The risk of bronchial asthma exacerbations among smokers with asthma-chronic obstructive pulmonary disease overlap after inpatient treatment

Abstract

To assess the risk of exacerbations of bronchial asthma (BA) in smoking patients with the asthma-chronic obstructive pulmonary disease (COPD) overlap (ACO) after inpatient treatment. 36 smokers with ACO (main group) and 36 non-smoking patients (control group) with severe or moderate exacerbation of bronchial asthma were examined. Assessment of the severity of exacerbation of BA before treatment, levels of control and risk of exacerbations of BA after treatment was determined according to the Federal clinical guidelines for the diagnosis and treatment of BA (2016). Spirometry, monitoring of blood oxygenation using transcutaneous spectral pulse oximetry and enzyme immunoassay for determination of matrix metalloproteinases 9 were performed. Smoking experience, smoking index and pack/years index were taken into account in patients with ACO. The carboxyhaemoglobin level was analyzed by the carbon monoxide fraction in the exhaled air. For the first time in patients with the ACO, the ability of heavy tobacco smoking and associated decrease in blood oxygenation to potentiate the negative impact of other predictors on the risk of exacerbations of the underlying disease was revealed. In smoking patients with the ACO, for the first time, a direct association of higher levels of matrix metalloproteinases 9 (measured before inpatient treatment) with such a predictor of the risk of further exacerbations of the disease as more frequent detection of symptoms of uncontrolled BA was revealed. In non-smoking patients with BA, a direct relationship between increased sputum secretion and eosinophilia of blood and/or sputum (a predictor of exacerbation of BA) and the relative duration of episodes of decreased blood oxygenation was established. It was found that intensive and prolonged smoking increases the duration and reduces the effectiveness of inpatient treatment of patients with ACO, contributing to the preservation of air traps and low (forced expiratory volume in 1 second 60%) ventilation capacity of the lungs with the persistence of moderately reduced blood oxygenation; the risk of further exacerbations of BA in this phenotype of patients is significantly higher than in non-smoking patients with BA without combination with COPD.