González-Reimers Emilio, Quintero-Platt Geraldine, Martín-González Candelaria, Pérez-Hernández Onán, Romero-Acevedo Lucía, Santolaria-Fernández Francisco
Emilio González-Reimers, Geraldine Quintero-Platt, Candelaria Martín-González, Onán Pérez-Hernández, Lucía Romero-Acevedo, Francisco Santolaria-Fernández, Servicio de Medicina Interna, Hospital Universitario de Canarias, Universidad de La Laguna, Tenerife, 38320 Canary Islands, Spain.
World J Gastroenterol. 2016 May 14;22(18):4427-37. doi: 10.3748/wjg.v22.i18.4427.
Hepatitis C virus (HCV) infection is associated with increased thrombotic risk. Several mechanisms are involved including direct endothelial damage by the HCV virus, with activation of tissue factor, altered fibrinolysis and increased platelet aggregation and activation. In advanced stages, chronic HCV infection may evolve to liver cirrhosis, a condition in which alterations in the portal microcirculation may also ultimately lead to thrombin activation, platelet aggregation, and clot formation. Therefore in advanced HCV liver disease there is an increased prevalence of thrombotic phenomena in portal vein radicles. Increased thrombin formation may activate hepatic stellate cells and promote liver fibrosis. In addition, ischemic changes derived from vascular occlusion by microthrombi favor the so called parenchymal extinction, a process that promotes collapse of hepatocytes and the formation of gross fibrous tracts. These reasons may explain why advanced HCV infection may evolve more rapidly to end-stage liver disease than other forms of cirrhosis.
丙型肝炎病毒（HCV）感染与血栓形成风险增加有关。涉及多种机制，包括HCV病毒对内皮细胞的直接损伤，伴有组织因子激活、纤维蛋白溶解改变以及血小板聚集和激活增加。在晚期，慢性HCV感染可能发展为肝硬化，在这种情况下，门静脉微循环的改变最终也可能导致凝血酶激活、血小板聚集和血栓形成。因此，在晚期HCV肝病中，门静脉分支血栓形成现象的发生率增加。凝血酶形成增加可能激活肝星状细胞并促进肝纤维化。此外，微血栓导致的血管闭塞引起的缺血性改变有利于所谓的实质细胞消亡，这一过程促进肝细胞塌陷和粗大纤维束的形成。这些原因可能解释了为什么晚期HCV感染比其他形式的肝硬化更易迅速发展为终末期肝病。
