scholarly journals Association of Clonal Hematopoiesis with Chronic Obstructive Pulmonary Disease

Blood ◽  
2021 ◽  
Author(s):  
Peter Miller ◽  
Dandi Qiao ◽  
Joselyn Rojas-Quintero ◽  
Michael C. Honigberg ◽  
Adam S. Sperling ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Somatic Mutations ◽  
Hematopoietic Cells ◽  
Smoke Exposure ◽  
Smoking History ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Clonal Hematopoiesis ◽  
Severe Copd

Chronic obstructive pulmonary disease (COPD) is associated with age and smoking, but other determinants of the disease are incompletely understood. Clonal hematopoiesis of indeterminate potential (CHIP) is a common, age-related state in which somatic mutations in clonal blood populations induce aberrant inflammatory responses. Patients with CHIP have an elevated risk for cardiovascular disease, but the association with COPD remains unclear. We analyzed whole-genome and exome sequencing data to detect CHIP in 48,835 subjects, of whom 8,444 had moderate-to-very-severe COPD, from four separate cohorts with COPD phenotyping and smoking history. We measured emphysema in murine models in which Tet2 was deleted in hematopoietic cells. In COPDGene, individuals with CHIP had a risk of moderate-to-severe and severe or very severe COPD 1.6 and 2.2 times greater than non-carriers, respectively (adjusted 95% confidence intervals [CI], 1.1 to 2.2 and 1.5 to 3.2). These findings were consistent observed in three additional cohorts and meta-analyses of all subjects. CHIP was also associated with decreased FEV1% predicted in COPDGene (mean between group difference -5.7%; adjusted 95% CI, -8.8 to -2.6), a finding replicated in additional cohorts. Smoke exposure was associated with a small but significant increased risk of having CHIP (OR 1.03 per ten pack-years, 95% CI 1.01-1.05) in the meta-analysis of all subjects. Inactivation of Tet2 in mouse hematopoietic cells exacerbated emphysema development and inflammation in cigarette smoke exposure models. Somatic mutations in blood cells are associated with the development and severity of COPD, independent of age and cumulative smoke exposure.

scholarly journals Paraoxonase 1 and Chronic Obstructive Pulmonary Disease: A Meta-Analysis

Antioxidants ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 1891
Author(s):  
Jun Watanabe ◽  
Kazuhiko Kotani ◽  
Alejandro Gugliucci
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Meta Analysis ◽  
Paraoxonase 1 ◽  
Pon1 Activity ◽  
Chronic Obstructive ◽  
Healthy Controls ◽  
Obstructive Pulmonary Disease ◽  
Paraoxonase Activity ◽  
Severe Copd

Oxidative stress is a driving factor in the pathophysiology of chronic obstructive pulmonary disease (COPD). While paraoxonase 1 (PON1) is an antioxidant enzyme and a potential biomarker of this disease, data regarding the status of PON-1 in COPD are inconclusive. In this regard, to shed light on this issue, we performed a meta-analysis of data on PON1 activity in COPD. Electronic databases (MEDLINE, Embase and CENTRAL) were searched for available studies on PON1 activity in patients with stable COPD published before October 2021. A meta-analysis was performed using random-effects models. Twelve studies (12 studies on paraoxonase and three on arylesterase) were identified. Patients with COPD had lower levels of paraoxonase activity (standard mean difference [SMD] −0.77, 95% confidence interval [CI] −1.35 to −0.18) and arylesterase activity (SMD −1.15, 95% CI −1.95 to −0.36) in comparison to healthy controls. In subgroup analyses, paraoxonase activity was lower in patients of studies as consisted of mainly non-severe COPD (SMD −1.42, 95% CI −2.04 to −0.79) and, by contrast, slightly higher in patients of studies including severe COPD (SMD 0.33, 95% CI 0.02 to 0.64) in comparison to healthy controls. Arylesterase activity showed a similar trend. Overall, PON1 activity was lower in patients with COPD, suggesting that PON1-related antioxidant defense is impaired in COPD. Future studies are warranted.

scholarly journals Prevalence of obstructive sleep apnea among patients with chronic obstructive pulmonary disease

2021 ◽  
Vol 15 (1) ◽  
Author(s):  
Osama Ibrahim Mohammad ◽  
Ahmed Gouda Elgazzar ◽  
Shymaa Mohammad Mahfouz ◽  
Marwa Elsayed Elnaggar
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Pulmonary Disease ◽  
Chronic Obstructive ◽  
Obese Patients ◽  
Obstructive Pulmonary Disease ◽  
Copd Patients ◽  
Obstructive Sleep ◽  
Severe Copd

