Chronic Obstructive Pulmonary Disease Smokers Research Articles

Identification of Molecular Markers Associated with COPD in non-smokers and smokers: A Bioinformatics Analysis

Even though the proportional burden of COPD among never-smokers is significant in both developing and developed nations, accounting for around 30% of all COPD in the community, there is little awareness of the prevalence of COPD in this population. Understanding the molecular processes that underlie COPD in nonsmokers is essential.

Identification of novel candidate genes in East Asian COPD patients by the functional summary-based imputation and the unified test for molecular signatures: a transcriptome-wide association study

Identification of novel candidate genes in East Asian COPD patients by the functional summary-based imputation and the unified test for molecular signatures: a transcriptome-wide association study

The concept of detection of dynamic lung hyperinflation using cardiopulmonary exercise testing.

Dynamic lung hyperinflation (DLH) caused by air trapping, which increases residual air volume, is a common cause of shortness of breath on exertion in chronic obstructive pulmonary disease (COPD). DLH is commonly evaluated by measuring the decrease in maximal inspiratory volume during exercise, or using the hyperventilation method. However, only few facilities perform these methods, and testing opportunities are limited. Therefore, we investigated the possibility of visually and qualitatively detecting DLH using data from a cardiopulmonary exercise test (CPET). Four men who underwent symptom-limiting CPET were included in this study, including a male patient in his 60s with confirmed COPD, a 50s male long-term smoker, and 2 healthy men in their 20s and 70s, respectively. We calculated the difference between the inspiratory tidal volume (TV I) and expiratory tidal volume (TV E) per breath (TV E-I) from the breath-by-breath data of each CPET and plotted it against the time axis. No decrease in TV E-I was observed in either of the healthy men. However, in the patient with COPD and long-term smoker, TV E-I began to decrease immediately after the initiation of exercise. These results indicate that DLH can be visually detected using CPET data. However, this study was a validation of a limited number of cases, and a comparison with existing evaluation methods and verification of disease specificity are required.

Investigating the comorbidity of COPD and tuberculosis, a computational study

Recent research has shown that people who suffer from chronic obstructive pulmonary disease (COPD) have a greater propensity to contract and develop tuberculosis (TB) than the general population. Not only is the hazard ratio for contracting active tuberculosis triple that of the general population for those with COPD, but that the probability of death from any cause during the first year was double that of the tuberculosis population as a whole. This observation suggests that patients with COPD are less likely to progress to latent tuberculosis infection (LTBI) and are more likely to develop active tuberculosis than the general population. While similar susceptibility rates to TB are known to occur in populations with other ailments of the lung, particularly HIV, emphysema or asthma, patients with COPD (both emphysema and chronic bronchitis) are statistically more at risk for the disease. To examine the comorbidity effects of COPD on tuberculosis disease and granuloma formation, the process by which Mycobacterium tuberculosis (Mtb) is either contained or disseminates, we used a multi-scale model that integrates pathophysiological and immunopathological aspects of COPD and TB. Depicting chronic obstructive pulmonary disease smoker and non-smoker populations, we integrate agent-based models (ABM) of cellular immune response, physiological models of pulmonary capacity for COPD smoker/non-smoker, systems biology models of macrophage immune response to Mtb, and metabolic models to capture intracellular and extracellular Mtb metabolism and proliferation. We use our model to investigate key drivers of disease outcomes of clearance, granuloma-based containment, and disseminated disease in individuals with COPD and TB for smoking and non-smoking populations.

