Ghanima Waleed, Holme Pål André, Tjønnfjord Geir E
Hematologisk seksjon, Medisinsk avdeling, Sykehuset Østfold Fredrikstad, 1603 Fredrikstad, Norway.
Tidsskr Nor Laegeforen. 2010 Nov 4;130(21):2120-3. doi: 10.4045/tidsskr.09.1119.
Immune thrombocytopenia (ITP) is caused by immune-mediated platelet destruction and reduced platelet production. The aim of this review article is to provide an updated overview of pathophysiology and new therapeutic modalities in ITP.
The article is based on literature identified through a non-systematic search in PubMed and our own clinical experience.
ITP is diagnosed in patients with platelet count < 100 × 10(9)/l after excluding other causes of thrombocytopenia. Anti-platelet autoantibodies are important in the platelet destruction mechanism, but other important mechanisms have been identified in recent years. Patients with very low platelet count < 30 × 10(9)/l are particularly susceptible to bleeding complications. The goal of treatment so far has been to increase the platelet count to a level that reduces the risk of serious bleeding. Thrombopoietin receptor agonists are new therapeutic agents that target the thrombopoietin receptor to increase platelet production. These drugs are shown to be effective in treatment of ITP.
New knowledge about pathophysiological mechanisms, such as sub-optimal platelet production in ITP, has led to the development of new therapeutic options which focus on stimulation of platelet production.
免疫性血小板减少症（ITP）是由免疫介导的血小板破坏和血小板生成减少引起的。这篇综述文章的目的是提供ITP病理生理学和新治疗方式的最新概述。
本文基于通过在PubMed上进行非系统检索以及我们自己的临床经验所确定的文献。
在排除其他血小板减少原因后，血小板计数<100×10⁹/L的患者被诊断为ITP。抗血小板自身抗体在血小板破坏机制中很重要，但近年来已发现其他重要机制。血小板计数极低<30×10⁹/L的患者特别容易发生出血并发症。迄今为止，治疗的目标是将血小板计数提高到降低严重出血风险的水平。血小板生成素受体激动剂是靶向血小板生成素受体以增加血小板生成的新型治疗药物。这些药物已被证明对ITP治疗有效。
关于病理生理机制的新知识，如ITP中血小板生成不足，已导致开发出专注于刺激血小板生成的新治疗选择。
