U.O di Diagnostica Ematochimica, Dipartimento di Patologia e Medicina di Laboratorio, Azienda Ospedaliero-Universitaria di Parma, Via Gramsci 14, 43126, Parma, Italy.
J Thromb Thrombolysis. 2012 Oct;34(3):360-6. doi: 10.1007/s11239-012-0753-3.
The pathogenesis of venous and arterial thrombosis is complex and multifaceted, entailing a multitude of risk factors, which only marginally overlap between the two vessels districts. Along with conventional and universally recognized risk factors, thrombosis might also develop as a consequence of unusual, atypical, unsuspected and even paradoxical conditions. Although the term "paradoxical embolism" is typically used to identify an embolization process that originates from the low-pressure venous system and may generate ischemic stroke or peripheral arterial occlusion through a cardiac or pulmonary shunt, there are additional clinical circumstances whereby the risk of thrombosis is surprising, unpredicted or even neglected. In this article we thereby analyze the prevalence, as well as the pathogenesis, of thrombosis associated with apparently paradoxical triggers such as during factor replacement therapy in haemophiliacs or in patients with von Willebrand disease; in patients with inherited clotting factor deficiencies especially involving factor XII, factor VII, fibrinogen; or in those with a prolonged activated partial thromboplastin time for the presence of lupus anticoagulant.
静脉和动脉血栓形成的发病机制复杂且多方面，涉及多种风险因素，这两种血管区域的风险因素仅有轻微的重叠。除了传统的和普遍公认的风险因素外，血栓也可能由于异常、非典型、未被怀疑甚至矛盾的情况而发生。尽管“反常栓塞”一词通常用于识别源自低压静脉系统的栓塞过程，该过程可能通过心脏或肺分流导致缺血性中风或外周动脉闭塞，但在其他临床情况下，血栓形成的风险是出人意料的、无法预测的，甚至被忽视。在本文中，我们分析了与看似矛盾的触发因素相关的血栓形成的患病率和发病机制，例如在血友病或血管性血友病患者中进行因子替代治疗时；在遗传性凝血因子缺乏症患者中，特别是涉及因子 XII、因子 VII、纤维蛋白原时；或在狼疮抗凝剂存在时，由于活化部分凝血活酶时间延长而导致的血栓形成。
