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Thrombocytopenia associated with liver cirrhosis and hepatitis C viral infection: role of thrombopoietin.

机译:与肝硬化和丙型肝炎病毒感染相关的血小板减少症:血小板生成素的作用。

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BACKGROUND/AIMS: Thrombocytopenia in chronic liver diseases has traditionally been considered a consequence of platelet pooling and destruction in spleen. We tried to evaluate the influence of thrombopoietin, the physiological regulator of thrombopoiesis, on the origin of this thrombocytopenia. METHODOLOGY: We determined serum thrombopoietin levels by ELISA in thrombocytopenic patients with liver cirrhosis (n = 32) and with chronic hepatitis C viral infection (n = 23). A group of 43 healthy subjects was used as a control. RESULTS: Liver cirrhosis patients presented slightly, but not significantly, lower serum thrombopoietin levels (104 +/- 56 pg/mL) than controls (121 +/- 58 pg/mL) or patients infected with chronic hepatitis C virus (125 +/- 40 pg/mL). No correlations were found between serum thrombopoietin concentrations and liver tests or hematological parameters. CONCLUSIONS: We conclude that low thrombopoietin production may play a role, along with hypersplenism, in the development of thrombocytopenia in patients with liver cirrhosis. Normal thrombopoietin levels exclude a defect in thrombopoietin production as a possible etiology for the thrombocytopenia in patients with chronic hepatitis C viral infection. However, a direct viral megakaryocyte infection or an immune mechanism could explain this thrombocytopenia, according to the thrombopoietin levels detected.
机译:背景/目的:慢性肝病中的血小板减少症传统上被认为是血小板积聚和脾脏破坏的结果。我们试图评估血小板生成素(血小板生成的生理调节剂)对这种血小板减少症起源的影响。方法:我们通过ELISA测定了患有肝硬化(n = 32)和慢性丙型肝炎病毒感染(n = 23)的血小板减少症患者的血清血小板生成素水平。一组43名健康受试者被用作对照。结果:肝硬化患者的血清血小板生成素水平(104 +/- 56 pg / mL)较对照组(121 +/- 58 pg / mL)或慢性丙型肝炎病毒(125 + / -40 pg / mL)。血清血小板生成素浓度与肝脏检查或血液学参数之间无相关性。结论:我们得出结论,血小板减少素的产生可能与脾功能亢进一起在肝硬化患者的血小板减少症的发生中起作用。正常的血小板生成素水平排除了血小板生成素产生的缺陷,作为慢性丙型肝炎病毒感染患者血小板减少的可能病因。然而,根据检测到的血小板生成素水平,直接病毒巨核细胞感染或免疫机制可以解释这种血小板减少症。

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