affect CXCL8 signaling in primary human non-COPD and COPD airway cells. Methods: Airway smooth muscle (ASM) cells, a pivotal cell type in COPD, were isolated from the small airways of heavy smokers with and without COPD. Histone acetylation and DNA methylation were inhibited before the TGF-β1 stimulation of cells. Subsequently, CXCL8 production and the abundance and activation of pertinent transcription regulatory proteins (NF-κB, p38 MAPK and JNK) were analyzed. Results: TGF-β1-stimulated CXCL8 release from ASM cells from 'healthy' smoker subjects was significantly modulated by DNA methylation (56.32 pg/mL and 56.60 pg/mL) and acetylation inhibitors (27.50 pg/mL and 48.85 pg/mL) at 24 and 48 h, respectively. However, modulation via the inhibition of DNA methylation (34.06 pg/mL and 43.18 pg/mL) and acetylation (23.14 pg/mL and 27.18 pg/mL) was observed to a lesser extent in COPD ASM cells. These changes were associated with differences in the TGF-β1 activation of NF-κB and MAPK pathways at 10 and 20 min. Conclusions: Our findings offer insight into differential epigenetics in controlling COPD ASM cells and provide a foundation warranting future studies on epigenetic differences associated with COPD diagnosis. This would provide a scope for developing therapeutic interventions targeting signaling and epigenetic pathways to improve patient outcomes. [ABSTRACT FROM AUTHOR]

Introduction: Chronic obstructive pulmonary disease (COPD) is a condition characterized by airflow obstruction which can lead to physical and psychosocial challenges, with a higher prevalence in developing countries. Non-pharmacological interventions for this group of people include pulmonary rehabilitation as well as music interventions. Although music technology was recommended to adjust to the user's breathing capacity for music-making and to gather information about their performance, music therapy trials used acoustic wind instruments for their rehabilitation. This interdisciplinary project aims to develop a dedicated electronic wind instrument for people with COPD. Method: This project follows a systematic prototype methodology that includes product research, instrument development, and user validation. Based in Brazil, our team has decided on an electronic ocarina based on its cultural features, its popularity as a digital application, and its potential for respiratory training. Unlike existing technologies, the prototype intends to be dedicated and a low-cost solution. Results: The development process includes decision making about the appropriate mouthpiece, sensors, Arduino, pushbuttons, 3-D printing projects, building a MIDI interface and a dedicated software. This is an ongoing project, and our team is in the MIDI interface development stage. We aim to run the first hardware trial with users so that we can integrate their feedback into the functional prototype and the dedicated software for the following trials. Discussion: This project's strengths rely on the innovation of building viable electronic wind instruments that can facilitate self-management of people with COPD in developing countries, where access to healthcare can be challenging. [ABSTRACT FROM AUTHOR]

Climate change and air pollution are pressing public health concerns, necessitating monitoring of their impact, particularly on respiratory diseases like obstructive lung diseases. This retrospective study analyzed medical records of patients hospitalized at the Warmia and Mazury Centre for Pulmonary Diseases in Olsztyn, Poland (2012–2021) for asthma and chronic obstructive pulmonary disease (COPD) exacerbations. Data included meteorological factors such as temperature, humidity, wind speed, precipitation, and levels of PM2.5 and PM10. The Humidex was utilized to assess thermal discomfort, considering various meteorological and thermal seasons. Findings indicated seasonal variability in asthma and COPD exacerbations. During winter, poorer air quality due to higher PM2.5 and PM10 levels correlated with increased exacerbations (r = 0.283, p < 0.05; r = 0.491, p < 0.001). In summer, discomfort from meteorological conditions led to more hospital admissions. Humidex values strongly correlated with admissions for obstructive diseases (R2 = 0.956 for asthma; R2 = 0.659 for COPD), with July and August showing statistically higher admission rates (p < 0.05). The study highlights the significant impact of air pollution and meteorological conditions on exacerbations of asthma and COPD, with Humidex serving as a valuable predictor during summer months. [ABSTRACT FROM AUTHOR]

Supplemental Digital Content is Available in the Text. Background: Chronic obstructive pulmonary disease (COPD) is a costly chronic disease affecting more than 15 million Americans. The prevalence among US veterans is 3 times higher than the general population. Local problem: The Veteran Health Administration developed a standardized, evidence-based COPD educational tool called Green Light to Go (GLTG) designed to educate patients on managing their COPD symptoms at home. Despite the availability of this resource, inpatient education on COPD self-management practices is highly variable across different medical teams. This quality improvement (QI) initiative sought to standardize inpatient COPD patient education using the GLTG tool. This initiative also assessed whether patients receiving standardized patient education during their index hospitalization had lower COPD 30-day readmission rates. Method: The QI initiative followed the LEAN methodology and the A3 framework. The team performed rapid tests of change (plan-do-study-act cycles) to increase the percentage of veterans receiving COPD education. Interventions: The interventions implemented for this QI initiative focused on clinical, patient, and system improvements. Results: This initiative standardized COPD patient education and increased the percentage of veterans receiving (a) daily COPD education from 0% to 66%, (b) verbal COPD education on discharge from a baseline of 20% to 100%, (c) receipt of written educational material on discharge from 20% to 100%, and (d) the cohort all-cause 30-day readmission rate declined from 19.3% to 14.3%. Conclusions: Given the substantial economic burden of COPD readmissions on the health care system and patients, evidence-based educational interventions may potentially improve outcomes and reduce hospital readmissions in this veteran population. [ABSTRACT FROM AUTHOR]

Background and Objective: There is no strong evidence on the optimal duration of pulmonary rehabilitation (PR) programmes. The aim of the study was to determine whether an 8‐week PR programme was equivalent to a 12‐week PR programme in improving endurance exercise capacity in people with chronic obstructive pulmonary disease (COPD). Methods: Participants with COPD were randomized to either an 8‐week (8‐wk Group) or 12‐week (12‐wk Group), twice weekly, supervised PR programme consisting of endurance and strength training and individualized self‐management education. Between group comparisons were made at completion of each programme (i.e., week 8 or week 12), for both programmes at week 12, and at 6–12‐month follow‐up. The primary outcome was endurance exercise capacity measured by the endurance shuttle walk test (ESWT) with the minimally important difference of 186 s set as the equivalence limit. Results: Sixty‐six participants [mean (SD); age 69 (7) years, FEV1 48 (17) %predicted] were randomized (33 per group). Between‐group comparisons demonstrated that the ESWT time was equivalent for the 12‐wk Group compared to the 8‐wk Group at programme completion [mean (95% CI)] [71 s (−61 to 203)], week 12 [70 s (−68 to 208)], and 6–12‐month follow‐up [93 s (−52 to 239)], though superiority of the 12‐wk Group could not be ruled out at each time point. Conclusion: Equivalence was shown between 8‐and 12‐week PR programmes for endurance exercise capacity, but superiority could not be ruled out for the 12‐wk Group. Decisions about programme duration may depend on local waitlist times, healthcare budgets and patient preference. In people with COPD, an 8‐week and 12‐week PR programme were equivalent at improving endurance exercise capacity at programme completion, week 12 and 6–12‐month follow‐up, though superiority of the 12‐week PR programme could not be ruled out. [ABSTRACT FROM AUTHOR]