Socioeconomic disparity in the association between fine particulate matter exposure and papillary thyroid cancer

BackgroundLimited data exists suggesting that cumulative exposure to air pollution in the form of fine particulate matter (aerodynamic diameter ≤ 2.5 μm [PM2.5]) may be associated with papillary thyroid carcinoma (PTC), although this relationship has not been widely established. This study aims to evaluate the association between PM2.5 and PTC and determine the subgroups of patients who are at the highest risk of PTC diagnosis.MethodsUnder IRB approval, we conducted a case-control study of adult patients (age ≥ 18) newly diagnosed with PTC between 1/2013–12/2016 across a single health care system were identified using electronic medical records. These patients were compared to a control group of patients without any evidence of thyroid disease. Cumulative PM2.5 exposure was calculated for each patient using a deep learning neural networks model, which incorporated meteorological and satellite-based measurements at the patients’ residential zip code. Adjusted multivariate logistic regression was used to quantify the association between cumulative PM2.5 exposure and PTC diagnosis. We tested whether this association differed by gender, race, BMI, smoking history, current alcohol use, and median household income.ResultsA cohort of 1990 patients with PTC and a control group of 6919 patients without thyroid disease were identified. Compared to the control group, patients with PTC were more likely to be older (51.2 vs. 48.8 years), female (75.5% vs 46.8%), White (75.2% vs. 61.6%), and never smokers (71.1% vs. 58.4%) (p < 0.001). After adjusting for age, sex, race, BMI, current alcohol use, median household income, current smoking status, hypertension, diabetes, COPD, and asthma, 3-year cumulative PM2.5 exposure was associated with a 1.41-fold increased odds of PTC diagnosis (95%CI: 1.23–1.62). This association varied by median household income (p-interaction =0.03). Compared to those with a median annual household income <$50,000, patients with a median annual household income between $50,000 and < $100,000 had a 43% increased risk of PTC diagnosis (aOR = 1.43, 95%CI: 1.19–1.72), and patients with median household income ≥$100,000 had a 77% increased risk of PTC diagnosis (aOR = 1.77, 95%CI: 1.37–2.29).ConclusionsCumulative exposure to PM2.5 over 3 years was significantly associated with the diagnosis of PTC. This association was most pronounced in those with a high median household income, suggesting a difference in access to care among socioeconomic groups.

Excessive Facial Wrinkling Is Associated with COPD Occurrence-Does COPD Damage Skin Beauty and Quality?

The aim of this study was to investigate facial wrinkling in COPD patients, its relationship with lung function parameters, and the differences in wrinkling between COPD patients and smokers without COPD. The study included 56 patients with COPD with smoking history and 84 controls. Wrinkle intensity was measured and classified using Daniell's grading system, and the total length of wrinkles was also estimated. The predominant grades of Daniell's scale were IV-V for COPD patients (89.3% of current and 75.0% of former smokers), III-V for controls who currently smoke (89.2%), and II-III for former (92.9%) and never smokers (100%) controls. These distributions were statistically significantly different, but current and former smokers with COPD and COPD former smokers and control current smokers did not differ. In terms of the total length of wrinkles, the COPD patients possessed significantly longer wrinkles than the control subgroups (all p-values were <0.004). Negative correlations between wrinkle length and lung parameters were found. This phenomenon seems to be independent of smoking, but the length of wrinkles is related to lung function parameters. It seems that not only smoking but also COPD damages skin beauty and quality.

Comparison of Serum CRP, Total Cholesterol, Magnesium and Uric Acid in Smoker and Non Smoker Patients with COPD: A Cross-sectional Study

