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[肝素诱导的血小板减少症:血液透析中的发病机制、临床表现及管理]

[Heparin-induced trombocytopenia: pathogenesis, clinical manifestations and management in hemodialysis].

作者信息

Esposito Pasquale, Libetta Carmelo, Borettaz Ilaria, Barone Marisa, Canevari Michele, Martinelli Claudia, Montagna Francesca, Romeo Salvatore, Margiotta Elisa, Calatroni Marta, La Porta Edoardo, Dal Canton Antonio

出版信息

G Ital Nefrol. 2014 May-Jun;31(3).

Abstract

Heparin has remained the most commonly used anticoagulant in hemodialysis patients (HD). Its use is usually safe but, in some cases, important adverse effects can occur. Heparin-induced thrombocytopenia (HIT) is an immuno-mediated condition due to the formation of PF4/heparin/IgG complex leading to the activation of platelets and coagulative cascade. The consequent prothrombotic hypercoagulable state may cause venous or arterial thrombosis, skin gangrene and acute platelet activation syndrome. Clinical and laboratory findings may be suggestive for HIT, but formal diagnosis requires the demonstration of the presence of circulating antibodies. Clinical management is complex including the withdrawal of any form of heparin and the administration of anticoagulants. In addition, since anticoagulation is routinely required to prevent clotting of the dialysis lines and membranes, in HD patients presenting HIT it is mandatory to establish heparin-free anticoagulation strategies. Thus, the use of citrate, direct thrombin inhibitors or eparinods have been proposed as alternative anticoagulation approaches in HIT. Here, we review the most important pathogenic factors and clinical features of HIT occurring in HD patients.

摘要

肝素一直是血液透析患者(HD)中最常用的抗凝剂。其使用通常是安全的,但在某些情况下,可能会出现重要的不良反应。肝素诱导的血小板减少症(HIT)是一种免疫介导的疾病,由于形成PF4/肝素/IgG复合物,导致血小板和凝血级联反应激活。随之而来的血栓前高凝状态可能导致静脉或动脉血栓形成、皮肤坏疽和急性血小板激活综合征。临床和实验室检查结果可能提示HIT,但正式诊断需要证明循环抗体的存在。临床管理很复杂,包括停用任何形式的肝素并给予抗凝剂。此外,由于常规需要抗凝以防止透析管路和膜的凝血,在出现HIT的HD患者中,必须建立无肝素抗凝策略。因此,有人提出使用柠檬酸盐、直接凝血酶抑制剂或类肝素作为HIT的替代抗凝方法。在此,我们综述了HD患者中发生HIT的最重要致病因素和临床特征。

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