Chronic obstructive pulmonary disease (COPD) is a type of lung disease marked by permanent damage to tissues in the lungs. Over time, chronic obstructive pulmonary disease (COPD) can make breathing difficult due to permanent lung damage. COPD encompasses two main conditions chronic bronchitis, where inflammation and scarring narrow the large airways, and emphysema, where the tiny air sacs in the lungs are damaged. The widespread lung condition, chronic obstructive pulmonary disease (COPD), is largely preventable and treatable, affecting people of all genders globally. There are many studies estimating the burden of COPD in men and women, however, only a few studies have estimated the prevalence of COPD in women aged more than 40 years. Women are equally susceptible to COPD, as they are exposed more to domestic smoke, but they are often neglected and the disease goes unnoticed, which makes them more vulnerable to respiratory failure following a respiratory infection. To gain a comprehensive understanding, this review explores the existing research through a narrative analysis of primary research articles retrieved from PubMed. In total 15 relevant papers were extracted and reviewed. The review finds significant differences exist in the prevalence of COPD among women 40 years of age and older, with greater rates found in rural areas. Women have more severe symptoms and higher fatality rates; contributing factors to this increase are exposure to biomass fuels and growing smoking rates. [ABSTRACT FROM AUTHOR]

Introduction: Asthma and COPD are among the leading causes of morbidity and mortality, impacting over 260 million people and causing over 3 million deaths globally (Momtaz-Manesh, S. et al., 2023). Pulmonary symptoms can impair tolerance and increase the negative attribution of anxiety sensations. Reciprocally, anxiety associated with dyspnea can induce hyperventilation. This perpetuates a cycle of symptom exacerbation and poor treatment adherence. Managing labored breathing is challenging due to its subjective nature. Dyspnea is a sufferer's endless pursuit to breathe, rendering its experience as truly, "Sisyphean." Aim: This study explored the role of anxiety sensitivity and distress tolerance in dyspnea among adults with asthma and COPD (N = 107). A single-group cross-sectional research design was used. Data from pulmonologist-diagnosed adults with asthma and COPD were collected across various clinics in Delhi-NCR. Results: It was found that anxiety sensitivity, distress tolerance and dyspnea were strongly correlated. Also, an increase in anxiety sensitivity was strongly predictive of dyspnea severity. Further, distress tolerance acted as a partial mediator between anxiety sensitivity and dyspnea. Conclusions: Improving distress tolerance can act as an adjuvant in effective dyspnea management. [ABSTRACT FROM AUTHOR]

Chronic obstructive pulmonary disease (COPD) is a pervasive and incapacitating respiratory condition, distinguished by airway inflammation and the remodeling of the lower respiratory tract. Central to its pathogenesis is an intricate inflammatory process, wherein macrophages exert significant regulatory functions, and High mobility group box 1 (HMGB1) emerges as a pivotal inflammatory mediator potentially driving COPD progression. This study explores the hypothesis that HMGB1, within macrophages, modulates COPD through inflammatory mechanisms, focusing on its influence on macrophage polarization. Our investigation uncovered that HMGB1 is upregulated in the context of COPD, associated with an enhanced proinflammatory M1 macrophage polarization induced by cigarette smoke. This polarization is linked to suppressed cell proliferation and induced apoptosis, indicative of HMGB1's role in the disease's inflammatory trajectory. The study further implicates HMGB1 in the activation of the Nuclear factor kappa‐B (NF‐κB) signaling pathway and chemokine signaling within macrophages, which are likely to amplify the inflammatory response characteristic of COPD. The findings underscore HMGB1's critical involvement in COPD pathogenesis, presenting it as a significant target for therapeutic intervention aimed at modulating macrophage polarization and inflammation. [ABSTRACT FROM AUTHOR]

Background: Because alpha-1 antitrypsin deficiency is severely underrecognized and delayed diagnosis is associated with harm, strategies to enhance early detection of alpha-1 antitrypsin deficiency are needed. Methods: The study intervention was placing a reminder to test for alpha-1 antitrypsin deficiency within an electronic medical record health maintenance dashboard that houses prompts to providers to implement guideline-based recommendations. This recommendation was for all patients assigned a diagnosis of COPD based on relevant International Classification of Diseases, Tenth Revision codes. The rate of testing for and detecting individuals with alpha-1 antitrypsin deficiency was assessed in 12 one-month intervals before and after implementing the dashboard. Results: After the prompt, whereas testing was still performed in only a small percentage of guideline-concordant instances, the rate of testing for alpha-1 antitrypsin deficiency increased 3.8-fold (ie, from 1.2% to 4.6%, P <.05). This did not result in detection of new patients with alpha-1 antitrypsin deficiency. The rate of testing increased both for alpha-1 antitrypsin serum levels and genotypes in each month after the intervention, though the rate of genotype testing was 2–5-fold lower than the rate of testing for serum level. Conclusions: The results of this preliminary study of a detection strategy for alpha-1 antitrypsin deficiency show that placing a reminder to test for alpha-1 antitrypsin deficiency when indicated in an electronic medical record health maintenance dashboard significantly increased the frequency of testing. Still, that only 4.6% of those in whom testing for alpha-1 antitrypsin deficiency was indicated were tested in the post-intervention period shows that, as for all other alpha-1 antitrypsin deficiency–targeted detection interventions to date, the impact of the intervention was marginal and that other strategies remain needed to mitigate underrecognition. A focus on combining targeted detection strategies (eg, coupling enhanced awareness with free testing) and population-based screening for alpha-1 antitrypsin deficiency is suggested. [ABSTRACT FROM AUTHOR]

Background: Appropriate hospital-to-home transitional care has been recognized for its positive impact on health care usage and health outcomes in patients with COPD. However, there is limited research assessing its effects on patient-centered outcomes, focusing on patient symptoms and experiences. Methods: This single-blind randomized controlled trial included subjects diagnosed with COPD at one of 2 university hospitals in South Korea. The study included 179 subjects (transitional care group [transitional care], 87; usual care group [usual care], 92). The transitional care received transitional care comprising post-discharge care planning, personalized education, breathing exercises, telephone counseling, home visits, and referral to social services. We analyzed the effects of these interventions by comparing breathing symptoms and various patient-centered outcomes between the 2 groups. Results: The Modified Medical Research Council scores (mean [SD], transitional care 1.3 [1.06], usual care 1.82 [1.1], P =.002) and COPD Assessment Test scores (transitional care 6.32 [5.5], usual care 9.43 [7.16], P =.001) in the intervention group demonstrated more significant improvement than did those in the usual care. Following intervention, the subjects exhibited enhanced awareness of their disease, an increased frequency of inhaler use (transitional care 49.69 [1.67], usual care 46.86 [7.92], P =.002), and lower depression and anxiety scores. Additionally, the transitional care outperformed the usual care in the domain of subject experience during hospitalization (transitional care 39.34 [6.14], usual care 37.5 [5.61], P =.036), preparedness before discharge (transitional care 34.54 [4.96], usual care 32.3 [5.09], P =.003), and post-discharge management (transitional care 34.72 [4.36], usual care 30.29 [4.26], P =.003). Conclusions: Evidence-based transitional care services can exert positive effects on patient-centered indices. Our findings can be used as evidence of the need to establish patient-centered transitional care as a form of universal care for patients with COPD. [ABSTRACT FROM AUTHOR]

