Analysis of risk factors and consequences for concurrent obstructive sleep apnea in chronic obstructive pulmonary disease patients

Background“Overlap syndrome” refers to obstructive sleep apnea (OSA) combined with chronic obstructive pulmonary disease (COPD), and has poorer outcomes than either condition alone. We aimed to evaluate the prevalence and possible predictors of overlap syndrome and its association with clinical outcomes in patients with COPD.MethodsWe assessed the modified Medical Research Council dyspnea scale (mMRC), Epworth sleepiness scale (ESS), COPD assessment test (CAT), Hospital Anxiety and Depression Scale (HADS), Charlson Comorbidity Index (CCI), and STOP-Bang questionnaire (SBQ) and performed spirometry and full overnight polysomnography in all patients. An apnea–hypopnea index (AHI) ≥ 5 events per hour was considered to indicate OSA. Risk factors for OSA in COPD patients were identified by univariate and multivariate logistic regression analyses.ResultsA total of 556 patients (66%) had an AHI ≥ 5 events per hour. There were no significant differences in age, sex ratio, mMRC score, smoking index, number of acute exacerbations and hospitalizations in the last year, and prevalence of cor pulmonale between the two groups (all p > 0.05). Body mass index (BMI), neck circumference, CAT score, CCI, ESS, HADS, and SBQ scores, forced expiratory volume (FEV)1, FEV1% pred, FEV1/forced vital capacity ratio, and prevalence of hypertension, coronary heart disease, and diabetes were all significantly higher and the prevalence of severe COPD was significantly lower in the COPD-OSA group compared with the COPD group (p < 0.05). BMI, neck circumference, ESS, CAT, CCI, HADS, hypertension, and diabetes were independent risk factors for OSA in COPD patients (p < 0.05). SBQ could be used for OSA screening in patients with COPD. Patients with severe COPD had a lower risk of OSA compared with patients with mild or moderate COPD (β = − 0.459, odds ratio = 0.632, 95% confidence interval 0.401–0.997, p = 0.048).ConclusionPatients with overlap syndrome had a poorer quality of life, more daytime sleepiness, and a higher prevalence of hypertension and diabetes than patients with COPD alone. BMI, neck circumference, ESS, CAT, CCI, HADS, hypertension, and diabetes were independent risk factors for OSA in patients with COPD. The risk of OSA was lower in patients with severe, compared with mild or moderate COPD.

<b>Background:</b> The diagnosis of COPD is based on spirometry¹. A CXR can be reported as suggestive of COPD but is not diagnostic. This could inadvertently cause confusion or worry. <b>Aim:</b> We examined the frequency of COPD on CXR reports and whether this correlates with a spirometric diagnosis of COPD and the severity of COPD. <b>Method:</b> Patients were referred from general practice to a direct access spirometry service. All patients had a CXR within 3 months of spirometry. Patients were classified as not COPD, mild, moderate or severe COPD. X-ray reports were then reviewed. <b>Results:</b> 183 patients all over the age of 40 (mean 65.7yrs) were found. Spirometry classified them as not COPD (101), mild COPD (35), moderate COPD (37) or severe COPD (10). The COPD patients were more likely to be male 48/82 vs 42/101 and older 68 years vs 63.8 years. Average FEV1 of the COPD and non COPD groups were 1.94L (75% predicted) and 2.7L (104.6% predicted) respectively. Patients with COPD were more likely to have COPD mentioned on their CXR report, 29/82 vs 13/101. Chi² 12.95, p= 0.0003. There was no difference in CXR reporting between the mild (12/35), moderate (14/37) and severe (3/10) COPD subcategories. Chi² 0.24, p= 0.88. The sensitivity and specificity for CXR report as diagnostic for COPD is 35% and 87% respectively. <b>Conclusions:</b> Patients who have COPD were more likely to get a radiological diagnosis of COPD on CXR reporting. One third of patients with positive x-ray reports did not have COPD on spirometry. This has the potential to cause misdiagnosis and errors in care for a sizeable number of patients. <b>

