Pathophysiology of portal hypertension in HCV-related cirrhosis - Putative role of assessment of portal pressure gradient in Peginterferon-treated patients

Chronic HCV infection is the leading aetiologic factor for cirrhosis, end-stage liver disease, hepatocellular carcinoma and liver transplantation worldwide. Pegylation of alfa interferons has improved the management of this disease. Interferon treatment has antifibrotic and immunomodulatory activities. Recent evidence supports the contention that Hepatitis C virus-related cirrhosis of the liver should no more be considered an irreversible disease; fibrosis is a potentially reversible process. Fibrosis and even cirrhosis reversal have been previously demonstrated either in experimental or clinical studies of other liver diseases. Development of portal hypertension is the main drive to the complications of advanced liver diseases: prognosis worsens significantly when portal hypertension becomes clinically significant. It is thus conceivable that within therapeutic trials involving patients with advanced fibrosis of the liver, measurement of the hepatic venous pressure gradient, the gold standard in the clinical assessment of portal hypertension and its management, could provide information on the portal pressure-lowering effects of interferon treatment affecting the fibrosis score. This can be accomplished by either sustained virological response either by fibrosis reduction achieved by chronic low-dose Peginterferon administration. If the introduction of drug therapy with non-selective beta blockers in the treatment of portal hypertension represents a milestone in the treatment of patients with cirrhosis and high-degree portal hypertension, the next step must then be prophylactic reversal of initial portal hypertension prompted by either HCV eradication and pharmacological inhibition of fibrosis progression by long-term Peginterferon before higher degrees of portal hypertension ensue. (C) 2005 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.