Division of Gastroenterology, Hepatology and Nutrition, Department of Internal Medicine, The University of Texas Health Science Center at Houston, 6431 Fannin Street, MSB 4.234, Houston, TX 77030-1501, USA.
Nat Rev Gastroenterol Hepatol. 2012 Sep;9(9):539-49. doi: 10.1038/nrgastro.2012.123. Epub 2012 Jul 3.
Hepatopulmonary syndrome (HPS) is a serious vascular complication of liver disease that occurs in 5-32% of patients with cirrhosis. The presence of HPS markedly increases mortality. No effective medical therapies are currently available and liver transplantation is the only established treatment option for HPS. The definition and diagnosis of HPS are established by the presence of a triad of liver disease with intrapulmonary vascular dilation that causes abnormal arterial gas exchange. Experimental biliary cirrhosis induced by common bile duct ligation in the rat reproduces the pulmonary vascular and gas exchange abnormalities of human HPS and serves as a pertinent animal model. Pulmonary microvascular dilation and angiogenesis are two central pathogenic features that drive abnormal pulmonary gas exchange in experimental HPS, and thus might underlie HPS in humans. Defining the mechanisms involved in the microvascular alterations of HPS has the potential to lead to effective medical therapies. This Review focuses on the current understanding of the pathogenesis, clinical features and management of HPS.
肝肺综合征(HPS)是肝脏疾病的一种严重血管并发症,发生于 5-32%的肝硬化患者中。HPS 的存在显著增加了死亡率。目前尚无有效的医学治疗方法,肝移植是 HPS 的唯一既定治疗选择。HPS 的定义和诊断是通过存在肝病三联征和肺内血管扩张来确定的,这会导致动脉气体交换异常。在大鼠中通过胆总管结扎诱导的实验性胆汁性肝硬化再现了人类 HPS 的肺血管和气体交换异常,是一种相关的动物模型。肺微血管扩张和血管生成是驱动实验性 HPS 中异常肺气体交换的两个中心致病特征,因此可能是人类 HPS 的基础。确定 HPS 微血管改变所涉及的机制有可能导致有效的医学治疗方法。这篇综述重点介绍了对 HPS 的发病机制、临床特征和治疗的最新理解。