Clinical Course Of Chronic Obstructive Pulmonary Disease Research Articles

Protein N-glycosylation in the bronchoalveolar space differs between never-smokers and long-term smokers with and without COPD.

Chronic obstructive pulmonary disease (COPD) kills millions of people annually and patients suffering from exacerbations of this disorder display high morbidity and mortality. The clinical course of COPD is associated with dysbiosis and infections, but the underlying mechanisms are poorly understood. Glycosylation of proteins play roles in regulating interactions between microbes and immune cells, and knowledge on airway glycans therefore contribute to the understanding of infections. Furthermore, glycans have biomarker potential for identifying smokers with enhanced risk for developing COPD as well as COPD subgroups. Here, we characterized the N-glycosylation in the lower airways of healthy never-smokers (HNS, n=5) and long-term smokers (LTS) with (LTS+, n=4) and without COPD (LTS-, n=8). Using mass spectrometry, we identified 57 highly confident N-glycan structures whereof 38 oligomannose, complex, and paucimannose type glycans were common to BAL samples from HNS, LTS- and LTS+ groups. Hybrid type N-glycans were identified only in the LTS+ group. Qualitatively and quantitatively, HNS had lower inter-individual variation between samples compared to LTS- or LTS+. Cluster analysis of BAL N-glycosylation distinguished LTS from HNS. Correlation analysis with clinical parameters revealed that complex N-glycans were associated with health and absence of smoking whereas oligomannose N-glycans were associated with smoking and disease. The N-glycan profile from monocyte-derived macrophages differed from the BAL N-glycan profiles. In conclusion, long-term smokers display substantial alterations of N-glycosylation in the bronchoalveolar space, and the hybrid N-glycans identified only in long-term smokers with COPD deserve to be further studied as potential biomarkers.

Comparative characteristics of TRP channels expression levels on the macrophages of patients with chronic obstructive pulmonary disease

Introduction. Macrophages are one of the key cells in the pathogenesis of chronic obstructive pulmonary disease (COPD), mediating the primary immune response and coordinating the further reaction of the immune system upon contact with cigarette smoke and air pollutants. It is known that some TRP channels expressed on macrophages are receptors for dust particles and cigarette smoke components.Aim. To study the features of TRPV1, TRPV4, TRPA1 and TRPM8 channels expression on monocyte-derived macrophages and alveolar macrophages of COPD patients and smokers without bronchial obstruction.Materials and methods. Expression of TRP channels at the mRNA level was studied in monocyte-derived macrophages obtained from 8 COPD patients and 6 healthy smokers by quantitative reverse transcription PCR. Expression of TRP channels at the protein level was studied on alveolar macrophages of 39 COPD patients and 8 healthy smokers by indirect flow cytometry.Results. It was found that under in vitro conditions, monocyte-derive macrophages of COPD patients were distinguished by a significant 4.8-fold increase in the number of TRPV1 transcripts (p=0.009). At the same time, the expression of the TRPV1 protein on the alveolar macrophages of COPD patients was also significantly higher when compared to the cells of smokers from the control group (14.1 [6.4‒21.2]% vs. 6.1 [2.1‒9.8]%, p=0.006). In addition, we found that TRPV4 expression was increased among active smokers with COPD, and the expression of TRPA1 and TRPM8 channels correlated with some lung function parameters.Conclusion. The obtained results suggest that the increased expression of TRPV1 on macrophages may be a marker of the disease and contribute to its development, while the expression of TRPV4, TRPA1 and TRPM8 may influence the clinical course of COPD.

Clinical course of COPD in patients with Arg16Gly (rs1042713) polymorphism of ADRB2 gene.

