Mild-moderate Chronic Obstructive Pulmonary Disease Research Articles

Haemodynamic compensations for exercise tissue oxygenation in early stages of COPD: an integrated cardiorespiratory assessment study

BackgroundCardiovascular comorbidities are increasingly being recognised in early stages of chronic obstructive pulmonary disease (COPD) yet complete cardiorespiratory functional assessments of individuals with mild COPD or presenting with COPD risk...

Activation of CD8+ T Cells in Chronic Obstructive Pulmonary Disease Lung.

Rationale: Despite the importance of inflammation in chronic obstructive pulmonary disease (COPD), the immune cell landscape in the lung tissue of patients with mild-moderate disease has not been well characterized at the single-cell and molecular level. Objectives: To define the immune cell landscape in lung tissue from patients with mild-moderate COPD at single-cell resolution. Methods: We performed single-cell transcriptomic, proteomic, and T-cell receptor repertoire analyses on lung tissue from patients with mild-moderate COPD (n = 5, Global Initiative for Chronic Obstructive Lung Disease I or II), emphysema without airflow obstruction (n = 5), end-stage COPD (n = 2), control (n = 6), or donors (n = 4). We validated in an independent patient cohort (N = 929) and integrated with the Hhip+/- murine model of COPD. Measurements and Main Results: Mild-moderate COPD lungs have increased abundance of two CD8+ T cell subpopulations: cytotoxic KLRG1+TIGIT+CX3CR1+ TEMRA (T effector memory CD45RA+) cells, and DNAM-1+CCR5+ T resident memory (TRM) cells. These CD8+ T cells interact with myeloid and alveolar type II cells via IFNG and have hyperexpanded T-cell receptor clonotypes. In an independent cohort, the CD8+KLRG1+ TEMRA cells are increased in mild-moderate COPD lung compared with control or end-stage COPD lung. Human CD8+KLRG1+ TEMRA cells are similar to CD8+ T cells driving inflammation in an aging-related murine model of COPD. Conclusions: CD8+ TEMRA cells are increased in mild-moderate COPD lung and may contribute to inflammation that precedes severe disease. Further study of these CD8+ T cells may have therapeutic implications for preventing severe COPD.

Physical Activity and Symptom Burden in COPD: The Canadian Obstructive Lung Disease Study.

The relationship between symptom burden and physical activity (PA) in chronic obstructive pulmonary disease (COPD) remains poorly understood with limited data on undiagnosed individuals and those with mild to moderate disease. The primary objective was to evaluate the relationship between symptom burden and moderate-to-vigorous intensity PA (MVPA) in individuals from a random population-based sampling mirroring the population at large. Baseline participants of the Canadian Cohort Obstructive Lung Disease (n=1558) were selected for this cross-sectional sub-study. Participants with mild COPD (n=406) and moderate COPD (n=331), healthy individuals (n=347), and those at risk of developing COPD (n=474) were included. The Community Healthy Activities Model Program for Seniors (CHAMPS) questionnaire was used to estimate MVPA in terms of energy expenditure. High symptom burden was classified using the COPD Assessment Test ([CAT] ≥10). Significant associations were demonstrated between high symptom burden and lower MVPA levels in the overall COPD sample (β=-717.09; 95% confidence interval [CI]=-1079.78, -354.40; p<0.001) and in the moderate COPD subgroup (β=-694.1; 95% CI=-1206.54, -181.66; p=0.006). A total of 72% of the participants with COPD were previously undiagnosed. The undiagnosed participants had significantly higher MVPA than those with physician diagnosed COPD (β=-592.41 95% CI=-953.11, -231.71; p=0.001). MVPA was found to be inversely related to symptom burden in a large general population sample that included newly diagnosed individuals, most with mild to moderate COPD. Assessment of symptom burden may help identify patients with lower MVPA, especially for moderate COPD and for relatively inactive individuals with mild COPD.

