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肝素诱导的血小板减少症:肾脏替代治疗中使用肝素时一种罕见但严重的并发症。

Heparin-induced thrombocytopenia: an uncommon but serious complication of heparin use in renal replacement therapy.

作者信息

Charif Rawya, Davenport Andrew

机构信息

University College London Centre for Nephrology, Royal Free Hospital, London, UK.

出版信息

Hemodial Int. 2006 Jul;10(3):235-40. doi: 10.1111/j.1542-4758.2006.00101.x.

Abstract

Heparin-induced thrombocytopenia (HIT) is an uncommon but potentially life-threatening complication of heparin therapy. Hemodialysis and hemofiltration patients are regularly exposed to heparin, which is used for extracorporeal anticoagulation. Type II HIT (HIT-II) is the rarer immune-mediated form and is of huge clinical significance. The clinical manifestation of HIT-II is characteristically with venous and arterial thrombotic events. However, systemic and pulmonary reactions have been reported. Type II HIT is due to antibodies to the heparin-platelet factor 4 complex, which induce a cascade of events leading to thrombocytopenia and thrombosis. Nowadays, with increasing availability of functional and immunoassay tests for HIT-associated antibodies, HIT diagnosis can be confirmed more readily. Hence, it is important to rapidly recognize, diagnose, and manage this syndrome early in hemodialysis patients with thrombocytopenia to avoid serious consequences resulting in morbidity and mortality. We report a case of HIT-II manifesting atypically as a "pseudopulmonary embolus" in a hemodialysis patient and discuss the clinical management of HIT.

摘要

肝素诱导的血小板减少症(HIT)是肝素治疗中一种不常见但可能危及生命的并发症。血液透析和血液滤过患者经常接触用于体外抗凝的肝素。II型HIT(HIT-II)是较罕见的免疫介导形式,具有重大临床意义。HIT-II的临床表现特征为静脉和动脉血栓形成事件。然而,也有全身性和肺部反应的报道。II型HIT是由针对肝素-血小板因子4复合物的抗体引起的,该抗体引发一系列导致血小板减少和血栓形成的事件。如今,随着针对HIT相关抗体的功能和免疫测定试验越来越容易获得,HIT的诊断可以更容易地得到证实。因此,对于血小板减少的血液透析患者,早期快速识别、诊断和处理该综合征以避免导致发病和死亡的严重后果非常重要。我们报告一例血液透析患者中表现为非典型“假性肺栓塞”的HIT-II病例,并讨论HIT的临床处理。

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