The ADBR2 gene has been studied for its possible relationship with the development and clinical course of chronic obstructive pulmonary disease (COPD), including response to beta-2 agonists, with existing data being contentious on the subject. So, the purpose of this study was to look into the potential impact of the arginine-16-glycine (Arg16Gly) polymorphism on the clinical course and drug utilization in COPD patients. Data show that patients with Arg16Arg have a lower number of hospital admissions for exacerbations (p=0.048), but only in the total number of exacerbations, including those treated out-patients (p=0.086). Each glycine (Gly) copy was associated with a higher number of exacerbations (OR: 0.25; 95% CI: 0.00-055; p=0.048). The number of exacerbations after LABA/LAMA treatment was similar across groups, indicating that all ADRB2 variants responded well to the treatment. Furthermore, there were no statistically significant differences in mMRC and CAT values across all study visits. Interestingly, groups differed in their use of antibiotics (AB) at all visits, with Arg16Arg being associated with the least amount of AB use. There was also a link discovered between clycine copies and increased use of glucocorticoids. As a result, Arg16Gly is involved in the clinical course of COPD as well as the utilization of drug groups. Based on the findings, we can speculate that the cross-talk between the ADRB2 gene and the corticosteroid receptor is altered in patients with the Gly16Gly genotype.

Does the Gln27Gln polymorphism of the adrenoreceptor beta 2 gene affect the clinical course of chronic obstructive pulmonary disease?

Introduction: Many recent guidelines have highlighted the importance of genetic factors in chronic obstructive pulmonary disease (COPD) development. Adrenoreceptor beta 2 (ADRB2) is believed to be linked to the response to beta 2 agonists. However, the data for this gene remains controversial. In our study we aimed to investigate the impact of the Gln27Glu gene polymorphism of ADRB2 on the clinical course of COPD. Methods: 100 patients were included into the study. We assessed GOLD group, number of exacerbations, hospitalizations, modified Medical Research Council (mMRC) dyspnea and COPD assessment test (CAT) scores, and the utilization of antibiotics, glucocorticoids, and xanthines in these patients, as well as genetic testing at inclusion. All patients had their medication changed to tiotropium/olodaterol. Results: Groups did not differ according to age, sex, smoking status, pack-years, or COPD duration. We found that patients with the Gln27Gln polymorphism had the lowest GOLD grading, D. No difference was found in the number of exacerbations, hospitalizations, and out-patient exacerbations in the year prior to inclusion and the study year. Tiotropium/olodaterol were comparable in all study groups in reducing exacerbations and hospitalizations. There was no significant difference in mMRC and CAT values between the groups. We found that Gln27Gln patients required less antibiotics at inclusion and less glucocorticoids at the end of the study. Tiotrpium/olodaterol showed variable results for different genotypes regarding the reduction in use of different drugs. Conclusion: This ADRB2 polymorphism was associated with the progression of COPD as it is linked to a more severe phenotype, requiring greater use of antibiotics and glucocorticoids. This indicates potential crosstalk at the cellular level between ADRB2 and glucocorticoid receptors and should be investigated further.

Когнитивные особенности хронической обструктивной болезни легких у пациентов с алкогольной зависимостью

Chronic obstructive pulmonary disease (COPD) is a significant public health problem due to its widespread prevalence. It becomes a medical and social burden for both society and the patient. To what extent comorbid alcoholism is able to influence the features of the clinical course of COPD remains an open issue. The study aimed to reveal the impact of alcoholism on the level of COPD subjective symptoms in patients with different compliance. Materials and methods. 147 men with COPD in the age of 40―88 years were examined. The study relied on spirometry criteria, mMRC, CAT, domestic questionnaire of adherence to therapy, 6-minutes walking tests. It also established the stage of alcohol disease. The inhalation therapy was clarified during the interview, the episodic and systemic omissions fixed. Results and discussion. We observed the trend to subjective COPD symptoms underestimation in patients with the II, III stages of alcohol disease. Alcohol disease did not affect subjective symptoms in patients with stages III, IV of COPD. The compliance level and subjective symptoms severity showed no interrelation in patients suffering from alcoholism. This emphasized the absent association between the high level of compliance and critical self-state perception in patients with concomitant diseases. Regardless of the concomitant dependence, systemic omissions were rarely observed in patients receiving inhalers with a lower dosage frequency. Conclusion. The poor informativity of mMRC dyspnea scale and CAT-test was demonstrated in patients with mild and moderate COPD and severe alcoholism. The high level of compliance showed no impact on this tendency. Using single dose per day regimen was associated with a better compliance to recommendations, regardless of alcohol adherence.

