The aim of the work was to study clinical and pathophysiological features of endothelial dysfunction, structural and functional state of the left heart in patients with bronchial asthma (BA). The study included 290 patients. 250 of them presented with moderate or severe BA during exacerbation and within 12 months after the onset of observation, 40 healthy volunteers served as controls. The endothelial function was disturbed in 63 and 74% of the patients with moderate and severe BA respectively. They showed reduced endothelium-dependent vasodilation in combination with a significant increase of the plasma sDC31/ sPECAM-1 level. It is concluded that patients with BA develop structural and functional changes in the left ventricular myocardium proportional to the severity of BA which leads to diastolic dysfunction.
We examined 192 patients in 18 72 years with persistent bronchial asthma (BA). The patients were divided into two groups: 1st group mild severe BA (n=103) and the 2nd group was severe BA (n=89). The most frequent factors of disease decline were viral infection, stress, late referral to a doctor. The control rate in the real clinical practice still low: not control disease course was registered in 89.3% patients in 1th group and in all patients in 2nd group. The main reason of not control disease course was absence or not adequate basic anti inflammation therapy. We can get objective result, that similar interpret in all patients to estimate the control rate of BA and the efficiency of anti asthmatic therapy by ACT test.
We studied the role of CD38/АDP-ribosyl cyclase in development of inflammation in bronchial asthma, and relationship of its expression to the levels of cytokines in blood serum. We assessed expression of СD38 in peripheral blood lymphocytes in severe and mild bronchial asthma. We found the elevated expression of CD38 in peripheral blood lymphocytes in patients of both groups in an exacerbation in comparison with control group. Elevated expression of CD38, presumably, contributes to interactions of activated lymphocytes with endothelial cells due to CD38-CD31 interactions (the latter serves as a non-substrate ligand of CD38). As a result, endothelial cells are damaged, soluble form of CD31 (sPECAM-1) is released, and endothelial dysfunction is developed. These events lead to alterations in endothelium-dependent regulation of vessel wall elasticity and increasing of its rigidity.