Avasthi Deepti, Zerilli Nicholas, Shaikh Fahad, Jamil Taimoor, Ishtiaq Daniyal, Avasthi Salil
Internal Medicine, Mercy Health - St. Vincent's Medical Center, Toledo, USA.
Pulmonary and Critical Care Medicine, Mercy Health - St. Vincent's Medical Center, Toledo, USA.
Cureus. 2025 May 1;17(5):e83309. doi: 10.7759/cureus.83309. eCollection 2025 May.
Portal hypertension, a complication of chronic liver disease, results from an elevated pressure gradient between the portal vein and the inferior vena cava. While non-selective beta-blockers are established for reducing portal pressure, the efficacy of losartan, an angiotensin II receptor blocker, remains debated. This study evaluated losartan's impact on portal pressure and liver fibrosis in patients with cirrhosis and portal hypertension. The goal of this meta-analysis was to appraise evidence on the role of losartan in reducing portal pressure and associated clinical outcomes in cirrhotic patients with portal hypertension. A comprehensive literature search was conducted in PubMed, Cochrane Library, Medline, and Web of Science. All the research and literature review were conducted from August 20th, 2024, through August 31st, 2024 (within one month of the paper's submission). The Risk of Bias Visualization Tool (Robvis 2.0) and Risk Of Bias In Non-randomized Studies - of Interventions (ROBINS-I) were used to assess study quality. Data were extracted and analyzed using Microsoft Excel. Among 426 potential studies, 12 met the inclusion criteria. Both losartan and propranolol reduced hepatic venous pressure gradient (HVPG), with some studies suggesting a more pronounced effect of losartan. A meta-analysis found no significant difference in HVPG reduction (p = 0.22), but losartan significantly reduced wedged hepatic venous pressure (WHVP) compared to propranolol (p = 0.03). Losartan also affected mean arterial pressure, renal function, and hepatic fibrosis. Losartan shows potential in treating portal hypertension by reducing portal pressure and fibrosis. It may be particularly beneficial in the treatment of liver cirrhosis by addressing both hemodynamic and structural components and improving sodium handling in complex cases.
门静脉高压是慢性肝病的一种并发症，由门静脉与下腔静脉之间的压力梯度升高所致。虽然非选择性β受体阻滞剂已被证实可降低门静脉压力，但血管紧张素II受体阻滞剂氯沙坦的疗效仍存在争议。本研究评估了氯沙坦对肝硬化和门静脉高压患者门静脉压力和肝纤维化的影响。这项荟萃分析的目的是评估氯沙坦在降低门静脉高压的肝硬化患者门静脉压力及相关临床结局方面作用的证据。在PubMed、Cochrane图书馆、Medline和科学网进行了全面的文献检索。所有的研究和文献综述均在2024年8月20日至2024年8月31日期间进行（在论文提交后的一个月内）。使用偏倚风险可视化工具（Robvis 2.0）和非随机干预研究中的偏倚风险（ROBINS-I）来评估研究质量。使用Microsoft Excel提取和分析数据。在426项潜在研究中，12项符合纳入标准。氯沙坦和普萘洛尔均降低了肝静脉压力梯度（HVPG），一些研究表明氯沙坦的效果更显著。一项荟萃分析发现，在降低HVPG方面无显著差异（p = 0.22），但与普萘洛尔相比，氯沙坦显著降低了肝静脉楔压（WHVP）（p = 0.03）。氯沙坦还影响平均动脉压、肾功能和肝纤维化。氯沙坦在通过降低门静脉压力和纤维化来治疗门静脉高压方面显示出潜力。通过解决血流动力学和结构成分问题以及改善复杂病例中的钠处理，它在肝硬化治疗中可能特别有益。