Background: Respiratory syncytial virus (RSV) infection is a common cause of hospital admission. The association between chronic obstructive pulmonary disease (COPD) exacerbation and RSV infection is not well studied. Objective: To analyze the hospitalizations of patients with COPD and RSV infection in Spain between 2018 and 2022. Methods: The data used were obtained from the Spanish Hospital Discharge Database. We selected subjects aged ≥40 years diagnosed with COPD, admitted to the hospital from 1 January 2018 to 31 December 2022. The COPD population that met the selection criteria was subdivided based on the presence of an ICD-10 code for RSV infection. To obtain comparable populations, for each subject with COPD and RSV infection, a subject without an RSV code was selected, with the COPD code in the same diagnostic position (1 to 20), as well as the same year of admission, sex, and age. Results: Among subjects aged ≥40 years, 1,429,288 were identified as having COPD, of whom 5673 also had RSV infection. The number of hospitalizations with COPD and RSV infection increased during the study period. The proportion of RSV infection among patients admitted for COPD increased significantly over time, from 0.32% in 2018 to 0.65% in 2022, p < 0.001. In-hospital mortality (IHM) increased over time, but the differences were not significant (6.23% in 2018 vs. 6.79% in 2022). Patients with COPD and RSV infection had, compared with those without RSV infection, a higher use of mechanical ventilation, both invasive (3.44% vs. 1.34%, p < 0.001) and noninvasive (8.09% vs. 4.51%, p < 0.001) and a higher proportion of intensive care unit (ICU) admission (7.21% vs. 3.9%, p < 0.001). After multivariate adjustment, a significant increase in IHM was found from 2018 to 2022 in subjects with and without RSV infection. The presence of RSV infection was associated with a higher mortality (OR 1.22; 95% CI 1.01–1.46). Conclusions: The proportion of RSV infection among patients admitted for COPD increased significantly over time. Patients with COPD and RSV infection had, compared with those without RSV infection, a higher severity, a higher use of mechanical ventilation, and a higher proportion of ICU admission. The presence of RSV infection was associated with IHM. These results can help to identify patients at higher risk and make decisions to avoid the increased risk of hospitalization and mortality in this population. [ABSTRACT FROM AUTHOR]

Background and Objectives: The aging population has led to a rise in cognitive impairments, including dementia, often associated with multimorbidity. Early diagnosis of cognitive decline is crucial, especially in primary care, where time constraints and the limitations of diagnostic tools may hinder accurate detection. This study aims to assess the cognitive functions of multimorbid patients using the Mini-Mental State Examination (MMSE) and the Lithuanian version of the General Practitioner Assessment of Cognition (LT-GPCOG). We hypothesized that the LT-GPCOG would perform similarly to the MMSE in suspecting cognitive impairments. Materials and Methods: This cross-sectional study, conducted from 2021 to 2022, included 796 patients aged 40–85, with arterial hypertension and at least one other chronic disease, recruited from seven Lithuanian primary health care centers. Cognitive function was assessed using the MMSE and LT-GPCOG, and statistical analyses were performed using SPSS to determine the association between cognitive impairment and various demographic and clinical variables. Results: Out of 796 participants, 793 completed the study. Cognitive impairment was suspected in 5.1% of participants based on MMSE and 4.2% based on the LT-GPCOG. Statistically significant associations were found between cognitive impairment and chronic obstructive pulmonary disease (COPD) (p = 0.008 and p = 0.003) in both tests and chronic kidney disease (CKD) (p = 0.005) while testing with the MMSE. Lower education and unemployment were also correlated with cognitive impairment (p = 0.008 and p < 0.001). Conclusions: The findings suggest that regular cognitive assessments should be integrated into the management of multimorbid patients, particularly those with COPD and CKD. The LT-GPCOG proved to be an efficient alternative to the MMSE in primary care settings, demonstrating comparable diagnostic accuracy. Further studies are also needed to assess the sensitivity and specificity of the LT-GPCOG test. [ABSTRACT FROM AUTHOR]

Background and Objectives: Despite the significant impacts of cognitive impairment on patients with chronic obstructive pulmonary disease (COPD), there is limited information available on healthcare workers' (HCWs) perceptions, current practice, and barriers to managing COPD patients with cognitive impairment. Materials and Methods: A cross-sectional questionnaire was distributed to HCWs in Saudi Arabia between April and December 2023. The collected responses were analysed using descriptive statistics and logistic regression models. Results: A total of 890 participants, including nursing, physical, and respiratory therapists, completed the online questionnaire. Over two-thirds of the study participants indicated not having sufficient knowledge or adequate training in managing cognitive impairment in patients with COPD. The majority of HCWs perceive cognitive impairment to underdiagnose COPD (83%), underestimate COPD severity (81%), exacerbate COPD symptoms (80%), and interfere with self-management (81%) and pulmonary rehabilitation (81%). However, less than 45% (n = 394) reported having the potential to recognise signs of cognitive impairment during patient encounters. Logistic regression analysis revealed that male healthcare practitioners were more likely to recognise cognitive impairment than females (OR: 1.48; 95% CI: 1.13 to 1.95; p < 0.001). Physical and respiratory therapists were more likely to identify cognitive impairment compared to nurses. Additionally, having more years of experience (≥10 years, OR: 1.63; 95% CI: 1.02 to 2.61; p = 0.001) and adequate knowledge of cognitive impairment (OR: 6.23; 95% CI: 4.18 to 9.29; p = 0.001) were strongly associated with better recognition. Confidence in managing cognitively impaired COPD patients was low, attributed to poor training (64%), inadequate knowledge (64%), and the absence of standardised procedures (58%). Conclusions: HCWs agreed upon the negative impacts associated with cognitive impairment in patients with COPD. However, the potential of recognising signs of cognitive impairment and confidently dealing with the existence of cognitive impairment in COPD is not optimal, owing to poor training and limited knowledge. A focus should be given to managing comorbidities alongside COPD. [ABSTRACT FROM AUTHOR]

Aim: This study aimed to evaluate the effect of partially edentulous ()PED condition on lung function through spirometry tests and comparison of airflow rates between dentulous and PED subjects. Settings and Design: The study design was a cross-sectional study conducted in the department of prosthodontics. Materials and Methods: Twenty-eight dentulous and 28 PED patients with an age range of 25–50 years were included in the study. Patients with missing more than 3 posterior teeth were considered PED. All have undergone spirometric evaluation. Statistical Analysis Used: Independent t-test was used. Results: In all three spirometric measures (forced vital capacity [FVC], forced expiratory volume in 1 s [FEV1], and peak expiratory flow rate [PEFR]), the PED participants had significantly lower FVC, FEV1 (P = 0.0005), and PEFR (P = 0.032) airflow rates than dentulous participants, and males had higher airflow rates than females. Conclusions: FVC, FEV1, and PEFR airflow rates were lower in PED individuals. The lower airflow rates could suggest the possible tendency to develop chronic obstructive pulmonary disease (COPD). [ABSTRACT FROM AUTHOR]

Rationale: Disability and loss of function are acknowledged as important problems for people living with chronic obstructive pulmonary disease (COPD), but there is a need for validated tools to assess them. Objectives: The Late-Life Function and Disability Instrument (LLFDI) was originally validated for community-dwelling older adults. The full instrument has not been validated to assess disability and loss of function in people with COPD. Methods: People with COPD from six European countries completed the LLFDI as part of an observational study. Its validity was assessed in terms of 1) levels and distribution of LLFDI domain and subdomain scores; 2) floor and ceiling effects; 3) instrument structure (three domains, seven subdomains) by confirmatory factor analysis; and 4) construct validity by convergent validity, which is based on Spearman correlation with COPD-relevant and related constructs (functional exercise capacity, severity of dyspnea, and COPD-related health status), and known-groups validity, which is based on the distribution of LLFDI scores according to COPD-meaningful groups (disease severity, age groups, and use of a walking aid). Results: The study included 605 participants (ages 68 ± 8 yr, 37% female; FEV1 = 54 ± 20 % predicted). Most had impaired disability and function levels. We observed no floor effects and a ceiling effect in only two subdomains. Confirmatory factor analysis showed a moderate model fit for all LLFDI domains. Most of the correlations met our hypotheses (73%), with moderate to strong correlations for the function domain (rmin-max = 0.25–0.70), followed by the disability limitation domain (rmin-max = 0.15–0.54), and weakest correlations in the disability frequency domain (rmin-max = 0.04–0.41). The disability limitation and function domains differed by disease severity, age group, and use of a walking aid. The disability frequency domain differed by disease severity and use of a walking aid, but not by age groups. Conclusions: The LLFDI, a valid patient-reported outcome to investigate disability and function, has proven good construct validity in people with COPD. Clinical trial registered with the ISRCTN registry (ISRCTN no. 12051706); . [ABSTRACT FROM AUTHOR]