Objectives: This study aimed to determine the role of Cardiopulmonary Exercise Testing (CPET) in uncovering the mechanisms of exercise intolerance in mild-to-severe stable chronic obstructive pulmonary disease (COPD) patients and to correlate the spirometry, 6-min walk test (6MWT), and COPD assessment test (CAT) scoring with the exercise capacity in stable COPD patients. This study was conducted at tertiary referral medical college hospital in South India. Methodology: This was a prospective and observational study conducted among all eligible subjects with stable COPD attending outpatient clinic at PSG Institute of Medical Sciences and research over 1 year during 2021–2022. All patients with a history suggestive of asthma, patients with clinically evident active pulmonary tuberculosis, ongoing or recent exacerbations of COPD within 2 weeks prior to enrolment in the study, and coexisting condition that are contraindicated or render forced expiratory maneuver difficult to perform were excluded from the study. A thorough history was taken and systemic examination was performed. Patients with spirometry postbronchodilator forced expiratory volume in 1 s (FEV1)/ Forced vital capacity (FVC) &lt;0.70 was allowed for the study in accordance with the GOLD recommendations. Based on postbronchodilator FEV1, patients who met the criteria were categorized as mild, moderate, severe, and extremely severe. For all qualified participants, the CAT questionnaire, 6MWT, and MMRC grades were evaluated. The treadmill procedure was then used to perform CPET in all individuals. Results: Thirty patients enrolled in our study were subjected to CPET using treadmill protocol and the variables and the nine panel plot were analyzed. The variables tested were minute ventilation, maximum oxygen uptake, anaerobic threshold, breathing reserve, VE/VCO 2 , oxygen pulse, and the maximum heart rate. In mild COPD, ventilatory inefficiency was the primary cause, while moderate and severe stages show overlapping cardiovascular, metabolic, and deconditioning factors contributed to dyspnea. VO 2 max was not significantly correlated with spirometry but showed meaningful associations with CAT score, MMRC grade, and 6-min walk distance. In practice, simpler tools can approximate CPET with readily available questionnaires and 6MWT to assess exercise tolerance in stable COPD patients. Conclusion: CPET is helpful in delineating the causes of exercise limitation in mild and moderate COPD patients. In severe COPD, there may be an overlap of various causes of exercise limitation and specific tests are warranted to know the exact cause of exercise limitation. The maximum oxygen uptake correlates well with MMRC dyspnea grade, CAT score, and 6 min walk distance. CPET can be useful in suggesting individually tolerated and tailored pulmonary rehabilitation program in mild and moderate COPD. Overall, CPET remains a valuable objective measure of exercise intolerance in COPD, but the strong correlations with dyspnea scores and 6MWD highlight that validated symptom/field tests can serve as practical alternatives to assess functional limitation, especially in the resource-constrained settings.

BackgroundChronic obstructive pulmonary disease (COPD) is a great public health burden worldwide. Few studies have focused on pain problems in patients with mild and moderate COPD in Chinese community settings.MethodsA cross-sectional study of 283 patients with mild and moderate COPD was conducted in six communities that were randomly sampled in Pudong New Area of Shanghai, China, in 2016. A face-to-face interview was conducted to collect data on personal characteristics and health conditions. The short form McGill Pain Questionnaire and the COPD assessment test (CAT) were applied to evaluate pain problems and health status, respectively.ResultsAmong 283 subjects, more than one third (37%) had pain problems indicated by the present pain intensity (PPI) scale. COPD patients aged <65 years with exacerbation in the past 12 months or a CAT score of ≥10 had a significantly higher score in affective dimension. Female sex, COPD severity, and length of disease were significantly related to higher scores of the sensory dimension. Those with moderate COPD or a CAT score of ≥10 had significantly higher scores of visual analog scale than those with mild COPD or a CAT score <10. Patients with moderate COPD had a higher rank of PPI than those with mild COPD.ConclusionPain was common in patients with mild and moderate COPD in the community settings of Shanghai, China. Severity of COPD and CAT score were significantly related to the prevalence of pain. Intervention measures should be developed to improve pain problems for COPD patients.

Chronic obstructive pulmonary disease (COPD) is a major cause of chronic morbidity and mortality throughout the world. According to global initiative for chronic obstructive lung disease, COPD is defined as FEV1/FVC<70% by spirometry. COPD affects pulmonary blood vessels, right ventricle as well as left ventricle, leading to development of pulmonary hypertension, cor-pulmonale, right ventricular dysfunction as well as left ventricular dysfunction. The significance of the right ventricular performance is recognized as one of the factors determining the clinical course and prognosis in COPD, but a potential role of the left ventricle is, however, less studied. The aim of this study was primarily to evaluate left ventricular function in COPD patients by echocardiography and to study the correlation between echocardiography findings and the severity of COPD based on GOLD1 criteria. A total of 100 patients were selected for this study, including 72 male patients and 28 female patients, aged 50–70 years, from outpatient department of medicine department, medical wards, TB and chest ward of Dr Baba Sahib Ambedkar Hospital, Delhi, considering the exclusion and inclusion criteria. In mild COPD group, only one patient was found to have systolic dysfunction out of 52 patients (1.92%), in moderate COPD group, 2 patients had systolic dysfunction out of 32 patients (6.25%), whereas in severe COPD, six patients had systolic dysfunction out of 16 patients (37.5%). So, in total, 9% patients had systolic dysfunction. 28% of patients were found to have left ventricular diastolic dysfunction in our study. COPD patients have a high prevalence of left ventricular diastolic dysfunction, which is associated with disease severity. A clear correlation was found between value of fractional shortening (FS) of left ventricle (a measure of contractility), and severity of COPD and FS value significantly decreased as the severity of COPD increased. In this study, ejection fraction (EF) was found to be preserved in mild and moderate COPD, albeit mean EF was found to be reduced in moderate COPD. In severe COPD group, EF was significantly lowered.

