Изменение концентрации биомаркеров дисфункции эндотелия при приеме ингибиторов тирозинкиназы I и II поколений у пациентов с хроническим миелолейкозом как фактор риска развития сердечно-сосудистых осложнений

CML), the accepting inhibitors tyrosine of kinases (TKI) I and the II generations (TKI1 and TKI2 respectively), and development of arterial hypertension. Material and methods . Examination of 137 patients with CML in the chronic phase (CP) is conducted, the median of age — 47 years. 24 of them were with for the first time the verified diagnosis of CML and earlier did not accept TKI, they have made group of control. Other patients accepted TKI: 39 patients — imatinib 400 mg/day, 36 — dasatinib 100 mg/day, 38 — nilotinib 800 mg/day) more than 6 months. In biochemical analysis of blood indicators of lipidic range were defined. Level detection of ET-1 and VEGF was made by means of enzyme immunoassay. To all patients measurement of the heart rate (HR) and the arterial blood pressure (ABP) on both hands at an interval of 2 minutes from previous was once taken. Results . In group of patients from CML accepting nilotinib authentically significant increase in levels of systolic and diastolic ABP (р<0,001) in comparison with group of control, with group of the patients accepting imatinib and dasatinib is noted. The most serious changes of lipidic range are noted at the patients accepting nilotinib. In all groups statistically significant increase in level of C-reactive protein, fibrinogen, homocysteine, endothelin-1 and VEGF in comparison with group of control is revealed. The most expressed changes are found in group of the patients accepting nilotinib, values of parameters of C-reactive protein, fibrinogen, homocysteine, endothelin-1 and VEGF are changed authentically (р<0,001) and statistically significantly differ in comparison with group for the first time of the revealed patients with CML and groups of reception of imatinib and dazatinib. Conclusion . As a result of the conducted research endothelium variation of a function at patients from CML accepting TKI1 and TKI2 is revealed. The above-stated indicators can be used as additional diagnostic criteria for assessment of risk of development of arterial hypertension in patients with CML at reception of TKI.