Impaired alveolar epithelial regeneration in patients with idiopathic pulmonary fibrosis (PF) or chronic obstructive pulmonary disease is attributed to telomere dysfunction in type II alveolar epithelial cells (A2Cs). Genetic susceptibility, aging, and toxicant exposures, including tobacco smoke (TS), contribute to telomere dysfunction in A2Cs. Here we investigated whether improvement of telomere function plays a role in CSP7 (Cav1 scaffolding domain peptide)–mediated protection of A2Cs against ongoing senescence and apoptosis during bleomycin-induced PF as well as alveolar injury caused by chronic TS exposure. We found a significant telomere shortening in A2Cs isolated from idiopathic PF and chronic obstructive pulmonary disease lungs in line with other studies. These cells showed increased p53 in addition to its posttranslational modification with induction of activated caspase-3 and β-galactosidase, suggesting a p53-mediated loss of A2C renewal. Further, we found increased expression of SIAH-1, a p53-inducible E3 ubiquitin ligase known to downregulate TRF2 (telomere repeats binding factor 2). Consistent with the loss of TRF2 and upregulation of TRF1, TERT (telomerase reverse transcriptase) was downregulated in A2Cs. A2Cs from fibrotic lungs of mice repeatedly instilled with bleomycin or isolated from a chronic TS exposure–induced lung injury model showed reduced telomere length; induction of p53, PAI-1, SIAH1, and TRF1; as well as loss of TRF2 and TERT, which were reversed in wild-type mice after treatment with CSP7. Interestingly, PAI-1−/− mice, or those lacking microRNA-34a expression in A2Cs, resisted telomere dysfunction, whereas uPA−/− mice failed to respond to CSP7 treatment, suggesting p53-microRNA-34a feed-forward induction and that the p53-uPA pathway contributes to telomere dysfunction. [ABSTRACT FROM AUTHOR]

Patients with multiple sclerosis (MS) face a heightened risk of developing chronic obstructive pulmonary disease (COPD). Despite this widely reported association, the pathogenic contributors and processes that may favor the development of COPD in MS patients have yet to be identified. Recent studies have suggested peripheral blood leukocytes as a potential link between COPD and autoimmune disorders. Therefore, this study aimed to unveil shared molecular signatures between MS and COPD using blood transcriptomes. To this end, gene expression datasets obtained from MS and COPD blood specimens were retrieved from the Gene Expression Omnibus (GEO) database. By integrating datasets belonging to each disorder, differentially expressed genes (DEGs) were determined for each disease. Then, the protein-protein interaction (PPI) network was constructed for shared DEGs between MS and COPD. Subsequently, the network was analyzed to identify hub genes and key regulatory miRNAs. The integrated data for MS encompassed 51 samples (28 from MS patients and 23 from controls), and the integrated data for COPD included 450 samples (275 from COPD patients and 175 from controls). A total of 246 genes were found to exhibit identical directions of expression in both MS and COPD. By applying a high confidence threshold (0.7), a PPI network with 74 nodes was constructed. TP53, H4C6, SNRPE, and RPS11 were identified as hub genes according to the degree measure. In addition, 8 miRNAs were identified as key regulators, each interacting with 6 mRNAs. Among these miRNAs, miR-218-5p and miR-142-5p have been previously reported to contribute to the pathogenesis of these diseases, and here they were identified as key regulators of the shared PPI network, suggesting a potential epigenetic link between MS and COPD. In conclusion, the results highlighted the potential role of peripheral blood leucocytes as a bridge between MS and COPD. These findings broaden our understanding of pathogenic contributors linking MS and COPD. While this transcriptomics study identified multiple key players, such as TP53, miR-218-5p, and miR-142-5p, the assessment of their therapeutic efficacy demands further experimental studies. [ABSTRACT FROM AUTHOR]

Background: The effects of camel milk in inflammation and systemic oxidative stress of cigarette smoke (CS)-induced chronic obstructive pulmonary disease (COPD) associated with small airway inflammation in rats were investigated. Methods: 35 male Wistar rats were randomly divided into five groups: (a) control, (b) CS-exposed rats, c and (d) CS-exposed rats treated with the 4 and 8 mL/kg camel milk, and (e) CS-exposed rats treated with 1 mg/kg dexamethasone. Results: Total and differential WBC counts, serum level of TNF- α and malondialdehyde (MDA) level in serum and homogenized tissues of the heart, kidney, liver, and testicle were significantly increased, but catalase (CAT), superoxide dismutase (SOD) and thiol levels were significantly decreased in CS-exposed rats (p < 0.01 to p < 0.001). Treatment with dexamethasone and both doses of camel milk improved all measured variables compared to the COPD group (p < 0.05 to p < 0.001). The improvements of most variables in the treated group with high dose of camel milk were higher than the effect of dexamethasone (p < 0.05 to p < 0.001). These findings suggest that camel milk has a therapeutic potential for treating systemic oxidative stress and inflammatory induced by CS. Conclusion: Therefore, camel milk might be effective in attenuating the effects of CS-induced systemic inflammation and oxidative stress. [ABSTRACT FROM AUTHOR]

Chronic obstructive pulmonary disease (COPD) is a type of lung disease marked by permanent damage to tissues in the lungs. Over time, chronic obstructive pulmonary disease (COPD) can make breathing difficult due to permanent lung damage. COPD encompasses two main conditions chronic bronchitis, where inflammation and scarring narrow the large airways, and emphysema, where the tiny air sacs in the lungs are damaged. The widespread lung condition, chronic obstructive pulmonary disease (COPD), is largely preventable and treatable, affecting people of all genders globally. There are many studies estimating the burden of COPD in men and women, however, only a few studies have estimated the prevalence of COPD in women aged more than 40 years. Women are equally susceptible to COPD, as they are exposed more to domestic smoke, but they are often neglected and the disease goes unnoticed, which makes them more vulnerable to respiratory failure following a respiratory infection. To gain a comprehensive understanding, this review explores the existing research through a narrative analysis of primary research articles retrieved from PubMed. In total 15 relevant papers were extracted and reviewed. The review finds significant differences exist in the prevalence of COPD among women 40 years of age and older, with greater rates found in rural areas. Women have more severe symptoms and higher fatality rates; contributing factors to this increase are exposure to biomass fuels and growing smoking rates. [ABSTRACT FROM AUTHOR]

Background: Patients with advanced chronic non-malignant conditions often experience significant symptom burden. Therefore, overcoming barriers to interprofessional collaboration between general practitioners (GPs) and specialist palliative home care (SPHC) teams is essential to facilitate the timely integration of palliative care elements. The KOPAL trial aimed to examine the impact of case conferences between GPs and SPHC teams on symptom burden and pain in patients with advanced chronic heart failure, chronic obstructive pulmonary disease, and dementia. Methods: The cluster-randomised controlled trial compared a structured palliative care nurse visit followed by an interprofessional case conference to usual care. Data were collected from GPs at baseline and 48 weeks, while standardised patient interviews were conducted at baseline, 6, 12, 24, and 48 weeks. Results: We analysed 172 patients from 49 German GP practices. Both groups showed marginal improvement in symptom burden; however, no statistically significant between-group difference was found ( =-0.561, 95% CI: -3.201–2.079, p =.68). Patients with dementia experienced a significant pain reduction ( =2.187, 95% CI: 0.563–3.812, p =.009). Conversely, the intervention did not have a significant effect on pain severity ( =-0.711, 95% CI: -1.430 − 0.008, p=.053) or pain interference ( =-0.036, 95% CI:-0.797 − 0.725, p=.926) in other patient groups. Conclusions: The intervention showed promise in the timely introduction of palliative care elements to address pain management in patients with dementia. Further studies are needed to identify and effectively address symptom burden and pain in other patient groups. Trial registration: German Clinical Trials Register: https://www.drks.de/DRKS00017795 (Registration date: 9th January 2020). [ABSTRACT FROM AUTHOR]

