Association of Short-Term Pollen Exposure With Lung Function in COPD Patients.

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

No More Equivalence Trials for Antibiotics in Exacerbations of COPD, Please

Nearly 16 million Americans, and more than 250 million people around the world, live with chronic obstructive pulmonary disease (COPD) and millions more remain undiagnosed. The COPD Foundation has been monitoring the global pandemic of a disease caused by the recently identified coronavirus family member SARS-CoV-2 named coronavirus disease 2019 (COVID-19). On April 17th, 2020 the World Health Organization (WHO) reported 2,078,605 confirmed cases and 139,515 deaths globally. 1 The COVID-19 pandemic has put patients with COPD and other comorbidities at a high risk for poor outcomes as noted by the U.S. Centers for Disease Control and Prevention (CDC). 2 Although there is limited published data on COVID-19 in COPD individuals (only 15 out of > 4815 PubMed references on April 17th), a recent article in the European Respiratory Journal evaluated 1590 laboratory-confirmed hospitalized cases in China

Antibiotics Should be Given Only to Patients with Moderate-To-Severe COPD

Objective: To analyze the differences in pulmonary function and inflammatory indicators between patients with chronic obstructive pulmonary disease (COPD) and those with persistent airflow limitation (PAL) asthma, and to explore the influencing factors of acute exacerbation in patients with COPD and PAL asthma. Methods: A total of 192 patients with stable COPD and PAL asthma who visited the Department of Respiratory and Critical Care Medicine of the Shanghai General Hospital of Shanghai Jiao Tong University School of Medicine from January 2021 to December 2022 were prospectively included. Among them, 143 were male and 49 were female; the age ranged from 40 to 87 years [(63.4±12.1) years]; 92 were in the COPD group and 100 were in the PAL asthma group. The differences in lung function and inflammatory markers between the COPD group and the PAL asthma group were compared. The disease exacerbation of COPD and PAL asthma patients was evaluated every 3 months. After 12 months of follow-up, 138 patients completed the acute exacerbation assessment, including 105 males and 33 females; the age was (64.9±10.2) years; 66 were in the COPD group and 72 were in the PAL asthma group. Multivariate logistic regression models were used to analyze the influencing factors of acute exacerbation in COPD and PAL asthma. Results: The percentage of predicted forced expiratory flow at 75% of forced vital capacity (FEF75%Pred), the percentage of predicted mid-expiratory flow between 25% and 75% of forced vital capacity (FEF25-75%Pred), and the neutrophil-to-lymphocyte ratio (NLR) in the PAL asthma group were all lower than those in the COPD group (all P<0.05); the eosinophil count, lymphocyte count, fractional exhaled nitric oxide (FeNO), and the proportion of patients with type 2 inflammation were all higher in the PAL asthma group than in the COPD group (all P<0.05). The improvement rates of forced expiratory volume in one second (ΔFEV1%), forced vital capacity (ΔFVC%), forced expiratory flow at 50% of forced vital capacity (ΔFEF50%), forced expiratory flow at 75% of forced vital capacity (ΔFEF75%), and mid-expiratory flow between 25% and 75% of forced vital capacity (ΔFEF25-75%) in the COPD group were all lower than those in the PAL asthma group (all P<0.05). There were 22 cases (33.3%) of acute exacerbation in the COPD group. There were 25 cases (34.7%) of acute attack in the PAL asthma group. A lower baseline FEV1%Pred (OR=0.934, 95%CI: 0.892-0.979) and a higher NLR (OR=1.185, 95%CI: 1.003-1.400) were risk factors for acute exacerbation in COPD patients within one year; a lower baseline FEV1%Pred (OR=0.896, 95%CI: 0.823-0.976), higher ΔFEF75% (OR=1.038, 95%CI: 1.011-1.066), and type 2 inflammation (OR=7.534, 95%CI: 1.254-45.246) were risk factors for acute attacks in PAL asthma patients within one year. Conclusions: Patients with PAL asthma have more prominent type 2 inflammation features and stronger reversibility of small airways. Lower FEV1%Pred and higher NLR are risk factors for acute exacerbation in COPD patients, while lower FEV1%Pred, higher ΔFEF75%Pred and type 2 inflammation are risk factors for acute attacks in PAL asthma patients.