BackgroundThe COPD (chronic obstructive pulmonary disease) assessment test (CAT) is a recently introduced, simple to use health status instrument, which takes less time to complete than better-established health status instruments...

Asthma and chronic obstructive pulmonary disease (COPD) continue to have considerable impact on disease burden and mortality worldwide. Early diagnosis still remains a challenge, with low uptake of spirometry in many countries. Implementing best practice management for airways disease is a critical goal for health-care systems—the management now includes pharmacological and non-pharmacological approaches to the lung disease, as well as recognition and treatment of comorbidities. Finally, the pathogenesis of airways disease continues to be fertile field of investigation, in order to better prevent disease, slow progression and identify relevant biomarkers. A large number of studies published in Respirology in 2012 have addressed all of these important clinical and scientific issues, and made major contributions to advance this field and hopefully improve outcomes for patients with asthma and COPD. Despite years of research, the origins of asthma remain obscure. Although there is clearly a genetic disposition to developing asthma, gene-association studies have so far failed to reveal clear insights into the development of asthma (reviewed in Respirology in 20111), indicating that asthma is likely to result from a complex interaction between genes and environment. Moreover, marked changes in the prevalence of asthma in recent decades indicate that changing environmental exposures must be to blame. Air pollution is known to exacerbate asthma symptoms and has been one of the factors suspected of causing the disease in the first place. Gowers et al. reviewed the association between air pollution and asthma for the Department of Health in the United Kingdom.2 In fact, they found little evidence for an association between pollution and asthma prevalence. If anything, time trends indicated a negative rather than positive association, but there is some evidence for an increased incidence of asthma in people living very close to roads carrying heavy traffic. The overall impact of this traffic pollution on asthma incidence is not likely to be large. Air pollution of different kind was studied by Havstad et al. who studied the impact of early-life exposure to environmental tobacco smoke on the development of atopy by 2–3 years in a cohort of children.3 Using propensity score matching, they found that tobacco smoke exposure increased the risk of positive skin prick or specific immunoglobulin E (IgE) tests in children whose mothers were not atopic, but paradoxically decreased the risk in those with a positive history of maternal atopy. This interaction between maternal atopy and the effect of environmental tobacco smoke on children's risk for atopy may help to explain some of the conflicting data from previous studies. An accompanying editorial emphasizes that exposing children to tobacco smoke should of course be avoided because of the many other adverse effects,4 but the paper, like that of Gowers et al.,2 demonstrates the need to better understand how genes and environment interact to cause atopy. Other changes in lifestyle and exposures may also help to explain increases in asthma prevalence. The well-recognized association between asthma and obesity was reviewed in Respirology and the mechanism for the association continues to elude researchers.5 Changing dietary exposures could be part of the explanation. A novel association between soft drink consumption, tobacco smoking and airway disease was reported by Shi et al.6 In a large cross-sectional telephone survey of Australian adults, consumption of more than half a litre a day of soft drinks was associated with both asthma and COPD. The association was only apparent among smokers in whom soft drinks and smoking appeared to have additive effects. If these findings are confirmed in other studies, they suggest a lifestyle intervention to prevent airways disease. One of the problems in identifying the origins of asthma is that clinical asthma comprises a number of distinct phenotypes. It has recently been proposed that these phenotypes represent truly different diseases with different causes (also called ‘endotypes’) rather than simply being different and variable expressions of the same underlying pathology.7 Defining asthma phenotypes on the basis of the cellular profile of induced sputum has become increasingly important as studies indicate that eosinophilic airway inflammation responds better to corticosteroid treatment than neutrophilic inflammation.8 Phenotypes are increasingly used to target novel asthma treatments, such as the anti-interleukin (IL)-5 monoclonal antibody targeted to eosinophilic asthma.9 Specific treatments for non-eosinophilic asthma have not been established however. Choi et al. studied sputum inflammatory profiles in patients with refractory asthma requiring high-dose corticosteroid therapy selected from a large asthma cohort.10 Those with persistent airway obstruction had a longer duration of asthma and had predominantly neutrophilic inflammation, whereas refractory asthma without persistent airway obstruction was more likely to be eosinophilic. The authors suggest that this provides a rationale for developing new medications for individualized treatment in these patients. However, two studies in Respirology show that eosinophilic airway inflammation varies over time even in the absence of corticosteroid treatment. Hancox et al. found that the eosinophilic/non-eosinophilic classification was not stable over time in two clinical asthma treatment trails: even though the sputum phenotype was determined at a time when the patients were not taking any steroid treatment, nearly all patients with ‘non-eosinophilic asthma’ had raised sputum eosinophils at some point.11 Similarly, the study of Bacci et al. (discussed in the Airway Biology section) provided evidence that inflammatory phenotypes based on sputum cell analysis are not stable over time.12 Another report last year found that sputum phenotypes are not stable in children either.13 Hence, characterization of asthma and long-term treatment decisions should not be based on a single sputum specimen.14 Induced sputum analysis remains valuable for assessing patients with difficult asthma, but the resources required to obtain and analyse frequent sample will inhibit its widespread use. Although not yet established in the management of asthma, measuring of exhaled nitric oxide (eNO) offers a more practical way to monitor airway inflammation than monitoring of induced sputum.15 Affordable handheld electrochemical nitric oxide analysers are now available, making this a realistic possibility for many services. Kim et al. compared eNO measurements using the handheld Niox Mino (Aerocrine AB, Solna, Sweden) electrochemical analyser with a Sievers (GE Analytical Instruments, Boulder, CO, USA) chemiluminesence analyser.16 Correlation between the two machines was good (r = 0.88), but agreement in absolute values was only moderate: the Mino tended to give about 15% lower readings. The handheld machines are convenient but differences between machines need to be taken into account when interpreting eNO values. Although measuring airway inflammation is appealing, more simple clinical assessments remain the mainstay of asthma management. Ko et al. found that a single measurement of the Asthma Control Test—a score based on a simple 5-item questionnaire—correlated with asthma control assessments by physicians and predicted exacerbations and emergency health-care use over the following 6 months in a cohort of patients attending tertiary care in Hong Kong.17 The baseline Asthma Control Test score was better at predicting exacerbations than lung function, peak flow or eNO measurements. Simple management of asthma was also supported by a large randomized control trial comparing adjustment of inhaled steroid doses using eNO, clinical physician guidance and patient symptom-based adjustment using inhaled corticosteroids (ICS) each time they required β-agonist. No difference was found between the strategies, with the trends favouring patient symptom-led adjustment.9 Improvements in computed tomography (CT) scanning technology and lower radiation doses have enabled the use of high-resolution scans to study airway structure and differentiate between diseases, sites of inflammation and treatment response without the need for tissue biopsies.18 Kurashima et al. found that airway lumens were smaller in the 3rd- to 6th-generation bronchi in asthma but not COPD, whereas both diseases demonstrated airway wall thickening.19 These small airway diameters correlated with lung function in asthma not COPD. Hoshino and Ohtawa used high-resolution CT scans to assess changes in large airway remodelling before and after 24 weeks treatment with combination long-acting β-agonist (LABA) and ICS or ICS alone in a double-blind randomized controlled trial.20 Combination therapy reduced airway wall thickness and increased the airway luminal area to a greater extent than ICS alone. The improvements in airway wall thickness in the combination group correlated with reductions in sputum eosinophils and improvements in forced expiratory volume in 1 s (FEV1). The mechanisms for this positive interaction between ICS and LABA are not known, but the findings offer hope that airway remodelling can effectively treated and/or prevented by combination therapy. An accompanying editorial by King and Farah emphasizes the need for confirmatory and long-term studies as well as investigations of the effects on smaller airways that remain beyond the resolution of the scans.21 The findings of Hoshino and Ohtawa of a positive interaction between LABA and ICS on remodelling is relevant to the current concerns over the safety of LABA in asthma.20 Among the most controversial issues this year is the American Food and Drug Administration requirement that the manufacturers of LABA undertake large safety studies of the combination on LABA with ICS. It is accepted that using LABA without ICS is not acceptable in asthma, but it has been suggested that these large safety studies of combination therapy are futile because they will not be powered to address the question of whether they cause a small excess of asthma deaths.22 In the meantime, a recent meta-analysis demonstrates that withdrawing LABA once asthma control has been achieved, as currently recommended by the Food and Drug Administration, leads to a deterioration in control.23 Cough-variant asthma is another well-recognized but poorly understood phenotype. Ohkura et al. compared coughing during methacholine-induced bronchoconstriction in patients with cough-variant asthma (but normal cough sensitivity to capsaicin challenge) and normal controls.24 Patients with cough-variant asthma had increased cough during even mild methacholine-induced bronchoconstriction. After treatment with inhaled steroids, the number of coughs diminished to be similar to normal controls, indicating that increased cough sensitivity to bronchoconstriction is a feature of this disease variant, but that it responds to anti-inflammatory treatment. For non-asthmatic refractory chronic cough, an exciting discovery this year was that gabapentin is an effective treatment in a double-blind randomized controlled trial.25 Gabapentin is an anticonvulsant that is also used to treat neuropathic pain, suggesting that its effect on chronic cough may be due to suppression of central cough reflexes. The paradigm of Th1- versus Th2-mediated inflammation would suggest that asthma (predominantly a Th2 disease) would be less uncommon in sarcoidosis—regarded as a Th1 disorder. However, Wilsher et al. found that the prevalence of positive specific IgE tests for common aeroallergens (34%) and a history of asthma (21.5%) were similar in patients with sarcoidosis to that reported in the general population.26 In another study from the same group, Young et al. found that 44% of patients with sarcoidosis had airway hyperresponsiveness to histamine (a direct airway challenge), whereas only 11% were hyperresponsive to an indirect challenge using hypertonic saline.27 Hyperresponsiveness to histamine was more common in those with lower baseline FEV1 values and those with fibrotic and reticular patterns on lung CT. The findings suggest that the high prevalence of histamine responsiveness in patients with sarcoidosis is likely to be distinct from asthma (because of the low prevalence of hypertonic saline responsiveness) and is more likely to be due