Hepatic Hemodynamic Laboratory, Liver Unit, Hospital Clínic-IDIBAPS, University of Barcelona, C.Villarroel 170, 08036, Barcelona, Spain.
Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBEREHD), Instituto de Salud Carlos III, Barcelona, Spain.
Hepatol Int. 2018 Feb;12(Suppl 1):1-10. doi: 10.1007/s12072-017-9827-9. Epub 2017 Oct 24.
Portal hypertension is a key complication of portal hypertension, which is responsible for the development of varices, ascites, bleeding, and hepatic encephalopathy, which, in turn, cause a high mortality and requirement for liver transplantation.
This review deals with the present day state-of-the-art preventative treatments of portal hypertension in cirrhosis according to disease stage. Two main disease stages are considered, compensated and decompensated cirrhosis, the first having good prognosis and being mostly asymptomatic, and the second being heralded by the appearance of bleeding or non-bleeding complications of portal hypertension.
The aim of treatment in compensated cirrhosis is preventing clinical decompensation, the more frequent event being ascites, followed by variceal bleeding and hepatic encephalopathy. Complications are mainly driven by an increase of hepatic vein pressure gradient (HVPG) to values ≥10 mmHg (defining the presence of Clinically Significant Portal Hypertension, CSPH). Before CSPH, the treatment is limited to etiologic treatment of cirrhosis and healthy life style (abstain from alcohol, avoid/correct obesity…). When CSPH is present, association of a non-selective beta-blocker (NSBB), including carvedilol should be considered. NSBBs are mandatory if moderate/large varices are present. Patients should also enter a screening program for hepatocellular carcinoma. In decompensated patients, the goal is to prevent further bleeding if the only manifestation of decompensation was a bleeding episode, but to prevent liver transplantation and death in the common scenario where patients have manifested first non-bleeding complications. Treatment is based on the same principles (healthy life style..) associated with administration of NSBBs in combination if possible with endoscopic band ligation if there has been variceal bleeding, and complemented with simvastatin administration (20-40 mg per day in Child-Pugh A/B, 10-20 mg in Child C). Recurrence shall be treated with TIPS. TIPS might be indicated earlier in patients with: 1) Difficult/refractory ascites, who are not the best candidates for NSBBs, 2) patients having bleed under NSBBs or showing no HVPG response (decrease in HVPG of at least 20% of baseline or to values equal or below 12 mmHg). Decompensated patients shall all be considered as potential candidates for liver transplantation.
Treatment of portal hypertension has markedly improved in recent years. The present day therapy is based on accurate risk stratification according to disease stage.
门静脉高压是门静脉高压的一个关键并发症，它导致静脉曲张、腹水、出血和肝性脑病的发展，进而导致高死亡率和需要进行肝移植。
本综述根据疾病阶段讨论了目前肝硬化门静脉高压的预防治疗方法。主要考虑两种疾病阶段，代偿期和失代偿期肝硬化，前者预后良好，大多无症状，后者以门静脉高压的出血或非出血并发症的出现为特征。
代偿期肝硬化的治疗目的是预防临床失代偿，更常见的事件是腹水，其次是静脉曲张出血和肝性脑病。并发症主要是由于肝静脉压力梯度（HVPG）增加到≥10mmHg（定义为存在临床显著门静脉高压，CSPH）。在 CSPH 之前，治疗仅限于肝硬化的病因治疗和健康的生活方式（戒酒、避免/纠正肥胖等）。当存在 CSPH 时，应考虑使用非选择性β受体阻滞剂（NSBB），包括卡维地洛。如果存在中/大静脉曲张，NSBB 是必需的。患者还应进入肝细胞癌筛查计划。在失代偿期患者中，如果唯一的失代偿表现是出血发作，则目标是预防进一步出血，但在患者首先出现非出血并发症的常见情况下，目标是预防肝移植和死亡。治疗基于相同的原则（健康的生活方式……），如果可能，将 NSBB 与内镜套扎联合使用，如果存在静脉曲张出血，则联合给予辛伐他汀（Child-Pugh A/B 患者每天 20-40mg，Child C 患者每天 10-20mg）。复发应用 TIPS 治疗。对于以下患者，TIPS 可能更早适用：1）难治性腹水患者，他们不是 NSBB 的最佳人选，2）在 NSBB 下出血或 HVPG 无反应（HVPG 下降至少基线的 20%或下降到等于或低于 12mmHg）的患者。所有失代偿期患者均应被视为肝移植的潜在候选者。
近年来，门静脉高压的治疗有了显著改善。目前的治疗方法是根据疾病阶段进行准确的风险分层。
