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首页> 外文期刊>European Heart Journal - Case Reports >Successful treatment with rivaroxaban of an extended deep vein thrombosis complicated by pulmonary embolism in a patient with familial antithrombin III deficiency: a case report
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Successful treatment with rivaroxaban of an extended deep vein thrombosis complicated by pulmonary embolism in a patient with familial antithrombin III deficiency: a case report

机译:用家族性抗凝血酶III缺乏患者患者肺栓塞的肺栓塞复杂化的rivaroxaban成功治疗:案例报告

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Background Patients with low levels of antithrombin III (AT III) are at an increased risk of developing arteriovenous thromboembolic disease. Case summary We report a case of a 28-year-old woman who presented with a 1-week history of spontaneous right calf pain and swelling. A heterozygous AT III deficiency, phenotypically expressed as deep vein thrombosis, was reported in the patient’s mother and sister. Blood workup revealed residual AT III activity at 58% with normal protein C and protein S levels. Computed tomographic angiography (CTA) revealed subsegmental bilateral pulmonary embolism (PE) and deep vein thrombosis in the right leg extending into the inferior vena cava up to the confluence of the left renal vein. Placement of an inferior vena cava filter was not considered. Given the patient’s haemodynamic stability, anticoagulant therapy with 15?mg of rivaroxaban twice a day was initiated instead. Echocardiography after 10?days of treatment revealed complete resolution of the thrombus located in the inferior vena cava, while CTA revealed complete resolution of the PE. Discussion Patients with AT III deficiency are likely to be heparin-resistant and will require higher heparin doses or the administration of AT III replacement therapy for the treatment of thrombosis, both of which are associated with an increased risk for haemorrhagic complications. Direct factor Xa inhibition by rivaroxaban provided an alternative mechanism for anticoagulation, which was found to be particularly useful in this patient with familial AT III deficiency, deep vein thrombosis, and PE.
机译:抗凝血酶III水平较低(III)的背景患者处于发育动静脉血栓栓塞疾病的风险增加。案例摘要我们举报了一个28岁女性的案例,他们介绍了一周的自发右小牛肉疼痛和肿胀。在患者的母亲和姐姐中报道了III缺乏的杂合,表达型为深静脉血栓形成。血液掉效果在III活性下显示58%,具有正常的蛋白C和蛋白质S水平。计算机断层摄影血管造影(CTA)显示右腿右腿部的副段双侧肺栓塞(PE)和深静脉血栓形成,延伸到左肾静脉的汇合中。不考虑放置下腔静脉筛过滤器。鉴于患者的血液动力学稳定性,抗凝治疗含有15μmmg的rivaroxaban,而是替代地进行两次。超声心动图10?天数的治疗后显示出位于下腔静脉的血栓的完全分辨率,而CTA揭示了PE的完全分辨率。讨论患有III缺乏症的患者可能是肝素抗性,需要更高的肝素剂量或在III替代疗法治疗血栓形成,这两者都与出血性并发症的风险增加有关。 Rivaroxaban的直接因素Xa抑制为抗凝提供了一种替代机制,该抗凝机制在本患者中特别有用III缺乏,深静脉血栓形成和PE。

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