Course Of Chronic Obstructive Pulmonary Disease Research Articles

Pulmonary embolism work-up in chronic obstructive pulmonary disease exacerbations: what is the best strategy for clinicians?

Acute exacerbations of chronic obstructive pulmonary disease (COPD) are important events in the natural course of COPD, as they increase morbidity and mortality. Acute pulmonary embolism may mimic the symptoms of COPD exacerbations. However, the exact prevalence of pulmonary embolism in unexplained exacerbations of COPD is unclear based on the current data. This review provides a practical approach to patients with COPD complaining of worsening respiratory symptoms. A randomized clinical trial has shown that a routine pulmonary embolism diagnostic work-up does not improve care of patients with acute exacerbations of COPD. However, review of the recent literature suggests that a nonnegligible proportion of otherwise unexplained exacerbations of COPD may be caused by pulmonary embolism. To date, nevertheless, there are limited studies developing and validating clinical models that might aid in the identification of patients requiring additional tests for the diagnosis of pulmonary embolism. Until new evidence becomes available, we believe that a routine diagnostic strategy for pulmonary embolism is not appropriate for patients with acute exacerbations of COPD. Recommendations for routine pulmonary embolism diagnostic work-up necessitate further development of prognostic models and conduct of clinical trials that assess important health outcomes.

Peculiarities of granulocyte-macrophage and macrophage colony-stimulating factors receptors expression in subpopulations of peripheral blood monocytes of patients with chronic obstructive pulmonary disease

Introduction. To analyze of the severity of respiratory symptoms in patients with chronic obstructive pulmonary disease (COPD), depending on the presence of an exacerbation or novel coronavirus infection (NCVI), taking into account the activity of acute phase blood parameters.Materials and methods. The medical documentation of 162 patients with COPD was studied, which were divided into 3 groups: group 1 (n=61) ‒ COPD and NCVI, group 2 (n=53) – stable COPD, group 3 (n=48) ‒ COPD exacerbation. The severity of respiratory symptoms was assessed using points. To assess the activity of inflammation the following biochemical indicators were used ‒ C-reactive protein (CRP) and fibrinogen (g/L).Results. According to the severity of cough and the intensity of dyspnea on the mMRC scale, the first, second and third groups did not differ statistically (p=0.07). Patients of the first group (82.5%) characterized by the absence of classical criteria for exacerbation of COPD. In terms of the severity of sputum production, the first, second and third groups are statistically different (p=0.0001). The first, second and third groups differ significantly in the level of serum CRP (p=0.0001) and fibrinogen (p=0.009). According to the results of the correlation analysis, some relationships found between respiratory symptoms and the level of CRP and fibrinogen.Conclusion. The clinical feature of the associated course of stable COPD and NCVI is the presence of severe dyspnea and the absence of classic criteria for exacerbation of COPD. Systemic inflammation in NCVI and stable COPD are more pronounced than in isolated stable COPD or exacerbation and correlates with cough and dyspnea. Practitioners for the differential diagnosis of NCVI in stable COPD can use the data obtained.

Clinical case of indacaterol / glycopyrronium bromide prescription in a patient with severe copd and concomitant pathology

Combinations of inhaled glucocorticosteroids (IHGC) and long-acting bronchodilator inhalers (LABA inhalers) have been widely used to treat chronic obstructive pulmonary disease (COPD) over the past two decades. Prescription of these drugs was based on large studies showing that this therapeutic regimen was more effective compared to placebo and monotherapy. The article presents a clinical case report of a patient with severe course of COPD and coronary heart disease (CHD). Up-to-date concepts of using dual bronchodilator therapy when switching from combinations of inhaled glucocorticosteroids and long-acting bronchodilator inhalers (IHGC/LABA) is discussed. A patient with COPD and coronary artery disease, atrial fibrillation while using IHGC/LABA had progressive respiratory failure, frequent exacerbations, and acute symptomatology. As there is evidence that the use of IHGC/LABA has a number of limitations in the combined course of COPD and cardiovascular diseases, first of all in coronary artery disease and arrhythmias, it was recommended to replace therapy with a combination of dual bronchodilators – a long-acting muscarinic antagonist (LAMA) and a long-acting β agonist (LABA). The therapy resulted in stabilization of the condition, reduction of clinical symptoms, and absence of cardiovascular complications. It has been concluded that the dual bronchodilator therapy with a combination of glycopyrronium bromide and indacaterol is prioritized in COPD, including COPD combined with cardiovascular pathology; no increase in cardiovascular events in patients with COPD combined with coronary artery disease is observed; Breezhaler inhaler is user-friendly for the patients and has advantages over other delivery devices.