Background: Anemia is a prevalent comorbidity in COPD associated with increased morbidity. However, the significance of longitudinal anemia status and variation in anemia status trends over time in COPD are not known. Furthermore, individuals with COPD and smoking history often have multiple comorbidities, in particular cardiovascular disease. The objective of this study was to evaluate the association between longitudinal anemia status and COPD outcomes, accounting for comorbid cardiovascular disease. Methods: Serial hemoglobin measures and clinical outcomes were obtained in former smokers with moderate to severe COPD from two clinical studies over a 6-to-9-month period. In the first analysis, the association between repeated measures of time-varying anemia status and outcomes was assessed by generalized estimating equations adjusted for covariates including cardiovascular disease. In the second analysis, each participant's anemia risk profile during the study period was characterized as high versus low anemia risk-growth rate. Mean differences in the progression of COPD outcomes over time between the two groups were assessed using a generalized linear mixed model. Effect modification by baseline coronary artery calcium (CAC) burden was explored. Results: There were 159 individuals with mean age of 66.5 years (± 8.3) and mean FEV1% predicted of 51.4% (± 17.0), of which 41% were ever-anemic during the study period. Repeated measures of anemia status were associated with higher St. George's Respiratory Questionnaire (SGRQ) scores (β 2.5, 95% CI: 0.1,4.8, p = 0.04), lower 6-minute walk distance (6MWD) (β -38.6, 95% CI: -67.7,-7.4, p = 0.02), and higher rate of moderate-to-severe exacerbations over the prospective follow-up period (IRR 1.8, 95% CI: 1.1,2.8, p = 0.02). There was effect modification by CAC burden such that with higher burden the mean difference in COPD outcome by anemia status was greater for a subset of symptom scores. Participants with profiles of increasing anemia risk had higher estimated rates of decline in the FEV1% predicted and 6MWD and increase in SGRQ scores compared to those with stable or decreasing anemia risk. Conclusions: Longitudinal anemia status trends may be predictive of COPD disease trajectory. Anemia status by repeated measures analysis is associated with COPD morbidity with potentially stronger associations in the setting of high CAC burden. [ABSTRACT FROM AUTHOR]

Background: Alveolar macrophages (AMs) modulate pulmonary inflammation in chronic obstructive pulmonary disease (COPD), contributing to its progression. The PPARγ/RXRα heterodimer influences AM polarization induced by cigarette smoke (CS). Although PPARγ agonists suppress CS-induced M1 macrophage polarization, the impact of RXRα agonists on this process has not been determined. This study explored the effects and mechanisms of the RXRα agonist bexarotene on macrophage polarization in a COPD mouse model. Methods: C57BL/6 mice were assigned to the control, model, bexarotene, or model + bexarotene group. The COPD model was induced by CS exposure and intraperitoneal injection of cigarette smoke extract (CSE), followed by intraperitoneal administration of bexarotene. Additionally, MH-S cells were exposed to CSE and bexarotene. Lung tissues were subjected to hematoxylin-eosin staining, and emphysema and inflammatory scores were assessed. Cytokine levels and cell differentials in bronchoalveolar lavage fluid were measured, and macrophage polarization was evaluated using immunohistochemistry, flow cytometry, and qPCR. Results: Bexarotene effectively reduced inflammatory scores, cytokine levels, and neutrophil counts and ameliorated emphysema and M1 polarization of AMs in COPD model mice. Furthermore, while CSE exposure reduced PPARγ expression and the transcriptional activity of AMs, bexarotene enhanced the transcriptional response of PPARγ to CSE. HO-1 was identified as a potential target of PPARγ; its levels were assessed in AMs, revealing that bexarotene mitigated the CSE-induced reduction in HO-1. Notably, the effect of bexarotene was partially inhibited by the PPARγ inhibitor. Conclusions: Our results indicated that bexarotene may curb inflammation and M1 polarization in COPD through activation of the PPARγ/HO-1 pathway. [ABSTRACT FROM AUTHOR]

Background: With the frequent occurrence of extreme weather worldwide, non-optimal temperature increased the risk of death from respiratory diseases. The burden of non-optimal temperature on chronic obstructive pulmonary disease (COPD) was quantitatively assessed, and its influencing factors were discussed to provide a basis for the prevention and treatment of COPD. Methods: Based on GBD 2019, we characterized the age-standardized mortality rate (ASMR) and years of life lost rate (ASYR) of COPD attributable to non-optimal temperature in three groups of countries at different isotherms (China and USA, South Africa and Australia, Iraq and Portugal) between 1990 and 2019. We constructed the age-period-cohort model to analyze age, period and cohort effects on mortality and the Bayesian age-period-cohort model to predict ASMR in six countries. We analyzed the relationship of socio-demographic index (SDI) with ASMR and ASYR by restricted cubic spline and quantile regression using data from 21 GBD regions. Results: ASMR of COPD attributable to non-optimal temperature in 2019 was 11.03/100,000 (China), 5.62/100,000 (USA), 2/100,000 (Australia), 0.93/100,000 (Iraq), 3.74/100,000 (Portugal), 4.13/100,000 (South Africa). Low temperature had a greater impact on COPD. The mortality showed an increasing trend with age, the period effect only showed a decreasing trend in China, and cohort effect showed a decreasing trend. The higher COPD burden was concentrated in areas with SDI values of 0.39–0.78. Implied quantile regression of mortality to SDI fit was meaningful at P5 and P75, and ASYR was at P5, P25, P75, and P95. We predicted an upward trend in COPD ASMR over the next 25 years only in the USA. Conclusions: In COPD burden caused by non-optimal temperature, low temperature played a more important role, and it was affected by sex, age, period, cohort and SDI. Over the next 25 years, ASMR in COPD was predicted to decline in all countries except the USA. [ABSTRACT FROM AUTHOR]

Background Purpose Methods Results Conclusion Respiratory function is impaired in chronic obstructive pulmonary disease (COPD). Automation of multi‐volume CT‐based measurements of different components of breathing‐related airway deformations will help understand multi‐pathway impairments in respiratory mechanics in COPD.To develop and evaluate multi‐volume chest CT‐based automated measurements of breathing‐related radial and longitudinal expansion of individual airways between inspiratory and expiratory lung volumes.We developed a method to compute breathing‐related airway deformation metrics and applied it to total lung capacity (TLC) and functional residual capacity (FRC) chest CT scans. The computational pipeline involves: (1) segmentation of airways; (2) skeletonization of airways; (3) labeling of anatomical airway segments at TLC and FRC; and (4) computation of radial and longitudinal expansion metrics of individual airways across lung volumes. Radial expansion (∆CSA) of an airway is computed as the percent change of its cross‐sectional area (CSA) between two lung volumes. Longitudinal expansion (∆L) of an airway is computed as the percent change in its airway path‐length from the carina between lung volumes. These measures are summarized at different airway anatomic generations. Agreement of automated measures with their manually derived values was examined in terms of concordance correlation coefficient (CCC) of automated measures with those derived using manual outlining. Intra‐class correlation coefficient (ICC) of automated measures from repeat CT scans (n = 37) was computed to assess repeatability. The method was also applied to a set of participants from the Genetic Epidemiology of COPD (COPDGene) Iowa cohort, distributed across COPD severity groups (n = 4 × 60).The CCC values for the automated ∆CSA measure with manually derived values were 0.930 at the trachea, 0.898 at primary bronchi, and greater than 0.95 at pre‐segmental and segmental airways; these CCC values were consistently greater than 0.95 for ∆L at all airway generations. ICC values for repeatability of ∆CSA were 0.974, 0.950, 0.943, and 0.901 at trachea, primary bronchi, pre‐segmental, and segmental airways, respectively; these ICC values for ∆L were 0.973, 0.954, and 0.952 at primary bronchi, pre‐segmental, and segmental airways, respectively. ∆CSA values were significantly reduced (p < 0.001) with increasing COPD severity at each of primary bronchi, pre‐segmental, and segmental airways. Significantly lower ∆L values were observed for moderate (p = 0.042 at pre‐segmental and p = 0.037 at segmental) and severe (p = 0.019 at pre‐segmental and p < 0.001 at segmental) COPD groups as compared to the preserved lung function group. Body mass index (BMI) and smoking status were found to significantly associate with ∆CSA at segmental airways (r = 0.17 and −0.19, respectively; significance threshold = 0.13), while age and sex were significantly associated with ∆L (r = −0.21 and −0.17, respectively); COPD severity was significantly associated with both ∆CSA and ∆L (r = −0.35 and −0.22, respectively).Our CT‐based automated measures of breathing‐related radial and longitudinal expansion of airways are repeatable and in agreement with manually derived values. Automation of different airway mechanical biomarkers and their observed significant associations with age, sex, BMI, smoking, and COPD severity establish an effective tool to investigate multi‐pathway impairments of respiratory mechanics in COPD and other lung diseases. [ABSTRACT FROM AUTHOR]