to airway remodelling caused by granulomatous airway inflammation. The development of COPD is related to both genetic and environmental factors. For genetic factors, a recent study by Guan et al. from China found that D2S388-5 microsatellite polymorphism located upstream of the surface lung surfactant protein B gene on chromosome 2 may be associated with susceptibility to COPD in Xinjiang Kazakhs.28 Another genetic factor, nucleotide-binding and oligomerization domain (NOD) 2 genes polymorphism, has also been found to have some potential association with COPD in a study from Japan. The distribution of NOD2 rs1077861 genotypes differed between COPD patients and non-COPD smokers and was associated with a lower FEV1 % predicted value in the TT when compared with the TA/AA genotypes.29 For environmental factors, exposure to noxious particles or gases is associated with the development of COPD.30 A study from Johannessen et al. found that exposure to environmental tobacco smoking during childhood was associated with COPD and respiratory symptoms in adulthood mainly in women in a cross-sectional study in Norway. In men, the most important risk factor is still acting smoking.31 The relationship of air pollution and COPD is reviewed by Ko and Hui.32 Outdoor air pollution (such as ambient air pollution) and indoor pollution (such as second-hand smoking and biomass fuel combustion exposure) are associated with the development of COPD and outdoor air pollution is a significant environmental trigger for acute exacerbation of COPD. Zeng et al. reviewed the aetiology of COPD in non-smoking subjects and risk factors may include genetic factors, long-standing asthma, outdoor air pollution, environmental smoke exposure, biomass smoke, occupational exposure, diet, recurrent respiratory infection in early childhood and tuberculosis.33 Interestingly, statins34 and even soft drink consumption6 have been found to have association with COPD. A cross-sectional study from Japan found that the prevalence of airflow limitation among patients who used statins was approximately five times lower than that among patients who did not use statins. However, statin use was not significantly associated with a lower prevalence of airflow limitation in multivariate analysis.34 Statins thus cannot be advocated for prevention of airflow obstruction at this stage. A study from South Australia assessed the relationship between soft drink consumption and presence of asthma/COPD in over 16 000 subjects.6 and noted the odds ratio for having COPD was 1.79 (95% confidence interval: 1.32–2.43) in multivariate analysis by comparing those who consumed more than half a litre of soft drink per day with those who did not consume soft drinks. The reason behind these associations is unclear and a causative relationship cannot be drawn from these studies. Comorbidities are common in COPD patients and the latest Global Initiative for Chronic Obstructive Lung Disease (GOLD) guideline has also emphasized that comorbid illness in COPD patients should be managed appropriately.30 The link between COPD and coronary artery disease is strong and complex. Coronary artery disease has a strong effect on the severity and prognosis of COPD and vice versa, including acute exacerbations.35 Ito and colleagues found that depression and sleep disorders were both common in patients with COPD.36 McSharry et al. found that sleep quality is poor in severe COPD patients with reduced sleep efficiency and reduced percentage of rapid eye movement sleep. There was a significant association between daytime hypoxaemia and sleep efficiency.37 However, depression, but not sleep disorder, is an independent risk factor for exacerbations and hospitalizations among COPD patients.36 The economic burden of COPD is huge and a recent study from Singapore showed that in 2009, COPD admissions represented 3.4% of all hospital discharges. Hospitalization was found to be the major cost driver, accounting for 73% of the total COPD burden, Between 2005 and 2009, attendances at primary care clinics, emergency departments and specialist clinics accounted for 3%, 5% and 17% of overall COPD costs, respectively.38 There are some new developments in the assessment of COPD using tools like CT and exercise tests. Degree of hyperinflation39 and airway dimensions18, 19 in COPD patients can be measured using CT parameters. Tanabe and colleagues applied a novel CT index to assess lung volume. This DLV% index measures the ratio of lung volume region adjacent to the diaphragm dome (D) to total lung volume (LV). Using this index, it was found that a reduced lung volume around the diaphragm correlated with lung hyperinflation and health-related quality of life, independent of emphysema severity.39 A recent study by Galban et al. adapted the parametric response map, a voxel-wise image analysis technique, for assessing COPD phenotype. In their study, whole-lung CT scans acquired at inspiration and expiration of COPD patients were analysed. Parametric response map identified the extent of functional small airways disease and emphysema as well as provided CT-based evidence that supports the concept that functional small airways disease precedes emphysema with increasing COPD severity.40 Phenotyping COPD by image biomarkers is currently under investigation and offers potential development of personalized therapy for COPD patients. There are also different field and laboratory tests for measuring exercise capacity in COPD patients. Hill and colleagues compared the 6-min walk test, incremental shuttle walk test and endurance shuttle walk test with a ramp cycle ergometer test in a group of patients with moderate COPD and found that these tests all elicited a similar peak rate of oxygen uptake and heart rate response. This suggested that that both self- and externally paced field tests can progress to high intensities.41 Field tests can probably offer a reasonable alternative for the evaluation of patients with moderate COPD.42 The revised was published in were indicated as the or in the treatment of all of patients with COPD. A new of and long-acting have as the most effective for control in patients with COPD. et al. reported the of one such when compared with in patients from 6 for found that provided significant and improvements in and in COPD with that reported in other from clinical indicate that may prevent acute exacerbations of However, the underlying mechanism for this effect is et al. showed that treatment in patients with COPD the and of both and by and This a effect of the in by the of and by the airway The long-term safety of this and its in to other treatment need evaluation before it a acute exacerbation of it is difficult for physicians to differentiate COPD from heart common and comorbidities. and colleagues the of for the diagnosis of in patients with severe acute exacerbations of COPD and in 2 care found that the was more in patients with normal function sensitivity and than those in and required adjustment of the to a et al. in a trial of patients with acute COPD and from heart compared treatment with versus reported more rapid in with the combination treatment but difference in This is a to the and treatment of heart during apparent COPD and sleep disorders are common and important in severe Ito et al. in a study of COPD patients and normal that only depression but not sleep disorders is associated with the increased risk of exacerbations and The management of and depression was the of a by and colleagues in they treatment with the of clinical on this important of COPD with sputum to exacerbations and poor quality of in patients with COPD. In a et al. that inhaled treatment may improve the quality of in patients with by sputum studies are to the of this is an important goal in patients with COPD.30 It quality of and the of greater and pulmonary is an effective way to in COPD long-term monitoring and of at is to the of any exercise In this et al. found that a value was correlated with severe This may be a practical of patients can and to with are and is a intervention for patients with acute exacerbations of COPD who to to treatment. It may be as the current of care in this clinical Moreover, in patients with COPD on the of and mortality from to However, there is a need to improve the practical assessment of the response to in the acute In this et al. reviewed the of for the of during acute However, they were to positive from randomized The clinical may be that of may not be a of response to and should continue to on parameters. the disease the treatment of COPD become less effective and symptoms become more for such patients need to early to complex with about values and for care including of et in a of the the approaches to care at the of in patients with severe interaction susceptibility to airway diseases such as asthma and COPD. association studies have found associations of specific single with the development of asthma or COPD. in Respirology have also on genetic of airway A meta-analysis of studies of the polymorphism in found increased risk of asthma in or with A genetic association study of COPD patients and non-COPD in Japan single in the genes and recognition that The A of single polymorphism rs1077861 in NOD2 was associated with increased risk of COPD, and NOD2 gene in with studies such as these interaction in inflammation and in the development of airway smoking is the major cause of other causes include air pollution and occupational In the development of childhood asthma, an and respiratory are The link between respiratory and Th2 has been demonstrated in asthma in with respiratory in induced airway inflammation and by and reduced to infection may also to asthma pathogenesis and as by studies of airway in In a of asthma, the as an for to by has been as a risk factor for In the Respirology on obesity and respiratory Farah and potential mechanisms for the effects of obesity in including of from tissue and changes that lung have found increased of tissue in patients with The of asthma is by Th2 IgE and cell with of the airway In non-eosinophilic asthma in some patients. In a study of patients with non-eosinophilic asthma of patients also had sputum during over 6 This was more common when they were treated with the alone without inhaled compared with This in Respirology supports the of LABA for asthma and the potential of airway inflammatory phenotype. The airway inflammation of COPD is by and A number of studies in Respirology have on other of are a of that and function more like but also link to the of were lower in the of patients with stable COPD and decreased during acute is a recognition that A study of lung tissue showed that from COPD patients and smokers had increased protein of compared with smoke exposure in increased of and increased and exposure to the smoke could inflammatory to and other of recognition in the Other have also been in COPD. of was in small airway of COPD patients and compared with in with gene of and from that had high Hence, of in the airways could to susceptibility to in the of COPD patients and Airway remodelling is an important feature of chronic In a study in airway of was increased in patients with severe asthma, compared with mild asthma or and was induced following bronchoconstriction with or has been to be for and is a potential of airway remodelling in The pathogenesis of COPD is by a response to environmental to lung that for inflammation, These have been in a number of studies in Respirology in the of may have effects in specific protein of was measured in the lung tissue of COPD with mainly in and was increased in sputum of COPD correlated with of lung function, and correlated with sputum and In another study, and tissue of were measured in from COPD patients and non-COPD of and as well as tissue of 1 and were increased in COPD, the of COPD is by acute as disease A study of patients with an exacerbation of COPD measured inflammatory biomarkers at and before of and were at the of the correlated with exacerbation severity and were reduced by the time of but not to normal of biomarkers behind clinical and could be in monitoring COPD studies into treatment in airways disease. In an asthma study, single in the region of the gene were associated with in a association study of subjects from clinical Although the function of is as yet in of by in airway increased protein of the suggesting a for in In the Respirology on into recent developments in tissue in to the The large airways have been for tissue with and or or In development of for the small airways has been more because of the and number of of the of lung will help to advance this the hope of for lung