Introduction: Chronic Obstructive Pulmonary Disease (COPD) is a common and treatable disease characterised by progressive airflow limitation and tissue destruction. Smoking is a common risk factor but non smokers can also develop COPD. There may be change in serum level of inflammatory marker, oxidative stress markers, bio-markers among these patients. In this study smoker and non smoker group in COPD patients studied and may helpful for comparing levels and to corelate with severity of disease and also for group specific management. Aim: To evaluate the level of Serum C-Reactive Protein (CRP), total cholesterol, Magnesium (Mg++), and uric acid in COPD patients and also, to compare these parameters in smoker and non smoker patients with COPD. Materials and Methods: This cross-sectional study was conducted in Department of Biochemistry and Department of Pulmonary Medicine at People’s College of Medical Sciences and Research Centre, Bhopal, Madhya Pradesh, India, from October 2021 to December 2022. A total of 100 COPD patients, aged between 40 to 60 years were included and divided into two groups: 50 smokers and 50 non smokers. Parameters such as CRP, Mg++, total cholesterol and uric acid, were estimated by autoanalyser. Data were statistically analysed using unpaired t-test. Results: In smokers, mean age was 53.08±5.89 years, whereas in non smokers, mean age was 53.9±4.84 years. Out of the 100 subjects, 50 were smokers (F=6 and M=44) and 50 were non smokers (F=6 and M=44). In the present study, observed increased CRP levels and cholesterol levels, low serum magnesium, and normal uric acid in smoker compared to non smokers COPD. There was significant difference in cholesterol (p-value=0.044), serum magnesium (p-value=0.001) and CRP levels (p-value=0.0001) but there was no significant difference in uric acid (p-value=0.989). Conclusion: Smokers with COPD had increased level of CRP, Cholesterol and low level of Magnesium as compared to non smoker COPD patients. This may attribute that smokers COPD patients are in risk of developing recurrent exacerbations and more disease severity

Impact of Marijuana Smoking on COPD Progression in a Cohort of Middle-Aged and Older Persons.

Limited data are available regarding marijuana smoking's impact on the development or progression of chronic obstructive pulmonary disease (COPD) in middle-aged or older adults with a variable history of tobacco cigarette smoking. We divided ever-tobacco smoking participants in the SubPopulations and InteRmediate Outcomes In COPD Study (SPIROMICS) into 3 groups based on self-reported marijuana use: current, former, or never marijuana smokers (CMSs, FMSs or NMSs, respectively). Longitudinal data were analyzed in participants with ≥2 visits over a period of ≥52 weeks. We compared CMSs, FMSs, and NMSs, and those with varying amounts of lifetime marijuana use. Mixed effects linear regression models were used to analyze changes in spirometry, symptoms, health status, and radiographic metrics; zero-inflated negative binomial models were used for exacerbation rates. All models were adjusted for age, sex, race, baseline tobacco smoking amount, and forced expiratory volume in 1 second (FEV1) %predicted. Most participants were followed for ≥4 years. Annual rates of change in FEV1, incident COPD, respiratory symptoms, health status, radiographic extent of emphysema or air trapping, and total or severe exacerbations were not different between CMSs or FMSs versus NMSs or between those with any lifetime amount of marijuana use versus NMSs. Among SPIROMICS participants with or without COPD, neither former nor current marijuana smoking of any lifetime amount was associated with evidence of COPD progression or its development. Because of our study's limitations, these findings underscore the need for further studies to better understand longer-term effects of marijuana smoking in COPD.

Associations of Smoking, Cytomegalovirus Serostatus, and Natural Killer Cell Phenotypes in Smokers With and At Risk for COPD.

Chronic obstructive disease (COPD) risk factors, smoking and chronic infection (Cytomegalovirus (CMV)) may mold NK cell populations. What is not known is the magnitude of effect of CMV seropositivity imparts on populations in smokers with and at-risk for COPD. We investigate the independent influence of CMV seropositivity on NK cell populations and differential effects when stratifying by COPD and degree of smoking history. Descriptive statistics determine relationship between cytotoxic NK cell populations and demographic and clinical variables. Multivariable linear regression and predictive modeling was performed to determine associations between positive CMV serology and proportions of CD57+ and NKG2C+ NK cells. We dichotomized our analysis by those with a heavy smoking history, COPD, and describing the effect size of CMV seropositivity on NK cell populations. When controlled for age, race, sex, pack-years smoked, body-mass index, and lung function, CMV+ serostatus was independently associated with a higher proportion of CD57+, NKG2C+, and NKG2C+CD57+ NK cells. CMV+ serostatus was the sole predictor of larger NKG2C+ and CD57+NKG2C+ populations. Associations are more pronounced in those with COPD and heavy smokers. Among Veterans who are current and former smokers, CMV+ serostatus was independently associated with larger CD57+ and NKG2C+ populations, with a larger effect in heavy smokers and those with COPD, and was the sole predictor for increased expression of NKG2C+ and CD57+NKG2C+ populations. These findings may be broadened to include the assessment of longitudinal NK cell population change, accrued inflammatory potential, and further identification of pro-inflammatory NK cell population clusters.