Similar programmed death ligand 1 (PD-L1) expression profile in patients with mild COPD and lung cancer

Programmed Death Ligand 1 (PD-L1) is crucial in regulating the immunological tolerance in non-small cell lung cancer (NSCLC). Alveolar macrophage (AM)-derived PD-L1 binds to its receptor, PD-1, on surveilling lymphocytes, leading to lymphocyte exhaustion. Increased PD-L1 expression is associated with cigarette smoke (CS)-exposure. However, the PD-L1 role in CS-associated lung diseases associated with NSCLC, such as chronic obstructive pulmonary disease (COPD), is still unclear. In two different cohorts of ever smokers with COPD or NSCLC, and ever and never smoker controls, we evaluated PD-L1 expression: (1) via cutting-edge digital spatial proteomic and transcriptomic profiling (Geomx) of formalin-fixed paraffin-embedded (FFPE) lung tissue sections (n = 19); and (2) via triple immunofluorescence staining of bronchoalveolar lavage (BAL) AMs (n = 83). PD-L1 mRNA expression was also quantified in BAL AMs exposed to CS extract. PD-L1 expression was increased in the bronchiolar wall, parenchyma, and vascular wall from mild-moderate (GOLD 1–2) COPD patients compared to severe-very severe (GOLD 3–4) COPD patients and controls. Within all the COPD patients, PD-L1 protein expression was associated with upregulation of genes involved in tumor progression and downregulation of oncosuppressive genes, and strongly directly correlated with the FEV1% predicted, indicating higher PD-L1 expression in the milder vs. more severe COPD stages. In bronchioles, PD-L1 levels were strongly directly correlated with the number of functionally active AMs. In BAL, we confirmed that AMs from patients with both GOLD 1–2 COPD and NSCLC had the highest and similar, PD-L1 expression levels versus all the other groups, independently from active cigarette smoking. Intriguingly, AMs from patients with more severe COPD had reduced AM PD-L1 expression compared to patients with mild COPD. Acute CS extract stimulation increased PD-L1 mRNA expression only in never-and not in ever-smoker AMs. Lungs from patients with mild COPD and NSCLC are characterized by a similar strong PD-L1 expression signature in bronchioles and functionally active AMs compared to patients with severe COPD and controls. Active smoking does not affect PD-L1 levels. These observations represent a new resource in understanding the innate immune mechanisms underlying the link between COPD and lung cancer onset and progression and pave the way to future studies focused on the mechanisms by which CS promotes tumorigenesis and COPD.

Study of Nocturnal Oxygen Desaturation in Chronic Obstructive Pulmonary Disease Patients

Background: Abnormal sleep architecture with decreased rapid eye movement sleep and arousals during the periods of nocturnal oxygen desaturation (NOD) are seen in patients with chronic obstructive pulmonary disease (COPD) with significant consequences. This study was done to evaluate the prevalence of NOD and other sleep-related disorders in COPD patients. Patients and Methods: This prospective cross-sectional study was conducted in the sleep laboratory of our tertiary center over 1 year. Fifty COPD patients were enrolled in this study. They were classified into mild COPD and moderate COPD, according to the Global Initiative for Obstructive Lung Disease (GOLD) classification. Complete history, physical examination, and relevant laboratory investigations were taken. All patients were subjected to overnight polysomnography. Results: Eight patients had mild COPD, whereas 42 patients had moderate COPD. Mean sleep efficiency was decreased with an average of 71.08% with a significant difference between mild and moderate COPD cases. Minimal SpO2, average SpO2, SpO2

Assessment of thyroid function tests in patients with chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease (COPD), a group of diseases of distinct aetio-pathological consideration with different phenotypic presentations where smoking is the leading cause, all share the ultimate result of airflow limitation. This study aimed to evaluate thyroid function tests (TFT) in patients with COPD. Pulmonary function tests (PFT) were performed for 30 patients with obstructive lung disease and fifteen healthy control individuals. We measured SPO2 to confirm COPD and assess the severity of the disease and assessed TT3, TT4, and TSH using the ELISA test. The values of VC, FVC, and FEV in the first second and PEF, TSH, and SPO2 were lower in the COPD group than in the control group (P-value=0.001). In severe COPD (FEV1<50%), there was a significant reduction in T3 but not T4 or TSH compared to mild-moderate COPD patients. Thyroid dysfunction was observed in patients with COPD pointing to a metabolic response; patients with lower weight indices had a lower TSH and, consequently, T3.

