Bleeding and thrombotic complications are common problems in patients with chronic liver disease. P-selectin is platelet activation marker that has been shown to be involved in thrombogenesis as well as bleeding disorders and may represent a possible link between inflammation and thrombosis through its adhesion to P-selectin glycoprotein ligand-1(PSGL-1, CD162) on leukocytes. PSGL-1 is a disulfide-bonded homodimeric mucin-like glycoprotein on leukocytes that interacts with P-, L-, and E-selectin. Thrombomodulin is a trasmembrane endothelial receptor involved in protein C pathway and may play a role in regulation of coagulation and inflammation processes. In order to investigate the clinical and pathogenic role of sP-selectin, CD162 and serum thrombomodulin in chronic liver disease, they were measured in 35 patients with chronic liver disease divided into; portal vien thrombosis group (PVT)(n=14), hematemesis group (n=11) and conservative treatment group (n=10). sP-selectin was significantly elevated in all patient groups as a part of inflammatory and immunological reactions that take place in patients with chronic liver disease. However among the 3 studied groups, the patients with hematemesis showed the highest elevation, may be due to hyperactivity of platelets, while in the PVT the lowest increase in sP-selectin level was recorded. This could be due to consumption of sP-selectin during clot formation. However, decrease surface expression of CD162 on neutrophils was detected in all our studied groups; this may be due to leukocyte activation and endtoxemia occurring in chronic liver disease. Thrombomodulin was significantly elevated in all patient groups and portal PVT showed the highest increase due to its hypersecretion from the activated endothelium with thrombus formation. However, marked elevation of thrombomodulin in patients with chronic liver disease could be one of hepatoma markers.