Вплив поліморфізму C79G (rs1072714) та A46G (rs1042713) гена ADRB2 на клінічний перебіг ХОЗЛ

Аbstract. Chronic obstructive pulmonary disease (COPD) is a prevalent disease, that can be prevented and treated. Genetic factors play an important role in the COPD development. The aim of our study was to found ADRB2 gene polymorphism prevalence among patients with COPD, and assessment of its relation with the COPD development and clinical course. Materials and methods. 100 patients with COPD were included into the study. Source documentation, clinical and historical data were collected during study visits. Blood samples for ADRB2 gene testing were taken in all patients. All patients were treated according to GOLD guidelines, which included a combination of long-acting beta-2 agonists and long-acting anticholinergic drugs. According to the genetic analysis all patients were divided into 3 groups C79C/G46G (Haplotype 1) — 23 patients (23 %), C79G/A46G (Haplotype 2) — 26 patients (26 %), G79G/A46A (Haplotype 3) — 26 patients (26 %). Results. In correlation analysis there was a weak negative correlation between Haplotype 1 and total amount of exacerbations (r = -0.245, p = 0.032) and hospitalizations (r = -0.248, p = 0.032), and haplotype 3 had weak positive correlation with the amount of out-patient exacerbations (r = 0.263, p = 0.023). An average amount of antibiotic courses in group 1 was (1.09 ± 0.2), in group 2 — (1.69 ± 0.18), in group 3 — (2.00 ± 0.22), this difference was statistically significant (р = 0.005). There also was a significant difference in the duration of antibiotic treatment, which was (8.61 ± 1.55) in group 1, (12.88 ± 1.62) days in group 2 and (14.42 ± 1.68) days in group 3 (р = 0.036). Conclusions. ADRB2 gene polymorphism affects clinical course of COPD, which manifest in the different need in the administration of antibiotics in study groups, and also in the tendency towards different amount of exacerbations and rate of glucocorticoid use. Key words: COPD, gene ADRB2, exacerbations, antibiotics.

Features of the COPD course in patients with different alleles of C79G (rs1072714) of ADRB2 gene

Chronic obstructive pulmonary disease (COPD) is a widely spread disease, that can be prevented and treated. As it was mentioned in the GOLD guidelines, genetic factors have a prominent impact on the development of COPD. A great amount of different genes is involved into the development of COPD. They influence processes of inflammation, fibrosis and regulation of airways reactivity. Polymorphism of ADRB2 gene is of a particular interest as it is associated with the development of COPD and response to beta-2 agonists, which are the main drugs used in the treatment of COPD. The aim of our study was to investigate an impact of the polymorphism of ADRB2 gene on the clinical course of COPD. We collected source data, medical history in all patients in order to assess smoking status and smoking experience, clinical group of COPD according to GOLD classification, total amount of exacerbations, exacerbations treated in in-patient and out-patient conditions, data about use of antibiotics, glucocorticosteroids and methylxanthines. Blood was collected in all patients for the genetic analysis of ADRB2 gene polymorphism. Among COPD patients 65 (65 %) had changes in ADRB2 gene. 26 patients (26 %) had mutation and 39 patients (39 %) had polymorphism of ADRB2 gene, which indicate possible relation of ADRB2 gene with the COPD development. Patients of group 1, C79C allele carriers, had milder COPD course, which presented with the significant difference in the of GOLD D patients in this group (17.14±7.13 %) and group 2, C79G allele carriers, (58.97±8.15 %) and group 3, G79G allele carriers, (34.61±9.59 %). Group 1 patients had lower amount of exacerbations (2.543±0.281) when compared to group 3 (2.963±0.273), and lower amount of hospital admissions (1.031±0.154) when compared to group 2 (1.332±0.167). Group 1 patients also used less antibiotics then other groups. So, ADRB2 gene polymorphism in C79G positions is a prognostic factor of the severity of COPD course. It is associated with the greater amount of exacerbations and hospitalizations and also greater antibiotic use.