Impact of pulmonary rehabilitation training on Chronic Obstructive Pulmonary Disease (COPD) and asthma patients

The objective of this study is to assess the impact of pulmonary rehabilitation training in the management of asthma and chronic obstructive pulmonary disease patients. A 6-month prospective interventional study was conducted in a tertiary care hospital that included participants above 18 to less than 70 years of age admitted to the general medicine ward with the diagnosis of mild-moderate chronic obstructive pulmonary disease and asthma without any other comorbidity or concurrent illness. The rehabilitation procedure consisted of breathing exercises and endurance training. Parameters like FEV1, FVC, modified medical research council scale, modified BORG grade, 6-minute walk test, and questionnaire like SF-36 were measured and compared with post-training results. A total of 80 patients were enrolled in the study. The pre and post-rehabilitation comparison in both COPD and asthma patients showed significant results in terms of improved dyspnea (FEV1, FVC, FEV1/FVC ratio; p=0.001) evident with modified Medical Research Council scores and modified BORG grades followed by significant differences in distance covered during 6-minute walk test (p=0.001) and health-related quality of life (SF-36 scores; p=0.001). Conclusion: Pulmonary rehabilitation significantly improved exercise tolerance, perception of dyspnea, health-related quality of life, and psychosocial behavior. Inclusion of pulmonary rehabilitation in COPD and asthma patients is essential to palliate the disease burden, reduce the rate of hospitalizations and improves the quality of life of a patients.

An Evaluation of quantitative body composition on thoracic computed tomography and the effect on clinical severity in patients with chronic obstructive pulmonary disease

The aim of this study was to evaluate the effect on disease severity of the quantitative measurements of pectoral muscle area (PMA), pectoral muscle index (PMI), pectoral muscle density (PMD), subcutaneous adipose tissue (SAT) and mediastinal adipose tissue (MAT) taken on thoracic computed tomography (CT) of patients with chronic obstructive pulmonary disease (COPD), according to the Global Initiative for Chronic Obstructive Lung Disease (GOLD) classification. A retrospective screening was made of patients diagnosed with COPD and applied with thoracic CT and respiratory function tests. For patients with obstructive findings, a record was made of height, weight, body mass index, and smoking history (packet/year). On thoracic axial CT images, the PMA, PMI, PMD, SAT, and MAT values at the aortic arch level were calculated quantitatively using OsiriX software (Pixmeo, Switzerland). The patients were grouped as A-B-C-D according to the GOLD 2018 guidelines. Then two groups were formed as mild-moderate COPD (GOLD A-B) and severe COPD (GOLD C-D). The relationship was evaluated between clinical severity and quantitative body composition values according to the GOLD classification. A total of 80 patients diagnosed with COPD were included in the study comprising 61 males and 19 females. The GOLD A-B group included 43 (53.75%) patients and the GOLD C-D group, 37 (46.25%) patients. No significant difference was determined between the two groups in respect of the PMA, PMI, and PMD values (p=0.001). A statistically significant difference was determined between the groups in respect of the SAT and MAT values (p=0.001, p=0.002, respectively). A cutoff value of &lt;30.04 in PMD (0.964; 95%CI:0.928-1) showed the best performance in predicting the mild-moderate COPD patients (GOLD A-B) with 92% sensitivity and 93% specificity. The results of this study demonstrated that PMD showed the best quantitative body composition performance in the differentiation of mild-moderate and severe COPD disease.

