The Effect of Obesity on the State of Platelet-plasma Hemostasis in Patients with Essential Hypertension in Combination with Non-alcoholic Fatty Liver Disease
Keywords:hypertension, non-alcoholic fatty liver disease, obesity, platelet-plasma hemostasis
Obesity, being one of the main modified risk factors for the development of pathology of the cardiovascular system, determines its rapid progression, more severe course and a high incidence of complications. With the prevalence of obesity, the incidence of hypertension (HT), non-alcoholic fatty liver disease (NAFLD), and, as a result, cardiovascular events increases.
The objective: To increase the efficiency of early diagnosis of thrombophilic changes in the blood in patients with essential hypertension and concomitant obesity, combined with non-alcoholic fatty liver disease.
Materials and methods. The study was conducted on the clinical base of the Department of Propedeutics of Internal Medicine No. 1 of the Bogomolets National Medical University in Kiev Clinical Hospital on railway transport No. 2 Branch «Center for Health Protection» of PJSC «Ukrainian Railway». 152 patients were examined: 72 men and 80 women. The patients were divided into groups: Group I – patients with stage II hypertension without signs of liver damage (46 people); Group II – patients with NAFLD without HT (54 people); Group III – patients with stage II HD with NAFLD (52 people).
Results. In the group of NAFLD patients without concomitant hypertension, the effect of obesity was observed both on the platelet count and on their mean volume. The platelet count was significantly higher in the presence of obesity – it was 16 % (<0.05) more, the MPV levels were also higher in NAFLD patients with a BMI ≥30 kg/m2 – by 2 % (p<0,05). The degree of adrenaline-induced aggregation was significantly increased only in obese patients –– by 40 % (p<0.001) compared with controls, and by 18 % with non-obese patients. During the exitox test in the NAFLD group in the obesity subgroup, a 9.5 % shortening of the clot formation time was revealed (p<0.05). In the group of combined course of NAFLD and HT II stage the division of patients by BMI made it possible to reveal the depression of anticoagulant activity of antithrombin III was less by 10.5 % (p<0.01), and protein C by 23.2 % (p<0.001) in obese patients.
Conclusion. Addition of obesity to hypertension and to the comorbid course of hypertension with NAFLD increased the thrombogenic activity of the blood, affecting various stages of hemostasis. However, the indicators of platelet-plasma hemostasis in patients with independent NAFLD did not actually differ from patients with obesity and BM I<30 kg/m2, which indicates similar pathophysiological mechanisms of prothrombotic changes in obesity and NAFLD.
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