Markers of hemostasis and inflammation in brucellosis infection

Abstract

Annotation. The relevance of the problem of brucellosis infection at the present stage determines the need to continue vector research to study the pathogenesis of the disease, including markers of inflammation and hemostasis, and the processes of development of endothelial dysfunction. The object of the study was patients diagnosed with acute brucellosis who were undergoing inpatient treatment in an infectious diseases hospital. The purpose of the study is to determine the level of markers of inflammation and hemostasis: coagulation factors (XII, X, V, II), endothelin-1, nitric oxide and its metabolites (nitrites (NO2-/nitrates (NO3-)), von Willebrand factor, vasculoendothelial factor, in the serum/blood plasma of patients with acute brucellosis and identification of a pathophysiological connection with the possible development of endothelial dysfunction. Results. An increase in the synthesis of vasculoendothelial factor (344.7±6.8 IU/ml), endothelin-1 (3.89±0.24 pg/ml), nitric oxide and its metabolites (nitrites (NO2- 207.4±11, 0 µmol/l; nitrates (NO3 - 170.9±10.2 µmol/l), (p≤0,001), indicating endothelial dysfunction. A decrease in plasma-coagulation factors of hemostasis was noted in patients with acute brucellosis (factor XII concentration was 50.6±14.0 %; factor X 50.4±13.1%; factor V 38.8±11.0%; factor II 60.9±14.5% compared to the control group, (p≤0,05)), which is possibly due to a protective reaction that prevents thrombus formation and bleeding, but leading to disruption of the maintenance of endothelial cell homeostasis - a “containment strategy” – a protective and adaptive reaction aimed at reducing the intensity of the systemic inflammatory response.