Dyspnoea and symptom burden in mild–moderate COPD: the Canadian Cohort Obstructive Lung Disease Study

Studies assessing dyspnoea and health-related quality of life (HRQoL) in chronic obstructive pulmonary disease (COPD) have focussed on patients in clinical settings, not the general population.The aim of this analysis was to compare the prevalence and severity of dyspnoea and impaired HRQoL in individuals with and without COPD from the general population, focussing on mild–moderate COPD.Analysis of the 3-year Canadian Cohort Obstructive Lung Disease (CanCOLD) study included four subgroups: mild COPD (Global Initiative for Chronic Obstructive Lung Disease (GOLD) 1); moderate COPD (GOLD 2); non-COPD smokers; and non-COPD never-smokers. The primary outcome was dyspnoea (Medical Research Council (MRC) scale), and the secondary outcome was HRQoL (COPD Assessment Test (CAT) score; Saint George's Respiratory Questionnaire (SGRQ) score). Subgroups were analysed by sex, physician-diagnosed COPD status and exacerbations.1443 participants (mild COPD (n=397); moderate COPD (n=262(; smokers (n=449) and never-smokers (n=335)) were studied. People with mild COPD were more likely to report more severe dyspnoea (MRC 2 versus 1) than those without COPD (OR (95% CI) 1.42 (1.05–1.91)), and non-COPD never-smokers (OR (95%CI) 1.64 (1.07–2.52)). Among people with mild COPD, more severe dyspnoea was reported in women versus men (MRC2 versus 1; OR (95% CI) 3.70 (2.23–6.14)); people with, versus without, physician-diagnosed COPD (MRC2 versus 1; OR (95% CI) 3.27 (1.71–6.23)), and people with versus without recent exacerbations (MRC2 versus 1; ≥2 versus 0 exacerbations: OR (95% CI) 3.62 (1.02–12.86); MRC ≥3 versus 1; 1 versus 0 exacerbation: OR (95% CI): 9.24 (2.01–42.42)). Similar between-group differences were obtained for CAT and SGRQ scores.Careful assessment of dyspnoea and HRQoL could help identify individuals for earlier diagnosis and treatment.

Reducing the use of inhaled corticosteroids in mild-moderate COPD: an observational study in east London

Inhaled corticosteroids (ICS) are often prescribed for worsening breathlessness, exacerbation frequency or lung function in chronic obstructive pulmonary disease (COPD). In mild-moderate disease and infrequent exacerbations, treatment risks may outweigh benefits and ICS may be withdrawn safely under supervision. A systematic ICS deprescribing programme for patients with mild-moderate COPD was introduced in an east London Clinical Commissioning Group (CCG) in April 2017. Primary care patient record analysis found that prescribing fell from 34.9% (n = 701) in the 18 months pre-intervention to 26.9% (n = 538) by the second year of implementation, decreasing 0.84% per quarter post intervention (p = 0.006, linear regression). The relative decrease was greater than the comparison CCG (23.0% vs. 9.9%). Only South Asian ethnicity was associated with increased cessation (odds ratio 1.48, confidence interval (CI) 1.09–2.01), p = 0.013, logistic regression). Patient outcome data were not collected. A primary care-led programme comprising local education, financial incentivisation and consultant support led to a significant decrease in ICS prescribing.

Oxidative stress and Nrf2 expression in peripheral blood mononuclear cells derived from COPD patients: an observational longitudinal study