Abstract Background The conjunction of chronic obstructive pulmonary disease (COPD) and obstructive sleep apnea (OSA) is known as overlap syndrome (OS). The coexistence of these diseases has cardiovascular morbidity and mortality. The aim of this study is to assess the prevalence of OSA in COPD patients. One hundred COPD patients (obese and non-obese) performed sleep questionnaires and polysomnograms. Results OSA prevalence in COPD was 50% and it increases with increasing disease severity (P < 0.001). The highest prevalence of OSA was found in obese patients with severe COPD; 90.5% of these patients have OSA. In the OSA group, obese patients were found to have significantly higher STOP-Bang Questionnaire (SBQ), Epworth Sleep Scale (ESS), modified medical research council (mMRC) dyspnea scale, apnea-hypopnea index (AHI), respiratory disturbance index (RDI), and oxygen desaturation index (ODI). Both obese and non-obese COPD patients showed significant positive correlations between AHI and smoking index (SI), SBQ, ESS, mMRC, ODI, and neck circumference (NC). Conclusions From this study, it can be concluded that moderate and severe COPD patients had a higher diagnosis of sleep-disordered breathing. Also, obese-COPD patients are more susceptible to develop OSA. Trial registration Name of the registry: Benha University Protocol Record Benha U123, Obstructive Sleep Apnea Prevalence in Patients With Chronic Obstructive Pulmonary Diseases. Trial registration number: NCT04903639. Date of registry: 5/22/2021 (retrospective study).

scholarly journals Morphological and functional erythrocyte parameters in smokers with chronic obstructive pulmonary disease

2008 ◽  
pp. 48-52
Author(s):  
E. V. Privalova ◽  
T. V. Vavilova ◽  
N. A. Kuzubova
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Smoking History ◽  
Chronic Obstructive ◽  
Bronchial Obstruction ◽  
Obstructive Pulmonary Disease ◽  
Compensatory Reaction ◽  
Copd Patients

The aim of this study was to investigate morphological and functional erythrocyte parameters in smokers with chronic obstructive pulmonary disease (COPD). We measured erythrocyte parameters (RBC, HGB, HCT, MCV, MCH, MCHC, RDW-SD) using the automatic hematological analyzer Sysmex XT-2000i. Sixty-nine patients participated in the study. The patients were divided into 3 groups: 34 patients with COPD (mean age 63 yrs, median smoking history 36 packyrs); 15 smokers without bronchial obstruction (mean age 56 yrs, median smoking history 28 packyrs) and 20 nonsmokers of the sane age without bronchial obstruction. Smokers with COPD and smokers without bronchial obstruction had significantly higher erythrocyte parameters compared to those of nonsmokers. Smokers demonstrated higher HGB level that could be as a compensatory reaction to nicotine-related preclinical hypoxia. Marked increase in RBC number and anisocytosis (RDW-SD) reflected the erythron activation in smokers with COPD. These results suggest that measurement of erythrocyte parameters could be useful to assess symptomatic erythrocytosis in COPD patients.

scholarly journals Decreased plasma epidermal growth factor (EGF) levels in patients with severe chronic obstructive pulmonary disease

Pneumologia ◽  
2019 ◽  
Vol 68 (1) ◽  
pp. 21-26
Author(s):  
Retno AS Soemarwoto ◽  
Andika Chandra Putra ◽  
Syazili Mustofa ◽  
◽  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Pulmonary Disease ◽  
Plasma Levels ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Copd Patients ◽  
Epidermal Growth ◽  
Severe Copd

Abstract Background Chronic mucus hypersecretion is a common feature in chronic obstructive pulmonary disease (COPD) and is associated with epidermal growth factor (EGF) activity. Aberrant EGF and its receptor signalling can cause airway hyperproliferation, increase in mucous cell differentiation and mucus hyperproduction. Furthermore, it can also promote subepithelial fibrosis and excessive collagen deposition in COPD. The objective of this research was to investigate the plasma levels of EGF in smokers with COPD in comparison with clinically healthy smokers. In addition, the relationship between the plasma levels of EGF and clinical features was investigated. Methods A cross-sectional study included 82 clinically stable male patients with mild-to-very severe COPD (mean age: 64.5±8.6 years), and the control group consisted of 86 healthy male smokers (mean age: 61.6±9.5 years). To define COPD, we performed spirometry and classified COPD using Global Initiative for Chronic Obstructive Lung Disease (GOLD) classification. We analyzed the levels of EGF by enzyme-linked immunosorbent assay in plasma. Results The mean serum levels of EGF were significantly lower in smokers with COPD than those in controls (69.30 and 83.82 pg/mL, respectively, p = 0.046). The plasma levels of EGF were significantly different (p = 0.004) between mild COPD and moderate-to-very severe COPD. There were no significant differences between the levels of EGF in plasma of spontaneous sputum producers (COPD patients) vs. nonsputum producers (p = 0.101) and between nonexacerbated COPD and exacerbated COPD patients(p = 0.138). Conclusions There is a significant difference in the plasma levels of EGF in male smokers with COPD as compared with male healthy smokers. Our findings suggest that the plasma levels of EGF may contribute to the pathogenesis of COPD.

