免疫性血小板减少症患者凝血代偿机制的研究进展  

Advances in coagulation compensation mechanisms of patients with immune thrombocytopenia

作　　者：肖燕杰 刘述川[1] 张莹[1] Xiao Yanjie;Liu Shuchuan;Zhang Ying(Department of Hematology ,First Affiliated Hospital of Harbin Medical University Harbin 150001,Heilongjiang Province ,China)

机构地区：[1]哈尔滨医科大学附属第一医院血液内科,150001

出　　处：《国际输血及血液学杂志》2019年第1期36-40,共5页International Journal of Blood Transfusion and Hematology

基　　金：哈尔滨市科学技术局2016年哈尔滨市应用技术研究与开发基金(2016RAXYJ105);黑龙江省教育厅科研基金(11541227).

摘　　要：免疫性血小板减少症(ITP)为一种获得性自身免疫性出血性疾病,该病涉及血小板破坏增加与血小板生成不足导致的血小板计数减少,伴或者不伴出血的临床表现。ITP患者血小板计数减少可以导致机体凝血功能障碍引起出血,但是出血情况的严重程度并不完全与血小板计数减少程度呈正相关关系。部分患者血小板计数即使极低亦无明显出血现象,这表明存在额外的机制代偿凝血功能,并改善这些患者的出血情况。笔者拟就近年有关ITP患者凝血代偿机制的研究进展进行综述。Immune thrombocytopenia (ITP) is an acquired autoimmune hemorrhagic disease involving increased platelet destruction and insufficient platelet production, leading to thrombocytopenia, with or without clinical manifestations of bleeding. Although thrombocytopenia may cause coagulation dysfunction and hemorrhagic complications, the bleeding severity is not certainly proportional to the number of platelets. In some cases, there is no significant bleeding symptom even the platelet count is extremely low, which suggests there are additional compensatory mechanisms to control or ameliorate the bleeding complications in ITP patients. The present article aims to review recent investigations on the compensatory mechanisms of coagulation function in the patients with ITP.

关 键 词：血小板减少 微粒体 磷脂酰丝氨酸类 凝血致活酶 血小板膜糖蛋白类 凝血酶 白细胞介素6 

分 类 号：R558.2[医药卫生—血液循环系统疾病]