ВЛИЯНИЕ КУРЕНИЯ НА ПОКАЗАТЕЛИ ОКИСИ УГЛЕРОДА И ОКСИДА АЗОТА В ВЫДЫХАЕМОМ ВОЗДУХЕ У ПАЦИЕНТОВ С ХРОНИЧЕСКОЙ ОБСТРУКТИВНОЙ БОЛЕЗНЬЮ ЛЕГКИХ

To date, points of view regarding the effect of smoking on the indicators of exhaled air are very contradictory, especially with regard to the examination of patients with chronic obstructive pulmonary disease (COPD) suffering from tobacco dependence. Basically, a comparative analysis is carried out by researchers solely on the fact of the presence of tobacco dependence, without taking into account the indicator of the smoking index (CI), as such, or the data obtained from the examination of smoking COPD patients and healthy volunteers are compared. Objective: to evaluate the change in the concentration of carbon monoxide (CO), nitric monoxide (NO) and carboxyhemoglobin (COHb) in the exhaled air of patients with COPD, depending on the status of smoking and CI. Material and research methods. 96 patients with COPD were examined, the average age of which was 54.6±5.9 years, the duration of the disease was 15±4.8 years. 70 patients (72.9%) who participated in the study suffered from tobacco dependence, while CI ≤10 pack-year was observed in 2.8% of them, 11-20 pack-year in 42.9%, 21-30 pack-year in 40.0% and &gt;30 pack-year in 14.3%. As part of a comprehensive examination, all patients underwent determination of CO (ppm) and COHb (%) in exhaled air using the MicroCO device (Micro medica, UK) and the level of NO was assessed using the Niox Mino analyzer (Aerocline, Sweden). The results of the study. During the analysis of the obtained data, we noted an increase in the average concentration of CO in the exhaled air in all smoking patients, while the increase in the indicator was directly proportional to the CI. A similar picture was observed with respect to the COHb level. The concentration of NO in the exhaled air, on the contrary, showed a tendency to decrease with increasing CI. A comparative analysis of the obtained data was carried out in three groups: I - non-smoking patients with COPD (n=26), II - patients with COPD with an IC of 11-20 pack-years (n=30) and III – patients with COPD with an IC of 21-30 pack-years (n=28). In terms of peripheral blood saturation, significant differences compared with the group of non-smokers were found in patients with IC 11-20 pack-years and with IC 21-30 pack-years, while there were no statistically significant differences between these groups of smoking patients. The CO level in smokers, regardless of CI, was significantly higher than in non-smokers, while in COPD patients with CI 21-30 pack-year it was also significantly higher than in patients with CI 11-20 pack-year. The COHb index in smokers with COPD was also significantly higher than in non-smokers, but when comparing data in the group with IC 11-20 pack-years and IC 21-30 pack/years, no statistically significant differences were found. In terms of NO in exhaled air, statistically significant differences were noted when comparing data in the group of non-smoking patients with COPD with the results obtained in groups of patients with IC 11-20 pack-years and with IC 21-30 pack-years, as well as when comparing data in these groups of smokers among themselves. Conclusions. The study revealed a statistically significant increase in the level of CO in the exhaled air, depending on the status of smoking and CI. It was determined that the smoking factor in COPD patients affects the level of NO in the exhaled air, causing its significant decrease in COPD patients with CI &gt;10 pack-year compared to non-smoking COPD patients.

Cleavage of Occludin by Cigarette Smoke-Elicited Cathepsin S Increases Permeability of Lung Epithelial Cells.