BackgroundA persistent low inflammatory-oxidative status and the inadequacy of the antioxidant nuclear factor-E2-related factor 2 (Nrf2) have been implicated in chronic obstructive pulmonary disease (COPD) progression. Therefore this study was aimed to assess the association between lung function decline and oxidative-inflammatory markers and Nrf2 signaling pathway expression in peripheral blood mononuclear cells (PBMCs) over time.Methods33 mild-moderate COPD outpatients (mean age 66.9 ± 6.9 years) were age-sex matched with 37 no-COPD subjects. A clinical evaluation, blood sampling tests and a spirometry were performed at baseline and after a mean follow-up of 49.7 ± 6.9 months.ResultsIn COPD, compared to no-COPD, we found a faster lung function decline at follow-up. Although similar prevalence of smoking, hypertension, diabetes and dyslipidemia, systemic markers of inflammation (hs-CRP and white blood cells, WBCs) and oxidative stress (8-isoprostane) were significantly increased in COPD at follow-up, while the antioxidant glutathione (GSH) was significantly reduced. Moreover the expression of Nrf2 and of Nrf2-related genes heme oxygenase (HO)-1 and glutamate-cysteine ligase catalytic (GCLC) subunit in PBMCS were significantly down-regulated in COPD at follow-up, whereas no changes were observed in no-COPD. The percent variation (Δ) of FEV1 detected after the follow-up in COPD patients was directly correlated with ΔNrf2 (r = 0.826 p < 0.001), ΔHO-1 (r = 0.820, p < 0.001) and ΔGCLC (r = 0.840, p < 0.001). Moreover ΔFEV1 was also directly correlated with ΔGSH (r = 0.595, p < 0.01) and inversely correlated with Δ8-iso (r = − 0.587, p < 0.01) and with baseline smoking history (r = − 0.39, p < 0.03). No correlation was found between ΔFEV1, ΔCRP and ΔWBCs. By means of hierarchical stepwise multiple linear regression, taking into account other baseline key factors related to FEV1, ΔNrf2, ΔHO-1and ΔGCLC were found to be significant predictors of ΔFEV1, explaining 89.5% of its variance.ConclusionsAlthough our results must be confirmed in larger trial they suggest that the down-regulation of Nrf2/ARE gene expression in PBMCs may be one of the determinants of FEV1 decline and of COPD progression. Therefore the future possibility to counteract Nrf2 decline in COPD patients may help in reducing the negative effects of the oxidative stress-induced progression of the disease.

Acute air pollution exposure alters neutrophils in never-smokers and at-risk humans.

Outdoor air pollution exposure increases chronic obstructive pulmonary disease (COPD) hospitalisations, and may contribute to COPD development. The mechanisms of harm, and the extent to which at-risk populations are more susceptible are not fully understood. Neutrophils are recruited to the lung following diesel exhaust exposure, a model of traffic-related air pollution (TRAP), but their functional role in this response is unknown. The purpose of this controlled human-exposure crossover study was to assess the effects of acute diesel exhaust exposure on neutrophil function in never-smokers and at-risk populations, with support from additional in vitro studies.18 participants, including never-smokers (n=7), ex-smokers (n=4) and mild-moderate COPD patients (n=7), were exposed to diesel exhaust and filtered air for 2 h on separate occasions, and neutrophil function in blood (0 h and 24 h post-exposure) and bronchoalveolar lavage (24 h post-exposure) was assessed.Compared to filtered air, diesel exhaust exposure reduced the proportion of circulating band cells at 0 h, which was exaggerated in COPD patients. Diesel exhaust exposure increased the amount of neutrophil extracellular traps (NETs) in the lung across participants. COPD patients had increased peripheral neutrophil activation following diesel exhaust exposure. In vitro, suspended diesel exhaust particles increased the amount of NETs measured in isolated neutrophils. We propose NET formation as a possible mechanism through which TRAP exposure affects airway pathophysiology. In addition, COPD patients may be more prone to an activated inflammatory state following exposure.This is the first controlled human TRAP exposure study directly comparing at-risk phenotypes (COPD and ex-smokers) with lower-risk (never-smokers) participants, elucidating the human susceptibility spectrum.

Advance care planning in COPD: guidance development for healthcare professionals

ObjectivesTo examine current practices, attitudes and levels of confidence related to advance care planning (ACP) in patients with chronic obstructive pulmonary disease (COPD) among healthcare professionals working in Ireland. This...

The effect of carotid chemoreceptor inhibition on exercise tolerance in chronic obstructive pulmonary disease: A randomized-controlled crossover trial.