scholarly journals Association of NLRP1 Coding Polymorphism with Lung Function and Serum IL-1β Concentration in Patients Diagnosed with Chronic Obstructive Pulmonary Disease (COPD)

Genes ◽  
2019 ◽  
Vol 10 (10) ◽  
pp. 783 ◽  
Author(s):  
Ozretić ◽  
da Silva Filho ◽  
Catalano ◽  
Sokolović ◽  
Vukić-Dugac ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Lung Function ◽  
Pulmonary Disease ◽  
Minor Allele ◽  
Fine Tuning ◽  
Airflow Limitation ◽  
Smoking History ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
The Impact

Chronic obstructive pulmonary disease (COPD) is a chronic disease characterized by a progressive decline in lung function due to airflow limitation, mainly related to IL-1β-induced inflammation. We have hypothesized that single nucleotide polymorphisms (SNPs) in NLRP genes, coding for key regulators of IL-1β, are associated with pathogenesis and clinical phenotypes of COPD. We recruited 704 COPD individuals and 1238 healthy controls for this study. Twenty non-synonymous SNPs in 10 different NLRP genes were genotyped. Genetic associations were estimated using logistic regression, adjusting for age, gender, and smoking history. The impact of genotypes on patients’ overall survival was analyzed with the Kaplan–Meier method with the log-rank test. Serum IL-1β concentration was determined by high sensitivity assay and expression analysis was done by RT-PCR. Decreased lung function, measured by a forced expiratory volume in 1 s (FEV1% predicted), was significantly associated with the minor allele genotypes (AT + TT) of NLRP1 rs12150220 (p = 0.0002). The same rs12150220 genotypes exhibited a higher level of serum IL-1β compared to the AA genotype (p = 0.027) in COPD patients. NLRP8 rs306481 minor allele genotypes (AG + AA) were more common in the Global Initiative for Chronic Obstructive Lung Disease (GOLD) definition of group A (p = 0.0083). Polymorphisms in NLRP1 (rs12150220; OR = 0.55, p = 0.03) and NLRP4 (rs12462372; OR = 0.36, p = 0.03) were only nominally associated with COPD risk. In conclusion, coding polymorphisms in NLRP1 rs12150220 show an association with COPD disease severity, indicating that the fine-tuning of the NLRP1 inflammasome could be important in maintaining lung tissue integrity and treating the chronic inflammation of airways.

scholarly journals Chronic Cigarette Smoke Exposure Primes NK Cell Activation in a Mouse Model of Chronic Obstructive Pulmonary Disease

2010 ◽  
Vol 184 (8) ◽  
pp. 4460-4469 ◽  
Author(s):  
Gregory T. Motz ◽  
Bryan L. Eppert ◽  
Brian W. Wortham ◽  
Robyn M. Amos-Kroohs ◽  
Jennifer L. Flury ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Mouse Model ◽  
Pulmonary Disease ◽  
Cigarette Smoke ◽  
Cell Activation ◽  
Nk Cell ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease

scholarly journals CT-measured lung air-trapping is associated with higher carotid artery stiffness in individuals with chronic obstructive pulmonary disease

2018 ◽  
Vol 125 (6) ◽  
pp. 1760-1766 ◽  
Author(s):  
Rachel E. Luehrs ◽  
John D. Newell ◽  
Alejandro P. Comellas ◽  
Eric A. Hoffman ◽  
Kelsey Warner ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Carotid Artery ◽  
Pulmonary Disease ◽  
Smoking History ◽  
Chronic Obstructive ◽  
Cvd Risk ◽  
Air Trapping ◽  
Obstructive Pulmonary Disease ◽  
Copd Patients ◽  
Artery Stiffness