The role of serum chloride ion in the prognosis of COPD

Antibiotics for treatment and prevention of exacerbations of chronic obstructive pulmonary disease

Management of chronic obstructive pulmonary disease: Moving beyond the asthma algorithm

Chronic Obstructive Pulmonary Disease, Neutrophils and Bacterial Infection: A Complex Web Involving IL-17 and IL-22 Unravels

Chronic Obstructive Pulmonary Disease (COPD) patients have alterations in body composition. Bioelectrical impedance analysis (BIA) evaluates body composition, hydration status, and fluid distribution. Subjects with fluid disturbances have been found to have lower FEV1, respiratory muscle strength, and poor prognosis. We aimed to evaluate the effect of hydration status and fluid distribution on pulmonary function in COPD patients. A cross-sectional study, 180 patients with a confirmed diagnosis of COPD were included. Patients with asthma, advanced renal or liver disease, acute HF, exacerbation of COPD, or pacemakers were excluded. Hydration status variables (TBW, ECW, ICW) and disturbance of fluid distribution [impedance ratio (IR) > 0.84 and phase angle (PhA)] were evaluated by BIA. Pulmonary function was assessed by spirometry. The mean population age was 71.55 ± 8.94 years; 55% were men. Subjects were divided into two groups according to the IR ≥ 0.84 or < 0.84. The group with higher IR ≥ 0.84 had lower FEV1, FVC, FEV1/FVC, DLCO and, PhA compared to those with IR < 0.84. After adjusting for confounding variables TBW, ECW, IR ≥ 0.84, PhA, and resistance/height increase were associated with decreased FEV1. In the same way, with IR ≥ 0.84, edema index ≥ 0.48, trunk and abdominal IR were negatively associated with FVC, and PhA had a positive association with FVC. Fluid distribution, especially IR and PhA, could be a useful parameter for predicting pulmonary function in COPD patients.

PurposeWNT/β-catenin signal pathway is a potential hope for lung tissue repair. We investigated the levels of Dickkopf‐1 (DKK1), an endogenous inhibitor of WNT/β-catenin signal pathway, in chronic obstructive pulmonary disease (COPD) patients and airway inflammation.Patients and MethodsCollected the demographic and clinical characteristics of 36 healthy controls, 25 stable COPD patients and 10 acute exacerbation of COPD (AECOPD) patients, then performed pulmonary function and detected serum DKK1 levels. After over-expression of DKK1, detect the levels of DDK1, lipoprotein-related protein 6 (LRP6) and inflammatory factors in bronchial epithelial cells stimulated with cigarette smoke extract (CSE).ResultsSerum DKK1 were reduced in stable COPD patients compared to healthy controls (3866.72 ± 775.33 pg/mL vs 5317.61 ± 1317.20 pg/mL, p<0.0001), but there was no significant difference between stable and acutely exacerbated patients (3866.72 ± 775.33 pg/mL vs 3482.10 ± 841.25 pg/mL, p>0.05). DKK1 was positively correlated with FEV1 (r = 0.570, p<0.0001), FEV1/FVC (rho = 0.590, p<0.0001), FEV1/Pre (r = 0.517, p<0.0001). Multiple linear regression analysis also suggested that FEV1 levels were higher with increasing DKK1. In vitro, elevated IL-6, IL-8, TNF-α and decreased DKK1, LRP6 were found in Beas-2B cells after CSE treatments, and increased LRP6 and decreased inflammatory factors were found after overexpression of DKK1. Andrographolide restored the CSE-induced decrease in DKK1 and increase in IL-6 and IL-8.ConclusionDKK1 levels were decreased in COPD patients and positively correlated with lung function, overexpression of DKK1 and andrographolide attenuated airway cell inflammation, both suggesting a potential role in pathophysiology and providing a disease-specific biomarker pattern.