Effect of Treatment with Inactive Vitamin D on the Intracranial Blood Flow in Patients with Chronic Obstructive Pulmonary Disease

The goal of the work was to assess the dynamics of ultrasound parameters of renal blood flow in patients with chronic obstructive pulmonary disease (COPD) and the initial stages of chronic kidney disease (CKD) upon treatment with inactive vitamin D. The study included 264 patients with COPD the second to fourth degrees of severity in combination with CKD of stages I–II: 135 patients in the main group and 129 patients in the control group. Each group was divided into four subgroups according to the FEV1 and vitamin D levels. Native vitamin D was prescribed according to a scheme allowing the maintenance of vitamin D at a level of >34.3 ng/mL during the year for the main group and in accordance with the recommendations of the Russian Association of Endocrinologists for the control group. An ultrasound of the kidneys with calculation of the resistance index (RI) and albuminuria level were carried out for all patients upon inclusion in the study and after its completion. A decrease in the severity of albuminuria from A3 to A2 was revealed in 24.1% (16), and an increase in the glomerular filtration rate (GFR) was observed in 42.9% (58) patients of all patients in the main group. A statistically significant decrease in the renal artery resistance index was recorded in the group of patients with moderate COPD (GOLD 2) and vitamin-D deficiency in the main group (p < 0.05). The maintenance of vitamin-D levels more than 34.3 ng/mL over 12 months in patients with COPD in combination with CKD stages I–II was associated with a decrease in the severity of albuminuria, an increase in the GFR, and a statistically significant decrease in the RI of renal arteries of patients with moderate clinical course of COPD (GOLD 2) and vitamin-D deficiency.

SO080NOVEL EVIDENCE OF THE “PULMO-RENAL INTERACTION” AS A DISEASE DRIVER IN PATIENTS WITH CKD AND COPD

Abstract Background and Aims Chronic kidney disease (CKD) and chronic obstructive pulmonary disease (COPD) represent a global public health problem worldwide. As such, both conditions are associated with high disease-related morbidity and mortality. However, it is unclear whether the presence of CKD aggravates the clinical course of COPD and vice versa. Method In a novel murine model of cigarette smoke (CS)-induced lung injury combined with an adenine nephropathy model, kidney and lung inflammation, and fibrosis were studied. Moreover, in 2,314 patients with stable COPD enrolled in the prospective, multi-centre COSYCONET study, urinary Dickkopf-3 (DKK3), a biomarker of kidney injury and CKD progression was quantified. The association between urinary DKK3 and trajectories of forced expiratory pressure in 1 second (FEV1) and estimated glomerular filtration rate (eGFR) during a median follow-up of 37.1 months, exercise capacity, risk of exacerbation, and mortality was determined. Results In the CKD-COPD animal model, the presence of kidney injury was associated with increased systemic and pulmonary inflammation, impaired pulmonary function, as well as more severe damage of the lung architecture. Moreover, CS enhanced kidney fibrosis. Accordingly, in the COPD patients from the COSYCONET study, higher urinary DKK3 was associated with declining FEV1 during follow-up (OR 3.36, 95% CI 2.22-5.08). Moreover, high urinary DKK3 was associated with higher risk for exacerbation (OR 1.24, 95% CI 1.03-1.50), lower 6-minute walking distance, and higher all-cause mortality (HR 1.49, 95% CI 1.08-2.05). Importantly, high urinary DKK3 was associated with declining eGFR during follow-up (OR 2.23, 95% CI 1.22-4.07) independently from baseline kidney function and proteinuria, which was confirmed by a machine learning approach. Conclusion These data uncover a novel pathophysiological link between CKD and COPD. Patient with COPD and concomitant CKD are at high risk for worsening pulmonary function and adverse outcomes. Elevated urinary DKK3 allows identification of COPD patients with progressive CKD. Measurement of urinary DKK3 in patients with COPD may therefore represent a novel tool for risk stratification and the identification of patients, who might in particular benefit from preventive therapeutic strategies to prevent progression of COPD and CKD as well.

Serum Alpha-1 Antitrypsin Levels and the Clinical Course of Chronic Obstructive Pulmonary Disease.