Patients with chronic obstructive pulmonary disease (COPD) have an exaggerated ventilatory response to exercise, contributing to exertional dyspnea and exercise intolerance. We recently demonstrated enhanced activity and sensitivity of the carotid chemoreceptor (CC) in COPD which may alter ventilatory and cardiovascular regulation and negatively affect exercise tolerance. We sought to determine whether CC inhibition improves ventilatory and cardiovascular regulation, dyspnea and exercise tolerance in COPD. Twelve mild-moderate COPD patients (FEV1 83 ± 15 %predicted) and twelve age- and sex-matched healthy controls completed two time-to-symptom limitation (TLIM) constant load exercise tests at 75% peak power output with either intravenous saline or low-dose dopamine (2 μg·kg-1·min-1, order randomized) to inhibit the CC. Ventilatory responses were evaluated using expired gas data and dyspnea was evaluated using a modified Borg scale. Inspiratory capacity maneuvers were performed to determine operating lung volumes. Cardiac output was estimated using impedance cardiography and vascular conductance was calculated as cardiac output/mean arterial pressure (MAP). At a standardized exercise time of 4-min and at TLIM; ventilation, operating volumes and dyspnea were unaffected by dopamine in COPD patients and controls. In COPD, dopamine decreased MAP and increased vascular conductance at all time points. In controls, dopamine increased vascular conductance at TLIM, while MAP was unaffected. There was no change in time to exhaustion in either group with dopamine. These data suggest that the CC plays a role in cardiovascular regulation during exercise in COPD; however, ventilation, dyspnea and exercise tolerance were unaffected by CC inhibition in COPD patients.

&lt;p&gt;Low FEV1 Is Associated With Increased Risk Of Cachexia In COPD Patients&lt;/p&gt;

BackgroundChronic obstructive pulmonary disease (COPD) has been introduced as a major public health problem. It has been suggested that disruption in function or some adipokines and serum proteins' signaling could play crucial roles in lung diseases. This study's purpose was to investigate the association between serum levels of S100A1, ZAG, and adiponectin with FEV1 in COPD patients.MethodsIn this cross-sectional study, 90 clinically stable outpatient males with age ranging from 40 to 70 years with COPD diagnosis – FEV1/FVC < 70% – were divided into two groups: mild–moderate COPD patients; FEV1 ≥ 50 (n=52) VS severe and very severe COPD patients; FEV1 < 50 (n=38). The serum levels of ZAG, S100A1, and adiponectin were measured by the use of enzyme-linked immunosorbent assay.ResultsIn the present study, lower FEV1 was significantly associated with increased risk of cachexia (OR = 5.76, 95% CI: 2.28–14.54). The serum level of ZAG was significantly higher in the mild–moderate COPD patients in comparison with the severe–very severe COPD patients (p<0.035). However, the resting metabolic rate (RMR) level was significantly higher in FEV1<50 group compared to FEV1≥50 group (p<0.024). Also, strong positive associations between serum S100A1–ZAG, serum adiponectin–ZAG, and serum adiponectin–S100A1 (β>0.800, p<0.001) were shown.ConclusionIn the present study, we found that low FEV1 was associated with increased risk of cachexia in COPD patients. Additionally, lower serum level of ZAG and higher RMR were observed in patients with severe–very severe COPD as compared to mild–moderate COPD. Therefore, it could be claimed that there is a mechanistic chain of causality between FEV1, serum ZAG, RMR, and cachexia.

The expression and clinical significance of migration inhibitory factor in human pulmonary tissues with chronic obstructive pulmonary disease

Objective To investigate the expression of macrophage migration inhibitory factor (MIF) in pulmonary tissues from patients with chronic obstructive pulmonary disease (COPD) and the relationship with its clinical features. Methods One hundred and eighty patients who underwent pulmonary bullectomy lobectomy due to pneumatocele from January 2015 to September 2018 in Longgang Central Hospital were enrolled and classified into patients without COPD (control group)and patients with COPD (COPD group), with 90 patients each group. According to the lung function parameters, 90 patients with COPD were divided into the mild COPD group, the moderate COPD group, and the severe COPD group. The levels of mRNA and protein of MIF were measured with RT-PCR, ELISA and Western blot. One-way ANOVA, Pearson correlation analysis and SNK-q test were used to analyze the results with SPSS 18.0, and P<0.05 was considered statistically significant. Results The level of MIF in pulmonary tissues from the control group was obviously lower than those in the COPD group (P<0.05). The level of MIF in pulmonary tissues in the severe COPD group was obviously higher than those in pulmonary tissues in the mild COPD, moderate COPD and control groups (P<0.05). MIF was positively correlated with the lung function parameters (P<0.05). Conclusion The high expression of MIF in pulmonary tissues is closely related to the severity of COPD. Key words: Migration inhibitory factor; Chronic obstructive pulmonary disease; Real time-PCR; ELISA; Western blot

