医学
肝移植
肝病
凝血病
凝血因子
内科学
纤溶
肝功能
移植
因子V
血小板生成素
胃肠病学
凝结
门脉高压
免疫学
肝硬化
血栓形成
生物
造血
遗传学
干细胞
标识
DOI:10.3748/wjg.v12.i48.7725
摘要
The liver is an essential player in the pathway of coagulation in both primary and secondary haemostasis.Only von Willebrand factor is not synthetised by the liver, thus liver failure is associated with impairment of coagulation.However, recently it has been shown that the delicate balance between pro and antithrombotic factors synthetised by the liver might be reset to a lower level in patients with chronic liver disease.Therefore, these patients might not be really anticoagulated in stable condition and bleeding may be caused only when additional factors, such as infections, supervene.Portal hypertension plays an important role in coagulopathy in liver disease, reducing the number of circulating platelets, but platelet function and secretion of thrombopoietin have been also shown to be impaired in patients with liver disease.Vitamin K deficiency may coexist, so that abnormal clotting factors are produced due to lack of gamma carboxylation.Moreover during liver failure, there is a reduced capacity to clear activated haemostatic proteins and protein inhibitor complexes from the circulation.Usually therapy for coagulation disorders in liver disease is needed only during bleeding or before invasive procedures.When end stage liver disease occurs, liver transplantation is the only treatment available, which can restore normal haemostasis, and correct genetic clotting defects, such as haemophilia or factor V Leiden mutation.During liver transplantation h a e m o r ra g e m a y o c c u r d u e t o t h e p r e -e x i s t i n g hypocoagulable state, the collateral circulation caused by portal hypertension and increased fibrinolysis which occurs during this surgery.
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