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血小板消耗在肝硬化患者血小板减少症发展中的意义。

The significance of platelet consumption in the development of thrombocytopenia in patients with cirrhosis.

机构信息

Departments of Pathology, Osaka City University Graduate School of Medicine, Osaka, Japan.

出版信息

Am J Med Sci. 2013 Sep;346(3):199-203. doi: 10.1097/MAJ.0b013e31826e364d.

Abstract

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.

摘要

简介

肝硬化引起的血小板减少主要归因于由于脾功能亢进导致的血小板破坏/隔离加速,或者由于促血小板生成素水平降低。肝硬化相关高凝状态导致的血小板过度消耗也被认为是血小板减少症的一个发病因素。为了明确肝硬化患者血小板过度消耗(如静脉血栓形成和弥散性血管内凝血)是否导致血小板减少,进行了以下基于尸检的研究。

方法

回顾性检查了 99 例慢性肝病(80 例肝硬化和 19 例非肝硬化)的尸检。在尸检方案中检查血小板计数、脾脏重量和血栓并发症。在高倍显微镜下计数骨髓中的巨核细胞。进行单变量和多变量分析以评估这些因素在血小板减少症中的意义。

结果

肝硬化病例的血小板计数(88 ± 51×10/L)明显低于非肝硬化病例(150 ± 120×10/L)。肝硬化病例的巨核细胞计数(1.5 ± 0.6/高倍视野)也低于非肝硬化病例(1.9 ± 0.5/高倍视野)。肝硬化病例的脾脏重量(264 ± 179g)大于非肝硬化病例(142 ± 82g)。29 例有血栓并发症的患者血小板计数(70 ± 41×10/L)低于无这些并发症的患者(113 ± 80×10/L)。多变量分析显示,这 3 个因素(巨核细胞计数、脾脏重量和血栓并发症)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/隔离-消耗的失衡导致了肝硬化患者的血小板减少。不能忽视血小板过度消耗来解释这种复杂情况,尤其是在有重大血栓事件的患者中。

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