Angelo Bianchi Bonomi Hemophilia and Thrombosis Center, Department of Internal Medicine, IRCCS Cà Granda Ospedale Maggiore Policlinico Foundation and Università degli Studi di Milan, Milan, Italy.
J Thromb Haemost. 2011 Sep;9(9):1713-23. doi: 10.1111/j.1538-7836.2011.04429.x.
Decreased levels of most coagulation factors and thrombocytopenia are the main haemostatic abnormalities of cirrhosis. As a consequence, this condition was, until recently, considered as the prototype acquired coagulopathy responsible for bleeding. However, recent evidence suggests that it should, rather, be regarded as a condition associated with normal or even increased thrombin generation. The bleeding events that occur in these patients should, therefore, be explained by the superimposed conditions that frequently occur in this setting. Due to elevated levels of factor VIII (procoagulant driver) in combination with decreased protein C (anticoagulant driver), which are typically found in patients with cirrhosis, a procoagulant imbalance, defined as a partial resistance to the in vitro anticoagulant action of thrombomodulin, can be demonstrated. Whether this in vitro hypercoagulability is truly representative of what occurs in vivo remains to be established. However, the hypothesis that it may have clinical consequences is attractive and deserves attention. The possible consequences that we discuss herein include whether (i) cirrhosis is a condition associated with increased risk of venous thromboembolism or portal vein thrombosis; (ii) the hypercoagulability associated with cirrhosis has any other role outside coagulation (i.e. progression of liver fibrosis); and (iii) anticoagulation should be used in cirrhosis. Although apparently provocative, considering anticoagulation as a therapeutic option in patients with cirrhosis is now supported by a rationale of increasing strength. There may be subgroups of patients who benefit from anticoagulation to treat or prevent thrombosis and to slow hepatic fibrosis. Clinical studies are warranted to explore these therapeutic options.
大多数凝血因子水平降低和血小板减少症是肝硬化的主要止血异常。因此，直到最近，这种情况仍被认为是导致出血的获得性凝血障碍的典型代表。然而，最近的证据表明，它应该被视为与正常甚至增加的凝血酶生成相关的情况。因此，应该用这种情况下经常发生的叠加情况来解释这些患者发生的出血事件。由于肝硬化患者通常存在因子 VIII 水平升高（促凝剂驱动因素）和蛋白 C 减少（抗凝剂驱动因素），因此可以证明存在促凝失衡，定义为对血栓调节蛋白体外抗凝作用的部分抵抗。这种体外高凝状态是否真的代表体内发生的情况仍有待确定。然而，这种假设可能具有临床意义，值得关注。我们在此讨论的可能后果包括：（i）肝硬化是否是静脉血栓栓塞或门静脉血栓形成风险增加的情况；（ii）肝硬化相关的高凝状态在凝血以外是否有任何其他作用（即肝纤维化的进展）；和（iii）是否应该在肝硬化中使用抗凝剂。虽然这似乎具有挑衅性，但考虑到抗凝作为肝硬化患者的治疗选择，现在有越来越多的理由支持这种选择。可能有一些患者亚组从抗凝治疗中获益，以治疗或预防血栓形成并减缓肝纤维化。需要进行临床研究来探索这些治疗选择。
