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Reticulated platelets as a marker of megakaryopoiesis in liver cirrhosis; relation to thrombopoietin and hepatocyte growth factor serum concentration.

Anatol Panasiuk, D Prokopowicz, Janusz Żak, Bozena Panasiuk

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Abstract

BACKGROUND/AIMS: Thrombocytopenia often accompanies chronic liver diseases. It can occur due to the decrease in blood platelet production by megakaryocytes, the increase in peripheral destruction, or splenic sequestration. METHODOLOGY: We estimate the reticulated platelets by use of flow cytometry in patients with liver cirrhosis with thrombocytopenia (n-24, platelets median (M)-77g/L), with normal platelet count (n-16, platelets M-193g/L) and in healthy (n-27, platelets M-242g/L). The level of reticulated platelets was determined in whole peripheral blood stained with thiazole orange and incubated with monoclonal antibodies anti-CD41. RESULTS: Patients with liver cirrhosis and thrombocytopenia revealed significantly lower reticulated platelet levels than patients without thrombocytopenia and healthy subjects (M-1.0% vs. 1.5% vs. 2.0% respectively). The correlation between reticulated platelet level and platelet count, serum level of thrombopoietin and hepatocyte growth factor in liver cirrhosis was not established. An inverse correlation was noted between reticulated platelets and thrombopoietin (r - 0.6, p<0.01) and hepatocyte growth factor (r - 0.5, p<0.01) in the control group. A positive correlation between platelet count in liver cirrhosis and serum level of thrombopoietin (r - 0.35, p<0.05) and hepatocyte growth factor (r - 0.48, p<0.01) was observed. CONCLUSIONS: Our studies showed that decreased production of platelets by megakaryocytes due to low thrombopoietin concentration could be a possible cause of thrombocytopenia in liver cirrhosis.

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BACKGROUND/AIMS: Thrombocytopenia often accompanies chronic liver diseases. It can occur due to the decrease in blood platelet production by megakaryocytes, the increase in peripheral destruction, or splenic sequestration. METHODOLOGY: We estimate the reticulated platelets by use of flow cytometry in patients with liver cirrhosis with thrombocytopenia (n-24, platelets median (M)-77g/L), with normal platelet count (n-16, platelets M-193g/L) and in healthy (n-27, platelets M-242g/L). The level of reticulated platelets was determined in whole peripheral blood stained with thiazole orange and incubated with monoclonal antibodies anti-CD41. RESULTS: Patients with liver cirrhosis and thrombocytopenia revealed significantly lower reticulated platelet levels than patients without thrombocytopenia and healthy subjects (M-1.0% vs. 1.5% vs. 2.0% respectively). The correlation between reticulated platelet level and platelet count, serum level of thrombopoietin and hepatocyte growth factor in liver cirrhosis was not established. An inverse correlation was noted between reticulated platelets and thrombopoietin (r - 0.6, p<0.01) and hepatocyte growth factor (r - 0.5, p<0.01) in the control group. A positive correlation between platelet count in liver cirrhosis and serum level of thrombopoietin (r - 0.35, p<0.05) and hepatocyte growth factor (r - 0.48, p<0.01) was observed. CONCLUSIONS: Our studies showed that decreased production of platelets by megakaryocytes due to low thrombopoietin concentration could be a possible cause of thrombocytopenia in liver cirrhosis.

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Available abstract

BACKGROUND/AIMS: Thrombocytopenia often accompanies chronic liver diseases. It can occur due to the decrease in blood platelet production by megakaryocytes, the increase in peripheral destruction, or splenic sequestration. METHODOLOGY: We estimate the reticulated platelets by use of flow cytometry in patients with liver cirrhosis with thrombocytopenia (n-24, platelets median (M)-77g/L), with normal platelet count (n-16, platelets M-193g/L) and in healthy (n-27, platelets M-242g/L). The level of reticulated platelets was determined in whole peripheral blood stained with thiazole orange and incubated with monoclonal antibodies anti-CD41. RESULTS: Patients with liver cirrhosis and thrombocytopenia revealed significantly lower reticulated platelet levels than patients without thrombocytopenia and healthy subjects (M-1.0% vs. 1.5% vs. 2.0% respectively). The correlation between reticulated platelet level and platelet count, serum level of thrombopoietin and hepatocyte growth factor in liver cirrhosis was not established. An inverse correlation was noted between reticulated platelets and thrombopoietin (r - 0.6, p<0.01) and hepatocyte growth factor (r - 0.5, p<0.01) in the control group. A positive correlation between platelet count in liver cirrhosis and serum level of thrombopoietin (r - 0.35, p<0.05) and hepatocyte growth factor (r - 0.48, p<0.01) was observed. CONCLUSIONS: Our studies showed that decreased production of platelets by megakaryocytes due to low thrombopoietin concentration could be a possible cause of thrombocytopenia in liver cirrhosis.

Key concepts: Thrombopoietin, Platelet, Cirrhosis, Internal medicine, Thrombopoiesis, Hepatocyte, Growth factor, Mean platelet volume

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