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Current concepts in thrombotic thrombocytopenic purpura.血栓性血小板减少性紫癜的当前概念。
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本文引用的文献

1
Localization of ADAMTS13 to the stellate cells of human liver.ADAMTS13在人肝脏星状细胞中的定位。
Blood. 2005 Aug 1;106(3):922-4. doi: 10.1182/blood-2005-01-0152. Epub 2005 Apr 26.
2
Binding of ADAMTS13 to von Willebrand factor.ADAMTS13与血管性血友病因子的结合。
J Biol Chem. 2005 Jun 10;280(23):21773-8. doi: 10.1074/jbc.M502529200. Epub 2005 Apr 11.
3
ADAMTS13 is expressed in hepatic stellate cells.ADAMTS13在肝星状细胞中表达。
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4
Does cryosupernatant plasma improve outcome in thrombotic thrombocytopenic purpura? No answer yet.冷冻上清血浆能否改善血栓性血小板减少性紫癜的预后？尚无答案。
Br J Haematol. 2005 Apr;129(1):79-86. doi: 10.1111/j.1365-2141.2005.05418.x.
5
Complement factor H mutation in familial thrombotic thrombocytopenic purpura with ADAMTS13 deficiency and renal involvement.
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6
Shiga-toxin-producing Escherichia coli and haemolytic uraemic syndrome.产志贺毒素大肠杆菌与溶血尿毒综合征
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7
The spacer domain of ADAMTS13 contains a major binding site for antibodies in patients with thrombotic thrombocytopenic purpura.ADAMTS13的间隔区包含血栓性血小板减少性紫癜患者抗体的主要结合位点。
Thromb Haemost. 2005 Feb;93(2):267-74. doi: 10.1160/TH04-05-0301.
8
Functional evolution of ADAMTS genes: evidence from analyses of phylogeny and gene organization.ADAMTS基因的功能进化：系统发育和基因组织分析的证据
BMC Evol Biol. 2005 Feb 4;5:11. doi: 10.1186/1471-2148-5-11.
9
Inherited dysregulation of the complement system.补体系统的遗传性调节异常。
Bull Mem Acad R Med Belg. 2004;159(Pt 2):195-8.
10
Anti-Factor H autoantibodies associated with atypical hemolytic uremic syndrome.与非典型溶血性尿毒症综合征相关的抗补体因子H自身抗体
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血栓性血小板减少性紫癜的当前概念。

Current concepts in thrombotic thrombocytopenic purpura.

作者信息

Tsai Han-Mou

机构信息

Division of Hematology, Albert Einstein College of Medicine and Montefiore Medical Center, Bronx, New York 10467, USA.

出版信息

Annu Rev Med. 2006;57:419-36. doi: 10.1146/annurev.med.57.061804.084505.

DOI:10.1146/annurev.med.57.061804.084505
PMID:16409158
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2426955/
Abstract

Recent advances have demonstrated that thrombotic thrombocytopenic purpura (TTP), characterized by widespread thrombosis in the arterioles and capillaries, is caused by deficiency of a circulating zinc metalloprotease, ADAMTS13. Two types of TTP are recognized: autoimmune TTP, caused by inhibitory antibodies of ADAMTS13, and hereditary TTP, caused by genetic mutations of ADAMTS13. This article reviews the characteristics and function of ADAMTS13, the mechanism by which ADAMTS13 deficiency may lead to thrombosis, and the causes of ADAMTS13 deficiency. It also discusses how the new knowledge may improve the diagnosis and treatment of this previously mysterious disorder.

摘要

最近的研究进展表明，血栓性血小板减少性紫癜（TTP）以小动脉和毛细血管广泛血栓形成为特征，是由循环中的锌金属蛋白酶ADAMTS13缺乏所致。TTP分为两种类型：由ADAMTS13抑制性抗体引起的自身免疫性TTP和由ADAMTS13基因突变引起的遗传性TTP。本文综述了ADAMTS13的特征和功能、ADAMTS13缺乏导致血栓形成的机制以及ADAMTS13缺乏的原因。还讨论了这些新知识如何改善对这种以前神秘疾病的诊断和治疗。