Natural Killer Cells as a Further Insight into the Course of Chronic Obstructive Pulmonary Disease.

The role of natural killer (NK) cells in chronic obstructive pulmonary disease (COPD) pathogenesis has been discussed but is not yet clearly understood. This current study aimed to evaluate the associations between immunophenotypes, degrees of maturity, and the expression level of functional receptors of NK cells in the lung environment present in bronchoalveolar lavage fluid (BALF), and an attempt was made to determine their relationship in the course and progression of COPD. A total of 15 COPD patients and 14 healthy smokers were included. The clinical parameters of COPD were evaluated. In both groups, NK cells using monoclonal antibodies directly conjugated with fluorochromes in flow cytometry were assessed in the peripheral blood. Additionally, NK cells using the same method were assessed in BALF in the COPD subgroup. The blood's NK cells differed from the estimated group's maturity and receptor expression. Functional receptors CD158b+, CD314+, and CD336+ expressed by NK cells were significantly interlinked with age, RV, TLC, 6MWT, smoking, and the number of exacerbations. These results confirm the essential role of NK cells in COPD pathogenesis. Additionally, the relationship between clinical parameters and NK cell expression may indicate its participation in the disease progression and exacerbation and allow for a better understanding of NK cell biology in COPD.

СОВРЕМЕННЫЕ АСПЕКТЫ СОЧЕТАННОГО ТЕЧЕНИЯ ХРОНИЧЕСКОЙ ОБСТРУКТИВНОЙ БОЛЕЗНИ ЛЕГКИХ И АРТЕРИАЛЬНОЙ ГИПЕРТЕНЗИИ: В ФОКУСЕ НАРУШЕНИЕ ФУНКЦИИ ПОЧЕК

Abstract. This literature review examines the relationship between the combined course of chronic obstructive pulmonary disease (COPD) and arterial hypertension (AH) in the context of functional renal impairment that develops against the background of the disease. Features of the combined course of COPD and hypertension can also lead to an increased risk of developing renal dysfunction. For example, both diseases can cause tissue hypoxia. Studying the features of the combined course of these conditions may be useful for developing more effective programs for the prevention and treatment of complications in the cardiovascular, respiratory and urinary systems. This will reduce the risk of disability, improve the quality of life of patients and extend their lives. Thus, studying the effect of the combined course of COPD and hypertension on renal functional disorders is an important area of research that can benefit patients and help in more effective prevention and treatment of these diseases.

Impact of Body Mass Index on Risk of Exacerbation in Patients With COPD: A Systematic Review and Meta-Analysis.

The objective of this review is to synthesize current evidence of the association between body mass index (BMI) categories and the risk of exacerbation in patients with chronic obstructive pulmonary disease (COPD). A systematic search was conducted across 3 electronic databases: PubMed, Embase, and Scopus. Eligible studies must have reported on the association between BMI (either as continuous or categorical) and risk of COPD exacerbation, as defined according to recognized clinical criteria. Observational studies (cohort, case-control, cross-sectional) were eligible for inclusion. The Newcastle Ottawa Scale (NOS) was used to evaluate the methodological quality. Combined effect sizes were reported as relative risk (RR) and corresponding 95% confidence intervals (CI). A total of 11 studies were included. Of them, 4 studies were prospective, 4 were retrospective cohorts in design, 2 were cross-sectional studies, and one study was a secondary data analysis from a randomized trial. Compared to patients with a normal BMI, underweight patients had an increased risk of COPD exacerbation (RR 1.90, 95% CI: 1.03, 3.48; N=7, I2=94.2%). Overweight and obese BMI status was associated with a similar risk of exacerbation. Our findings report that underweight, but not overweight or obese patients, have an increased risk of COPD exacerbation, compared to individuals with a normal BMI. This differential association emphasizes the need for nuanced investigations into the underlying mechanisms of the impact of BMI on the course of COPD. Further research is needed to inform personalized interventions and improve COPD management strategies.

