Portal hypertension (PHT) is a frequent and severe complication of cirrhosis. PHT may lead to the development of various complications with high mortality. Liver transplantation is the gold standard as a surgical curative treatment for end-stage liver disease. Theoretically, etiological treatment focusing on the pathophysiology of the underlying disease should be the objective of the nonsurgical management of cirrhotic PHT. Chronic viral hepatitis is the major etiology of cirrhosis and PHT. In cirrhotic patients with chronic hepatitis B virus infection, antiviral therapies can suppress viral replication, ameliorate hepatic inflammation, regress fibrosis, and restore liver functional reserve. Moreover, they can delay the progression of liver cirrhosis and ameliorate the severity of PHT. In patients with hepatitis C virus-induced liver cirrhosis, interferon and ribavirin combination therapy provide a favorable long-term prognosis, including lower rates of liver-related and non-liver-related deaths, hepatic decompensation, and hepatocellular carcinoma, particularly in those who have successful eradication of the virus after therapy. In patients with PHT, direct antivirals (DAAs) for hepatitis C virus infection have good safety profiles and excellent viral suppression. Moreover, DAAs can reduce hepatic venous pressure gradient. However, these effects are stronger during the earlier stage of liver cirrhosis. Abstinence is the cornerstone of etiological treatment for alcoholic liver disease. The effects of pharmacological treatments are not satisfactory, and additional studies are mandatory.
Keywords: Alcoholic liver disease; Hepatitis B; Hepatitis C; Liver cirrhosis; Portal hypertension.