Sleep disturbance in patients with mild-moderate chronic obstructive pulmonary disease.

Although sleep problems have an important impact on daily life and health outcome measures in patients with chronic obstructive pulmonary disease (COPD), patterns of sleep disturbance in patients with mild-moderate COPD remain unknown. The aim of this study was to investigate patterns of sleep disturbance and factors associated with sleep impairment in patients with mild-moderate COPD. This prospective cross-sectional study enrolled 148 male patients with COPD. At enrolment, all patients completed a disease-specific sleep measure, the COPD and Asthma Sleep Impact Scale (CASIS) to assess sleep impairment. Health-related quality of life (HRQL) was measured using the St. George's Respiratory Questionnaire (SGRQ) and the 36-item Short-Form health survey (SF-36). Anxiety and depression status were assessed using the Hospital Anxiety and Depression Scale (HADS). Self-efficacy was measured by the COPD Self-Efficacy Scale (CSES). The mean age of the subjects was 67years [standard deviation (SD)=8.11]. The proportion of patients who indicated that they had a bad night's sleep was 33.1%. Univariated analysis showed that CASIS score was significantly correlated with the modified Medical Research Council (mMRC) dyspnea scale, SGRQ, SF-36 Physical Component Summary, SF-36 Mental Component Summary, HADS-anxiety, HADS-depression and CSES scores (all P<0.05). In a multivariate analysis, SGRQ and CSES were independently associated with CASIS score. Poorer HRQL and lower self-efficacy are significantly associated with sleep disturbance and perhaps may be improved by better sleep quality. Future research is required to enhance sleep quality in patients with mild-moderate COPD.

Multi-level immune response network in mild-moderate Chronic Obstructive Pulmonary Disease (COPD)

BackgroundChronic Obstructive Pulmonary Disease (COPD) is associated with an abnormal pulmonary and systemic immune response to tobacco smoking. Yet, how do immune cells relate within and between these two biological compartments, how the pulmonary infiltrate influences the lung transcriptome, and what is the role of active smoking vs. presence of disease is unclear.MethodsTo investigate these questions, we simultaneously collected lung tissue and blood from 65 individuals stratified by smoking habit and presence of the disease. The immune cell composition of both tissues was assessed by flow cytometry, whole lung transcriptome was determined with Affymetrix arrays, and we used Weighted Gene Co-expression Network Analysis (WGCNA) to integrate results.ResultsMain results showed that: (1) current smoking and the presence of COPD were both independently associated with a reduction in the proportion of lung T cells and an increase of macrophages, specifically those expressing CD80 + CD163+; (2) changes in the proportion of infiltrating macrophages, smoking status or the level of airflow limitation were associated to different WGCNA modules, which were enriched in iron ion transport, extracellular matrix and cilium organization gene ontologies; and, (3) circulating white blood cells counts were correlated with lung macrophages and T cells.ConclusionsMild-moderated COPD lung immune infiltrate is associated with the active smoking status and presence of disease; is associated with changes in whole lung tissue transcriptome and marginally reflected in blood.