Oxidative and nitrosative stress — the leading mechanisms of chronic pancreatitis and chronic obstructive pulmonary disease interaction and inducers of their progression

Background. The frequency of chronic pancreatitis (CP) comorbidity with chronic obstructive pulmonary disease (COPD) has significantly increased recently. It may be accompanied by changes in oxidant-antioxidant homeostasis and activates a cascade of reactions of mutual burdening of these pathologies. The purpose of the current research was to evaluate the intensity of lipid peroxidation, oxidative modification of proteins and the state of individual factors of the antioxidant defense system in the development and course of CP, depending on the comorbid COPD. Materials and methods. Three hundred and seventeen patients were examined, including 62 patients with CP alone (group 1), 132 CP patients with comorbid COPD (group 2), 123 patients with COPD alone (group 3). The content in blood of isolated double bonds in compounds, conjugated dienes, ketodienes and conjugated trienes, malonic aldehyde, nitrites/nitrates, reduced glutathione, the activity of catalase, glutathione-S-transferase, glutathione peroxidase were evaluated in all patients. Results. In CP patients with comorbid COPD, the maximum oxidative stress intensity among the compared groups was registered. There was a reliable increase in the content of malonic aldehyde — by 2.0 times (p < 0.05), isolated double bonds — by 2.2 times (p < 0.05), conjugated dienes — by 1.9 times (p < 0.05), ketodienes and conjugated trienes — by 1.9 times (p < 0.05), nitrites/nitrates — by 2.6 times (p < 0.05). A reliable decrease in reduced glutathione content of erythrocytes was detec­ted: in group 1 — by 1.5 times, in group 2 — by 1.9 times (p < 0.05), in group 3 — by 1.2 times (p < 0.05). The compensatory increase in the activity of glutathione-S-transferase, glutathione peroxidase and blood catalase was revealed: in group 1 — by 1.3, 1.2 and 1.5 times (p < 0.05); in group 2 — by 1.5, 1.3 and 1.8 times (p < 0.05), in group 3 — by 1.2, 1.2 and 1.4 times, respectively (p < 0.05). Conclusions. The comorbid course of CP and COPD is accompanied by the maximum intensity of oxidative and nitrosative stress compared to the isolated course of the disease. An increase was detected in intermediate and final metabolites of peroxide oxidation in the blood, oxidative modification of proteins, nitrites/nitrates in the blood against the background of a deep imbalance of antioxidant defense factors, an increase in ceruloplasmin content in the blood, which requires the administration of antioxidant agents to correct detected disorders and prevent the progression of both comorbid diseases.

Analyses of Factors Associated with Acute Exacerbations of Chronic Obstructive Pulmonary Disease: A Review.

Acute exacerbations of chronic obstructive pulmonary disease (AECOPD) is the exacerbation of a range of respiratory symptoms during the stable phase of chronic obstructive pulmonary disease (COPD). AECOPD is thus a dangerous stage and key event in the course of COPD, as its deterioration and frequency seriously affects the quality of life of patients and shortens their survival. Acute exacerbations occur and develop due to many factors such as infection, tobacco smoke inhalation, air pollution, comorbidities, airflow limitation, various biomarkers, history of previous deterioration, natural killer cell abnormalities, immunoglobulin G deficiency, genetics, abnormal muscle and nutritional status, negative psychology, and seasonal temperature changes. There is relatively limited research on the impact of the role of standardized management on the alleviation of AECOPD. However, with the establishment of relevant prevention and management systems and the promotion of artificial intelligence technology and Internet medical approaches, long-term effective and standardized management of COPD patients may help to achieve the quality of life and disease prognosis in COPD patients and reduce the risk of AE.

