Background: Chronic liver disease is a worldwide common pathology characterized by an inflammatory and fibrotic process that may lead to progressive evolution from chronic hepatitis to cirrhosis. Monocytes play a crucial role in the pathogenesis of inflammation and fibrosis in chronic liver diseases. Also, blood platelet, by connecting hemostasis and inflammatory processes, participate in the pathogenesis of chronic liver diseases.Aim of the work: We aim to assess the expression of platelet monocyte aggregates and their relationship to both monocyte and platelet activation in peripheral blood in patients with HCV induced chronic liver disease in relation to the degree of hepatic insufficiency and haemostatic imbalance and their relevance in aggravating the acute attack of haematemesis in these patients.Subjects and Methods: This study was conducted on 60 patients classified according to Child Pugh classification to Child A (15 patients), B (15 patients), C (15 patients) and Child C during acute attack of haematemesis (15 patients), 15 healthy subjects served as normal controls. Immunophenotype characterization for identification of platelet monocyte aggregates (CD41/CD45) on activated blood monocytes (CD11b and CD14) and activated blood platelet populations (CD61and CD62P) in different groups studied was carried out by flowcytometric analysis using monoclonal antibodies anti-CD41/45, anti-CD11b, anti-CD14, anti-CD61 and anti-CD62P, respectively. The circulating blood levels of monocyte activation marker (MCP-1) and platelet activation markers (PF4 and sP-selectin) were also determined in different groups studied using immunological assays.Results: Our findings revealed that the activation of monocytes and platelets increased in stepwise fashion in conjunction with worsening severity of liver disease as assessed by Child Pugh staging. A marked decrease in platelet count concomitant with an increase in the surface expression of CD61 on peripheral blood platelets were also noticed in different groups of patients compared to healthy subjects, implicating that the platelet count drops in correlation with advancement of liver cirrhosis. Data demonstrated a significant increase in the surface expression of each of CD11b, CD14 and CD41/45 on peripheral blood monocytes revealing increased activation of peripheral blood monocytes in different groups studied compared to healthy subjects, especially cases during acute attack of hematemesis. Data also showed a significant progressive increase in the surface expression of CD62P and CD41/CD45 on peripheral blood platelets and in the circulating levels of sP-selectin and PF4, indicating increased activation of peripheral blood platelets, in different groups of patients compared to healthy subjects, especially cases during acute attack of hematemesis. Conclusion: The progressive increase in monocytes and platelets activation with the simultaneous formation of monocyte-platelet aggregates noticed in patients studied may contribute to progressive liver injury in these patients. Monocytes play a crucial role in the pathogenesis of liver damage and liver cirrhosis, and as platelets, by connecting haemostasis and inflammatory processes, participate in pathogenesis of chronic liver diseases. We, therefore, may conclude that the blockage of platelet and monocyte activation may diminish thrombocytopenia and liver cirrhosis intensification in patients with chronic hepatitis C virus.