Department of Medicine, Division of Hospice and Palliative Care, North Shore University Hospital, Manhasset, NY, USA.
Department of Medicine, Division of Hematology and Oncology, State University New York (SUNY) Downstate Medical Center, Brooklyn, NY, USA.
Am J Case Rep. 2020 May 29;21:e922498. doi: 10.12659/AJCR.922498.
BACKGROUND Heparin, often used as an anticoagulant, acts by binding to antithrombin III. Indeed, heparin binds to a variety of proteins other than antithrombin III. Among them, platelet factor 4 can bind and neutralize the anticoagulant activity of heparin. Upon binding with heparin, platelet factor 4 undergoes a conformational change and expresses immunogenic neo-epitopes that induce the generation of antibodies of the platelet factor 4 heparin complex. This immune reaction may lead to thrombocytopenia and venous, arterial, or microvascular thrombosis. However, the risk of such complications is quite variable, as it is affected not only by the source and dose of heparin and the clinical condition (e.g., cardiovascular surgery and orthopedic surgery) of the patient, but also the molecular size of the heparin formulation. Venous, arterial, and small-vessel thrombosis can lead to leg swelling, pulmonary embolism, stroke, skin necrosis, or gangrene requiring limb amputation or intestinal resection. Myocardial infarction due to coronary thrombosis also occurs, although it is less common and can be readily recognized. CASE REPORT Heparin-induced thrombocytopenia (HIT) is a potentially life-threatening complication of heparin therapy. We report the case of a 67-year-old woman who developed ST-segment elevation myocardial infarction and thrombocytopenia within 10 days of prophylactic enoxaparin therapy after undergoing bilateral total knee replacement surgery. She also had peripheral arterial and venous thrombosis. With thrombolysis and argatroban anticoagulation therapy, she recovered without residual sequelae. CONCLUSIONS Thrombocytopenia with coronary and other vascular thrombosis is a potentially serious complication of heparin therapy. A trend of decreased platelet count, decreased platelet count by 30% or more, and/or occurrence of any type of thrombosis should raise the suspicion of HIT. This case demonstrates that early recognition and prompt treatment of HIT can be life-saving.
肝素通常用作抗凝剂，通过与抗凝血酶 III 结合发挥作用。事实上，肝素还可以与除抗凝血酶 III 以外的多种蛋白质结合。其中，血小板因子 4 可以与肝素结合并中和其抗凝活性。与肝素结合后，血小板因子 4 发生构象变化，并表达免疫原性新表位，诱导血小板因子 4 肝素复合物抗体的产生。这种免疫反应可能导致血小板减少以及静脉、动脉或微血管血栓形成。然而，这种并发症的风险差异很大，不仅受肝素的来源和剂量以及患者的临床状况（例如心血管手术和骨科手术）的影响，还受肝素制剂的分子大小的影响。静脉、动脉和小血管血栓形成可导致腿部肿胀、肺栓塞、中风、皮肤坏死或坏疽，需要截肢或肠切除术。也会发生由于冠状动脉血栓形成导致的心肌梗死，尽管这种情况较少见，但很容易识别。病例报告：肝素诱导的血小板减少症（HIT）是肝素治疗的一种潜在危及生命的并发症。我们报告了一例 67 岁女性的病例，她在双侧全膝关节置换术后接受依诺肝素预防性治疗 10 天内出现 ST 段抬高型心肌梗死和血小板减少症，同时还患有周围动静脉血栓形成。经过溶栓和阿加曲班抗凝治疗后，她恢复良好，没有遗留后遗症。结论：伴有冠状动脉和其他血管血栓形成的血小板减少症是肝素治疗的一种潜在严重并发症。血小板计数下降趋势、血小板计数下降 30%或更多、和/或任何类型的血栓形成都应引起对 HIT 的怀疑。本例表明，早期识别和及时治疗 HIT 可以挽救生命。