Оценка температуры выдыхаемого воздуха у пациентов с различным течением хронической обструктивной болезни легких

INTRODUCTION: Chronic obstructive pulmonary disease (COPD) is an important medical problem of modern society. COPD is characterized by a heterogeneous course due to individual trajectories of pulmonary function decline, differences in the frequency of exacerbations and comorbidity. The exhaled air temperature is a parameter associated with the activity of local inflammation in the respiratory tract in COPD and, accordingly, the nature of the course of the disease. AIM: To study peak values of exhaled air temperature in patients with heterogeneous COPD. MATERIALS AND METHODS: The exhaled air temperature was assessed in patients with COPD phenotype with frequent exacerbations in comparison with patients with stable COPD and rare exacerbations and a group of healthy individuals. RESULTS: It was shown that the peak values of exhaled air temperature decreased in patients with COPD with rare exacerbations compared with healthy controls (p < 0.01), but increased in patients with COPD with a phenotype of frequent exacerbations compared with both the control group (p < 0.01) and COPD with rare exacerbations (p < 0.01). CONCLUSION: The stable course of COPD with rare exacerbations is characterized by a decrease in the values of the exhaled air temperature compared with the healthy control, while in COPD patients with the phenotype of frequent exacerbations, the exhaled air temperature increased compared with the healthy control.

The effect of <i>TRPV1</i> gene polymorphism on the development of progressive course of chronic obstructive pulmonary disease

Introduction. It is known that the course of chronic obstructive pulmonary disease (COPD) may vary depending on the rate of bronchial obstruction progression. It has been shown that TRPV1 channels play an important role in the formation of some pathological syndromes typical for COPD.Aim. To study the effect of single nucleotide polymorphisms (SNPs) of TRPV1 gene on the rate of bronchial obstruction progression in COPD patients.Materials and methods. We examined 103 patients with COPD, including 47 with rapid progression of bronchial obstruction (decrease in FEV1≥50 ml/year). SNPs rs460716, rs222749, rs222747, and rs8065080 were genotyped by LATE-PCR.Results. We established that rs460716 SNP had a significant effect on the development of progressive bronchial obstruction in COPD. The CC+TT genotypes were more common among patients with progressive disease (48.9% versus 23.2%), while the heterozygous genotype was protective (p=0.006). Differences remained significant after adjusting for sex, age, pack-year index and baseline FEV1 (OR 3.2; 95%CI [1.32; 7.57], p=0.009).Conclusion. The obtained results indicate a negative influence of the homozygous genotypes carriage for TRPV1 rs460716 SNP on the course of COPD.

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.

Analysis of the Comorbid Course of Chronic Obstructive Pulmonary Disease.

(1) Background. Chronic obstructive pulmonary disease (COPD) has a heterogeneous natural history, manifested both in the variability of clinical features and in association with various comorbid pathologies. Atherosclerotic cardiovascular disease (ASCVD) is of great clinical importance and contributes significantly to the natural history and prognosis of COPD. The present study aimed to evaluate the nature of the comorbid course of COPD during a 15-year follow-up. (2) Methods: A total of 170 male COPD patients were included in this study. Spirometry values, symptom severity, presence of risk factors, and comorbidities were considered. Prognostic factors were evaluated using the Kaplan-Meier method. (3) Results: ASCVD was the most common comorbidity and the main cause of death in patients with COPD. Patients with comorbid COPD and ASCVD had more severe dyspnea, higher frequency of COPD exacerbations, and worse survival than patients without ASCVD (p < 0.01). Among patients with COPD, the risk of death from ASCVD was higher in those older than 60 years (OR 3.23, 95% CI [1.72, 6.07]), those with rapidly declining FEV1 (OR 4.35, 95% CI [2.28, 8.30]), those with more than two exacerbations per year (OR 3.21, 95% CI [1.71, 6.11]), and those with a pack year index greater than 30 (OR 2.75, 95% CI [1.38, 5.51]. High Charlson comorbidity index scores in patients with COPD were associated with a more severe disease course, including severity of dyspnea, frequency of exacerbations, and multivariate index scores. A high Charlson comorbidity index score was an adverse prognostic factor. (4) Conclusions: ASCVD influences the course of the disease and is a major cause of mortality in COPD patients.

Implementation of pro- and anti-inflammatory mechanisms of sirtuin-1 in patients with chronic obstructive pulmonary disease and chronic coronary syndrome and their combination