Background: Alpha-1 antitrypsin deficiency (AATD) is associated with increased susceptibility to chronic obstructive pulmonary disease (COPD). AATD results from mutations in the SERPINA1 gene and over 500 rare mutations have been identified. Despite these findings and recommendations from major healthcare organizations, testing of COPD patients and their family members for AATD remains inadequate. Methods: We examined genotypes and clinical characteristics of COPD patients (index cases; n = 14) treated at Recep Tayyip Erdoğan University Chest Diseases Department and their relatives (n = 17). Results: When index cases were compared with screened relatives positive for AATD (n = 14), index cases were older and more predominantly male than screened relatives. Both groups had extensive smoking histories. All of the index cases and one of the screened relatives had been diagnosed with COPD. Clinical characterization of the COPD cases (14 index cases; 1 screened relative) showed that they had moderate to severe COPD with pre-treatment AAT levels of 0.59 ± 0.40 g/L (mean ± SD) and a COPD Assessment Test (CAT) score of 16.0 ± 8.12. The majority of these patients (73.3%) had panlobular emphysema. Five of the patients were treated with AAT augmentation which led to a decrease in the number of COPD exacerbations. Genotyping revealed that the most common rare allele identified in this population was MPalermo (c.227_229delTCT mutation on the M1(Val213) allelic background). Conclusions: More testing and research need to be done to identify the relative prevalence of rare AATD variants. Earlier identification could lead to more effective treatment of affected individuals and improvement in their quality of life. [ABSTRACT FROM AUTHOR]

Background: Pulmonary hypertension (PH) is a serious complication of chronic obstructive pulmonary disease (COPD), distinguished by pulmonary endothelial dysfunction. The extracellular cold-inducible RNA-binding protein (eCIRP) is a damage-associated molecular pattern (DAMP) that triggers inflammation and causes vascular endothelial dysfunction in COPD-PH. Methods: The expression levels of CIRP were compared in peripheral lung tissues among 40 individuals. Moreover, A prospective analysis was conducted on serum levels of eCIRP, interleukin (IL) 1β, IL-33, endothelin-1 (ET-1), and nitric oxide (NO) in 150 COPD patients and 50 healthy control individuals at Jiangsu Taizhou Peoples Hospital. The study aimed to compare these serum levels and correlations among COPD-PH group, COPD non-PH group and the normal group. Results: We found higher CIRP levels in COPD-PH compared to COPD non-PH and the normal in lung tissue samples. A prospective analysis showed higher serum levels of eCIRP, IL-1β, IL-33, and ET 1 in COPD-PH, while a noticeable reduction in NO levels. There exists a correlation between the severity of COPD-PH and elevated levels of eCIRP, proinflammatory cytokines like IL-1β and IL-33, along with indicators of endothelial dysfunction like endothelin-1 ET-1 and NO. Moreover, the serum eCIRP level demonstrated a notable positive correlation with the levels of IL-1β, IL-33, PCT, and ET-1, while displaying a negative correlation with NO and Peripheral Oxygen Saturation (SpO2). Moreover, the serum eCIRP level demonstrated a notable positive correlation with the levels of IL-1β, IL-33, PCT, and ET-1, while displaying a negative correlation with NO and SpO2. Moreover, an assessment of independent risk factors for COPD-PH with ROC curve analysis, gauged the predictive value of serum eCIRP, IL-1β, IL-33, ET-1, and NO levels in diagnosing COPD-PH. Elevated eCIRP, IL-33, and ET-1 levels significantly correlated with COPD-PH, highlighting eCIRP's strong predictive value for this condition. Conclusion: eCIRP levels could serve as a valuable biomarker for predicting endothelial dysfunction in COPD-PH. [ABSTRACT FROM AUTHOR]

Alpha-1 antitrypsin deficiency (AATD) is a genetic condition that predisposes a person to certain diseases over their lifetime, mainly including lung disease (in the form of emphysema) and liver disease (liver cirrhosis). Quality of life questionnaires are instruments designed to quantify the deterioration of a patient's health. Background/Objectives: This study aimed to assess whether certain quality of life tests that are routinely used in clinical practice can be useful for patients with AATD. Methods: A sample of AATD patients, with various genotypes, but with the common characteristic that they must have both altered alleles (Pi* ≠ M), participated in the study. Different quality of life tests were used, including the COPD Assessment Test (CAT), COPD and Asthma Sleep Impact Scale, the short form of the Short Form Health Survey, and EuroQol 5 dimensions, and were related to differing clinical and functional characteristics. Results: The sample was composed of 54 patients, and slightly more than half of the participants were women (57.4%), with a mean age of 51.5 ± 13.7. The main genotypes were Pi*SZ (43.4%) and Pi*ZZ (34%). In patients under 65 years of age (n = 47), those who were actively working could walk a greater distance in the walking test, namely, 573 m (511–629), compared to those who were not actively working, namely, 415.5 m (392–469; p < 0.001). Active non-workers had a worse CAT (13.6 ± 7.8 vs. 4.6 ± 4.3; p < 0.001). In total, 80% of non-working patients had exacerbations, but only 46. 9% of those who were active, although the association did not reach statistical significance (p = 0.068). Having a lower score in the physical component of SF-12 was related to suffering from lung disease (46.0 ± 11.4 vs. 38.4 ± 11.1 (p = 0.026)). Conclusions: Quality of life tests were able to detect differences and relate them to functional factors such as the distance covered in the walking test, being sensitive and specific in this regard. [ABSTRACT FROM AUTHOR]

Backgrounds: Despite the significant global health impact of cardiometabolic multimorbidity (CMM), our understanding of potential predictors associated with its development in smokers, remains limited. Objective: This study aimed to investigate whether a new COPD diagnosis and the rate of lung function decline serve as predictors for incident CMM (defined as having at least two of the following comorbidities: cerebro-cardiovascular diseases, hypertension, dyslipidemia, and diabetes mellitus) in smokers. Methods: An observational longitudinal analysis of prospectively collected data was conducted, including smokers without a previous COPD diagnosis and any cardiometabolic conditions. Sociodemographic and clinical data (body mass index, smoking history, respiratory symptoms, and hospital admissions) were collected at baseline. Lung function tests were performed at baseline and at the end of the follow-up period. The incidence of CMM, a new positive diagnosis of COPD, and the forced expiratory volume in 1 s (FEV1) annual rate of decline were prospectively registered. Adjusted Cox proportional hazard models were adopted to explore risk factors associated with the incidence of CMM. Results: From the 391 smokers included in the study, 207 (53%) were newly diagnosed with COPD, and 184 had a preserved spirometry at baseline (non-COPD group). After nearly a decade of follow-up, 34% (n = 133) of smokers developed CMM. This group was characterized by male predominance, older age, higher BMI and pack-years of smoking, lower post-FEV1, baseline COPD diagnosis, and a history of hospital admission. A positive diagnosis of COPD at baseline and a greater rate of lung function decline (ΔFEV1 ≥ 40 mL/year) were independent predictors for developing CMM. Conclusions: A new COPD diagnosis and an accelerated decline in lung function are significantly associated with the development of CMM in smokers. [ABSTRACT FROM AUTHOR]