PurposeAlpha-1 antitrypsin deficiency is associated with the development of chronic obstructive pulmonary disease (COPD), whereas increased levels of serum alpha-1antitrypsin occur in response to inflammation. The effects of alpha-1 antitrypsin levels on the clinical course of COPD had been unclear. We investigated the association of serum alpha-1 antitrypsin levels with the clinical course of COPD patients based on data from a 10-year prospective cohort study.Patients and methodsWe analyzed 278 COPD patients who participated in the Hokkaido COPD cohort study and who did not meet the criteria for alpha-1 antitrypsin deficiency. We divided the subjects into 3 groups according to quartiles of serum alpha-1 antitrypsin levels at baseline: lower group (<116 mg/dL, n = 66); middle group (116 to ≤141 mg/dL, n = 145); and higher group (>141 mg/dL, n = 67). The annual change in forced expiratory volume in 1 s (FEV1) and events of COPD exacerbation were monitored during the first 5 years, and mortality was followed-up during the entire 10 years.ResultsAt baseline, the higher group showed lower body mass index; higher computed tomography emphysema score; lower diffusing capacity; higher levels of acute-phase proteins; and higher blood neutrophil counts. Longitudinal analyses revealed that in the higher group, the annual decline in FEV1 was rapid and the 10-year mortality was higher, but there was no association between serum alpha-1 antitrypsin levels and time to first exacerbation.ConclusionCOPD subjects with higher serum alpha-1 antitrypsin levels were associated with a worse systemic inflammation status and higher 10-year mortality.

Metformin use mitigates the adverse prognostic effect of diabetes mellitus in chronic obstructive pulmonary disease

Background and objectiveAmong patients with chronic obstructive pulmonary disease (COPD), diabetes mellitus (DM) is a common comorbidity and is probably associated with increased systemic inflammation and worse prognosis. Metformin, with its pleiotropic anti-inflammatory and antioxidant actions, may offer theoretical benefits in COPD patients with DM. Thus, this study aimed to investigate the effects of DM and metformin use on mortality in the clinical trajectory of COPD.MethodsThis was a retrospective cohort study comprising patients with spirometry-confirmed COPD and an age of ≥40 years from 2008 to 2014. The primary outcome of interest was all-cause mortality. We evaluated the effects of DM on mortality through the clinical course of COPD and we also assessed the impact of metformin use on survival of the COPD population.ResultsAmong 4231 COPD patients, 556 (13%) had DM, and these patients had 1.62 times higher hazards of 2-year mortality than those without DM (95% confidence interval [CI], 1.15–2.28) after adjusting for age, gender, COPD stage, comorbidities and prior COPD hospitalization. Over a 2-year period, metformin users had a significantly lower risk of death (hazard ratio, 0.46; 95% CI, 0.23–0.92) compared with non-metformin users in patients with coexistent COPD and DM. Moreover, metformin users had similar survival to COPD patients without DM.ConclusionsThis study shows that DM is associated with an increased risk of death in COPD patients and metformin use seems to mitigate the hazard. Our findings suggest a potential role of metformin in the management of DM in COPD.

Resting hyperinflation and emphysema on the clinical course of COPD

The aim of this study is to clarify whether the combined evaluation of resting hyperinflation and emphysema confers any additional advantages in terms of predicting clinical outcomes in chronic obstructive pulmonary disease (COPD) patients. We included COPD patients from the Korean Obstructive Lung Disease (KOLD) cohort. Patients with a residual volume/total lung capacity (RV/TLC) over the upper limit of normal were defined as having resting hyperinflation, and those with an emphysema index >10% were defined as having emphysema. We investigated the impacts of resting hyperinflation and emphysema on exacerbations and mortality. A total of 310 COPD patients were analyzed over a mean of 61.1 months. After adjustment for covariates, resting hyperinflation was an independent predictor of earlier exacerbation (HR = 1.66, CI = 1.24–2.22), more frequent exacerbation (IRR = 1.35, CI = 1.01–1.81), and higher mortality (HR = 2.45, CI = 1.16–5.17) risk. Emphysema was also significantly associated with earlier exacerbation (HR = 1.64, CI = 1.15–2.35), and higher mortality (HR = 3.13, CI = 1.06–9.27) risk. Participants with both resting hyperinflation and emphysema had an additively higher risk of earlier exacerbations (HR = 1.71, 95% CI = 1.26–2.33) and mortality (HR = 3.75, 95% CI = 1.81–7.73) compared with those in other groups. In conclusion, resting hyperinflation and emphysema had additional worse impacts on exacerbations and mortality in COPD patients.

