6±2.2 mg/day in 50 patients) or propranolol group (mean dose 153.5± 100.2 mg/day in 49 patients). After randomization, 8 patients and 11 patients AZD6244 mouse were dropped out in carvedilol and propranolol group, respectively. The response was defined to achieve a fall in HVPG to < 12 mmHg or a 20% reduction from baseline values 6weeks after treatment. Results: There were no significant differences between carvedilol and propranolol group in age, sex, etiology, Child-Turcott-Pugh score, MELD score, HVPG, presence of ascites and baseline serum parameters. In per-protocol analysis,

the response rate in carvedilol and propranolol group was 54.8% (23/42) and 45.2% (16/38), respectively (p=0.258). In intent-to-treat analysis, the response rate in carvedilol and propranolol group were 46.0% and 32.7%, respectively (p=0.174) and the mean decrease of HVPG was 15.6±18.1% and 8.1 ±30.1%, respectively (p=0.188). There was no significant difference in adverse events between two groups. Conclusions: In this interim analysis, low dose of carvedilol showed similar efficacy in reducing portal pressure compared to propranolol in cirrhotic AZD6738 in vitro patients with severe

portal hypertension. This study was entered in the Clinical Research Information Service (CRiS) Clinical Trial Registry (KCT0000102). Disclosures: The following people have nothing to disclose: Joo Hyun Sohn, Tae Yeob Kim, Soon Ho Um, Yeon Seok Seo, Soon Koo Baik, Moon Young Kim, Jae Young Jang, Soung Won Jeong, Young Seok Kim, Sang Gyune Kim, Dong Joon Kim, Ki tae Suk, Woo Kyoung Jeong Ribavirin is a synthetic guanosine ifoxetine analogue with mild, transient antiviral effect on hepatitis C virus (HCV) replication, that maintains biochemical and histological improvements in chronic hepatitis C patients not responding to standard treatment with interferon-alfa/ribavirin (Hepatology 2003; 38: 66).

We designed a proof-of-concept trial to evaluate whether maintenance treatment with ribavirin in non-responder hepatitis C virus (HCV) cirrhosis patients is associated to a reduction in portal pressure. Patients: 42 patients with genotype 1 HCV cirrhosis and portal hypertension (hepatic venous pressure gradient, HVPG, >6 mmHg) were randomized to receive for 6 months ribavirin (1000-1200 mg/day) or colchicine (0.5 mg/12 h) in open-label conditions (NCT00840489). We studied before and at the end of treatment splanchnic and systemic hemodynamics, aminotransferases, and HCV viremia. Malonyldialdehyde (MDA) was measured in hepatic vein as a surrogate of oxidative stress and inflammation. Results: Ribavirin significantly decreased HVPG (Table) and calculated hepatic vascular resistance. HVPG decreased by −7.8±15% in the ribavirin group, and increased by +13.7±36% in the colchicine group (p<0.01). Systemic hemodynamics did not change in either group. Ribavirin reduced hemoglobin (from 13.8±1.8 to 12.0±1.9 g/dl, p<0.