10 Importantly, they found reversal of cirrhosis in 75 of 153 (49%) patients. Similar improvements in histology with SVR have been reported by others as well.11, 12 In addition to improvements in fibrosis, antiviral therapy may also directly affect HVPG. Rincon et al. studied 20 compensated patients with advanced fibrosis, by using liver biopsy and hepatic pressure measurements before and immediately after therapy with pegylated interferon and ribavirin.13

They found that all but one patient had a significant decrease in HVPG from baseline following antiviral mTOR inhibitor therapy and that those with SVR had a greater reduction than those with nonresponse. The benefits of reductions in HVPG with SVR were confirmed by Roberts et al. in 47 patients with cirrhosis.14 Although the Hepatitis C Antiviral Long-Term Treatment Against Cirrhosis (HALT-C) trial did not show overall benefit of maintenance interferon,15 improved clinical outcomes Saracatinib mw were observed in those with significant viral suppression without SVR.16 Taken collectively, these data suggest that those with chronic HCV and advanced fibrosis who achieve SVR have reduced clinical outcomes, including variceal bleeding.9 However,

the impact of SVR on the de novo development of varices was not specifically assessed in these analyses and remains unknown. In this issue of HEPATOLOGY, Bruno et al. addressed the impact of SVR on the development of esophageal varices in a subgroup analysis of a large prospective database of subjects with compensated HCV-induced cirrhosis.17 In this

study, consecutive HCV-positive subjects seen between January 1989 and December 1992 with compensated, Child A Meloxicam cirrhosis were screened for varices. Those with hepatitis B, human immunodeficiency virus, prior history of decompensation, or HCC within 6 months were excluded. Among the 352 patients screened, 218 who were free of varices at baseline and agreed to have follow-up endoscopy were included in the analysis. All 218 subjects had regular follow-up with surveillance ultrasound for HCC every 6 months and endoscopy every 3 years to identify de novo varices. Patients received HCV therapy as determined by current practice at that time, and SVR was defined as negative HCV RNA at 6 months after stopping therapy. The primary endpoints were development of de novo varices or HCC. Of the 218 patients, 149 (68%) received HCV therapy and 23% had SVR. During the median follow-up of 11.4 years, de novo varices developed in 67 patients and was similar in untreated (22 of 69, 32%) and treated (45 of 115, 32%) patients. The distribution of varices were small (F1, 76%) while 12% each had moderate (F2) or large (F3) varices. The median time between enrollment and detection of F3 varices (5 of 8 that bled) was 8 years (range, 3-17).