Relationship of chronic obstructive pulmonary disease severity with early and late mortality in elderly patients with hip fracture

IntroductionWe conducted a comparative study to compare patients with and without chronic obstructive pulmonary disease (COPD) and to analyze the effect of COPD severity on mortality in elderly patients with hip fractures who were diagnosed by pulmonologists. The purposes of this study were to compare early and late mortality after hip fracture between COPD and non-COPD patients and to assess risk factors of mortality after hip fractures in elderly patients with COPD. MethodsThis study included 1294 patients (1294 hips) who were diagnosed as having unilateral femoral neck or intertrochanteric fractures and who underwent surgery at two hospitals between 2004 and 2017. The patients were categorized into a non-COPD group (853 patients) and a COPD group (441 patients; mild-to-moderate [354 patients] and severe-to-very severe COPD subgroups [87 patients]). The cumulative crude mortality rate was calculated, and 30-day, 60-day, 3-month, 6-month, and 1-year mortality rates were compared between the non-COPD and COPD groups. Logistic regression analysis was conducted to identify independent factors associated with mortality. ResultsThe 30-day, 60-day, 3-month, 6-month, and 1-year postoperative cumulative mortality rates were 1.3%, 2.5%, 3.5%, 6.6%, and 10.7%, respectively, in the non-COPD group, and 2.9%, 5.7%, 7.7%, 11.8%, and 16.6%, respectively, in the COPD group (p = 0.049, p = 0.004, p = 0.002, p = 0.002, and p = 0.004, respectively). The 30-day, 60-day, 3-month, 6-month, and 1-year postoperative cumulative mortality rates in the severe-to-very severe COPD group were 4.6%, 6.9%, 11.5%, 20.7%, and 26.4%, respectively. In elderly patients with hip fracture, COPD increased the risk of mortality for 1.6 times and 1.7 times at 3 months and 1 year postoperative, respectively. In subgroup analysis, severe-to-very severe COPD was associated with 1.55-fold and 1.65-fold increased postoperative mortality risk at 6 months and 1 year respectively, as compared with mild-moderate COPD. ConclusionsIn elderly patients with hip fracture, the comparison between the COPD and non-COPD patients revealed that COPD was an independent factor of mortality at a minimum of 1-year follow-up, and COPD severity in patients with hip fracture was also a risk factor of 6-month and 1-year mortality.

Analysis of curative effect of adjuvant therapy with bronchoalveolar lavage on COPD patients complicated with pneumonia.

Clinical effect of adjuvant therapy with bronchoalveolar lavage on chronic obstructive pulmonary disease (COPD) patients complicated with pneumonia and its influence on the expression levels of inflammatory factors were studied. One hundred and twenty mild-moderate COPD patients complicated with pneumonia treated in the Department of Respiratory Medicine, The Sixth People's Hospital of Nantong from February 2016 to February 2017 were selected and randomly divided into three groups: One-time lavage group (n=40), two-time lavage group (n=40) and control group (n=40). Fasting peripheral blood was collected from all the patients in the morning. The lung function and blood gas analyses, and the detection of peripheral white blood cells (WBC), procalcitonin (PCT) and C-reactive protein (CRP) were performed. Moreover, the messenger RNA (mRNA) levels of interleukin-6 (IL-6), IL-8, tumor necrosis factor-α (TNF-α) and leukotriene B4 (LTB4) in lavage fluid were detected via reverse transcription-quantitative polymerase chain reaction. The lung functions of patients in the two-time lavage group were significantly improved compared with that in the one-time lavage group (p<0.01). pH and PaO2 in two-time lavage group were higher than those in the one-time lavage group (p<0.01). Peripheral WBC, PCT and CRP levels in the two-time lavage group were lower than those in the one-time lavage group (p<0.05). The mRNA levels of IL-6, IL-8, TNF-α and LTB4 in lavage fluid in two-time lavage group were lower than those in one-time lavage group (p<0.01). IL-6, IL-8, TNF-α and LTB4 expression levels in lavage fluid in two-time lavage group were lower than those in one-time lavage group (p<0.01). In conclusion, the adjuvant therapy with bronchoalveolar lavage improves the therapeutic effect on COPD patients complicated with pneumonia, which can significantly reduce the expression levels of inflammatory factors, and facilitate the control of pulmonary infection and recovery of lung function.