Cytokine profile in patients with both unstable angina and overweight

Abstract

The purpose include to study the indicators profile of cytokine (TNF-α, IL-1β, IL-4) in patients with both unstable angina and overweight. Materials and Methods: 57 patients were examined, of which unstable angina with obesity installed in 21 patients and unstable angina with overweight in 23 patients. The control group was - 13 people. The study was based in the Kharkiv Clinical hospital № 27. Indicators were studied cytokine profile: TNF-α, IL-1β, IL-4. The immunoassay kit produced by "Ukrmedservis" Ltd. (Ukraine) was used for the investigation of TNF-α, IL-1β, IL-4 parameters, using the manufacturer's instructions. Statistical processing of data was performed using the «Microsoft Exel» 2007 i Windows STATISTIKA 6.0. Results. The level of TNF-α in the patients with both unstable angina and overweight laid within the range 72,13 ± 6,03 pg / ml, significantly (p <0.01) differed from the level of healthy people - 41,4 ± 8,6 pg / ml. The average level for people with both unstable angina associated with obesity was 87,52 ± 7,15 pg / ml that went beyond the control point (p <0.01). The level of IL-1β in the patients with both unstable angina and overweight increased to 162,43 ± 21,71 pg / ml, which was significantly compared with the control - 42,86 ± 7,14 (p <0,01). The level of IL-1β in the patients with both unstable angina and obesity within range 203,85 ± 30,35 pg / ml, significantly increased than in the control group (p<0,01). The level of IL-4 for all patients with both unstable angina and overweight reduced to the range of 9,34 ± 2,11 pg / ml (p<0,01), thus being no different from the control value of 18,25 ± 1,75 (p> 0,1). The level of IL-4 for the patients struggling unstable angina and obesity went down to the range of 4,67 ± 2,05 pg / ml (p <0,05), that is, to the level significantly (p <0, 01) lower than the control value. Conclusions. Thus, activation of inflammation in obesity confirmed scalene change the content of cytokines (TNF-α, IL-1β, IL-4) and reflected the severity of the disease, the mechanism of which remains speculative.