Chronic obstructive pulmonary disease (COPD) is an irreversible disease mainly caused by smoking. COPD is characterized by emphysema and chronic bronchitis associated with enhanced epithelial permeability. Lung biopsies from smokers revealed a decreased expression level of occludin, which is a protein involved in the cohesion of epithelial tight junctions. Moreover, the occludin level correlated negatively with smoking history (pack-years), COPD grades, and cathepsin S (CatS) activity. Thus, we examined whether CatS could participate in the modulation of the integrity of human lung epithelial barriers. Cigarette smoke extract (CSE) triggered the upregulation of CatS by THP-1 macrophages through the mTOR/TFEB signaling pathway. In a co-culture model, following the exposure of macrophages to CSE, an enhanced level of permeability of lung epithelial (16HBE and NHBE) cells towards FITC-Dextran was observed, which was associated with a decrease in occludin level. Similar results were obtained using 16HBE and NHBE cells cultured at the air-liquid interface. The treatment of THP-1 macrophages by CatS siRNAs or by a pharmacological inhibitor restored the barrier function of epithelial cells, suggesting that cigarette smoke-elicited CatS induced an alteration of epithelial integrity via the proteolytic injury of occludin. Alongside its noteworthy resistance to oxidative stress induced by cigarette smoke oxidants and its deleterious elastin-degrading potency, CatS may also have a detrimental effect on the barrier function of epithelial cells through the cleavage of occludin. The obtained data emphasize the emerging role of CatS in smoking-related lung diseases and strengthen the relevance of targeting CatS in the treatment of emphysema and COPD.

Smoking induces shifts in cellular composition and transcriptome within the bronchial mucus barrier.

Smoking disturbs the bronchial-mucus-barrier. This study assesses the cellular composition and gene expression shifts of the bronchial-mucus-barrier with smoking to understand the mechanism of mucosal damage by cigarette smoke exposure. We explore whether single-cell-RNA-sequencing (scRNA-seq) based cellular deconvolution (CD) can predict cell-type composition in RNA-seq data. RNA-seq data of bronchial biopsies from three cohorts were analysed using CD. The cohorts included 56 participants with chronic obstructive pulmonary disease [COPD] (38 smokers; 18 ex-smokers), 77 participants without COPD (40 never-smokers; 37 smokers) and 16 participants who stopped smoking for 1 year (11 COPD and 5 non-COPD-smokers). Differential gene expression was used to investigate gene expression shifts. The CD-derived goblet cell ratios were validated by correlating with staining-derived goblet cell ratios from the COPD cohort. Statistics were done in the R software (false discovery rate p-value < 0.05). Both CD methods indicate a shift in bronchial-mucus-barrier cell composition towards goblet cells in COPD and non-COPD-smokers compared to ex- and never-smokers. It shows that the effect was reversible within a year of smoking cessation. A reduction of ciliated and basal cells was observed with current smoking, which resolved following smoking cessation. The expression of mucin and sodium channel (ENaC) genes, but not chloride channel genes, were altered in COPD and current smokers compared to never smokers or ex-smokers. The goblet cell-derived staining scores correlate with CD-derived goblet cell ratios. Smoking alters bronchial-mucus-barrier cell composition, transcriptome and increases mucus production. This effect is partly reversible within a year of smoking cessation. CD methodology can predict goblet-cell percentages from RNA-seq.

From Differential DNA Methylation in COPD to Mitochondria: Regulation of AHRR Expression Affects Airway Epithelial Response to Cigarette Smoke.

