Purpose: To elucidate the natural history of hypovascular nodules that appear hypointense on hepatocyte-phase gadoxetic acid-enhanced MR images by focusing on hypervascularization over time. Materials and Methods:In this study, 135 hypovascular nodules revealing no gadoxetic acid uptake in 53 patients were examined. All nodules were retrospectively examined using serial follow-up computed tomography (CT) and MRI examinations until hypervascularity was observed on arterial-phase dynamic CT or gadoxetic acid-enhanced MR images, or on CT during hepatic arteriography. Logistic regression analysis was used to investigate the association between hypervascularization and MR findings including a presence of fat assessed by a signal drop on opposed-phase T1-weighted images.Results: Of the 135 nodules, 16 underwent hypervascularization. The size of the nodules and the presence of fat in the nodules were independent indicators of hypervascularization. The 1-year cumulative risk of hypervascularization was 15.6%. This risk was significantly increased in the case of nodules >10 mm (37.6%, P < 0.01) and fatcontaining nodules (26.5%, P < 0.01).Conclusion: Hypovascular nodules that appear hypointense on hepatocyte-phase gadoxetic acid-enhanced MR images may progress to conventional hypervascular hepatocellular carcinoma. Nodules more than 10 mm in diameter and containing fat are at high risk for developing hypervascularization.

administration of double dose of Gd-EOB-DTPA provided better arterial enhancement of hepatocellular carcinomas in patients with chronic liver disease, and also improved the lesion-liver contrast in hepatocyte-phase images in patients with Child-Pugh class B disease.

Recently, microdomains of organelle membranes rich in sphingomyelin and cholesterol (called "lipid rafts") have been considered to act as a scaffold for the hepatitis C virus (HCV) replication complex. Using the HCV cell culture system, we investigated the effect of myriocin, a sphingomyelin synthesis inhibitor, on HCV replication. We also investigated the combined effect of myriocin with interferon (IFN) and myriocin with simvastatin. Myriocin suppressed replication of both a genotype 1b subgenomic HCV replicon (Huh7/Rep-Feo) and genotype 2a infectious HCV (JFH-1 HCV) in a dose-dependent manner (for subgenomic HCV-1b, maximum of 79% at 1000 nmol/L; for genomic HCV-2a, maximum of 40% at 1000 nmol/L). Combination treatment with myriocin and IFN or myriocin and simvastatin attenuated HCV RNA replication synergistically in Huh7/Rep-Feo cells. Our data demonstrate that the sphingomyelin synthesis inhibitor strongly suppresses replication of both the subgenomic HCV-1b replicon and the JFH-1 strain of genotype 2a infectious HCV, indicating that lipid metabolism could be a novel target for HCV therapy.

Y93H was detected frequently by deep sequencing in daclatasvir treatment-naïve patients. Importantly, it seems that the IL28B status of the patients may influence the presence of Y93H mutations, resulting in different treatment responses to daclatasvir.

Aim: Although the viral markers hepatitis B surface antigen (HBsAg) and hepatitis B core-related antigen (HbcrAg) could reflect intrahepatic hepatitis B virus (HBV) replication activity and constitute important biomarkers for hepatocellular carcinoma (HCC), the value of using these two markers in combination for assessing HCC risk has not been clarified in detail.Methods: Four hundred and forty-nine consecutive patients with chronic HBV infection were included in the study and the association of HBsAg and HBcrAg with HCC risk was investigated cross-sectionally, as well as longitudinally. Conclusions:Patients with low HBsAg/high HBcrAg values are at high risk of developing HBV-related HCC, according to this cross-sectional and longitudinal analysis, indicating that the combination of HBsAg and HBcrAg values is an excellent biomarker for assessing HCC risk.These authors contributed equally to this work.