A CONNECTION BETWEEN ARTERIAL HYPERTENSION, DYSLIPIDEMIA AND ACTIVITY OF INTERLEUKIN-1BETA AND INTERLEUKIN-6 IN TYPE 2 DIABETES MELLITUS

Abstract
To determine the relationship between blood pressure (BP), lipid metabolism and levels of IL-1beta and IL-6 in patients with type 2 diabetes mellitus (T2DM). A total of 96 patients with T2DM (mean age 52.74 ± 9.56, 38 women) and 20 healthy volunteers were examined. A systolic blood pressure (SBP, mmHg), diastolic blood pressure (DBP, mmHg), and mean arterial pressure (MAP) were measured; levels of total cholesterol (TC), high density lipoprotein cholesterol (HDL), triglycerides (TG) were determined by biochemical method (mmol/L), the level of low density lipoprotein cholesterol (LDL) was calculated by Friedwald's formula. The levels of IL-1-beta and IL-6 were determined by ELISA (ng/ml). SBP in main group - 141.76 ± 1.31, in control group - 120.75 ± 1.51; DAT - 88.43 ± 0.68 and 77.75 ± 0.85, respectively; MAP - 106.23 ± 0.87 and 92.08 ± 0.98, respectively. All the results in the studied groups were statistically significant. The study of cholesterol metabolism also revealed significant differences: TC in the main group was 5.29 ± 0.15, in the control group - 4,06 ± 0.05; TG 1.20 ± 0.02 and 1.3 ± 0.03, respectively; LDL 3.28 ± 0.14 and 2.01 ± 0.04, respectively. The levels of proinflammatory cytokines significantly differed in studied groups: IL-1beta in main group was 13,58 ± 0,29, control group - 8,12 ± 0,24; IL-6 12.37 ± 0.3 and 8.83 ± 0.22, respectively. Significant (p < 0.05) correlations were revealed in the main group: SBP and TC (R = 0.29), SBP and TG (R = 0.28), SBP and LDL (R = 0.28), SBP and IL-1beta (R = 0.41), SBP and IL-6 (R = 0.25); DBT and IL-1beta - (R = 0.25); MAP and TC (R = 0.26), MAP and TG (R = 0.29), MAP and LDL (R = 0.27), MAP and IL-1beta (R = 0.39), MAP and IL-6 (R = 0.28). There were no significant correlations in the control group. The revealed interrelations indicate that the risk of arterial hypertension is increased even with a slight elevation of BP in patients with T2DM. The reasons for this include not only the increase of vascular resistance and the decrease of the elasticity of the vascular wall, but also the progression of dyslipidemia and deployment of systemic inflammatory response due to the increased levels of proinflammatory cytokines IL-1beta and IL-6.