Background: Although chronic obstructive pulmonary disease(COPD) and interstitial lung abnormalities(ILAs) have distinct clinical manifestations, both diseases may coexist in a patient because they share similar risk factors such as smoking, male sex, and old age.The presence of ILAs, which may be an early or mild form of ILD, is notable among patients with COPD, and associated with poor prognosis. Objective: We aimed to elucidate the exacerbation rate and clinical outcomes according to ILAs in patients with COPD. Methods: A retrospective study was conducted between January 2015 and December 2023 of COPD patients who underwent chest CT imaging and longitudinal pulmonary function tests. We evaluated radiographic findings, history of COPD exacerbations, lung function changes and mortality rate in hospitalized patients to pulmonary and critical care medicine department of university hospital during the longituidinal follow-up. Results: Of 724 patients with COPD,286 patients had ILAs. Patients with ILAs were significantly older (p&amp;lt;0.01) and had lower FEV1(p&amp;lt;0.01), lower FVC(p&amp;lt;0.02), and lower DLCO (p&amp;lt;0.001) than patients without ILAs.During the mean follow-up period of 7.4 years, ILAs were associated significantly with the annual incidence of moderate to severe acute exacerbations of COPD (3.45+_1.24 vs 1.88+_0.86; p&amp;lt;0.002) and with the risk of frequent exacerbation (adjusted OR,2.89;p&amp;lt;0.02). COPD exacerbations in patients with ILAs commonly were non-infectious compared to patients with COPD without ILAs (OR 2.44[0.79-4.36]; p&amp;lt;0.002) in whom common exacerbations were related to with infectious factors. Patients with COPD associated with ILAs related to progressive ILAs and frequent exacerbations of COPD pulmonary function tests showed a significantly higher rate of annual decline in FEV1 and FVC than those showing no ILAs. ICU admission was hgiher in patients with ILAs(p&amp;lt;0.001) and the occurance of pulmonary hypertension also was hgiher in COPD patients with ILAs(OR 3.55[0.96-7.34]; p&amp;lt;0.001). Mortality rate was higher in COPD patients with ILAs (OR 2.45[0.84-5.75]; p&amp;lt;0.002) than in patients with COPD without ILAs (148/51.7% vs 94/ 21.4%;p&amp;lt;0.002). Conclusions:ILAs were associated significantly with moderate to severe acute exacerbations in patients with COPD, and commonly COPD exacerbation in patients were non-infectious.The frequent exacerbations of COPD and progression of ILAs were associated with an accelerated decline of lung function.COPD exacerbation and ILAs progression also were associated with an increased rate of ICU admission of patients and with significantly increased the mortality rate

IntroductionPatients with chronic obstructive pulmonary disease (COPD) frequently suffer from comorbidities. COPD severity may be evaluated by the Global initiative for chronic Obstructive Lung Disease (GOLD) combined risk assessment score (GOLD score). Spirometry, body plethysmography, diffusing capacity of the lung for carbon monoxide (DLCO), and high-resolution computed tomography (HR-CT) measure lung function and elucidate pulmonary pathology. This study assesses associations between GOLD score and measurements of lung function in COPD patients with and without (≤1) comorbidities. It evaluates whether the presence of comorbidities influences evaluation by GOLD score of COPD severity, and questions whether GOLD score describes morbidity rather than COPD severity.MethodsIn this prospective study, 106 patients with stable COPD were included. Patients treated for lung cancer were excluded. Demographics, oxygen saturation (SpO2), modified Medical Research Council Dyspnea Scale, COPD exacerbations, and comorbidities were recorded. Body plethysmography and DLCO were measured, and HR-CT performed and evaluated for emphysema and airways disease. COPD severity was stratified by the GOLD score. Correlation analyses: 1) GOLD score, 2) emphysema grade, and 3) airways disease and lung function parameters, described by: forced expiratory volume in the first second in percent of expected value (FEV1%), inspiratory capacity (IC%), total lung volume (TLC%), IC/TLC, and SpO2. Correlation analyses between subgroups and hierarchical cluster analysis were performed.ResultsSignificant associations were found between GOLD score and both emphysema grade (correlation coefficients [cc]: −0.2, P=0.03) and lung function parameters (cc: −0.5 to −0.7, P-values all <0.001) weakened in patients with >1 comorbidity (cc: −0.4 to −0.5, P-values all 0.001). Significant differences between subgroups were found in GOLD score and both FEV1% (cc: −0.2, P=0.02) and IC/TLC (cc: −0.2, P=0.02). Comorbidities were associated with GOLD score and composite measures in hierarchical cluster analysis.ConclusionThe presence of comorbidities influences the relationship between GOLD score and lung function measurements. GOLD score may be more representative of morbidity than of COPD severity.

