Warkentin T E, Kelton J G
Department of Laboratory Medicine, Hamilton Civic Hospitals (General Division), Ontario, Canada.
Am J Med. 1996 Nov;101(5):502-7. doi: 10.1016/s0002-9343(96)00258-6.
To determine the sites of thromboses (venous versus arterial circulation) that complicate the clinical course of immunemediated heparin-induced thrombocytopenia, and to determine the 30-day risk for thrombosis in patients who are initially recognized with isolated heparin-induced thrombocytopenia.
We analyzed objectively documented thrombotic events that complicated the clinical course of 127 patients with serologically confirmed heparin-induced thrombocytopenia identified in one medical community over a 14-year period. We classified heparin-induced thrombocytopenia patients into two groups: patients recognized with heparin-induced thrombocytopenia only after a new thrombosis had occurred, and patients initially recognized with isolated heparin-induced thrombocytopenia. We determined the subsequent 30-day risk for thrombosis for the cohort of patients initially recognized with isolated thrombocytopenia.
Heparin-induced thrombocytopenia was associated with the development of new venous thrombotic events and arterial thrombotic events in 78 and 18 patients, respectively (ratio venous/arterial thrombosis = 4:1). Pulmonary embolism was the most common life-threatening thrombotic event, occurring in 25% of all patients. Approximately half of all heparin-induced thrombocytopenia patients were recognized only after they had a complicating thrombotic event. Of the remaining 62-patient cohort initially recognized with isolated thrombocytopenia, the subsequent 30-day risk of thrombosis was 52.8%. The risk of thrombosis did not differ whether the heparin had been discontinued alone or whether warfarin had been substituted for the heparin.
Venous thrombosis complicates heparin-induced thrombocytopenia more frequently than does arterial thrombosis. The high risk of thrombosis in patients initially recognized with isolated thrombocytopenia suggests that conventional management approaches require reappraisal.
确定在免疫介导的肝素诱导的血小板减少症临床过程中并发血栓形成的部位（静脉循环与动脉循环），并确定最初被诊断为孤立性肝素诱导的血小板减少症患者发生血栓形成的30天风险。
我们分析了在一个医疗社区14年期间确诊的127例血清学确诊的肝素诱导的血小板减少症患者临床过程中并发的客观记录的血栓形成事件。我们将肝素诱导的血小板减少症患者分为两组：仅在新血栓形成后才被诊断为肝素诱导的血小板减少症的患者，以及最初被诊断为孤立性肝素诱导的血小板减少症的患者。我们确定了最初被诊断为孤立性血小板减少症患者队列随后30天的血栓形成风险。
肝素诱导的血小板减少症分别与78例和18例患者发生新的静脉血栓形成事件和动脉血栓形成事件相关（静脉/动脉血栓形成比例=4:1）。肺栓塞是最常见的危及生命的血栓形成事件，发生在所有患者中的25%。所有肝素诱导的血小板减少症患者中约一半仅在出现并发症性血栓形成事件后才被诊断出来。在其余最初被诊断为孤立性血小板减少症的62例患者队列中，随后30天的血栓形成风险为52.8%。无论肝素是单独停用还是华法林替代肝素，血栓形成风险均无差异。
静脉血栓形成比动脉血栓形成更常使肝素诱导的血小板减少症复杂化。最初被诊断为孤立性血小板减少症患者的高血栓形成风险表明，传统的管理方法需要重新评估。