One of the key pathogenetic aspects of chronic obstructive pulmonary disease (COPD) and chronic coronary syndrome (CCS) is endothelial dysfunction. Further study on this pathological process is relevant for a better understanding of the course and increasing the treatment effectiveness of these diseases. In this context, in recent years, there has been a growing body of evidence about sirtuins which, according to the latest research results, were capable of rebalancing vasoconstrictory and vasodilatory mediators, regulating the balance in the protease-antiprotease system, protecting endothelial cells from oxidative stress and may be useful in relation to the pathogenesis of COPD and CCS. Aim. To study changes in the levels of serum endothelial nitric oxide synthase (NOS3/eNOS) and sirtuin 1 (SIRT1) in patients with a combined course of COPD and CCS and with COPD or CCS alone. Materials and methods. In order to study endothelial dysfunction and the role of SIRT1 in the processes of its development, we examined 60 patients with combined course of COPD and with CCS or COPD alone. The control group included 10 apparently healthy individuals. Levels of SIRT1 and NOS3/eNOS were studied by enzyme-linked immunosorbent assay, and high-sensitivity C-reactive protein (hsCRP) – by immunoturbidimetric method; clinical data and medical records were analyzed. Commonplace statistical analyses were used. Results. The results have shown that the serum level of SIRT1 in patients with COPD and CCS was lower than that in the control group. The level of hsCRP was significantly higher in patients with the studied pathology than that in apparently healthy individuals and was the highest in patients with combined COPD and CCS. The study on serum NOS3/eNOS has showed the highest concentration in COPD patients, and it was significantly higher in all groups of patients with the studied pathology than that in healthy individuals. A direct correlation has been found between the serum level of SIRT1 and hsCRP and an inverse correlation – with the level of NOS3/eNOS. Conclusions. Thus, the pleiotropic effects and multifaceted molecular interactions of SIRT1 are a promising direction in the search for effective new therapeutic strategies in COPD and CCS.

Laboratory and instrumental characteristics of patients with chronic obstructive pulmonary disease and hypertension

The article defines the clinical-laboratory and clinical-instrumental features of the comorbid course of chronic obstructive pulmonary disease (COPD) and hypertension (HTN). The aim of the study was to determine the clinical, laboratory and instrumental features of the comorbid course of COPD and HTN. The study was carried out in accordance with the existing recommendations of bioethical norms and rules. All patients took part in the study of their own free will with the signing of informed consent. 125 patients aged 18–50 years were examined, who were divided into 3 groups: group I – 48 patients with COPD and HTN, group II – 47 patients with an isolated course of COPD, group III (control) – 30 practically healthy people. Medical and statistical calculation was performed using the IBM SPSS 25.0 software package. Calculated median (Me) levels and their 25.0% (LQ) and 75.0% (UQ) quartiles. The probability of differences was determined using the Man-Whitney U-test with a statistical significance threshold of 0.05 (p=0.05). According to the results of the study, an excess of systolic and diastolic blood pressure levels was significantly stated in comorbidity of COPD and HTN and in patients with isolated COPD. The presence of lymphocytopenia and monocytosis in such patients has been reliably established and significant protein loss in COPD has been determined. Significant predominances of biochemical values of the blood of patients with comorbidity of COPD and HNT and with isolated COPD compared to the control were significantly recorded. Significant decreases in the levels of external respiratory function in COPD (especially in its comorbidity with HNT) were noted and a significant predominance of Caspase-8 levels was determined in the following patients: in comorbidity of COPD and HTN – 3.79 [3.57; 3.84] U/l and in isolated COPD – 3.48 [2.99; 3.72] U/l. Keywords: patients with chronic obstructive pulmonary disease, comorbidity of arterial hypertension, clinical and laboratory characteristics, clinical and instrumental characteristics, caspase-8.

The Role of Smoking in the Mechanisms of Development of Chronic Obstructive Pulmonary Disease and Atherosclerosis.

Tobacco smoking is a major cause of chronic obstructive pulmonary disease (COPD) and atherosclerotic cardiovascular disease (ASCVD). These diseases share common pathogenesis and significantly influence each other's clinical presentation and prognosis. There is increasing evidence that the mechanisms underlying the comorbidity of COPD and ASCVD are complex and multifactorial. Smoking-induced systemic inflammation, impaired endothelial function and oxidative stress may contribute to the development and progression of both diseases. The components present in tobacco smoke can have adverse effects on various cellular functions, including macrophages and endothelial cells. Smoking may also affect the innate immune system, impair apoptosis, and promote oxidative stress in the respiratory and vascular systems. The purpose of this review is to discuss the importance of smoking in the mechanisms underlying the comorbid course of COPD and ASCVD.

