Pathophysiology of portal hypertension and implications for its pharmacological control.

Abstract

Bleeding from esophageal varices complicating portal hypertension is a major cause of morbidity and mortality in patients with chronic liver disease. Therapy has been directed towards obliteration of esophageal varices (endoscopic sclerotherapy, transhepatic sclerosis, or esophageal transection) or decompression of the portal vascular bed by the creation of surgical portasystemic shunts. The use of pharmacological agents to lower portal venous pressure (PVP) was for many years limited to intravenous or intraarterial vasopressin in the setting of acute variceal hemorrhage. However, since Lebrec et al.,1 reported the favourable effect of propranolol on PVP and on the incidence of rebleeding from the upper gastrointestinal tract in patients with portal hypertension,2 there has been an increasing interest in the potential use of a number of pharmacological agents in the short and long term management of patients with portal hypertension. The purpose of such therapy would be to reduce the incidence of complications of portal hypertension. These may include upper gastrointestinal bleeding, ascites via reduced ascitic fluid formation, and even portasystemic encephalopathy via improvement of hepatic perfusion and reduction of collateral shunting of blood.