Background: Chronic obstructive pulmonary disease (COPD) is associated with persistent airflow limitation and systemic deconditioning that reduce exercise tolerance and worsen functional outcomes. Low-cost adjunct exercise modalities that can augment rehabilitation effects remain clinically relevant. Objective: To determine the effects of adding isometric handgrip (IHG) exercise training to resistance training on lung function and functional exercise capacity in COPD patients. Methods: A single-center, parallel-group randomized clinical trial enrolled 48 ambulatory patients with GOLD stage II–III COPD and randomized them to IHG plus resistance training (n=24) or resistance training alone (n=24) for 8 weeks. Spirometry outcomes included forced expiratory volume in one second (FEV1), forced vital capacity (FVC), and FEV1/FVC ratio, and functional capacity was assessed with the 6-minute walk test (6MWT). Parametric analyses compared within-group pre–post changes and between-group post-intervention differences. Results: Both groups improved after intervention; however, the combined program produced larger post-intervention values. FEV1 was higher in the combined group (2.4047±0.4619 vs 1.9320±0.3823 L; MD 0.4727; 95% CI 0.2261–0.7193; p&lt;0.01) and FVC was higher (3.4688±0.5834 vs 3.0949±0.4941 L; MD 0.3739; 95% CI 0.0596–0.6882; p=0.021). 6MWT distance was also higher (422.94±31.03 vs 391.58±24.00 m; MD 31.36; 95% CI 15.24–47.48; p&lt;0.001). Conclusion: Adding IHG training to resistance exercise enhanced pulmonary function and walking capacity more than resistance training alone in GOLD II–III COPD. Keywords: Chronic obstructive pulmonary disease; isometric handgrip; resistance training; spirometry; FEV1; forced vital capacity; six-minute walk test; pulmonary rehabilitation.

Introduction: Controlling and preventing symptoms of exacerbations, shortness of breath, cough and mucus in the lungs are important goals of Chronic Obstructive Pulmonary Disease (COPD) treatment. Oscillating Positive Expiratory Pressure (OPEP) devices have been shown to improve clinical results. The conservation of energy and oxygen, as well as, the prevention of lung infections and reducing rehospitalisation may be facilitated by clearing the lungs. There are several airway clearance devices, that can be used to help clear excessive sputum. Aim: To identify the effect of aerobika device versus acapella device on rehospitalisation and lung functions in COPD patients. Materials and Methods: This systematic review was conducted in the Department of Physiotherapy at Acharya Vinoba Bhave Rural Hospital, Sawangi, Wardha, Maharashtra, India. The duration of the study was three months, from march 2022 to june 2022. Five databases (PubMed, scopus, web of science, google scholar) were searched from 2012 to 2022. Inclusion criteria consisted of studies on the effect of aerobika device and acapella device on rehospitalisation and lung functions only in COPD patients. Data extraction included baseline features, treatment intervention, training frequency, supervision level, breathlessness, acute exacerbation, and outcomes. High quality experimental trials and comparative studies were chosen for the study. Results: A total of 20 articles were extracted; five were utilised for the purpose of writing the review, emphasising the effect of aerobika device versus acapella device on rehospitalisation and lung functions in COPD patients. Studies had showed inconsistent results on the effect of aerobika device versus acapella device on rehospitalisation and lung functions in COPD patients. Conclusion: Rehospitalisation, readmission and length of the stay can be reduced by using both, aerobika and acapella devices. Both devices are effective in improving lung function in COPD patients.