The Significance of Platelet Consumption in the Development of Thrombocytopenia in Patients With Cirrhosis
The Significance of Platelet Consumption in the Development of Thrombocytopenia in Patients With Cirrhosis
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DOI：
10.1097/maj.0b013e31826e364d
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发表时间：
2013-09-01
影响因子：
3.1
通讯作者：
Wakasa, Kenichi
中科院分区：
文献类型：
--
作者：
Ikura, Yoshihiro;Ohsawa, Masahiko;Wakasa, Kenichi
简介：肝硬化血小板减少主要是由于脾功能亢进或血小板生成素水平降低导致血小板加速破坏/隔离。由于血小板减少症相关的高凝状态引起的血小板过度消耗也被认为是血小板减少症的一个病因。为了澄清是否过度血小板消耗（例如，静脉血栓形成和弥散性血管内凝血）有助于血小板减少症肝硬化，以下尸检为基础的studywasperformed.Methods：99例尸检慢性肝病（80肝硬化和19 noncardiac）进行了回顾性检查。在尸检方案中检查血小板计数、脾脏重量和血栓性并发症。高倍镜下计数骨髓巨核细胞。结果：肝硬化组血小板计数（88 ± 51 × 10（9）/L）明显低于非肝硬化组（150 ± 120 × 10（9）/L）。肝硬化患者的巨核细胞计数（1.5 +/-0.6/高倍视野）也低于非肝硬化患者（1.9 +/-0.5/高倍视野）。肝硬化组脾脏重量（264 ± 179 g）高于非肝硬化组（142 ± 82 g）。29例患者记录了血栓并发症，其血小板计数（70 +/- 41 x 10（9）/L）低于无这些并发症的患者（113 +/- 80 x 10（9）/L）。多因素分析显示，这3个因素（巨核细胞计数，脾脏重量，血栓并发症）与血小板计数独立相关。结论：这些结果表明，血小板生成-破坏/封存-消耗的失衡有助于肝硬化血小板减少症。不能忽略过度血小板消耗来解释这种复杂的情况，特别是在发生重大血栓事件的患者中。
Introduction:Thrombocytopenia in cirrhosis is mainly explained by accelerated platelet destruction/sequestration because of hypersplenism or by decreased thrombopoietin levels. Excessive platelet consumption because of cirrhosis-related hypercoagulability has also been assumed to be an etiopathologic factor in thrombocytopenia. To clarify whether excessive platelet consumption (eg, venous thrombosis and disseminated intravascular coagulation) contributes to thrombocytopenia in cirrhosis, the following autopsy-based study was performed.Methods:Ninety-nine autopsies of chronic liver disease (80 cirrhosis and 19 noncirrhosis) were examined retrospectively. Platelet count, weight of spleen and thrombotic complications were checked in autopsy protocols. Megakaryocytes in bone marrow were counted under high-power microscopic view. Univariate and multivariate analyses were performed to evaluate significances of these factors in thrombocytopenia.Results:The platelet count was significantly lower in the cirrhosis cases (88 51 x 10(9)/L) than in the noncirrhosis cases (150 +/- 120 x 10(9)/L). The megakaryocyte count was also lower in the cirrhosis cases (1.5 +/- 0.6 per high-power field) than in the noncirrhosis cases (1.9 +/- 0.5 per high-power field). The weight of the spleen was greater in the cirrhosis cases (264 +/- 179 g) than in the noncirrhosis cases (142 +/- 82 g). Thrombotic complications had been recorded in 29 cases, whose platelet count (70 +/- 41 x 10(9)/L) was lower than that of those without these complications (113 +/- 80 x 10(9)/L). Multivariate analysis revealed that these 3 factors (megakaryocyte count, weight of spleen, and thrombotic complications) were independently correlated with the platelet count.Conclusions:These results suggest that the imbalance of platelet production-destruction/sequestration-consumption contributes to thrombocytopenia in cirrhosis. Excessive platelet consumption cannot be ignored to explain this complex condition, especially in patients with major thrombotic events.