ANALYSIS OF THE STATE OF PLATELET AGGREGATION IN PREGNANT WOMEN WITH THROMBOPHILIA AND BURDENED OBSTETRIC HISTORY

Abstract

The analysis of platelet aggregation in pregnant women with thrombophilia and burdened obstetric history was performed. It has been determined that the development of adverse effects of pregnancy is significantly influenced by conditions such as placental abruption, fetal growth retardation, preeclampsia and fetal death, which are provoked by an abnormal vascular network of the placenta and hemostasis disorders caused by various thromboembolic disorders due to thrombophilia. Therefore, in recent years, the problem of thrombophilia has attracted much attention as a risk factor for pregnancy complications caused by various thromboembolic disorders, which are responsible for preeclampsia, fetoplacental insufficiency, fetal growth retardation and fetal loss, and others.

Given the above, the aim of the work was to analyze the state of platelet aggregation of pregnant women with thrombophilia and burdened obstetric history.

To achieve this goal, a study of pregnant women with thrombophilia and burdened obstetric history was conducted: 137 pregnant women, which were divided into two study groups – the main group, which included 101 pregnant women with a burdened obstetric history and thrombophilia, and the control group, which included 36 pregnant women with a burdened obstetric history without thrombophilia.

The analysis of platelet aggregation of pregnant women with thrombophilia and burdened obstetric history was performed. It was found that the degree of platelet aggregation with the addition of an inducer of adenosine diphosphate at a concentration of 0.0625 prevailed in the control group as compared with pregnant women with thrombophilia (26.3 [24.3; 28.4] % and 21,4 [14,6; 31,1] % in contrast to the aggregation time and its speed (which were lower in the controls (58.0 [54.0; 72.0] s and 22.9 [20.4; 24.9] min) as compared with the main group (71.0 [48.0; 530.5] s) (and 26.5 [14.5; 38.3] min)). It was found that at a concentration of adenosine diphosphate of 0.125, all indicators of platelet aggregation prevailed in the main group (degree of aggregation (35.4 [25.6; 52.5] %; U = 1236.0; p = 0.004), its time (115.0 [47.0; 324.0] s; U = 1623.5; p = 0.341) and speed (45.2 [32.1; 57.5] min; U = 968.5; p < 0.001) compared to the controls (30.1 [26.7; 31.2] %, 84,0 [78.0; 103.5] s and 26.4 [30.4; 35.8] min). It was determined that the concentration of adenosine diphosphate of 0.250 caused an increase in the aggregation time in the control group as compared to the main group (225.5 [196.5; 269.3] s and 181.0 [57.0; 347.0] s; U = 1554.5; p = 0,198) in contrast to the degree [43,3 [39,6; 48.8] % and 51.1 [35.4; 63.8] %; U = 1417.0; p = 0.050) and aggregation rates (57.8 [42.8; 67.0] min and 40.1 [34.4; 47.9] min; U = 786.5; p < 0.001). It was also found that the maximum concentration of adenosine diphosphate (0.500) caused a significant (U = 11178.0; p = 0.002) increase in the aggregation time in the controls (329.0 [269.5; 390.0] s) compared to the main group (211.0 [72.5; 381.0] s) in contrast to the degree and rate of aggregation [51.9 [50.1; 54.3] %; U = 1606.5; p = 0.300 and 42.7 (38.8; 49.4] min; U = 923.5; p < 0.001 and 55.1 [38.6; 69.0] % and 63.6 [44.7; 72.6] min).