Background: Microbial culture-independent sequencing techniques have advanced our understanding of host-microbiome interactions in health and disease. The purpose of this study was to explore the dysbiosis of airway microbiota in patients with moderate or severe chronic obstructive pulmonary disease (COPD) and compare them with healthy controls.Methods: The COPD patients were investigated for disease severity based on airflow limitations and divided into moderate (50%≤FEV1<80% predicted) and severe groups (FEV1<50% predicted). Spontaneous sputum samples were collected and, the V3-V4 regions of the 16S rRNA coding gene were sequenced to examine the microbiome profile of COPD and healthy participants.Results: A total of 45 sputum samples were collected from 17 severe COPD, 12 moderate COPD cases, and 16 healthy volunteers. The bacterial alpha diversity (Shannon and Simpson’s index) significantly decreased in the moderate and severe COPD groups, compared to healthy samples. A significantly higher proportion of Firmicutes and Actinobacteria were present in moderate COPD, and Proteobacteria numbers were comparatively increased in severe COPD. In healthy samples, Bacteroidetes and Fusobacteria were more abundant in comparison to both the COPD groups. Among the most commonly detected 20 bacterial genera,Streptococcus was predominant among the COPD sputum samples, whereasPrevotella was the top genus in healthy controls. Linear discriminant analysis (LDA>2) revealed that marker genera likeStreptococcus andRothia were abundant in moderate COPD. For severe COPD, the generaPseudomonasandLeptotrichia were most prevalent, whereasFusobacterium andPrevotella were dominant in the healthy group.Conclusions: Our findings suggest a significant dysbiosis of the respiratory microbiome in COPD patients. The decreased microbial diversity may influence the host immune response and provide microbiological biomarkers for the diagnosis and monitoring of COPD.