Mucins 5AC (MUC5AC) and 5B (MUC5B) are the major mucins providing the organizing framework for the airway's mucus gel. We retrieved bronchial mucosal biopsies and bronchial wash (BW) samples through bronchoscopy from patients with chronic obstructive pulmonary disease (n = 38), healthy never-smokers (n = 40), and smokers with normal lung function (n = 40). The expression of MUC5AC and MUC5B was assessed immunohistochemically. The mucin concentrations in BW were determined using the slot-blot technique. The immunohistochemical expression of MUC5AC and MUC5B was localized to goblet cells and submucosal glands. Smokers had higher MUC5AC and lower MUC5B goblet cell expression and higher concentrations of soluble MUC5AC in BW than never-smokers. The MUC5B expression in goblet cells correlated positively with expiratory air flows, diffusing capacity, and the dyspnoea score. Chronic bronchitis, emphysema, and the progression of chronic airflow limitation during a median follow-up time of 8.4 years were associated with higher MUC5AC and lower MUC5B expression in goblet cells. Sustainers, slow progressors, and rapid progressors of airflow obstruction differed in their MUC5B expression at baseline. Emphysema and bronchial wall thickening on CT at a follow-up visit were associated with lower MUC5B expression at baseline. Our findings strengthen the hypothesis that MUC5AC and MUC5B are yet another contributing factor to smoking-associated lung disease progression. [ABSTRACT FROM AUTHOR]

Background and Purpose: Physical activity is an effective therapeutic protocol for treating chronic obstructive pulmonary disease (COPD). However, the mechanisms underlying the benefits of physical activity in COPD are not fully elucidated. Experimental Approach: In a mouse model of COPD, analysis of biological markers and lung proteomics identified the molecular pathways through which exercise ameliorates COPD. Key Results: Exercise improved pulmonary function, emphysema, small airway disease, pulmonary inflammation, glucose metabolic dysregulation, and insulin resistance in COPD mice. Proteomic analysis revealed 430 differentially expressed proteins (DEPs) between the COPD and COPD + Exercise (COPD + Ex) groups. GO analysis indicated that the enriched pathways were predominantly related to the immune response, inflammatory processes, insulin secretion, and glucose metabolic processes. GO analysis revealed IL‐33 as a crucial target for the exercise‐related amelioration of COPD. KEGG analysis showed that DEPs were significantly enriched in primary immunodeficiency, the intestinal immune network for IgA production, and the NF‐κB signalling pathway. Exercise inhibited NF‐κB activation by suppressing the CD14/TLR4/MyD88 and TNF‐α/TNF‐R1/TRAF2/5 pathways in COPD mice. Exercise inhibited expression of BCR, IgM, IgD, IgG, IgE, and IgA by suppressing B‐cell receptor signalling. Exercise attenuated glucose metabolic dysregulation and insulin resistance through the suppression of proinflammatory mediators, including MHC I, MHC II, TNF‐α, IFN‐γ, and IL‐1β, while concurrently increasing insulin expression. The qRT‐PCR results were consistent with the proteomic results. Conclusion and Implications: In a mouse model, exercise improved COPD and its metabolic comorbidities through immune system regulation and inflammation suppression, offering insights into potential therapeutic targets. [ABSTRACT FROM AUTHOR]

Background: Rheumatoid arthritis (RA) and chronic obstructive pulmonary disease (COPD) are prevalent and incapacitating conditions, sharing common pathogenic pathways such as tobacco use and pulmonary inflammation. The influence of respiratory conditions including COPD on RA has been observed, meanwhile RA may constituting one of the risk factors for COPD. It unclear that whether a bidirectional associate between RA and COPD. Our study aims to explore the bidirectional relationship between RA and COPD. Methods: We systematically searched PubMed, Cochrane Library, and Embase for observational studies from the databases inception to February 20, 2024, utilizing medical subject headings (MeSH) and keywords. We included studies in which RA and COPD were studied as either exposure or outcome variables. Statistical analyses were conducted employing STATA software (version 14.0). The relationship was reported as odds ratios (OR) and corresponding 95% confidence intervals (CI). Publication bias was assessed using funnel plots and Egger's regression. Results: Nineteen studies with 1,549,181 participants were included. Risk of bias varied from low to moderate, with evidence levels rated as low or very low. Pooled analysis revealed a significant association between RA and increased COPD risk (OR=1.41, 95%CI 1.13 to 1.76, I2 = 97.8%, P =0.003). Subgroup analyses showed similar COPD risk elevations in both of genders, seropositive/seronegative RA, cohort and case control studies. Additionally, there was a significant RA risk increase among those with COPD (OR=1.36, 95%CI 1.05 to 1.76, I2 = 55.0%, P =0.022), particularly among females and seropositive RA, and cohort studies. Conclusion: The meta-analysis identifies a significant bidirectional association between RA and COPD, emphasizing mutually increased risk. Recognizing this connection may can inform proactive approaches to disease prevention and management, potentially reducing the public health burden and improving quality of life. Systematic Review Registration: https://www.crd.york.ac.uk/PROSPERO/ , identifier CRD42024518323. [ABSTRACT FROM AUTHOR]

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Background: Productive cough with sputum is a prominent sign generally associated with respiratory diseases, including chronic obstructive pulmonary disease (COPD). Airway clearance devices are an option for COPD management, but physicians' preferences for and clinical practice with them are not known. Objective: This study aims to explore preferences for and clinical practice with airway clearance devices among physicians in Saudi Arabia. Design: An observational, cross-sectional survey. Methods: A self-administered questionnaire was conducted between October 2022 and September 2023, which included a review of respiratory medication prescriptions by physicians for patients with COPD. The analysis was performed using the Statistical Package for the Social Sciences. Results: The participants were 445 physicians. The majority were female, accounting for 64.3% of the sample. Flutter and Acapella were the most commonly preferred airway clearance devices (45.8% and 20.7%, respectively). Among the participants, 12.6% reported unfamiliarity with any of the mentioned devices. Of the participants, 43.6% "usually" suggested the devices for patients with daily, difficult-to-clear, thick sputum, while 27% "sometimes" recommended them to COPD patients who had experienced four exacerbations or more. In routine clinical practice, physicians prescribe pharmacological therapies as the main treatment. The prescribing data showed that in the last year, there was no record of prescribed airway clearance devices for COPD by physicians. Conclusion: Family and pulmonary physicians prefer Flutter and Acapella devices, but a significant number of physicians are unaware of such devices. Prescribing data showed no record of prescribed airway clearance devices for COPD management. Further initiatives are needed to increase awareness in clinical practice. [ABSTRACT FROM AUTHOR]

