COPD: Journal of Chronic Obstructive Pulmonary Disease最新文献

Chronic obstructive pulmonary disease (COPD) is a major burden of healthcare worldwide. We aimed to determine the effects of PDE-5 inhibitors on clinical outcomes and haemodynamic parameters in patients with COPD. A PROSPERO-registered systematic review and meta-analysis (identification number CRD42021227578) were performed to analyse the effects of PDE-5 inhibitors in patients with COPD. Data were sourced from MEDLINE, EMBASE, Cochrane Register of Controlled Trials and "ClinicalTrials.gov." Randomised controlled trials (RCTs) comparing PDE-5 inhibitors with control in patients with COPD were included. Quality assessment was carried out using the Cochrane Collaboration's tool for assessing the risk of bias in randomised trials. The pooled mean difference of 6-minute walk distance (6MWD) and mean pulmonary arterial pressure based on inverse variance estimation were analysed with a fixed-effect model or random-effects model meta-analysis. Nine RCTs involving 414 patients were included in the review. There was no significant difference in 6MWD (mean difference = 22.06 metres, 95% confidence interval (CI), -5.80 to 49.91). However, there was a statistically significant difference between PDE-5 inhibitor and control groups in mean pulmonary artery pressure (mean difference = -3.83 mmHg, 95% CI, -5.93 to -1.74). Headaches were the most common adverse event, occurring significantly in the PDE-5 inhibitor intervention group (odds ratio 3.83, 95% CI, 1.49 to 9.86). This systematic review indicates that PDE-5 inhibitors do not improve exercise capacity despite some possible improvements in haemodynamic parameters in COPD patients.

Patients with chronic obstructive pulmonary disease (COPD) may have a limited level of physical activity in daily life (PADL) and health-related quality of life (HRQOL). The interrelationships of these variables should be measure by cluster analysis to characterize this population and enable rehabilitation programs to target each patient profile identified. This study investigates different phenotypes in COPD according to PADL and HRQOL. A cross-sectional study with cluster analysis was done, in which 76 people with COPD were submitted to measurements to characterize the sample on first day, followed by used of physical activity monitor, which was worn for 7 days. After 7 days, the six-minute walk test (6MWT) and HRQOL questionnaires were applied (St. George's Respiratory Questionnaire). The main results: three phenotypes were identified (A, B and C), with phenotype A who exhibited an inactive physical activity level and HRQOL scores above the value deemed satisfactory, phenotype B those with active physical activity level and poor HRQOL scores, and phenotype C subjects with inactive physical activity level and HRQOL scores but the value is close to cutoff point. To conclude, three phenotypes were found, with one indicating disproportionality between PADL and HRQOL.

Pulmonary rehabilitation (PR) is an essential method for Acute exacerbation in chronic obstructive pulmonary disease (AECOPD) recovery. We perform a meta-analysis to compare early PR with usual care. A literature search was performed through these databases: PubMed, MEDLINE database, Google Scholar, Cochrane, Embase from inception to July 2021. Eligible trials were clinical randomized controlled trials comparing the effects of early PR and usual care in AECOPD patients. The primary endpoint of this meta-analysis was FEV1% predicted, 6-min walk test (6MWD), modified Medical Research Council (mMRC) and George Respiratory Questionnaire-total (SGRQ-total). The secondary outcomes were borg dyspnea score, short-form 36 health survey questionnaire physical (SF-36 physical) and SF-36 mental. We included 13 RCTs with a total of 866 patients. There were no significant effects of the PR group on measures of FEV1% predicted (MD = 0.50, 95%CI -1.43 to 2.44, Z = 0.51, p = 0.61), borg dyspnea score (MD = -0.88, 95%CI -1.89 to 0.13, Z = 1.71, p = 0.09) and SF-36 mental (MD = 4.34, 95%CI -1.64 to 10.32, Z = 1.42, p = 0.16) compared with usual care. PR group achieved better 6MWD (MD = 97.58, 95%CI 17.21 to 177.96, Z = 2.38, p = 0.02), mMRC (MD = -0.36, 95%CI -0.52 to -0.21, Z = 4.56, p ˂ 0.00001), SGRQ-total (MD= -9.67, 95%CI -16.23 to -3.11, Z = 2.89, p = 0.004) and SF-36 physical (MD = 4.98, 95%CI 0.60 to 9.35, Z = 2.23, p = 0.03) compared with usual care group. Early PR in AECOPD patients would lead to better 6MWD, mMRC, SGRQ-total and SF-36 physical. But there were no significant effects of the PR group on measures of FEV1% predicted, borg dyspnea score and SF-36 mental.