Background: Microbial culture-independent sequencing techniques have advanced our understanding of host-microbiome interactions in health and disease. The purpose of this study was to explore the dysbiosis of airway microbiota in patients with moderate or severe chronic obstructive pulmonary disease (COPD) and compare them with healthy controls. Methods: The COPD patients were investigated for disease severity based on airflow limitations and divided into moderate (50%≤FEV1&lt;80% predicted) and severe groups (FEV1&lt;50% predicted). Spontaneous sputum samples were collected and, the V3-V4 regions of the 16S rRNA coding gene were sequenced to examine the microbiome profile of COPD and healthy participants. Results: A total of 45 sputum samples were collected from 17 severe COPD, 12 moderate COPD cases, and 16 healthy volunteers. The bacterial alpha diversity (Shannon and Simpson’s index) significantly decreased in the moderate and severe COPD groups, compared to healthy samples. A significantly higher proportion of Firmicutes and Actinobacteria were present in moderate COPD, and Proteobacteria numbers were comparatively increased in severe COPD. In healthy samples, Bacteroidetes and Fusobacteria were more abundant in comparison to both the COPD groups. Among the most commonly detected 20 bacterial genera, Streptococcus was predominant among the COPD sputum samples, whereas Prevotella was the top genus in healthy controls. Linear discriminant analysis (LDA&gt;2) revealed that marker genera like Streptococcus and Rothia were abundant in moderate COPD. For severe COPD, the genera Pseudomonas and Leptotrichia were most prevalent, whereas Fusobacterium and Prevotella were dominant in the healthy group. Conclusions: Our findings suggest a significant dysbiosis of the respiratory microbiome in COPD patients. The decreased microbial diversity may influence the host immune response and provide microbiological biomarkers for the diagnosis and monitoring of COPD.

