Risk factors for the exacerbation of esophageal varices or portosystemic encephalopathy after sustained virological response with IFN therapy for HCV-related compensated cirrhosis

Abstract

We aimed to identify risk factors contributing to the exacerbation of esophageal varices (EV) or portosystemic encephalopathy after hepatitis C virus (HCV) eradication with interferon (IFN) therapy in patients with compensated cirrhosis. Also, the prognosis after HCV eradication was analyzed. Fifty-two patients with sustained virological response to IFN treatment for HCV-related compensated cirrhosis were enrolled in this retrospective cohort study. At the achievement of HCV eradication, in 31 of the 52 patients (60%), feeding vessels for EVs (left gastric vein, posterior gastric vein, short gastric vein) were shown, and in 18 patients (35%) there were extrahepatic portosystemic shunts (paraesophageal vein, paraumbilical vein, and splenorenal shunt). Although the HCV eradication was successful, significant improvements were not observed in portosystemic collateral vessels 1year after HCV eradication, and EVs were exacerbated in 19 (36%) patients. The cumulative 1- and 3-year rates of EV exacerbation were 13% and 49%, respectively. By multivariate analysis, the existence of feeding vessels for EVs at HCV eradication was an independent predictive factor for the exacerbation of EVs (P=0.009). Seven patients who had an extrahepatic portosystemic shunt at HCV eradication developed portosystemic encephalopathy during follow up. The 1-, 3-, and 5-year incidences of portosystemic encephalopathy were 6, 21, and 34%, respectively. The cumulative 5-year survival rate of the cohort was 81%. Two patients died of hepatocellular carcinoma (HCC). Our findings suggest that the existence of radical portosystemic collateral vessels at successful HCV eradication increases the risk of the exacerbation of EVs and the incidence of portosystemic encephalopathy in patients with HCV-related cirrhosis.