ROLE OF IL-4, IL-6, IL-8, IL-10 CYTOKINES IN THE IMMUNOPATHOGENESIS OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE

Chronic obstructive pulmonary disease (COPD) is socially significant disease. COPD is based on chronic inflammatory process of respiratory tract, which determines steady progression of the bronchial obstruction. Studies of the role of cytokines in immune pathogenesis of COPD are of crucial importance. The biological mediators determine local, systemic inflammation, and pathophysiological effects of extra-systemic pathological manifestations. In this work, we studied spontaneous and induced production of IL-4, IL-6, IL-8, IL-10 cytokines by blood leukocytes from the patients with moderate and severe chronic obstructive pulmonary disease, beyond the exacerbation phase. It is shown that the evident role in formation of the inflammatory process in COPD belongs to the IL-6, IL-8. We have found a significant increase in both spontaneous and induced production of IL-6 and IL-8 (p &lt; 0.05) in the patients. Induced production of cytokines strongly suggests the reserve capabilities of immunocompetent cells in response to the pathogenic factor. Neutrophilic type of inflammation, manifesting as activation of granulocytes, mostly, neutrophils, in response to toxic agents (in particular, smoking) and bacterial pathogens, is primarily associated with IL-6 and IL-8. These results reflect the type and intensity of respiratory tract inflammation in patients with chronic obstructive pulmonary disease and its persistent course.High levels of the studied cytokines confirm their role in bronchial remodeling and contribute to irreversibility of bronchial obstruction in this disorder. The relationship between spontaneous and induced production of the studied cytokines and the clinical indices of the disease course has been shown. Statistically significant increase between frequency of COPD recurrences (more than 2 times pro year, p &lt; 0.05), and low FEV1values (p &lt; 0.05) were observed in patients with high values of spontaneous and induced production of IL-6 and IL-8. It may be associated with persistent course of neutrophilic inflammation of respiratory tract and progressive bronchial obstruction. IL-6 and IL-8 significantly contribute to pathogenetic mechanisms, determining the clinical course of COPD and may serve as markers of severity in this disorder. Certainly, the immune mechanisms of pathological inflammation in COPD are complex and multifaceted. Studies of clinical significance of induced cytokine production will help the physician when determining type and duration of treatment. Personalized approach to the therapy of patients with COPD depends on the phenotype of pathology, pattern, severity and intensity of inflammation.

A relationship between chronic obstructive pulmonary disease, obesity and melatonin level

This is a review of experimental and clinical studies investigated effects of obesity on clinical course of chronic obstructive pulmonary disease (COPD); pathophysiological mechanisms of this effect, and relationships between melatonin level and the course of COPD have been also discussed. Associations between severity of COPD, rate of exacerbations and blood levels of most important adipokines, such as leptin and adiponectin, and relationships between melatonin levels and those adipokines were published. Conflicting results were obtained in studies of effects of obesity on clinical course of COPD. The "obesity paradox", that is a reduction in mortality and milder bronchial obstruction in obese COPD patients, has been identified in several studies. Despite contradictory results, obesity is likely to improve prognosis of COPD due to decrease in the systemic inflammation. Levels of leptin and adiponectin increase in acute exacerbation of COPD and then decrease to the baseline. Moreover, melatonin is suggested to play a great role for COPD course, mostly due to antiinflammatory and antioxidant activities. According to results of several studies, melatonin could affect blood levels of adiponectin and lectin; this could indirectly influence on the systemic inflammation in COPD. Further studies are needed to elicit these relationships.

Anemia as a clinical marker of stable chronic obstructive pulmonary disease in the Korean obstructive lung disease cohort.