Background: Microbial culture-independent sequencing techniques have advanced our understanding of host-microbiome interactions in health and disease. The purpose of this study was to explore the dysbiosis of airway microbiota in patients with moderate or severe chronic obstructive pulmonary disease (COPD) and compare them with healthy controls. Methods: The COPD patients were investigated for disease severity based on airflow limitations and divided into moderate (50%≤FEV1<80% predicted) and severe groups (FEV1<50% predicted). Spontaneous sputum samples were collected and, the V3-V4 regions of the 16S rRNA coding gene were sequenced to examine the microbiome profile of COPD and healthy participants. Results: A total of 45 sputum samples were collected from 17 severe COPD, 12 moderate COPD cases, and 16 healthy volunteers. The bacterial alpha diversity (Shannon and Simpson's index) significantly decreased in the moderate and severe COPD groups, compared to healthy samples. A significantly higher proportion of Firmicutes and Actinobacteria were present in moderate COPD, and Proteobacteria numbers were comparatively increased in severe COPD. In healthy samples, Bacteroidetes and Fusobacteria were more abundant in comparison to both the COPD groups. Among the most commonly detected 20 bacterial genera, Streptococcus was predominant among the COPD sputum samples, whereas Prevotella was the top genus in healthy controls. Linear discriminant analysis (LDA>2) revealed that marker genera like Streptococcus and Rothia were abundant in moderate COPD. For severe COPD, the genera Pseudomonasand Leptotrichia were most prevalent, whereas Fusobacterium and Prevotella were dominant in the healthy group. Conclusions: Our findings suggest a significant dysbiosis of the respiratory microbiome in COPD patients. The decreased microbial diversity may influence the host immune response and provide microbiological biomarkers for the diagnosis and monitoring of COPD.

