An Ning and Yiwen Liu
Jiangxi Provincial Institute of Parasitic Diseases, China
Posters & Accepted Abstracts: J Bacteriol Parasitol
Objective: Schistosomiasis japonica is pathologically characterized by liver inflammation and fibrosis. Although coagulation, fibrinolysis and inflammation are affected and increased D-dimer levels have been noted, the mechanisms remain unclear. Methods: 150 patients with chronic schistosomiasis as chronic schistosomaiasis group, 90 patients with advanced schistosomiasis as advanced schistosomaiasis group and 69 healthy residents in this study as control group were taken. Liver function, blood coagulation, liver fibrosis and routine blood test data were gathered. ELISA technique was used to measure tissue-type plasminogen activator (t-PA) and urokinase (u-PA), plasmin/anti-plasmin complex (PAP), plasminogen (PLG), anti-thrombin (AT) and plasminogen activator inhibitor 1 (PAI1) levels. D-dimer levels were monitored using the immune turbidity method and coagulation factor VIII (FVIII) was measured using the coagulation method. Antithrombin III (AT-III), PLG, Protein S and Protein C activities were measured via the chromogenic substrate method. Results: Although the indicators of coagulation duration (prothrombin time (PT), activated partial thromboplastin time (APTT), thrombin time (TT) and fibrinogen (Fbg) level) were not significantly different between the case and control groups, the plasma levels D-Dimer, FVIII, PAP and plasmin activators (t-PA and u-PA ) were significantly increased in the cases compared to the controls. These levels were further elevated to the advanced patients compared with the chronic patients (P<0.05). Anti-coagulation proteins, including AT-III, PLG, PC and PS, and anti-plasmin activators (PAI1) were decreased in the patient cases compared with the healthy controls and these level was further decreased from the advanced patients compared with the chronic patients (P<0.01 ). Conclusion: Schistosoma induced specific pathological variations on concomitant increases in coagulation and fibrinolysis that led to the inhibition of infection-induced thrombi in the vessels and an increase in D-dimers to preserve blood flow.
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