COPD: Journal of Chronic Obstructive Pulmonary Disease最新文献

Chronic obstructive pulmonary disease (COPD) is a complex disease, and its pathogenesis is influenced by genetic factors. This study aimed to evaluate the role of IL5RA genetic variation in the risk of COPD. In this study, 498 patients with COPD and 498 normal controls were recruited. Subsequently, five SNPs (rs3804795, rs2290610, rs13097407, rs334782, and rs3856850) in the IL5RA gene were genotyped. Logistic analysis examined the association of five single nucleotide polymorphisms (SNPs) in IL5RA with the risk of COPD under various genetic models. Furthermore, the association between IL5RA and susceptibility to COPD was comprehensively analyzed with stratification based on age, sex, smoking, and alcohol consumption. Our study showed that IL5RA rs13097407 reduced susceptibility to COPD (OR = 0.43, p < 0.001, p (FDR)< 0.001). On the other hand, rs3856850 was associated with an increased risk of COPD (OR = 1.71, p = 0.002, p (FDR) = 0.002). Interestingly, the effect of IL5RA SNPs on susceptibility to COPD was found to be influenced by factors such as sex and smoking. IL5RA gene variants were significantly associated with susceptibility to COPD.

The Assessment of the Burden of COPD (ABC) tool facilitates shared decision-making and goal setting to develop a personalized care plan. In a previous trial (RCT), the ABC tool was found to have a significant effect on patients' Health-related Quality of Life (HRQoL). In this exploratory study we used data from the intervention group of the RCT to investigate if patients with health-related goals had an improved HRQoL compared to those without goals, and if the quality and types of goals differed for those who have a clinically meaningful improvement in HRQoL. We hypothesized that the quality and the type of the goal described in the ABC tool, relates to an improved HRQoL. We assessed the quality of the goals according to the Specificity, Measurability, Achievability, Relevance and Timeliness (SMART) criteria, and coded and counted each type of goal. We found that having a goal or not, did not differ significantly for those who had a clinically meaningful improved HRQoL versus those who had not, nor was the quality or type of goal significantly different. The most common types of goals were exercise more, smoke less, and improve weight. Based on the results, we speculate that when a clinically meaningful improvement in HRQoL is achieved, it is not related to a single component (i.e. goal setting as part of shared decision-making) but that the different components of the ABC tool (visualization of burden, shared decision making, utilization of tailored evidence based interventions, and regular monitoring of progress) may have a synergistic effect on disease cognition and/or behavior change. Noteworthy, the sample size was small while the calculated effect size was moderate, making it unlikely to find a significant effect.

Home exercises (HE) with minimal resources seem to be useful in individuals with COPD. The objective was to evaluate the effects of HE, on activities of daily living (ADL), dyspnea, on the health status(CAT) and quality of life (HRQoL) of individuals with COPD GOLD II to IV. Quasi-experimental study of the effects of HE, for 2 months, 3 times a week. Individuals with COPD(n = 45) were recruited, 37 started the protocol(9 did not complete it). 28 individuals (mean age 62.04 ± 5.8 years, FEV1: 44.7 ± 2.25%, FEV1/FVC 59.8 ± 6.9%) were evaluated before and after training. We observed improvements in the ADL-Glittre (4.9 ± 1.4 vs 3.9 ± 1.1 min; mean difference: -0.9 ± 0.2 min [95%CI: -1.3 to -0.2]; p = 0.008), as well as the mMRC score(2.8 ± 1.1 vs 2.07 ± 0.81; mean difference: 0.7 ± 0.3 [95%CI: -1.20.18 to -0.2]; p = 0.009), and in the CAT (25.6 ± 4.8 vs 18.9 ± 3.1; mean difference: -6.6 ± 3.4 [95%CI: -10.6 to -1.6]; p = 0.042). Analyzing the mean change before and after the intervention, a weak correlation was observed between ADL-Glittre and mMRC (r = 0.35; [95% CI 0.09; 0.56]; p = 0.009); moderate between ADL-Glittre and CAT (r = 0.52; [95% CI 0.30; 0.69]; p < 0.001) and between ADL-Glittre and SGRQ (r = 0.50; [95% CI 0 .27; 0.67]; p < 0.001). Individuals with COPD can benefit from HE performed autonomously and with minimal resources, as this proposal improves functional capacity for ADL, health perception and dyspnea.