Early stages of chronic obstructive pulmonary disease (COPD) are characterized by the loss and narrowing of terminal bronchioles in the lung, resulting in “air-trapping,” often occurring before overt emphysema manifests. Individuals with an airway-predominant phenotype of COPD display extensive lung air-trapping and are at greater cardiovascular disease (CVD) risk than COPD patients with an emphysema-predominant phenotype. We hypothesized that the degree of computed tomography (CT)-quantified lung air-trapping would be associated with greater aortic and carotid artery stiffness and lower endothelial function, known biomarkers of CVD risk. Lung air-trapping was associated with greater aortic stiffness (carotid femoral pulse wave velocity, CFPWV) ( r = 0.60, P = 0.007) and carotid β-stiffness ( r = 0.75, P = 0.0001) among adults with ( n = 10) and without ( n = 9) a clinical diagnosis of COPD and remained significant after adjusting for blood pressure (BP) and smoking history (pack-years) (carotid β-stiffness: r = 0.68, P < 0.01; CFPWV r = 0.53, P = 0.03). The association between lung air-trapping and carotid β-stiffness remained significant after additionally adjusting for age and forced expiratory volume 1(FEV1) ( r = 0.64, P = 0.01). In the COPD group only ( n = 10), lung air-trapping remained associated with carotid β-stiffness ( r = 0.82, P = 0.05) after adjustment for age, pack-years, and FEV1. In contrast, no association was observed between CFPWV and lung air-trapping after adjustment for BP, pack-years, age, and FEV1 ( r = 0.12, P = 0.83). Lung air-trapping was not associated with endothelial function (brachial artery flow-mediated dilation) in the entire cohort ( P = 0.80) or in patients with COPD only ( P = 0.71). These data suggest that carotid artery stiffness may be a mechanism explaining the link between airway-predominant phenotypes of COPD and high CVD risk. NEW & NOTEWORTHY Previous cross-sectional studies have demonstrated greater large elastic artery stiffness and lower endothelium-dependent dilation in chronic obstructive pulmonary disease (COPD) patients compared with controls. Furthermore, COPD patients with emphysema have greater aortic stiffness than non-COPD controls, and the degree of stiffness is associated with emphysema severity. The present study is the first to demonstrate that even before overt emphysema manifests, lung air-trapping is associated with carotid artery stiffness in COPD patients independent of blood pressure, age, or smoking history.

scholarly journals The Burden of Illness in Patients with Moderate to Severe Chronic Obstructive Pulmonary Disease in Canada

2012 ◽  
Vol 19 (5) ◽  
pp. 319-324 ◽  
Author(s):  
M Reza Maleki-Yazdi ◽  
Suzanne M Kelly ◽  
Sy S Lam ◽  
Mihaela Marin ◽  
Martin Barbeau ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Burden Of Illness ◽  
Patient Survey ◽  
Forced Expiratory Volume ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Global Initiative ◽  
One Year ◽  
Severe Copd

INTRODUCTION: No recent Canadian studies with physician- and spirometry-confirmed diagnosis of chronic obstructive pulmonary disease (COPD) that assessed the burden of COPD have been published.OBJECTIVE: To assess the costs associated with maintenance therapy and treatment for acute exacerbations of COPD (AECOPD) over a one-year period.METHODS: Respirologists, internists and family practitioners from across Canada enrolled patients with an established diagnosis of moderate to severe COPD (Global initiative for chonic Obstructive Lung Disease stages 2 and 3) confirmed by postbronchodilator spirometry. Patient information and health care resources related to COPD maintenance and physician-documented AECOPD over the previous year were obtained by chart review and patient survey.RESULTS: A total of 285 patients (59.3% male; mean age 70.4 years; mean pack years smoked 45.6; mean duration of COPD 8.2 years; mean postbronchodilator forced expiratory volume in 1 s 58.0% predicted) were enrolled at 23 sites across Canada. The average annual COPD-related cost per patient was $4,147. Across all 285 patients, maintenance costs were $2,475 per patient, of which medications accounted for 71%. AECOPD treatment costs were $1,673 per patient, of which hospitalizations accounted for 82%. Ninety-eight patients (34%) experienced a total of 157 AECOPD. Treatment of these AECOPD included medications and outpatient care, 19 emergency room visits and 40 hospitalizations (mean length of stay 8.9 days). The mean cost per AECOPD was $3,036.DISCUSSION: The current costs associated with moderate and severe COPD are considerable and will increase in the future. Appropriate use of medications and strategies to prevent hospitalizations for AECOPD may reduce COPD-related costs because these were the major cost drivers.

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