Butyrate inhibits iILC2-mediated lung inflammation via lung-gut axis in chronic obstructive pulmonary disease (COPD)

BackgroundThe study investigated the effects and underlying mechanisms of intestinal flora metabolite butyrate on inflammatory ILC2 cells (iILC2s)-mediated lung inflammation in chronic obstructive pulmonary disease (COPD).MethodsMouse models of COPD and acute exacerbation of COPD (AECOPD) were established. Flow cytometry was used to detect natural ILC2 cells (nILC2s) and iILC2s in lung and colon tissues. The 16s rRNA and GC-MS were used to detect microbial flora and short chain fatty acids (SCFAs) in feces. ELISA was used to detect IL-13 and IL-4. Western blot and qRT-PCR were used to detect the relative protein and mRNA levels, respectively. In vitro experiments were performed with sorted ILC2s from colon tissues of control mice. Mice with AECOPD were treated with butyrate.ResultsThe nILC2s and iILC2s in lung and colon tissues of AECOPD mice were significantly higher than control groups. The abundance of the flora Clostridiaceae was significantly reduced, and the content of SCFAs, including acetate and butyrate, was significantly reduced. The in vitro experiments showed that butyrate inhibited iILC2 cell phenotype and cytokine secretion. Butyrate treatment reduced the proportion of iILC2 cells in the colon and lung tissues of mice with AECOPD.ConclusionsThe nILC2s and iILC2s in the colon tissues are involved in the course of COPD. Decreased Clostridiaceae and butyrate in AECOPD mice caused the accumulation of iILC2 cells in the intestines and lungs. Supplementation of butyrate can reduce iILC2 in the intestine and lung tissues. Our data may provide new ideas for prevention and treatment of COPD.

The Role of Multidimensional Indices for Mortality Prediction in Chronic Obstructive Pulmonary Disease

(1) Background: Chronic obstructive pulmonary disease (COPD) is one of the most important respiratory diseases. It is characterised by a progressive course with individual differences in clinical presentation and prognosis. The use of multidimensional indices such as the BODE, eBODE, BODEX, CODEX, ADO, and Charlson Comorbidity Index has been proposed to predict the survival rate of COPD patients. However, there is limited research on the prognostic significance of these indices in predicting long-term survival rates in patients with COPD. The aim of this prospective cohort study was to investigate the prognostic value of the BODE, eBODE, BODEX, CODEX, ADO, COTE and Charlson Comorbidity Index in predicting 5- and 10-year survival in patients with COPD. (2) Methods: A total of 170 patients were included in the study and their clinical and functional characteristics of COPD progression, such as dyspnoea, body mass index and spirometry data, were evaluated. A Kaplan-Meier survival analysis was used to calculate 5- and 10-year survival rates. The predictive value of each index was assessed using Cox proportional hazards regression models. (3) Results: The 5-year survival rate was 62.35% and the 10-year survival rate was 34.70%. The BODE, eBODE, BODEX, CODEX, ADO, COTE and Charlson Comorbidity Index were all significantly associated with the 10-year survival rate of COPD patients (p < 0.05). The hazard ratios (HRs) for these indices were as follows: BODE (HR = 1.30, 95% confidence interval [CI] 1.21-1.39); eBODE (HR = 1.29, 95% CI 1.21-1.37); BODEX (HR = 1.48, 95% CI 1.35-1.63); CODEX (HR = 1.42, 95% CI 1.31-1.54); COTE (HR = 1.55, 95% CI 1.36-1.75); ADO (HR = 1.41, 95% CI 1.29-1.54); and Charlson Comorbidity Index (HR = 1.35, 95% CI 1.22-1.48). (4) Conclusions: The multidimensional indices are a useful clinical tool for assessing the course and prognosis of COPD. These indices can be used to identify patients at a high risk of mortality and guide the management of COPD patients.

