Vu et al. treated six patients with persistent kinase inhibitor Perifosine postsurgical bile leaks as a complication after hepatic lobectomy or cholecistectomy using NBCA glue for the obliteration of isolated segmental bile ducts in four cases [6]. Endoscopic treatment of biliary leakage by NBCA has been described by Seewald in nine patients in whom primary stent placement or nasobiliary drain was unsuccessful [7]. More recently, Romano et al. [8] described the use of a cyanoacrlylate in the treatment of a pancreatic fistula after distal pancreatectomy. The percutaneous interventional technique represents an effective valuable approach to reduce mortality and morbidity in the treatment of biliary complications after liver transplantation.

The use of NBCA in obliteration of a dilated bile duct seems to be a safe procedure with good results providing a less invasive option than hepatic resection above all in high-risk patients with posttransplant bile duct injuries, decreasing the morbidity associated with chronic external biliary drainage. Futher studies are needed to determine whether this approach is effective and safe and whether it could reduce hospital stay and costs. Abbreviations SLT: Split-liver transplantation GGT: g-glutamyl transpeptidase ALT: Alanine transaminase MRC: Magnetic resonance cholangiography PTC: Percutaneous transhepatic cholangiography NBCA: n-butyl cyanoacrylate
Hepatitis C virus (HCV) is the most common indication for liver transplantation (LT) in the US with almost universal recurrence following LT. The need for antiviral therapy is common with up to 30% of patients progressing to cirrhosis by 5 years [1].

Though the indication for antiviral therapy is based on histologic findings, the primary goal of treatment goal is serologically defined by a sustained viral response (SVR). The absence of HCV RNA in liver tissue at the end of treatment has been associated with SVR in HCV patients with chronic liver disease treated with interferon-based antiviral therapy [2]. A recently reported series in HCV LT patients suggested that the presence or absence of allograft HCV RNA following treatment predicted a relapse or SVR in patients with a loss of viremia at the end of treatment. All 7 patients with a negative hepatic HCV RT-PCR at the end of treatment had an SVR while 3 patients with HCV RT-PCR present had relapse [3].

However, SVR status has not uniformly resulted in histologic stabilization or fibrosis regression. It has been observed in a previous report that twenty percent Brefeldin_A of post LT HCV patients experienced fibrosis progression 3�C5 years following SVR [4, 5], while fibrosis regression has been described in treated patients without SVR [6]. Additionally, hepatic HCV RNA persistence has been described in patients with SVR [7]. The correlation of hepatic allograft HCV RNA detectability post LT with serum virologic endpoints and histologic outcomes remains uncertain.