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网织血小板作为肝硬化中巨核细胞生成的标志物;与血小板生成素和肝细胞生长因子血清浓度的关系。

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

作者信息

Panasiuk Anatol, Prokopowicz Danuta, Zak Janusz, Panasiuk Bozena

机构信息

Department of Infectious Diseases, Medical Academy of Bialystok, Poland.

出版信息

Hepatogastroenterology. 2004 Jul-Aug;51(58):1124-8.

PMID:15239259
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.

摘要

背景/目的:血小板减少症常伴随慢性肝病出现。其发生可能是由于巨核细胞产生血小板减少、外周破坏增加或脾内扣押所致。

方法

我们采用流式细胞术对肝硬化伴血小板减少症患者(n = 24,血小板中位数(M)= 77g/L)、血小板计数正常患者(n = 16,血小板M = 193g/L)及健康受试者(n = 27,血小板M = 242g/L)的网织血小板进行评估。用噻唑橙染色并与抗CD41单克隆抗体孵育后的全外周血来测定网织血小板水平。

结果

肝硬化伴血小板减少症患者的网织血小板水平显著低于无血小板减少症患者及健康受试者(分别为M = 1.0% 、1.5% 、2.0%)。肝硬化患者中网织血小板水平与血小板计数、血小板生成素血清水平及肝细胞生长因子之间未建立相关性。在对照组中,网织血小板与血小板生成素呈负相关(r = 0.6,p<0.01),与肝细胞生长因子也呈负相关(r = 0.5,p<0.01)。观察到肝硬化患者的血小板计数与血小板生成素血清水平呈正相关(r = 0.35,p<0.05),与肝细胞生长因子也呈正相关(r = 0.48,p<0.01)。

结论

我们的研究表明,由于血小板生成素浓度低导致巨核细胞产生血小板减少可能是肝硬化患者血小板减少症的一个潜在原因。

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