Cigarette smoking causes hypomethylation of the gene Aryl Hydrocarbon Receptor Repressor (AHRR), which regulates detoxification and oxidative stress-responses. We investigated whether AHRR DNA methylation is related to chronic obstructive pulmonary disease (COPD) and studied its function in airway epithelial cells (AECs). The association with COPD was assessed in blood from never and current smokers with/without COPD, and in AECs from ex-smoking non-COPD controls and GOLD stage II-IV COPD patients cultured with/without cigarette smoke extract (CSE). The effect of CRISPR/Cas9-induced AHRR knockout on proliferation, CSE-induced mitochondrial membrane potential and apoptosis/necrosis in human bronchial epithelial 16HBE cells was studied. In blood, DNA methylation of AHRR at cg05575921 and cg21161138 was lower in smoking COPD subjects than smoking controls. In vitro, AHRR DNA methylation at these CpG-sites was lower in COPD-derived than control-derived AECs only upon CSE exposure. Upon AHRR knockout, we found a lower proliferation rate at baseline, stronger CSE-induced decrease in mitochondrial membrane potential, and higher CSE-induced late apoptosis/necroptosis. Together, our results show lower DNA methylation of AHRR upon smoking in COPD patients compared to non-COPD controls. Our data suggest that higher airway epithelial AHRR expression may lead to impaired cigarette smoke-induced mitochondrial dysfunction and apoptosis/necroptosis, potentially promoting unprogrammed/immunogenic cell death.

Contribution of adaptive immunity to human COPD and experimental models of emphysema.

The pathophysiology of chronic obstructive pulmonary disease (COPD) and the undisputed role of innate immune cells in this condition have dominated the field in the basic research arena for many years. Recently, however, compelling data suggesting that adaptive immune cells may also contribute to the progressive nature of lung destruction associated with COPD in smokers have gained considerable attention. The histopathological changes in the lungs of smokers can be limited to the large or small airways, but alveolar loss leading to emphysema, which occurs in some individuals, remains its most significant and irreversible outcome. Critically, however, the question of why emphysema progresses in a subset of former smokers remained a mystery for many years. The recognition of activated and organized tertiary T- and B-lymphoid aggregates in emphysematous lungs provided the first clue that adaptive immune cells may play a crucial role in COPD pathophysiology. Based on these findings from human translational studies, experimental animal models of emphysema were used to determine the mechanisms through which smoke exposure initiates and orchestrates adaptive autoreactive inflammation in the lungs. These models have revealed that T helper (Th)1 and Th17 subsets promote a positive feedback loop that activates innate immune cells, confirming their role in emphysema pathogenesis. Results from genetic studies and immune-based discoveries have further provided strong evidence for autoimmunity induction in smokers with emphysema. These new findings offer a novel opportunity to explore the mechanisms underlying the inflammatory landscape in the COPD lung and offer insights for development of precision-based treatment to halt lung destruction.

THE SUBSEQUENT IMPACT OF COVID-19 FOR BOTH IMMUNE DYSREGULATION AND OPPORTUNISTIC INFECTIONS

THE SUBSEQUENT IMPACT OF COVID-19 FOR BOTH IMMUNE DYSREGULATION AND OPPORTUNISTIC INFECTIONS

Comparative characteristics of TRP channels expression levels on the macrophages of patients with chronic obstructive pulmonary disease

Introduction. Macrophages are one of the key cells in the pathogenesis of chronic obstructive pulmonary disease (COPD), mediating the primary immune response and coordinating the further reaction of the immune system upon contact with cigarette smoke and air pollutants. It is known that some TRP channels expressed on macrophages are receptors for dust particles and cigarette smoke components.Aim. To study the features of TRPV1, TRPV4, TRPA1 and TRPM8 channels expression on monocyte-derived macrophages and alveolar macrophages of COPD patients and smokers without bronchial obstruction.Materials and methods. Expression of TRP channels at the mRNA level was studied in monocyte-derived macrophages obtained from 8 COPD patients and 6 healthy smokers by quantitative reverse transcription PCR. Expression of TRP channels at the protein level was studied on alveolar macrophages of 39 COPD patients and 8 healthy smokers by indirect flow cytometry.Results. It was found that under in vitro conditions, monocyte-derive macrophages of COPD patients were distinguished by a significant 4.8-fold increase in the number of TRPV1 transcripts (p=0.009). At the same time, the expression of the TRPV1 protein on the alveolar macrophages of COPD patients was also significantly higher when compared to the cells of smokers from the control group (14.1 [6.4‒21.2]% vs. 6.1 [2.1‒9.8]%, p=0.006). In addition, we found that TRPV4 expression was increased among active smokers with COPD, and the expression of TRPA1 and TRPM8 channels correlated with some lung function parameters.Conclusion. The obtained results suggest that the increased expression of TRPV1 on macrophages may be a marker of the disease and contribute to its development, while the expression of TRPV4, TRPA1 and TRPM8 may influence the clinical course of COPD.