Background: Chronic obstructive pulmonary disease (COPD) significantly impacts respiratory and motor function, balance, and cognition, leading to muscle weakness and impaired exercise capacity. The impairments often result in challenges with daily activities, particularly those requiring dual-tasking. Objectives: The study investigated whether patients with severe COPD would exhibit more significant cognitive and motor performance decline during dual tasks compared to healthy controls. Design: This study employed a cross-sectional design to compare cognitive and motor performance in dual tasks between patients with severe COPD and healthy controls. Methods: We included 44 patients with severe COPD and 43 healthy individuals. Participants underwent various tests, including pulmonary function tests, six-minute walking tests, dual Timed Up and Go tests (TUG), dual single-leg stance tests (SLS), Berg Balance Scale assessments, and Falls Efficacy Scale International evaluations (FES-I). Results: The COPD group had significantly lower scores in the Berg Balance Scale (BBS; 44.79 ± 4.70 vs 52.67 ± 2.16, p < 0.0001) and longer times for the TUG test (12.44 s; [11.44, 13.50] vs 9.14 s; [7.91, 10.11], p < 0.0001) and shorter times for the SLS test (14.15 s; [12.31, 15.65] vs 26.20 s; [23.45, 30.88], p < 0.0001), indicating poorer functional mobility and balance. Furthermore, dual-task interference (DTI) outcomes revealed poorer performance in the COPD group (p < 0.0001). The fear of falling (FES-I) was increased in the COPD group. There was a significant positive correlation between DTI TUG and FES-I (r = 0.35, p = 0.01) and a negative correlation between DTI SLS and BBS (r = −0.41, p = 0.005) in the COPD group. Conclusion: The study reveals significant impairments in DTI and balance among patients with severe COPD. Patients with severe COPD performed worse in tests involving dual tasks. They had poorer balance overall compared to healthy controls, with longer times for the dual Timed Up and Go test and shorter times for the SLS test, indicating a higher susceptibility to DTI and a greater fear of falling. Plain language summary: How severe COPD affects balance and ability to perform two tasks at once: a cross-sectional study Why was the study done? Chronic obstructive pulmonary disease (COPD), a lung disease affecting many people, makes breathing more challenging and increases the risk of falling. This is because people with COPD often have weak muscles and trouble with balance. Doing two things simultaneously, like walking and talking, is essential for staying independent and avoiding falls, especially in older people. However, there isn't much research on how people with severe COPD do when trying to do two things at once while also keeping their balance. What did the researchers do? Our study compared people with severe COPD to healthy individuals. Both groups were tested on their lung function, walking distance, how fast they could stand up and walk, how long they could stand on one leg, and their confidence in not falling. What did the researchers find? The results showed that people with severe COPD did worse in tests that involved doing two things at once, like walking and talking, and had poorer balance overall. They were slower at standing up and walking, couldn't stand on one leg as long, scored lower on balance tests, and had a greater fear of falling compared to the healthy group. Adding simultaneously a second task, both groups presented a decrease in the performed tests, with severe COPD patients presenting an even higher decrease in the evaluation. What do the findings mean? In conclusion, our study shows that people with severe COPD have a much harder time with balance and doing two things at once compared to healthy people. Our study provides information regarding the multitasking ability of patients with severe COPD. [ABSTRACT FROM AUTHOR]

Background: Inflammation and nutrition are strongly linked to respiratory diseases, but the link between inflammation and nutrition-based indicators and chronic obstructive pulmonary disease (COPD) and its mortality has not been reported. Methods: We recruited adults no younger than 20 years old from the NHANES 1999–2018. Inflammation and nutrition-based indicators included NAR, PNI, MAR, RAR, HALP, and ALI. COPD were assessed through a self-report questionnaire. Participants' mortality rates were determined by association with the National Death Index. Results: A total of 46,572 individuals were collected in this study, including 1,549 COPD patients. NAR, MAR, and RAR were positively linked with the prevalence of COPD. However, PNI and HALP were negatively linked with the prevalence of COPD. In participants with COPD, the highest quartile of NAR (HR = 1.43 [1.04–1.97]), MAR (HR = 1.66 [1.23–2.26]), and RAR (HR = 2.45 [1.90–3.17]) were linked with an increased risk of all-cause mortality compared to the lowest quartile. However, the highest quartile of PNI (HR = 0.48 [0.38–0.61]) and HALP (HR = 0.56 [0.44–0.71]) were linked with a decreased risk of all-cause mortality compared to the lowest quartile. Randomized survival forests (RSF) showed that RAR had the strongest predictive power for all-cause mortality in COPD individuals among all indicators. Conclusion: We found that inflammation and nutrition-based indicators were linked to prognosis in COPD patients, with RAR having the highest predictive value. [ABSTRACT FROM AUTHOR]

Objective: The gut microbiota and its metabolites exert a significant influence on COPD, yet the underlying mechanisms remain elusive. We aim to holistically evaluate the role and mechanisms of the gut microbiota and its metabolites in COPD through network pharmacology and Mendelian randomization approaches. Methods: Employing network pharmacology, we identified the gut microbiota and its metabolites' impact on COPD-related targets, elucidating the complex network mechanisms involving the gut microbiota, its metabolites, targets, and signaling pathways in relation to COPD. Further, promising gut microbiota metabolites and microbiota were pinpointed, with their causal relationships inferred through Mendelian randomization. Results: A complex biological network was constructed, comprising 39 gut microbiota, 20 signaling pathways, 19 targets, and 23 metabolites associated with COPD. Phenylacetylglutamine emerged as a potentially promising metabolite for COPD treatment, with Mendelian randomization analysis revealing a causal relationship with COPD. Conclusion: This study illuminates the intricate associations between the gut microbiota, its metabolites, and COPD. Phenylacetylglutamine may represent a novel avenue for COPD treatment. These findings could aid in identifying individuals at high risk for COPD, offering insights into early prevention and treatment strategies. [ABSTRACT FROM AUTHOR]

Background: Exercise tolerance and health-related quality of life (HRQL) are enhanced in patients with chronic obstructive lung disease (COPD) by pulmonary rehabilitation. This study aimed to evaluate the effect of PR program both short and long course among stable COPD patients to improve their tolerance and outcome. Methods: This non randomized clinical study was carried out at Chest Disease Department at Pulmonary Rehabilitation Unit of Zagazig University Hospitals on 30 Stable COPD patients during the period from July 2023 to February 2024 to assess the effect of PR program both short and long course among stable COPD patients to improve their tolerance and outcome. Results: There is a significant improvement in pulmonary function tests (FEV1/FVC, FEV1, FVC) (predicted %), Oxygen saturation, 6MWD and Quality of life score after long PR course compared to short PR course. Also there was significant decrease in mMRC after long PR course compared to short PR course. Conclusions: Pulmonary Rehabilitation program should be conducted for all COPD patients, improving dyspnea, exercise tolerance, and quality of life and. For best results exercise should continue for long course of Pulmonary Rehabilitation. [ABSTRACT FROM AUTHOR]

ABSTRACT: Background: Chronic obstructive pulmonary disease (COPD) is a major health concern in India, with exacerbations leading to increased morbidity, mortality, and healthcare costs. Periodontal disease, a chronic inflammatory condition, may affect COPD outcomes by promoting systemic inflammation. This prospective cohort study aimed to investigate the association between periodontal inflammation and the risk of COPD exacerbations in the Indian population. Methods: A total of 2500 participants with established COPD from various regions of India were enrolled and followed for five years. Baseline assessments included comprehensive periodontal evaluations, with measurements of clinical parameters and inflammatory markers (C-reactive protein, interleukin-6). COPD exacerbations were defined as events requiring medical intervention, such as hospitalization, emergency room visits, or changes in medication. Results: Periodontal inflammation, measured by clinical attachment loss and elevated inflammatory markers, was significantly associated with a higher risk of COPD exacerbations (Hazard Ratio [HR] 2.3, 95% Confidence Interval [CI] 1.7–3.1), even after adjusting for confounders. Specific periodontal parameters and inflammatory markers were identified as strong predictors of future exacerbations. Conclusions: This study provides evidence that periodontal inflammation is an independent and potentially modifiable risk factor for COPD exacerbations in the Indian population. Addressing periodontal health as a part of COPD management may offer a novel approach to reduce the frequency and severity of exacerbations, thereby improving quality of life and clinical outcomes. [ABSTRACT FROM AUTHOR]