Anemia is a major co-morbidity in chronic obstructive pulmonary disease (COPD). However, the mechanism of development for anemia and the impact of anemia on the prognosis of COPD remain poorly understood. Therefore, this study attempted to evaluate the prognostic role of anemia on the clinical course of COPD and investigate the factors linked with the serum hemoglobin level in COPD. We analyzed 407 COPD patients enrolled in the Korean obstructive lung disease (KOLD) cohort at 16 hospitals in Korea recruited over 9 years. Multivariate Cox regression analysis was performed to find independent predictors of survival and multivariate logistic regression analyses were done to find independent factors. Anemic COPD were older with lower body mass index (BMI) (P<0.001), lower serum cholesterol level (P=0.001), lower serum albumin level (P<0.001), and shorter 6-minute walking distance (P=0.046) compared to non-anemic COPD. A multivariate Cox regression analysis revealed that age (P=0.002), BMI (P=0.001), post-bronchodilator forced expiratory volume in 1 second (FEV1) (P=0.007), 6-minute walk distance (P=0.008), anemia (P=0.025) were significant predictors for all-cause mortality. In multivariate regression analysis, older age (P<0.001), female gender (P=0.001), lower BMI (P=0.016), and lower serum albumin level (P<0.001) were independent factors associated with lower serum hemoglobin level. Our data showed that anemia was an independent risk factor for mortality in COPD, and aging, lower serum albumin level, and lower BMI were independent factors associated with lower serum hemoglobin level.

The association between serological features of chronic Chlamydia pneumoniae infection and markers of systemic inflammation and nutrition in COPD patients

Introduction: Chlamydia pneumoniae is an obligatory human pathogen involved in lower and upper airway infections, including pneumonia, bronchitis. Asymptomatic C. pneumoniae carriage is also relatively common. The association of C. pneumoniae infections with the chronic obstructive pulmonary disease (COPD) course is unclear.Objectives: The aim of the study was to investigate the association between chronic C. pneumoniae infection and clinical features of COPD, markers of inflammation and metabolic dysfunction.Patients and methods: The study included 59 patients with stable COPD who had no, or had ≥2 acute exacerbations during last year. The level of IgA and IgG antibody against C. pneumoniae, IL-6, IL-8, resistin, insulin, adiponectin and acyl ghrelin was measured in serum by enzyme-linked immunosorbent assay (ELISA).Results: No differences in clinical and functional data were observed between COPD patients without serological features of C. pneumoniae infection and chronic C. pneumoniae infection. The level of anti C. pneumoniae IgA significantly correlated with IL-8, IL-6, resistin concentration in group of frequent exacerbators. IgG level correlated negatively with acetyl ghrelin and body mass index (BMI) in patients without frequent exacerbations, in contrast to frequent COPD exacerbation group where significant correlations between IgG level and BMI was demonstrated. Serum IL-6 correlated positively with resistin and insulin and negatively with adiponectin in group of patients with serological features of chronic C. pneumoniae infection only.Conclusions: Our study showed that chronic C. pneumoniae infection does not influence the clinical course of COPD in the both study groups. Chronic C. pneumoniae infections might be associated with a distinct COPD phenotype that affects metabolic dysfunction.

National clinical guidelines on diagnosis and treatment of chronic obstructive pulmonary disease: a clinical decision-making algorithm

Treatment of patients with chronic obstructive pulmonary disease (COPD) is one of the most important tasks of clinical medicine due to high prevalence of and high mortality from COPD. Treatment of COPD as a heterogeneous disease requires different approaches depending on the severity and the clinical course of COPD. Clinical guidelines have become the principal document that regulates different aspects of management of COPD patients. Algorithms of management and clinical decision making are the crucial part of guidelines because they help achieving a balance between making the decision in different clinical situations and simple graphics. The simplified approach is important for implementation the algorithm into clinical practice. Different evidence-based therapeutic schemes proposed by experts of Russian Respiratory Society and other countries have been enclosed into this article with discussion about their strengths and limitations and possibility of practical use. The Russian algorithm reflects a current view on differentiated management of COPD patients and fits the requirements of Healthcare Ministry of Russian Federation and needs of achieving the optimal balance between high informative significance and a simple graphics of the scheme.