Existing comprehensive management strategies for COPD effectively relieve the symptoms of patients, delay the deterioration of lung function, and prevent the progression of COPD through various means and multidisciplinary interventions. However, there has been limited progress in therapies that address the underlying causes of COPD pathogenesis. Recent studies have identified specific changes in the gut and pulmonary microbiota in response to exposure to smoke that can cause or exacerbate CS-COPD by regulating the inflammatory immune response in the lungs through the gut-lung axis. As a convenient and controllable intervention, modifying the diet to include more dietary fiber can effectively improve the prognosis of CS-COPD. Gut microbiota ferment dietary fiber to produce short-chain fatty acids, which connect the microbial communities in the lung and gut mucosa across the gut-lung axis, playing an anti-inflammatory and immunosuppressive role in the lungs. Given that the effect of dietary fiber on gut microbiota was highly similar to that of quitting smoking on gut microbiota, we assume that microbiota might be a potential therapeutic target for dietary fiber to alleviate and prevent CS-COPD. This study examines the similarities between pulmonary and gut microbiota changes in the presence of smoking and dietary fiber. It also highlights the mechanism by which SCFAs link pulmonary and gut microbiota in CS-COPD and analyzes the anti-inflammatory and immunomodulatory effects of short-chain fatty acids on CS-COPD via the gut-lung axis.

Alpha-1 Antitrypsin deficiency (AATD) is a genetic condition that can lead to Chronic Obstructive Pulmonary Disease. The burden of psychological disease, its impact and contributing factors in patients with AATD are largely unknown. This study determined the prevalence of depression and anxiety in AATD and its clinical impact. All subjects with PiZZ/PiZnull (n = 635) and PiSZ (n = 111) genotypes within the AATD registry who had sufficient data to calculate pulmonary physiological and health status (HS) decline were grouped as those with or without a diagnosis of depression and/or anxiety. Univariate and multivariate analyses were performed on physiological, demographic and HS parameters. Depression and/or anxiety was present in 16.4% overall in both PiSZ and PiZZ/PiZnull cohorts and was associated with lower baseline pulmonary function and worse HS. In the multivariable analysis of the PiZZ/PiZnull cohort, a greater average decline in FEV₁% predicted was observed in those with depression and/or anxiety than those without (-1.53 SD ± 2.26 per year, -0.99 ± 1.79, respectively; p = 0.03) but there was no difference in HS decline (p = 0.33). No differences were seen in the PiSZ cohort. Dyspnoea (mMRC score) was generally worse in those with depression and/or anxiety than those without. Comorbidity burden did not differ between those with or without depression and/or anxiety. Disease severity and progression may be contributing to the prevalence of psychological factors in PiZZ/PiZnull patients. Patients who are declining rapidly should be actively monitored for psychological co-morbidity and treated by cognitive or pharmacological means.Supplemental data for this article is available online at https://doi.org/10.1080/15412555.2021.1991904 .

A concern of antibiotic use in chronic obstructive pulmonary disease (COPD) is the emergence and propagation of antimicrobial resistance (AMR). A systematic review was conducted to determine prevalence, pattern, risk factors and consequences of AMR in COPD. Bibliographic databases were searched from inception to November 2020, with no language restrictions, including studies of any design that included patients with COPD and reported prevalence and pattern of AMR. 2748 unique titles and abstracts were identified, of which 63 articles, comprising 26,387 patients, met inclusion criteria. Forty-four (69.8%) studies were performed during acute exacerbation. The median prevalence of AMR ranged from 0-100% for Pseudomonas aeruginosa, Moraxella catarrhalis, Klebsiella pneumoniae and Acinetobacter baumannii. Median resistance rates of H influenzae and S pneumoniae were lower by comparison, with maximum rates ≤40% and ≤46%, respectively, and higher for Staphylococcus aureus. There was a trend towards higher rates of AMR in patients with poorer lung function and greater incidence of previous antibiotic exposure and hospitalisation. The impact of AMR on mortality was unclear. Data regarding antimicrobial susceptibility testing techniques and the impact of other risk factors or consequences of AMR were variable or not reported. This is the first review to systematically unify data regarding AMR in COPD. AMR is relatively common and strategies to optimise antibiotic use could be valuable to prevent the currently under-investigated potential adverse consequences of AMR.Supplemental data for this article is available online at https://doi.org/10.1080/15412555.2021.2000957 .

