Asessment of platelet activation in coupled schistosomiasis and viral hepatitis infection: contribution to complexity of course and development of complications

This study assessed platelet activation and possible contribution to the pathogenesis of liver cirrthosis [LC], heaptocellular carcinoma [HCC] and portal vain thrombosis [PVT].forty five patients with LC caused by dual schistosomsis and viral hepatitis infections were enrolled in the study, 15 had LC only, 15 were complicated with HCC, and 15 were complicated with PVT, addition to healthy controls. Platelet morphological parameters including platelet count, platelet crit, mean platelet volume [MPV] and platelet distribution width [PDW], as well as platelet activation as evidenced by measuring soluble platelet selectin [sP-selectin] level and the release of beta thromboglobulin [beta-TG], transforming growth factor beta-1 [TGF-beta1] and platelet derived factor-AA [PDGF-AA] were evaluated. The results obtained revealed significant reduction in platelet count, platelet crit and MPV while PDW was significantly increased in all LC patients in comparison to controls. sP selectin, beta-TG, TGF-beta1 and PDGF-AA revealed significant increase in all diseased when compared to control group. Patients complicated with HCC or PVT demonstrated significant increase in the aforementioned parameters in comparison to patients with LC only patients with PVT showed significant increase versus HCC patients. These findings indicate that platelet activation is a prominent feature in LC and its serious complication HCC and PVT This activation can play an important role the in pathogenesis of LC, HCC and PVT in patients with mixed schistosomiasis and viral hepatitis infections such patients need careful medical attention and effective treatment. Stabilization of the activated platelets and the dual suppression of PDGF and TGF-beta1 could be new therapeutic strategies against LC and its sequels.

Relation between thrombin activatable fibrinolysis inhibitor and haemostatic alterations in patients with chronic liver disease and portal vein thrombosis

Recently, a new inhibitor of fibrinolysis was discovered which down regulates fibrinolysis after its activation by thrombin and was therefore named thrombin activatable fibrinolysis inhibitor [TAFI]. We aimed at evaluating TAFI level in chronic liver disease [CLD] and its relationship to important haemostatic parameters namely: tissue factor [TF], prothrombin fragment 1+2 [Fl+2], thrombomodulin [TM], protein C [PC], protein S [PS], thrombus precursor protein [TpP] and D-dimer [D-di] in a trial to clarify the role of TAFI in haemostatic alterations frequently encountered in CLD. The study included 35 CLD patients [Chid B or C], 15 [out of them] were complicated by portal vein thrombosis [PVT], in addition to 15 healthy controls. Significant reduction in TAFI level was detected in CLD patient with and without PVT in comparison to controls, however a significantly higher values were noticed in patients complicated by PVT when compared to those without thrombosis. Correlation analysis demonstrated a strong correlation between TAFI level and other measured parameters namely PT, PTT, PC, PS and D-dimer in PVT group. It could be concluded that TAFI plays a crucial role in regulation of coagulation and fibrinolysis. Reduced TAFI level in patients with CLD could result in up regulation of fibrinolysis. High TF level, associated with decreased natural anticoagulants namely PC and PS accompanied by a higher TAFI level and its increased activation could play a role in the development of PVT as a complication of CLD