Tokgoz Huseyin, Caliskan Umran, Demir Muzaffer
Department of Pediatric Hematology, Konya University Meram Faculty of Medicine, Konya, Turkey.
Blood Coagul Fibrinolysis. 2012 Dec;23(8):769-71. doi: 10.1097/MBC.0b013e328358afc9.
Heparin-induced thrombocytopenia (HIT) is a well described side effect of heparin therapy. A 12-year-old boy developed deep-vein thrombosis. Risk factors for initial thrombosis are antiphospholipid syndrome and heterozygous mutation for prothrombin G20210A. Anticoagulant therapy with warfarin for 12 months was effective, but discontinuation of warfarin after 12 months resulted in recurrence of thrombosis. Unfractionated heparin (UFH) was initiated during the acute period, but heparin-induced thrombocytopenia developed. Transition from UFH to fondaparinux resulted in successful anticoagulation for a period of platelet recovery. We report a case of HIT developing with a background of prothrombotic genetic risk factors and antiphospholipid syndrome. This case study highlights several difficulties in pediatric HIT cases.
肝素诱导的血小板减少症(HIT)是肝素治疗中一种广为人知的副作用。一名12岁男孩发生了深静脉血栓形成。初始血栓形成的危险因素是抗磷脂综合征和凝血酶原G20210A杂合突变。使用华法林进行抗凝治疗12个月有效,但12个月后停用华法林导致血栓复发。急性期开始使用普通肝素(UFH),但发生了肝素诱导的血小板减少症。从UFH转换为磺达肝癸钠后,在血小板恢复期间成功实现了抗凝。我们报告了一例在血栓形成前遗传危险因素和抗磷脂综合征背景下发生HIT的病例。本病例研究突出了儿科HIT病例中的几个难点。