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Acute exacerbations of chronic obstructive pulmonary disease (AECOPD) are associated with disease progression and increased risk of death. We need to better understand the phenotypes of AECOPD to improve treatment strategies. The main triggers of COPD exacerbations are viral and bacterial infections.The aim is to characterize the viral, bacterial, and viral-bacterial phenotypes of acute exacerbations in patients with COPD caused by industrial aerosol exposure or tobacco smoke.Methods. 180 subjects with established moderate and severe COPD who met the Global Initiative for Chronic Obstructive Lung Disease (GOLD) criteria, 2020 – 2021, and were hospitalized with AECOPD, were enrolled in this prospective observational study. The virus-induced, bacteria-induced, and virus-bacteria-induced AECOPD strata (n = 60 each) were formed. Each stratum included 30 patients with occupational COPD and 30 patients with COPD caused by tobacco smoke. Virus-induced AECOPDs were diagnosed by PCR of bronchoalveolar fluid. Length of hospital stay, symptoms, lung function, mean pulmonary artery pressure (mPAP), and type of inflammation were assessed. Cox proportional hazard regression was used to examine the relationships.Results. The length of hospital stay was highest in patients with virus-induced and virus-bacteria-induced exacerbations of occupational COPD, being equal to (Me, IQR) 16.5 (14 – 18) and 18 (16 – 20) days. The virus-induced exacerbations in occupational COPD and in COPD caused by tobacco smoke featured the highest bronchodilation coefficient, 10.9 (9.8 – 11,5)% and 9.2 (8.3 – 10.3)%, respectively, decrease in the diffusing capacity of the lungs (DLCO/Va) by 42 (40 – 45)% and 49 (47 – 52)%, increase in mPAP by 44 (39 – 45) и 33 (29 – 38) mmHg, and eosinophilic inflammation with blood eosinophil count of 425 (385 –527) and 350 (310 – 391) cells per μl (р > 0.01). Virus-bacteria-induced AECOPD in occupational COPD and in COPD caused by smoke were characterized by decrease in FEV1 by 40.2 (36.6 – 42.2)% and 31.0 (28.1 – 33.6%), decrease in DLCO/Va by 48 (44 – 50)% and 37 (35 – 41)%, increase in mPA by 43 (38 – 46) and 50 (45 – 54) mmHg, and eosinophilic-neutrophilic inflammation in 63.3 and 66.6% of patients. The mid-range FEV1, highest DLCO/Va, and neutrophilic inflammation were seen in patients with bacteria-induced AECOPD.Conclusion. Exacerbations of occupational COPD are characterized by more severe functional impairment and inflammation with high eosinophil count when these exacerbations have viral origin.
Acute exacerbations of chronic obstructive pulmonary disease (AECOPD) are associated with disease progression and increased risk of death. We need to better understand the phenotypes of AECOPD to improve treatment strategies. The main triggers of COPD exacerbations are viral and bacterial infections.The aim is to characterize the viral, bacterial, and viral-bacterial phenotypes of acute exacerbations in patients with COPD caused by industrial aerosol exposure or tobacco smoke.Methods. 180 subjects with established moderate and severe COPD who met the Global Initiative for Chronic Obstructive Lung Disease (GOLD) criteria, 2020 – 2021, and were hospitalized with AECOPD, were enrolled in this prospective observational study. The virus-induced, bacteria-induced, and virus-bacteria-induced AECOPD strata (n = 60 each) were formed. Each stratum included 30 patients with occupational COPD and 30 patients with COPD caused by tobacco smoke. Virus-induced AECOPDs were diagnosed by PCR of bronchoalveolar fluid. Length of hospital stay, symptoms, lung function, mean pulmonary artery pressure (mPAP), and type of inflammation were assessed. Cox proportional hazard regression was used to examine the relationships.Results. The length of hospital stay was highest in patients with virus-induced and virus-bacteria-induced exacerbations of occupational COPD, being equal to (Me, IQR) 16.5 (14 – 18) and 18 (16 – 20) days. The virus-induced exacerbations in occupational COPD and in COPD caused by tobacco smoke featured the highest bronchodilation coefficient, 10.9 (9.8 – 11,5)% and 9.2 (8.3 – 10.3)%, respectively, decrease in the diffusing capacity of the lungs (DLCO/Va) by 42 (40 – 45)% and 49 (47 – 52)%, increase in mPAP by 44 (39 – 45) и 33 (29 – 38) mmHg, and eosinophilic inflammation with blood eosinophil count of 425 (385 –527) and 350 (310 – 391) cells per μl (р > 0.01). Virus-bacteria-induced AECOPD in occupational COPD and in COPD caused by smoke were characterized by decrease in FEV1 by 40.2 (36.6 – 42.2)% and 31.0 (28.1 – 33.6%), decrease in DLCO/Va by 48 (44 – 50)% and 37 (35 – 41)%, increase in mPA by 43 (38 – 46) and 50 (45 – 54) mmHg, and eosinophilic-neutrophilic inflammation in 63.3 and 66.6% of patients. The mid-range FEV1, highest DLCO/Va, and neutrophilic inflammation were seen in patients with bacteria-induced AECOPD.Conclusion. Exacerbations of occupational COPD are characterized by more severe functional impairment and inflammation with high eosinophil count when these exacerbations have viral origin.
