Abstract

BACKGROUND One of the main pathogenetic aspects of the severe course of acute pancreatitis (AP) is endothelial dysfunction. Under normal physiological conditions, the endothelium has both anticoagulant and procoagulant properties. However, with the development of AP, endothelial dysfunction often begins as a diffuse activation of coagulation, which further potentiates the progression of the systemic inflammatory response syndrome (SIRS) and thereby complicates the course of AP. MATERIAL AND METHODS The present retrospective-prospective study included 78 patients; men — 52 (66.7%), women — 26 (33.3%) with severe AP. The mean age was 51.8±14.2 years. The patients were divided into two groups: the 1st group (n=39), based on a retrospective analysis of the data, included patients in whom the following hemostasis parameters were assessed: activated partial thromboplastin time, international normalized ratio, prothrombin. The second group (n=39) included patients in whom, in addition to the above, the following indicators were evaluated: fibrinogen, D-dimer, antithrombin III, protein C. CONCLUSION In the course of this study, it was found that routine methods for assessing the parameters of the hemostasis system, including the determination of only activated partial thromboplastin time, international normalized ratio, prothrombin, are uninformative and do not reflect the severity of the disease. A comprehensive comprehensive study of the coagulation system already in the early stages of the disease indicates an existing tendency to a severe course, which allows anticoagulant therapy to be immediately begun, thereby reducing the number of infectious complications, cases of multiple organ failure, and reducing mortality.

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