Current literature yields unequivocal results regarding the effect of body composition on physical function in patients with chronic obstructive pulmonary disease and disproportionately includes a majority of males. The purpose of this study was to determine whether specific body composition measures are significantly associated with physical function and exercise capacity in patients with chronic obstructive pulmonary disease with equal representation of males and females. Independent variables included sex, total body mass, total body lean and fat mass, appendicular total mass, and appendicular lean and fat mass. Dependent variables included peak oxygen consumption, 6-minute walk distance and self-reported physical function. Patients (n = 170) with dual-energy X-ray absorptiometry data, 6-minute walk distance, and self-reported physical function were used for these analyses. A sub-set of 145 of these patients with peak oxygen consumption data were also analysed. Hierarchical multiple regression analysis was used to determine if sex and body composition measures correlated with physical function and exercise capacity and if they explained additional variance after controlling for disease severity. After controlling for disease severity, appendicular lean mass, total body fat mass, and sex explained an additional 16.5% of the variance in peak oxygen consumption (p < 0.001). Appendicular lean mass explained an additional 8.9% of the variance in 6-minute walk distance (p < 0.001) and an additional 2.5% of the variance in self-reported physical function (p = 0.057). Body composition measures may further predict exercise capacity, 6-minute walk distance, and self-reported physical function in patients with chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease (COPD) is a difficult-to-cure disease that mainly affects the respiratory system. Inhaled anesthetic drug such as sevoflurane plays a controversial role in COPD by different concentration, but the underlying epigenetic mechanism remains unclear. Here, we prepared lipopolysaccharide (LPS)-induced COPD rat model, and isolated Alveolar type II (ATII) cells. We mainly focused DNA methylation on the promoter of COPD-related genes including Sftpa1, Napsa, Ca2, Sfta2, Lamp3, Wif1, Pgc, and Etv5. We observed COPD rat treated by sevoflurane with low (0.5%) and high (2%) concentrations displayed an opposite DNA methylation pattern. These six genes' promoter were all hypomethylated by 0.5% sevoflurane whereas hypermethylated by 2% sevoflurane, accompanied with the opposite transcriptional activity. We further verified that the DNMT1 binding ability contributed to DNA methylation these six genes' promoter. Moreover, we also captured DNMT1 and identified REC8 meiotic recombination protein (REC8) as the specific binding protein only existed in ATII cells treated with 0.5% sevoflurane rather than 2% and control. The binding ability of REC8 on these target genes' promoter showed highly positive correlation with DNMT1. In summary, we uncovered a potential epigenetic role of sevoflurane with low concentration in ATII cells of COPD that may help us deeply understand the pathogenesis and treatment mechanism of inhaled anesthesia drugs in COPD via a dose-dependent manner.

Because cigarette smoke can induce COPD/emphysema through accelerating senescence with or without an incomplete repair system. However, the pathogenesis of COPD following lung senescence induced by CS is not fully understood. Airspace enlargement and airway epithelial cell senescence are common finding during the COPD development. We investigated the lung tress response to CS and demonstrated that a stress-responsive transcription factor, FOXO3, was regulated by deacetylase. SIRT1 inhibited FOXO3 acetylation and FOXO3 degradation, leading to FOXO3 accumulation and activation in airway epithelial cells. CS exposure activated SIRT1 contributed to FOXO3 activation and functioned to protect lungs, as deletion of SIRT1 decreased CS-induced FOXO3 activation and resulted in more severe airway epithelial cells senescence airspace enlargement. Strikingly, deletion of FOXO3 during the development of COPD aggravated lung structural and functional damage, leading to a much more profound COPD phenotype. We show that deletion of FOXO3 resulted in decreased autophagic response and increased senescence, which may explain lung protection by FOXO3. Our study indicates that in the COPD, stress-responsive transcription factors can be activated for adaptions to counteract senescence insults, thus attenuating COPD development.

As a key adipokine, leptin has been extensively investigated for its potential role in the pathogenesis of chronic obstructive pulmonary disease (COPD). However, concordant conclusions have not been attained. In this study, we investigated the relationship between leptin and COPD using an integrative analysis that combined a Mendelian randomization (MR) study with transcriptomic data analysis. Here, the MR analysis was performed on the online platform MR-Base, and the bioinformatics analyses were performed with the aid of R Bioconductor packages. No evidence was found by the integrative analysis to support the association of the two attributes. All methods detected a null causal effect of leptin on COPD in the MR analysis. In particular, when the genetically predicted leptin level increased one unit, the risk of developing COPD was estimated as 0.999 (p = 0.943), 0.920 (p = 0.516), 1.002 (p = 0.885), and 1.002 (p = 0.906) by the Inverse Variance Weighted (IVW), MR-Egger, weighted median, and weighted mode method, respectively. Furthermore, no leptin-associated genes except one were identified as being differentially expressed between COPD and control in bioinformatics analysis. The observed association between leptin and COPD in previous observational studies may be attributable to unmeasured confounding effects or reverse causation.