Cigarette smoking-related inflammation, cellular stresses, and tissue destruction play a key role in lung disease, such as chronic obstructive pulmonary disease (COPD). Notably, augmented apoptosis and impaired clearance of apoptotic cells, efferocytosis, contribute to the chronic inflammatory response and tissue destruction in patients with COPD. Of note, exposure to cigarette smoke can impair alveolar macrophages efferocytosis activity, which leads to secondary necrosis formation and tissue inflammation. A better understanding of the processes behind the effect of cigarette smoke on efferocytosis concerning lung disorders can help to design more efficient treatment approaches and also delay the development of lung disease, such as COPD. To this end, we aimed to seek mechanisms underlying the impairing effect of cigarette smoke on macrophages-mediated efferocytosis in COPD. Further, available therapeutic opportunities for restoring efferocytosis activity and ameliorating respiratory tract inflammation in smokers with COPD were also discussed.

Blood eosinophils have been proposed as a surrogate biomarker of airway eosinophilia that can be used for treatment decisions in patients with COPD, mainly for the identification of candidates for the initiation or withdrawal of therapy with inhaled corticosteroids, as well as for the identification of patients at future risk of exacerbations. In this manuscript we review the recent literature on blood eosinophils in the management of patients with COPD, in an attempt to answer the major questions that are relevant for the practicing clinician. A growing body of evidence suggests that eosinophilic COPD may constitute a separate phenotype of the disease with distinct clinical features and blood eosinophils may represent a potential candidate surrogate marker for specific COPD patients. Several points still need to be clarified, including the role of eosinophils for the identification of candidates for future COPD therapies, yet blood eosinophils plausibly represent the most dependable and promising biomarker for the precision management of COPD today.

Leukotriene A₄ hydrolase (LTA₄H) is associated with inflammation and emphysema. Nevertheless, clinical implications of LTA₄H genetic polymorphism in chronic obstructive pulmonary disease (COPD) has been understudied to date. A prospective study was performed to investigate the clinical implications of LTA₄H genetic polymorphism in patients with COPD. AA, GA, and GG types of genetic polymorphism of LTA₄H were assayed in patients with COPD at the baseline. Then all patients were followed up for 12 months. At the baseline, the number of participants with AA, GA, and GG type of LTA₄H rs7971150 were 22 (14.2%), 43 (27.7%), and 90 (58.1%) in the COPD group (n = 155), whereas 55 (36.7%), 38 (25.3%), and 57 (38.0%) in the control group (n = 150) (p = 0.001). During the follow-up, the variations with respect to forced expiratory volume in one second (FEV₁), 6 min walking distance (6MWD), and BODE (body-mass index, obstruction, dyspnea, and exercise capacity) were similar between patients with AA and GA types, which were both lower than those of GG type. The patients with GG type had more hospitalizations than patients with AA (p = 0.001) and GA (p = 0.001) types, respectively. The cumulative hospitalization-free rate in patients with GG type was lower than those of patients with AA and GA types, respectively (p = 0.019). Compared with COPD patients with AA and GA types, patients with GG type were positively correlated with smoking, more hospitalizations, worse FEV₁, 6MWD, and BODE index. The current study suggests that GG type of LTA4H is a predisposing factor in COPD development, functional decline, and exacerbation of patients with COPD.

Although fibrinogen is a FDA qualified prognostic biomarker in COPD, it still lacks sufficient resolution to be clinically useful. Next to replication of findings in different cohorts also the combination with other validated biomarkers should be investigated. Therefore, the aim of this study was to confirm in a large well-defined population of COPD patients whether fibrinogen can predict mortality and whether a combination with the biomarker MR-proADM can increase prognostic accuracy. From the COMIC cohort study we included COPD patients with a blood sample obtained in stable state (n = 640) and/or at hospitalization for an acute exacerbation of COPD (n = 262). Risk of death during 3 years of follow up for the separate and combined biomarker models was analyzed with Cox regression. Furthermore, logistic regression models for death after one year were constructed. When both fibrinogen and MR-proADM were included in the survival model, a doubling in fibrinogen and MR-proADM levels gave a 2.2 (95% CI 1.3-3.7) and 2.1 (95% CI 1.5-3.0) fold increased risk of dying, respectively. The prediction model for death after 1 year improved significantly when MR-proADM was added to the model with fibrinogen (AUC increased from 0.78 to 0.83; p = 0.02). However, the combined model was not significantly more adequate than the model with solely MR-proADM (AUC 0.83 vs 0.82; p = 0.34). The study suggests that MR-proADM is more promising than fibrinogen in prediciting mortality. Adding fibrinogen to a model containing MR-proADM does not significantly increase the predictive capacity of the model.