Clinical course of occupational chronic obstructive pulmonary disease in workers exposed to dust

The aim of the study was to investigate staging and time of onset of pulmonary inflammation in workers exposed to dust. Methods. This prospective study involved patients (n = 483) with occupational chronic bronchitis (OCB) and chronic obstructive pulmonary disease (COPD). We analyzed medical history, lung function, blood biochemistry, and sputum culturing. Additionally, medical recordts of died patients (n = 180) with occupational lung disease were also analyzed. Results. First symptoms of chronic lung disease occurred after 17.1 ± 1.1 years of occupational hazard exposure in women and after 20.1 ± 1.2 years in smoking men. Occupational etiology of the disease was recognized 5 – 6 years later. Occupational COPD occurred earlier that OCB; this could be explained by genetic predisposition to this disease. Occupational COPD developed independently of respiratory infection excepting patients with concurrent diabetes mellitus. Conclusion. The clinical course of COPD is gradual with initial sighs of OCB followed by bronchial obstruction, probably, in genetically predisposed subjects. The disease occurred earlier in women than in men; this could be related to higher susceptibility of females to inhalational pollutants. The cause of death was lung malignancy in &gt; 50% of patients with occupational lung diseases. Lung tumors were diagnosed significantly later compared to non-pulmonary tumors.

Prevalence and impact of diabetes, hypertension, and cardiovascular diseases in chronic obstructive pulmonary diseases: A hospital-based cross-section study.

BackgroundChronic obstructive pulmonary disease (COPD) is associated with important chronic comorbid diseases, including diabetes, hypertension and cardiovascular diseases. As very limited data is available in India, the aim of the present study was to determine the relationship between COPD and the common, chronic comorbid conditions of diabetes mellitus (DM), hypertension (HTN), and cardiovascular diseases (CVD) and also to determine how these affect the clinical course of COPD.MethodsAll the COPD cohorts diagnosed as per Global Initiative for Chronic Obstructive Lung Disease-2013 (GOLD-2013) criteria were screened for DM, HTN, and CVD as per stipulated national and WHO guidelines.ResultsThe prevalence of DM, HTN, and CVD in the 2432 COPD subjects was 25.94%, 37.25%, and 13.93%, respectively. In multivariate analyses, very severe COPD was associated with a higher risk of DM (odds ratio [OR] 1.6, 95% confidence interval [CI] 1.2–2), HTN (OR 1.6, 95% CI 1.4–1.9), and CVD (OR 2.5, 95% CI 1.9–3.0).ConclusionA significant relationship was found between COPD and the presence of comorbid DM, HTN, and CVD. It was also found that subjects with advanced COPD were more likely to have at least two of these conditions and hugely affect the outcome of the disease. These findings suggest that the presence of COPD could provide a rationale to look for other comorbid disease and, conversely, that the presence of DM, HTN, or CVD might be the basis for the assessment of patients for airflow limitation and COPD as the tobacco smoking and advancing age were common risk factors.

COPD Surveillance—United States, 1999-2011

This report updates surveillance results for COPD in the United States. For 1999 to 2011, data from national data systems for adults aged ≥ 25 years were analyzed. In 2011, 6.5% of adults (approximately 13.7 million) reported having been diagnosed with COPD. From 1999 to 2011, the overall age-adjusted prevalence of having been diagnosed with COPD declined (P = .019). In 2010, there were 10.3 million (494.8 per 10,000) physician office visits, 1.5 million (72.0 per 10,000) ED visits, and 699,000 (32.2 per 10,000) hospital discharges for COPD. From 1999 to 2010, no significant overall trends were noted for physician office visits and ED visits; however, the age-adjusted hospital discharge rate for COPD declined significantly (P = .001). In 2010 there were 312,654 (11.2 per 1,000) Medicare hospital discharge claims submitted for COPD. Medicare claims (1999-2010) declined overall (P = .045), among men (P = .022) and among enrollees aged 65 to 74 years (P = .033). There were 133,575 deaths (63.1 per 100,000) from COPD in 2010. The overall age-adjusted death rate for COPD did not change during 1999 to 2010 (P = .163). Death rates (1999-2010) increased among adults aged 45 to 54 years (P < .001) and among American Indian/Alaska Natives (P = .008) but declined among those aged 55 to 64 years (P = .002) and 65 to 74 years (P < .001), Hispanics (P = .038), Asian/Pacific Islanders (P < .001), and men (P = .001). Geographic clustering of prevalence, Medicare hospitalizations, and deaths were observed. Declines in the age-adjusted prevalence, death rate in men, and hospitalizations for COPD since 1999 suggest progress in the prevention of COPD in the United States.