Sturtevant J M, Pillans P I, Mackenzie F, Gibbs H H
Department of Pharmacy, Princess Alexandra Hospital. Brisbane, Queensland, Australia.
Intern Med J. 2006 Jul;36(7):431-6. doi: 10.1111/j.1445-5994.2006.01106.x.
Heparin-induced thrombocytopenia (HIT) is a potentially serious adverse reaction caused by platelet-activating antibodies.
To describe experience with HIT.
Twenty-two patients identified by laboratory records of heparin-associated antibodies with a 50% or greater decrease in platelet count were reviewed in our 600-bed metropolitan teaching hospital from 1999 to April 2005.
There was an increase in the frequency of HIT diagnosed during the review period, which was associated with a rise in the number of requests for HIT antibodies. Thrombotic complications were identified in 14 of 22 patients with HIT. Mean age was 65 years, and 11 patients were men. Seven patients died and HIT was considered contributory in four. One patient required mid-forearm amputation. Unfractionated heparin was used in all cases and five patients also received enoxaparin. Mean time to HIT screen, reflecting when the diagnosis was first suspected, was 14 days. Platelet nadir ranged from 6 x 10(9)/L to 88 x 10(9)/L, with a percentage drop in platelet count of 67-96%. Alternative anticoagulation (danaparoid) was not used in three patients, two of whom died.
HIT is a potentially life-threatening complication of heparin therapy, associated with a fall in platelet count and a high incidence of thromboembolic complications. It is most frequently seen using unfractionated heparin therapy. The increase in frequency of HIT diagnosed in our hospital appears to be associated with a greater awareness of the entity, although detection is often delayed. Platelet count should be monitored in patients on heparin and the presence of antiplatelet antibodies determined if HIT is suspected. Treatment involves both discontinuation of heparin and the use of an alternative anticoagulant such as danaparoid because of the persisting risk of thrombosis.
肝素诱导的血小板减少症(HIT)是一种由血小板激活抗体引起的潜在严重不良反应。
描述肝素诱导的血小板减少症的诊疗经验。
回顾性分析1999年至2005年4月间在我院(一所拥有600张床位的都市教学医院)住院的22例患者,这些患者经实验室检查确诊为肝素相关抗体阳性且血小板计数下降50%或更多。
在回顾期间,肝素诱导的血小板减少症的诊断频率有所增加,这与肝素诱导的血小板减少症抗体检测需求的增加有关。22例肝素诱导的血小板减少症患者中有14例出现血栓并发症。患者平均年龄为65岁,其中11例为男性。7例患者死亡,4例被认为与肝素诱导的血小板减少症有关。1例患者需要进行前臂中段截肢。所有病例均使用了普通肝素,5例患者还接受了依诺肝素治疗。肝素诱导的血小板减少症筛查的平均时间(反映首次怀疑诊断的时间)为14天。血小板计数最低点在6×10⁹/L至88×10⁹/L之间,血小板计数下降百分比为67%至96%。3例患者未使用替代抗凝剂(达那肝素),其中2例死亡。
肝素诱导的血小板减少症是肝素治疗的一种潜在危及生命的并发症,与血小板计数下降和血栓栓塞并发症的高发生率相关。在使用普通肝素治疗时最为常见。我院肝素诱导的血小板减少症诊断频率的增加似乎与对该疾病的认识提高有关,尽管检测往往延迟。对接受肝素治疗的患者应监测血小板计数,如果怀疑肝素诱导的血小板减少症,应检测抗血小板抗体的存在。治疗包括停用肝素,并使用替代抗凝剂如达那肝素,因为仍存在血栓形成的风险。