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肝病中的止血、出血和血栓形成

Hemostasis, bleeding and thrombosis in liver disease.

作者信息

Flores Brisas, Trivedi Hirsh D, Robson Simon C, Bonder Alan

机构信息

Division of Internal Medicine, Beth Israel Deaconess Medical Center, Harvard University, 330 Brookline Avenue, 02215, Boston, USA.

Liver Center. Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, 02215, USA.

出版信息

J Transl Sci. 2017 May;3(3). doi: 10.15761/JTS.1000182. Epub 2017 Mar 4.

DOI:10.15761/JTS.1000182
PMID:30221012
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6136435/
Abstract

The presence of cirrhosis poses an increased risk of both thrombosis and bleeding in individuals with chronic liver disease. This duality is a result of a dynamic disequilibrium between procoagulant and anticoagulant states in individuals with cirrhosis. The mechanism of this imbalance in cirrhosis remains unclear. It is known that the progression of cirrhosis leads to decreased synthetic function and a concurrent lack of natural anticoagulants. Other proposed mechanisms contributing to this hemostatic imbalance include decreased platelet production, increased platelet destruction from hypersplenism, decreased synthesis of Vitamin K-dependent and independent clotting factors and anticoagulant factors, and alterations in purinergic signaling pathways. Given the current state of flux in our understanding of bleeding and thrombophilia in cirrhosis, the recommendations for treatment of these conditions are still evolving. We provide a current update on the proposed pathophysiology of altered hemostasis and thrombophilia in cirrhosis. We discuss recent studies in portal vein thrombosis (PVT) and venous thromboembolism (VTE), which are the common thrombotic consequences of cirrhosis, resulting in substantive morbidity and mortality. To address these, we discuss new prophylactic interventions and current treatment options to manage the heightened risk of thrombosis in cirrhosis, while limiting hemorrhagic complications.

摘要

肝硬化的存在会增加慢性肝病患者发生血栓形成和出血的风险。这种双重性是肝硬化患者促凝和抗凝状态之间动态失衡的结果。肝硬化中这种失衡的机制尚不清楚。已知肝硬化的进展会导致合成功能下降以及同时缺乏天然抗凝剂。导致这种止血失衡的其他机制包括血小板生成减少、脾功能亢进导致的血小板破坏增加、维生素K依赖性和非依赖性凝血因子及抗凝因子合成减少,以及嘌呤能信号通路的改变。鉴于目前我们对肝硬化出血和血栓形成倾向的理解尚不稳定,针对这些情况的治疗建议仍在不断发展。我们提供了关于肝硬化止血和血栓形成倾向改变的拟议病理生理学的最新情况。我们讨论了门静脉血栓形成(PVT)和静脉血栓栓塞(VTE)的最新研究,这两者是肝硬化常见的血栓形成后果,会导致严重的发病率和死亡率。为了解决这些问题,我们讨论了新的预防性干预措施和当前的治疗选择,以管理肝硬化中血栓形成风险增加的问题,同时限制出血并发症。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1bd/6136435/62a84b8cb26f/nihms885748f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1bd/6136435/1ba27b08875f/nihms885748f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1bd/6136435/05b6edb9753d/nihms885748f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1bd/6136435/62a84b8cb26f/nihms885748f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1bd/6136435/1ba27b08875f/nihms885748f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1bd/6136435/05b6edb9753d/nihms885748f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1bd/6136435/62a84b8cb26f/nihms885748f3.jpg

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The Complex Role of Anticoagulation in Cirrhosis: An Updated Review of Where We Are and Where We Are Going.
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