PHARMACOTHERAPY AND LUNG FUNCTION DECLINE IN PATIENTS WITH CHRONIC OBSTRUCTIVE PULMONARY DISEASE : A SYSTEMATIC REVIEW

Chronic obstructive pulmonary disease (COPD) is a long-term condition that affects millions of individuals all over the world and is a major contributor to the rise in hospital admission rates. According to projections made by the World Health Organization (WHO), COPD would become the third greatest cause of mortality worldwide by the year 2020. These patients are also very substantial consumers of the resources made available by the health and social care systems. Because there is now no treatment that can reverse the effects of COPD, patients are responsible for their own healthcare and the management of their condition. There is a correlation between the amount of cigarettes smoked and the degree to which COPD is present. The pathophysiology of COPD is intimately tied to the impact that cigarette smoke has on the lungs. Pharmacological trials that were carried out more than three decades ago with the use of short-acting bronchodilators or inhaled glucocorticoids did not succeed in demonstrating a statistically significant slower rate of FEV1 decline in comparison to the placebo group in their intention-to-treat populations. In light of these equivocal data, the belief that smoking cessation is the only treatment that can delay the course of COPD became widespread. Unfortunately, this pessimism has had a negative impact on how the general public views COPD and has decreased interest in alternative therapeutic techniques. Tiotropium had a greater FEV1 than the placebo, and it also reduced the annual reduction in FEV1 after bronchodilator usage in individuals with COPD who were in the GOLD stage 1 or 2 range. FEV1 drop might be stopped by FF or VI. The patients expressed satisfaction with the treatment, which resulted in fewer exacerbations. It seems like fluticasone furoate or vilanterol could slow down the drop in FEV1 levels.

The influence of systemic inflammatory markers on the development of obstetrical complications in pregnant women with chronic obstructive pulmonary disease

The increasing prevalence of chronic obstructive pulmonary disease (COPD) among the female half of the population is the reason for the increased interest of scientists in the course of COPD and its impact on pregnant women. At the same time, the chronic lung inflammatory process leads to the development of obstetrical and perinatal complications during pregnancy. The aim of our study is to establish the features of changes in the cytokine profile in pregnant women with COPD and their role in the development of obstetrical and perinatal complications. Materials and methods. 77 pregnant women with clinically and instrumentally verified signs of COPD were examined, who were divided into 2 subgroups depending on the degree of bronchial obstruction: IA – 43 pregnant women with FEV1 ≥80 %, IB – 34 pregnant women with FEV1 50–79 %. The control group consisted of 27 healthy pregnant women. The cytokine profile was determined and a correlational interaction with the degree of bronchial obstruction and the frequency of obstetrical and perinatal complications was established. Results. Our analysis of cytokine profile indicators in pregnant women with COPD at the stage of mild and moderate bronchoobstruction has shown a characteristic and significant increase in the level of pro-inflammatory cytokines (IL-1β, IL-6, IL-8, TNF-α) and a simultaneous decrease in the level of anti-inflammatory IL-10 (P ≤ 0.05). Dysregulation of the inflammatory response in COPD in pregnant women became the main basis for the development of obstetrical and perinatal complications. We have established that an increase in the degree of bronchoobstruction was also associated with a higher detection frequency of such pregnancy and childbirth complications as anemia by 3.1 times, the threat of preterm birth by 9 times, preeclampsia by 7 times, placental dysfunction by 3.4 times, intrauterine growth restriction by 8 times, premature birth by 3.5 times, premature rupture of membranes during labor by 4 times, and fetal distress by 3 times. Conclusions. In pregnant women with COPD, an increase in the level of pro-inflammatory cytokines – IL-1β (rI = -0.81, rII = -0.67), IL-6 (rI = -0.88, rII = -0.78), IL-8, TNF-α was found to be directly proportional to the degree of bronchial obstruction, and inversely proportional level of anti-inflammatory IL-10 (rI = 0.80, rII = 0.86), which can be an early prognostic criterion for the development of obstetrical and perinatal complications.

Treatment, diagnostics, and management of chronic obstructive pulmonary disease in women

Chronic obstructive pulmonary disease (COPD) poses a significant burden on women’s health. Insufficient attention is paid to this problem in scientific research and in clinical practice, although more and more information surfaces about the gender-associated differences in the treatment, diagnostics, and management of COPD.The aim of the review is to consider the most significant data currently available on the clinical signs, course, and outcomes of COPD in women and propose ways to achieve the best results in the diagnosis and treatment of this disease.Conclusion. There are biological and cultural differences between the clinical manifestations, course and outcome of COPD in men and women, and these differences impact the clinical practice. It is advisable to apply individualized diagnostic, organizational, and pharmacotherapeutic approaches to COPD in women, based on the knowledge of female-specific variances in the symptoms of the disease and the health status.