Viral respiratory infection is one of the main etiologic factors for acute exacerbations of COPD (AECOPD). The disease course after virus-associated AECOPD and the response to treatment have not been studied adequately.The aim was to evaluate the efficacy of single-inhaler triple therapy (SITT) of long-acting anticholinergic drugs (LAMA)/long-acting β2-agonists (LABA) of adrenergic receptors/inhaled glucocorticosteroids (ICS) on COPD symptoms, lung function, exercise tolerance, and inflammatory activity compared with multiple-inhaler triple therapy (MITT) after a virus-associated COPD exacerbation.Methods. This was an observational prospective cohort study of COPD patients (spirographус criterion) hospitalized for AECOPD with viral (n = 60) or viral-bacterial (n = 60) infection. The comparison group included patients with bacterial AECOPD (n = 60). Viral infection was diagnosed by PCR-RT of sputum or bronchoalveolar lavage fluid for RNAs of rhinovirus, RS virus, influenza A and B viruses, or SARS-CoV-2 virus. Bacterial infection was demonstrated by sputum purulence and/or procalcitonin test results and/or standard culture data. During AECOPD, blood cytokines were measured by ELISA. The patients were treated with SITT (investigational treatment) or MITT (comparison treatment) of LAMA/LABA/ICS in real-world clinical practice. The follow-up started 4 weeks after AECOPD regression and discharge from hospital.Results. After 52 weeks of treatment, FEV1 decline was smaller than in the SITT group. Differences from the MITT group were greater in patients with viral AECOPD (–69 (–75; –10) ml vs –75 (–78; –72) ml) or viral-bacterial AECOPD (–67.5 (–69; –37.25) ml vs –75.5 (–84; –70.25) ml). An increase in DLCO/Va, 6-minut walk test (6MWT) results, a decrease in bronchodilation coefficient, blood eosinophils and fibrinogen was seen only in subjects who received SITT and had viralor viral-bacterial AECOPD. A multiple regression model revealed a direct association between blood interleukin-5 and improvement in FEV1 (В = 0.848) and DLCO/Va (B=0.117) and a negative correlation with blood levels of amino-terminal propeptide of type-III procollagen and improvement in DLCO/Va (В = –0.021).Conclusion. SITT with LAMA/LABA/ICS was more effective in preventing FEV1 decline, increasing DLCO, 6MWT results, and decreasing airway inflammation in virus-associated or viral-bacterial AECOPD.
Introduction. Heart failure increases the severity of symptoms and worsens the prognosis of chronic obstructive pulmonary disease (COPD) in smokers. Professional COPD is a separate phenotype, which suggests dif erences in the pat ern of comorbidity. Professional COPD in combination with heart failure has not been studied enough. T e aim of the study was to determine the relationship of heart failure c clinical, functional and hygienic characteristics of professional COPD. Materials and methods. T e one-center observational study included 115 patients with occupational chronic obstructive pulmonary disease (OCOPD). T e comparison group of 103 patients with COPD, smokers of tobacco. T e diagnosis of COPD met the criterion of GOLD 2011–2019. OCOPD patients were exposed to aromatic hydrocarbons with an excess of MPC in the air of working zone is 1.5 to 6 times, or of inorganic dust in the range of 2 to 9.5 MPC. Heart failure was diagnosed on the basis of any signs of myocardial dysfunction in echocardiography and/or elevation of the N-terminal precursor of cerebral natriuretic peptide (NT-pro-BNP) serum more than 125 PG/ml. the Groups were comparable in sex, age, durationof COPD, duration of action of exogenous etiological factor, causes of heart failure. Clinical and functional characteristics of COPD and heart failure were evaluated. For comparisons between groups for quantitative parameters used covariance analysis or test Kruskall-Wallis for comparison, the share of χ2 criterion. Relationships were determined by logistic regression. Results. In patients with OCOPD, the heart failure rate was higher — 63 (54.8%) cases compared to 38 (36.9%) in the group of COPD Smoking (p=0.009). Biventricular failure prevailed (44 (38.3%) patients) with preserved ejection fraction(47 (40.9%) cases). Right ventricular failure was detected in 15 (13.0%) of the subjects, lef ventricular failure — in 4 (3.5%), p=0.002. Echocardiography revealed severe pulmonary hypertension and diastolic myocardial dysfunction in the OCOPD group. OCOPD in combination with heart failure was characterized by CAT index values of more than 10 points, low exercise tolerance, a signif cant rate of decline in FEV1, a decrease in the partial tension of arterial blood oxygen, severe exacerbations of COPD. In multivariate analysis of the development of heart failure in patients with OCOPD predicted: length of service, systolic pressure in the pulmonary artery, partial oxygen tension of arterial blood, the test distance of six-minute walk. Conclusions. 1. OCOPD is characterized by a probability of heart failure — 54.8%. Biventricular failure with preserved ejection f action and predominant violation of diastolic myocardial function prevails. 2. T e subphenotype of OCOPD in combination with heart failure is characterized by severe symptoms, hypoxemia of rest, severe exacerbations of COPD.
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