The aim of the research was to identify the frequency of development of the syndrome of post-exercise bronchial spasm in patients with asthma against physical load and the study of clinical-functional features of its course. 197 patients (122 women and 75 men) with mild persistent partially controlled and uncontrolled asthma were observed. The mean age of the patients was 36.1±0.73 years old; the mean height was 168.8±0.63 cm; the mean weight was 74.6±1.03 kg. The patients did not have strong obstructive disorders of the ventilation pulmonary function; forced expiratory volume for the first second (FEV1) was 91.6±2.5% from the predicted value. All the patients had clinical-anamnestic test and the assessment of apnoea degree by the scale of mMRC and identification of disease control by validated questionnaire Asthma Control Test; the airway response was evaluated in reaction to dosed physical load calculated and fulfilled at the research complex for ergospirometric studies OxyconPro (VIASYS Healthcare, Germany); basic study of the lung function at the device Easyone-PC (Switzerland) was done. As a result of the study post-exercise bronchial spasm was diagnosed in 18.3% of patients with asthma. Close positive correlation between the baseline FEV1 (in %) and bronchial response to the dosed physical load measured at the first minute of the recovery period (r=0.19; р<0.05) as well as the intensity of the further bronchial response at the 10th minute of the recovery period (r=0.19; р<0.05) was registered. The intensity of bronchial response at the 10th minute of the recovery period in patients with airway hyperresponsiveness to dosed physical load was directly related with the degree of asthma control (r=0.56; р˂0.05). It was found out that the degree of the asthma control correlated with the airway hyperresponsiveness to physical load.

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Heterogeneity of respiratory tract inflammation determines the clinical course and control of mild asthma. The aim of the research was to study the relationship between clinical and functional parameters and the form of bronchial inflammation in patients with mild persistent asthma against the background of standard basic anti-inflammatory therapy. In 198 patients with mild asthma (the mean age was 41.5±0.7 years old) against the background of maintenance therapy with low doses of inhaled glucocorticosteroids (ICS at a dose ≤500 mcg/day by beclomethasone dipropionate), there were determined the level of asthma control according to the questionnaire Asthma Control Test (ACT), lung function, airway reaction to 3-minute isocapnic hyperventilation with cold (-20ºC) air; there was done the collection of induced sputum (IS). The content of cells in cytograms of IS was assessed. The activity of myeloperoxidase (MPO) (in pixels) was measured by cytochemical method in neutrophilic and eosinophilic granulocytes. Group 1 (n=43; 22%) included patients with the eosinophilic pattern of bronchial inflammation, group 2 (n=155; 78%) included patients with mixed pattern of inflammation. In group 2, unlike the patients of group 1, in the inflammatory profile of infiltrate against the background of high neutrophil content (34.6±1.1 and 10.8±0.5%, respectively; p=0.000001), there was found an increased level of eosinophils (17.0±1.1 vs. 21.2±1.8%, respectively; p=0.048), and there was revealed a higher intragranular deposition of MPO (85.8±3.5 vs. 77.0±3.2 pixels, respectively; p=0.057). The mixed type of inflammation with the dominant neutrophil component and the greatest activity of MPO was associated with more pronounced clinical symptoms of the disease and low level of asthma control (16.0±0.7 vs. 18.7±0.4 ACT points, respectively; p=0.004), lung function decrease (FEV1 was 89.4±1.4 vs. 97.9±2.2%, respectively; p=0.005) and degree of FEV1 drop in response to bronchial provocation by cold air (-10.1±1.1 vs. -3.4±1.1%, respectively; p=0.002), due to insufficient anti-inflammatory effect of the used controller therapy. A discriminant equation is proposed, which can serve as an additional criterion for the effectiveness of anti-inflammatory therapy.

Introduction. The role of an alternative adenylate cyclase pathway of hormonal signal transmission under the action of synthetic glucocorticosteroids with the participation of endogenous stress-limiting activity of the adrenal cortex in conjunction with the adaptive capabilities of airway homeostasis in patients with asthma under conditions of osmotic stress has not been studied at present. Aim. To assess the dynamics of cortisol and cyclic adenosin monophosphate (cAMP) in asthma patients with different airway responses to hypoosmolar stimuli when using anti-inflammatory combination therapy with inhaled corticosteroids/long-acting β2 -agonists (ICS/LABA). Materials and methods. 96 patients diagnosed with asthma received combined anti-inflammatory therapy with ICS/LABA for 24 weeks. Group 1 included patients (n=18) with airway hyperresponsiveness to hypoosmolar stimulus, group 2 (n=78) – with no reaction of the bronchi to a 3-minute ultrasonic inhalation of distilled water. At baseline and at the end of treatment, the lung function was studied; to assess the regulatory function of glucocorticoids using non-genomic signaling pathways, the levels of cortisol in blood serum and cAMP in blood leukocytes were determined. Results. Patients of group 1 in comparison with the second one initially had a lower FEV1 ‒ 88.2±5.3 and 98.5±1.7%, respectively (p<0.05), after treatment in both groups there was a slight tendency to an increase in FEV1 (98.5±5.7 and 101.4±2.5%, respectively, p>0.05). The concentration of cortisol and cAMP at baseline and after 24 weeks of therapy in patients of group 1 was 588.7±32.0 and 495.0±48.7 nmol/L, 61.7±5.1 and 76.5±5, 2 pmol/106 cells (p<0.01); in group 2 − 610.5±20.1 and 522.2±15.60 nmol/L (p<0.001), 76.2±2.2 and 90.6±2.5 pmol/106 cells (p<0.001). Conclusion. In asthma patients with airway osmotic hyperresponsiveness, persistent adaptation to osmotic stress is traced, which is combined with a more significant impairment of the lung function and indicates insufficient therapeutic control over glucocorticoid regulation of osmotic stress by the selected volume of ICS/LABA therapy.

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