PLATELET-ENDOTHELIAL CELL ACTIVATION/INTERACTION IN CHRONIC LIVER DISEASE

Among the complex haemostatic disturbances in chronic liver disease (CLD), thrombocytopenia and defective platelet function are considered two of the frequent disorders which favour variceal bleeding; a serious complication endangering the patients lives. The aim of this study was to offer an answer to the puzzling question of whether the interaction of activated platelets and perturbed endo-thelial cells (ECs) contribute to thrombocytopenia and its precipitating mechanisms in patients with CLD. Sixty patients with CLD classified as Child A (n=15), Child B (n=15), Child C (n=15) and Bleeders (n=15), in addition to 15 healthy controls were enrolled in the study. Platelet count; platelet activation markers [platelet factor-4 (PF-4) and (5-thromboglobulin (β-TG)]; EC injury markers [sol-uble thrombomodulin (sTM) and von Willebrand factor (vWF)]; fibrinogen (Fgn), thrombin-antithrombin complex (TAT) and D-dimer were measured in all subjects. Data obtained helped us to elicit the presence of: platelet activation (significantly increased PF-4 β-TG in diseased groups as compared with controls) together with significant reduction in platelet count; EC injury (significant increased levels of sTM and vWF in diseased groups versus controls) as well as reduced plasma Fgn level together with the elevated TAT complex and D-dimer levels; reflecting activation of coagulation cascade with subsequent fibrinolysis and hence the occurrence of DIC. The association of activated platelets, injured ECs and DIC may suggest the possible implication of enhanced platelet-EC inter-action in the causation of thrombocytopenia in CLD. The prompt control of endotoxaemia known to occur in the late stages of CLD may be the key to rescue the patients from the deleterious effects of platelet activation, EC injury and coagulopathy.