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首页> 外文期刊>The American Journal of the Medical Sciences >The significance of platelet consumption in the development of thrombocytopenia in patients with cirrhosis
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The significance of platelet consumption in the development of thrombocytopenia in patients with cirrhosis

机译:血小板摄入对肝硬化患者血小板减少的发生的意义

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摘要

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 × 10/L) than in the noncirrhosis cases (150 ± 120 × 10/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 × 10/L) was lower than that of those without these complications (113 ± 80 × 10/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.
机译:简介:肝硬化中的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破坏/隔离加快所致。由于肝硬化相关的高凝性,血小板消耗过多也被认为是血小板减少症的病因。为了弄清血小板摄入过多(例如,静脉血栓形成和弥散性血管内凝血)是否会导致肝硬化中的血小板减少,我们进行了以下基于尸检的研究。方法:回顾性分析了九十九例慢性肝病(80例肝硬化和19例非肝硬化)的尸体。在尸检方案中检查血小板计数,脾脏重量和血栓形成并发症。高倍镜下计数骨髓中的巨核细胞。进行单因素和多因素分析以评估这些因素在血小板减少症中的意义。结果:肝硬化患者的血小板计数(88±51×10 / L)显着低于非肝硬化患者(150±120×10 / L)。肝硬化病例中的巨核细胞计数也较低(每高倍视野1.5±0.6),而非肝硬化病例(每高倍视野1.9±0.5)也较低。肝硬化病例的脾脏重量(264±179 g)比非肝硬化病例的脾脏重量(142±82 g)更大。记录有29例血栓形成并发症,其血小板计数(70±41×10 / L)低于无这些并发症的血小板计数(113±80×10 / L)。多变量分析显示这三个因素(巨核细胞计数,脾脏重量和血栓形成并发症)与血小板计数独立相关。结论:这些结果表明,血小板生产-破坏/螯合-消耗的不平衡导致了肝硬化中的血小板减少症。不能忽略过多的血小板消耗来解释这种复杂的情况,尤其是在有严重血栓事件的患者中。

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