Background: Microbial culture-independent sequencing techniques have advanced our understanding of host-microbiome interactions in health and disease. The purpose of this study was to explore the dysbiosis of airway microbiota in patients with moderate or severe chronic obstructive pulmonary disease (COPD) and compare them with healthy controls. Methods: The COPD patients were investigated for disease severity based on airflow limitations and divided into moderate (50%≤FEV1&lt;80% predicted) and severe groups (FEV1&lt;50% predicted). Spontaneous sputum samples were collected and, the V3-V4 regions of the 16S rRNA coding gene were sequenced to examine the microbiome profile of COPD and healthy participants. Results: A total of 45 sputum samples were collected from 17 severe COPD, 12 moderate COPD cases, and 16 healthy volunteers. The bacterial alpha diversity (Shannon and Simpson’s index) significantly decreased in the moderate and severe COPD groups, compared to healthy samples. A significantly higher proportion of Firmicutes and Actinobacteria were present in moderate COPD, and Proteobacteria numbers were comparatively increased in severe COPD. In healthy samples, Bacteroidetes and Fusobacteria were more abundant in comparison to both the COPD groups. Among the most commonly detected 20 bacterial genera, Streptococcus was predominant among the COPD sputum samples, whereas Prevotella was the top genus in healthy controls. Linear discriminant analysis (LDA&gt;2) revealed that marker genera like Streptococcus and Rothia were abundant in moderate COPD. For severe COPD, the genera Pseudomonas and Leptotrichia were most prevalent, whereas Fusobacterium and Prevotella were dominant in the healthy group. Conclusions: Our findings suggest a significant dysbiosis of the respiratory microbiome in COPD patients. The decreased microbial diversity may influence the host immune response and provide microbiological biomarkers for the diagnosis and monitoring of COPD.

Bronchodilatory effects of NVA237, a once daily long-acting muscarinic antagonist, in COPD patients

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

Nanocurcumin modulates Th17 cell responses in moderate and severe COPD patients

To assess the systemic bioactivity of fluticasone proprionate (FP) 2000 micro g daily on sensitive adrenal and bone markers in severe chronic obstructive pulmonary disease (COPD) patients with or without significant emphysema. Ten patients without emphysema (COPD group: age 55 years, FEV(1) 51% predicted and DL(CO) 83% predicted) and 10 patients with emphysema (COPDE group: age 59 years, FEV(1) 43% predicted and DL(CO) 49% predicted) received FP 2000 micro g daily via a spacer for 2 weeks. There was a 1-week washout period prior to FP treatment where patients were given salmeterol and oxitropium, after stopping their usual inhaled corticosteroids for the duration of the study. Measurements including overnight 10 h urinary cortisol excretion corrected for creatinine (OUCC) and serum osteocalcin concentrations were performed at baseline following washout and after 2 weeks of FP. Values for OUCC and serum osteocalcin concentrations pre- and post-FP were not significantly different between the COPD and COPDE groups. There was significant suppression of OUCC (nmol mmol(-1)) by FP treatment within the COPD group (P = 0.03): 7.86 vs 4.64 (95% CI on the difference 0.47, 5.98), and within the COPDE group (P = 0.006): 7.13 vs 4.27 (95% CI on the difference: 1.03, 4.69). Likewise, there was significant suppression of osteocalcin concentration (nmol l(-1)) by FP treatment within the COPD group (P = 0.04): 7.24 vs 6.34 (95% CI on the difference: 0.01, 1.78), and within the COPDE group (P = 0.03): 6.92 vs 5.72 (95% CI on the difference: 0.12, 2.29). Severe COPD patients who are receiving high dose FP are susceptible to the development of systemic adverse effects, irrespective of the presence of emphysema.