Gene Expression Trajectories from Normal Nonsmokers to COPD Smokers and Disease Progression Discriminant Modeling in Response to Cigarette Smoking.

Background Cigarette smoking (CS) is considered to the predominant risk factor contributing to the etiopathogenesis of chronic obstructive pulmonary disease (COPD); meanwhile, genetic predisposition likely plays a role in determining disease susceptibility. Objectives We aimed to investigate gene expression trajectories from normal nonsmokers to COPD smokers and disease progression discriminant modeling in response to cigarette smoking. Methods Small airway epithelial samples of human with different smoking status using fiberoptic bronchoscopy and corresponding rat lung tissues following 0, 3, and 6 months of CS exposure were obtained. The expression of the significant overlapping genes between human and rats was confirmed in 16HBE cells, rat lung tissues, and human peripheral PBMC using qRT-PCR. Binary logistic regression analysis was carried out to establish discrimination models. Results The integrated bioinformatic analysis of 8 human GEO datasets (293 individuals) and 9 rat transcriptome databases revealed 13 overlapping genes between humans and rats in response to smoking exposure during COPD progression. Of these, 5 genes (AKR1C3/Akr1c3, ERP27/Erp27, AHRR/Ahrr, KCNMB2/Kcnmb2, and MRC1/Mrc1) were consistently identified in both the human and rat and validated by qRT-PCR. Among them, ERP27/Erp27, KCNMB2/Kcnmb2, and MRC1/Mrc1 were newly identified. On the basis of the overlapping gene panel, discriminant models were established with the receiver operating characteristic curve (AUC) of 0.98 (AKR1C3/Akr1c3 + ERP27/Erp27) and 0.99 (AHRR/Ahrr + KCNMB2/Kcnmb2) in differentiating progressive COPD from normal nonsmokers. In addition, we also found that DEG obtained from each expression profile dataset was better than combined analysis as more genes could be identified. Conclusion This study identified 5 DEG candidates of COPD progression in response to smoking and developed effective and convenient discriminant models that can accurately predict the disease progression.

Proactive Electronic Visits for Smoking Cessation and Chronic Obstructive Pulmonary Disease Screening in Primary Care: Randomized Controlled Trial of Feasibility, Acceptability, and Efficacy.

BackgroundMost smokers with chronic obstructive pulmonary disease (COPD) have not yet been diagnosed, a statistic that has remained unchanged for over two decades. A dual-focused telehealth intervention that promotes smoking cessation, while also facilitating COPD screening, could help address national priorities to improve the diagnosis, prevention, treatment, and management of COPD. The purpose of this study was to preliminarily evaluate an integrated asynchronous smoking cessation and COPD screening e-visit (electronic visit) that could be delivered proactively to adult smokers at risk for COPD, who are treated within primary care.ObjectiveThe aims of this study were (1) to examine e-visit feasibility and acceptability, particularly as compared to in-lab diagnostic pulmonary function testing (PFT), and (2) to examine the efficacy of smoking cessation e-visits relative to treatment as usual (TAU), all within primary care.MethodsIn a randomized clinical trial, 125 primary care patients who smoke were randomized 2:1 to receive either proactive e-visits or TAU. Participants randomized to the e-visit condition were screened for COPD symptoms via the COPD Assessment in Primary Care to Identify Undiagnosed Respiratory Disease and Exacerbation Risk (CAPTURE). Those with scores ≥2 were invited to complete both home spirometry and in-lab PFTs, in addition to two smoking cessation e-visits. Smoking cessation e-visits assessed smoking history and motivation to quit and included completion of an algorithm to determine the best Food and Drug Administration–approved cessation medication to prescribe. Primary outcomes included measures related to (1) e-visit acceptability, feasibility, and treatment metrics; (2) smoking cessation outcomes (cessation medication use, 24-hour quit attempts, smoking reduction ≥50%, self-reported abstinence, and biochemically confirmed abstinence); and (3) COPD screening outcomes.ResultsOf 85 participants assigned to the e-visits, 64 (75.3%) were invited to complete home spirometry and in-lab PFTs based on CAPTURE. Among those eligible for spirometry, 76.6% (49/64) completed home spirometry, and 35.9% (23/64) completed in-lab PFTs. At 1 month, all cessation outcomes favored the e-visit, with a significant effect for cessation medication use (odds ratio [OR]=3.22). At 3 months, all cessation outcomes except for 24-hour quit attempts favored the e-visit, with significant effects for cessation medication use (OR=3.96) and smoking reduction (OR=3.09).ConclusionsA proactive, asynchronous e-visit for smoking cessation and COPD screening may offer a feasible, efficacious approach for broad interventions within primary care.Trial RegistrationClinicalTrials.gov NCT04155073; https://clinicaltrials.gov/ct2/show/NCT04155073

