One of the directions in the study of diseases is their phenotyping. Thus, understanding the peculiarities of bronchial asthma (BA) and various types of obesity phenotypes combination will not only provide a differentiated approach to treatment, but also achieve maximum therapeutic effect. The aim of this study was to evaluate clinical and laboratory features of various obesity phenotypes in BA patients at a young age in order to optimize antiasthmatic therapy and early diagnosis of cardiovascular complications. Methods . Patients with BA of different severity were examined (n = 164); the control group was made up of relatively healthy subjects (n = 40). The subjects were divided into groups with BMI (Body Mass Index); the 1 st group (n = 93) included patients with BMI 18.5–24.9 kg/m 2 ; the 2 nd group (n = 80) included BA patients with BMI 30–34.9 kg/m 2 (1st degree obesity). Overweight patients were detected, clinical and functional examination was performed, epicardial adipose tissue thickness (EATT) was measured by standard two-dimensional echocardiography (EchoCG), obesity degree, cytokine, adipokine, insulin levels, insulin resistance indices were determined. Results . According to the results of the study in patients with BA and metabolic fat obesity phenotype (MFOP) a significant disorder of adipokine balance was revealed, carbohydrate metabolism disorder was noted, and significantly higher insulin levels were observed, insulin resistance index (Homeostasis Model Assessment of Insulin Resistance – НОМА-IR) and decrease in insulin sensitivity index (ISI) relative to the group of patients with metabolically healthy obesity phenotype and control. Conclusion . It has been established that the EATT determined by the EchoCG method can serve as a predictor of MFOP and a risk factor for cardiovascular diseases.
AIM To study cytokine status and to reveal a possible relationship of clinical and functional indicators and systemic inflammation in patients with severe asthma to tobacco smoking. Subjects and methods. Examinations were made in 139 patients with severe asthma during its exacerbation and without the latter after 12 months. Groups 1 and 2 included 98 nonsmoking and 41 smoking patients with severe asthma, respectively. A control group consisted of 40 apparently healthy volunteers. External respiratory function, plasma TNF-α, IFN-γ, IL-2, IL-4, IL-6, IL-8, IL-10, C-reactive protein, and neutrophil elastase levels, and integral cytokine index were studied. RESULTS Systemic inflammation that was more marked on a disease exacerbation and mediated by elevated TNF-α, IL-2, and C-reactive protein levels was detected in severe asthma in both groups. The smoking patient group showed a statistically significant increase in IL-8 and neutrophil elastase levels, which may be indirectly indicative of the active participation of neutrophils in the development of chronic persistent inflammation. CONCLUSION Tobacco smoking is a clinically significant risk factor that aggravates both the course of asthma and the magnitude of inflammation during a disease exacerbation.
Background. To estimate interrelation of clinical and functional parameters and vessel tome regulating function of endothelium in patients with bronchial asthma. Methods. 126 patients with bronchial asthma have been examined, including 29 patients with mild bronchial asthma (the first group), 32 persons with moderate bronchial asthma (the second group), 40 respondents with severe asthma (the third group) and 25 patients with steroiddependent asthma (fourth group). The control group included 27 healthy volunteers. We have assessed the parameters of external respiration, vasodilatation function, and the levels of TNFa, IL4, sCD31 in the plasma. Results. The results of the research of vessel tome regulating function in patients with bronchial asthma are presented. The existence of endothelial function of an endothelium are characterized by disturbance of vasomotor activity of endothelium, rising of sCD31 and levels of cytokines (Il-4, TNFa) in plasma was revealed. These changes deteriorate within the ages and the course of bronchial asthma. Conclusion. We have demonstrated that endothelial dysfunction is developed even at the early stages of bronchial asthma.