Nelson J C, Lerner R G, Goldstein R, Cagin N A
Arch Intern Med. 1978 Apr;138(4):548-52.
Two patients with underlying thromboembolic disorders developed severe thrombocytopenia while receiving heparin sodium; one of these patients developed recurrence of the thrombocytopenia and possible heparin-induced pulmonary emboli when heparin was restarted. In a prospective study of patients receiving heparin in a coronary care unit (CCU), nine of 37 patients developed transient mild thrombocytopenia (platelet counts ranging from 88,000 to 150,000/cu mm). Heparin added to citrated platelet-rich plasma caused platelet aggregation in the two original patients. In three of six CCU patients tested, and in 17 of 87 other subjects, with maximum aggregation at concentrations of heparin likely to be present in vivo during therapy. We herein discuss evidence that suggests that heparin may cause or aggravate thrombosis by causing platelet aggregation. The occurrence of severe heparin-induced thrombocytopenia is well documented, and mild transient thrombocytopenia may be more common than has been recognized. Studies of heparin efficacy should take these responses into account.
两名患有潜在血栓栓塞性疾病的患者在接受肝素钠治疗时出现了严重血小板减少症；其中一名患者在重新使用肝素时血小板减少症复发，并可能出现肝素诱导的肺栓塞。在一项针对冠心病监护病房（CCU）中接受肝素治疗患者的前瞻性研究中，37名患者中有9名出现了短暂性轻度血小板减少症（血小板计数范围为88,000至150,000/立方毫米）。将肝素添加到枸橼酸化富血小板血浆中会导致最初两名患者的血小板聚集。在测试的6名CCU患者中的3名以及87名其他受试者中的17名中，在治疗期间体内可能存在的肝素浓度下出现了最大聚集。我们在此讨论表明肝素可能通过引起血小板聚集而导致或加重血栓形成的证据。严重的肝素诱导的血小板减少症的发生有充分记录，轻度短暂性血小板减少症可能比人们认识到的更为常见。肝素疗效的研究应考虑到这些反应。
