Blood platelet and monocyte activations and relation to stages of liver cirrhosis

Abstract

Aim: Bloob platelets (plt) and monocytes are the cells that play a crucial role in the pathogenesis of liver damage and liver cirrhosis (LC). In this paper, the analysis of mutual relationship between platelets and monocytes activation in LC was conducted. Methods: Immunofluorescent flow cytometry was used to measure the percentage of activated platelet populations (CD62P, CD63), the percentage of plt-monocyte aggregates (pma) (CD41/CD45), and activated monocytes (CD11b, CD14, CD16) in the blood of 20 volunteers and 40 patients with LC. Platelet activation markers: sP-selectin, platelet factor 4 (PF4), beta-thromboglobulin (βTG) and monocyte chemotactic peptide-1 (MCP-1) were measured and compared in different stages of LC. Results: Platelet activation with the increase in both βTG serum concentration and elevation of plt population (CD62P and CD63 as well as MIF CD62P and CD63) is elevated as LC develops and thrombocytopenia rises. There is a positive correlation between medial intensity of fluorescence (MIF) CD62P and MIF CD63 in LC. We did not show any relationship between monocyte activation and pma level. SP-selectin concentration correlates positively with plt count and pma, and negatively with stage of plt activation and MIF CD62P and MIF CD63. There was no correlation between MCP-1 concentration and plt, monocyte activation as well as pma level in LC. CD16 monocytes and MIF CD16 populations are significantly higher in the end stage of LC. A positive correlation occurs between the value of CD11b monocyte population and MIF CD14 and MIF CD16 on monocytes in LC. Conclusion: Platelet and monocyte activation plays an important role in LC. Platelet activation stage does not influence monocyte activation and production of plt aggregates with monocytes in LC. With LC development, thrombocytopenia may be the result of plt consumption in platelet-monocyte aggregates. © 2005 The WJG Press and Elsevier Inc. All rights reserved.