Role of X-ray in the Detection of Structural Changes Related to COPD in Smoker and Non-Smoker

Background: A entire of 10% of Chronic Obstructive pulmonary disease (COPD) are never Smokers because of occupational history positive like biogas and air pollution. And 90% of patients are Smokers. Smoking is main cause of COPD in worldwide. Aim: To determine the role of X-Rays in the Detection of Structural Changes Related to COPD in smokers and nonsmokers. Material and Method: This cross-sectional study was conceded out in Radiological department DHQ Medical institution Gujranwala. The duration of study was 4 months i.e. January 2022 to May 2022. Total no of patients was conduct in Radiology department with COPD are 100. Exclusion criteria included all patients who are not with COPD. Results: Total number of participants are 100 in out of which 10% are non-Smokers and 90% are Smokers. In which we evaluate the structural changes related to COPD. The Result shows hyper- inflated lungs (100%) occupy in smokers and never-smokers. And focal bullae are not occupying in smokers and never-smokers and Flattening of diaphragm are (8%) in non-smokers and (92%) in smokers Increase chest size in never-smokers are (1%) and in smokers are (99%) present. Tubular heart is (63%) in smokers and (37%) in non-smokers. Conclusion: In this prospective study 100 patients of COPD are involved of both genders. In which males are more common than females. The overall study rate of COPD in this study is 10/90 with higher occurrence in males in smokers.

Modeling the Health and Economic Burden of Chronic Obstructive Pulmonary Disease in China From 2020 to 2039: A Simulation Study

ObjectivesDespite a growing prevalence of respiratory diseases in recent decades in China, limited evidence is available on the health and economic burden of chronic obstructive pulmonary disease (COPD). We estimated the 20-year health and economic burden of COPD in China from 2020 to 2039. MethodsWe created a probabilistic dynamic open-cohort Markov model of COPD for the Chinese population aged ≥40 years. Projections of population growth and urbanization rates were obtained from the United Nations Population Division. Other parameter inputs including smoking prevalence, COPD prevalence and severity distributions, disease-related costs, and utility weights were obtained from the most recent published literature. We modeled number of COPD patients, excess mortality due to COPD, exacerbations, COPD-attributable losses of quality-adjusted life-years, and direct and indirect COPD costs over the 20 years. ResultsThe number of COPD patients was projected to increase from 88.3 million in 2020 to 103.3 million in 2039. The projected total losses of quality-adjusted life-years and the excess mortality due to COPD were, respectively, estimated to be 253.6 million and 3.9 million over the 20 years. The projected 20-year total discounted direct and indirect costs of COPD were, respectively, $3.1 trillion and $360.5 billion. The projected health and economic burden was higher in males and urban areas. ConclusionsCOPD is projected to inflict a substantial burden to the society and the health care system in China. Effective strategies for prevention and early management of COPD are needed to mitigate the forthcoming disease burden.