Role of the protein C system in aggravation of acute pancreatitis
World Journal of Biology Pharmacy and Health Sciences, 10 (3):
001–010 (June 2022)DOI: 10.30574/wjbphs.2022.10.3.0080
Abstract
The goal of the study was to identify risk factors for coagulation and fibrinolysis in aggravation of acute pancreatitis (AP) based on 11 markers and APACHE-II score.
The subjects were 42 patients with AP (12 severe AP and 30 mild AP) and 20 healthy controls. Measurements of antithrombin III (AT-III), plasminogen (Plg), platelet counts, lipopolysaccaride (LPS), thrombomodulin (TM), protein C (PC), activated protein C (APC), APC/PC ratio, free-protein S (f-PS), thrombin-antithrombin complex (TAT), and tissue-type plasminogen activator·PAI-1 (t-pA·PAI-1) complex and clinical scores were performed using ELISA kits and clinical examinations of patients.
Fluctuations of most markers in the course of AP indicated abnormal activation from onset to 3 days. After 7 days, non-survivor severe AP (SAP) cases showed abnormal marker reactivation, while survivor SAP and mild AP (MAP) cases had gradual normalization of markers. At 7 days after onset and during all stages of progression of AP, there were significant differences between non-survivor SAP and survivor SAP cases for 5 and 8 markers, respectively, but APC and t-pA·PAI-1 complex were common to both. The TAT/APC and t-pA·PAI-1/APC ratios, which reflect APC generation, were higher in survivor SAP than in non-survivor SAP cases. A decrease in APC generation leading to excessive thrombin synthesis may be a risk factor for coagulation and fibrinolysis in aggravation of AP.