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INTRODUCTION: Antiviral therapy improves hepatic fibrosis and reduces hepatocellular carcinoma (HCC) incidence. This study aimed to evaluate whether on-therapy changes in scores for fibrosis index based on 4 factors and aspartate aminotransferase-to-platelet ratio index are associated with HCC development and establish an HCC risk score model incorporating noninvasive fibrosis marker (NFM) response. METHODS: This multicenter study recruited 5,147 patients with chronic hepatitis B (4,028 for derivation cohort and 1,119 for validation cohort) who were given entecavir/tenofovir for >12 months between 2007 and 2018. A risk prediction model for HCC was developed using predictors based on multivariable Cox models, and bootstrapping was performed for validation. RESULTS: The 10-year cumulative HCC incidence rates were 12.6% and 13.7% in the derivation and validation cohorts, respectively. The risk of HCC significantly differed with early NFM response, with a marked reduction in HCC risk in patients achieving a significant decrease in NFM by 12 months (P < 0.001). NFMresponse, sex, age, and cirrhosis were independently predictive of HCC. Wedeveloped the Fibrosis marker response, Sex, Age, and Cirrhosis (FSAC) score based on regression coefficients of each variable. For the 10-year prediction of HCC, FSAC showed higher C-index values than PAGE-B, modified PAGE-B, CU-HCC, and REACH-B (0.84 vs 0.77, 0.80, 0.77, and 0.67, respectively; all P < 0.005). The predictive performance of FSAC was corroborated in the validation cohort, with higher C-index than other models (all P < 0.050). DISCUSSION: On-therapy changes in NFM are an independent indicator of HCC risk. FSAC incorporating NFM response is a reliable risk score for risk estimation for HCC with better performance than other models. [ABSTRACT FROM AUTHOR]

Background/Aims Transarterial radioembolization (TARE) is a form of radiation therapy performed by selective intra-arterial injection of microspheres loaded with Yttrium-90. TARE is known to be effective in the management of unresectable hepatocellular carcinoma (HCC). The aim of this study is to identify prognostic factors for overall survival (OS) and time to progression (TTP) in patients with HCC undergoing TARE. Methods This study included 73 consecutive HCC patients who underwent TARE from July 2009 to January 2018. The tumor responses to TARE were assessed according to modified Response Evaluation Criteria in Solid Tumors. Results The patients' baseline characteristics were as follows: median age was 66 years, 74% of male. The median tumor size was 9 cm and 41% of the patients had tumors larger than 10 cm. Multifocal HCCs identified in 58% and 26% of the patients showed infiltrative tumor. Sixty-three percent of the patients did not have portal vein tumor thrombus (PVTT), 10% had VP 1-2, and 27% had VP 3-4 of PVTT. Among 73 patients, five (7%) obtained complete response and 25 (34%) showed partial response at 3 months after TARE. Median OS was 27.6 months and TTP was 3.2 months. Multivariate analysis revealed that the absence of PVTT (hazard ratio [HR], 0.137; 95% confidence interval [CI], 0.057 to 0.331; p<0.001) was independent factor for OS. The absence of PVTT (HR, 0.330; 95% CI, 0.172 to 0.632; p=0.001) and tumor diameter ≤10 cm (HR, 0.287; 95% CI, 0.135 to 0.611, p=0.001) were independent prognostic factors for TTP. Conclusions TARE is an effective therapy for patients with advanced HCC. Absence of PVTT before TARE is an independent predictive factor for both OS and TTP. [ABSTRACT FROM AUTHOR]

Background/Aims Pegylated interferon (PEG-IFN) treatment with a high rate of off-therapy host immune control is still an attractive treatment for chronic hepatitis B virus (HBV) infection. There remains uncertain about the prognosis of sustained responder after PEG-IFN treatment who do not need nucleos(t)ides (NAs). We investigated the long-term outcomes of PEG-IFN treatment focused on tolerant patients without NAs up to 13 years. Methods A consecutive 172 patients treated with PEG-IFN for chronic hepatitis B or compensated liver cirrhosis between 2005 and 2014 were enrolled and finally 122 patients who fully completed PEG-IFN treatment were analyzed. The definition of response for PEG-IFN treatment at 6months posttreatment were as follows: hepatitis B e antigen (HBeAg) positive patients, achieve both virologic response (VR; <2,000 IU/mL of HBV DNA) and serologic response (HBeAg loss or seroconversion); HBeAg negative patients, reach VR. During follow-up period, we analyzed the number of patients with HBsAg loss, starting NAs due to viral activation and disease progression including liver cirrhosis and hepatocellular carcinoma (HCC). Results The median follow-up period of 122 patients were 7.2 years (range, 1.1 to 13.2 years). Of 122 patients, 43 patients (35.2%) had a response at 6 months posttreatment. During follow-up, 69 patients (56.6%) started NAs and the patients who had a response for PEG-IFN significantly lower rate of starting NAs (14/43 vs 55/79, p<0.001). HBsAg loss occurred in nine patients (7.4%) and sustained responders without further NAs treatment had significantly high rate of HBsAg loss compared to the patients with starting NAs (13.2% vs 2.9%, p=0.01). Eight patients (6.6%) developed disease progression including HCC (n=3). All of them were nonsustained responders who started NAs after PEG-IFN therapy compared to sustained responders (p=0.03). Conclusions Sustained responders without further NAs treatment after PEG-IFN treatment had a favorable clinical outcome in HBsAg loss and no disease progression up to 13 years. [ABSTRACT FROM AUTHOR]

Background/Aims Nonalcoholic fatty liver disease (NAFLD) is a metabolic-related disorder ranging from steatosis to steatohepatitis which may progress to fibrosis, cirrhosis and hepatocellular carcinoma. Micro RNAs (miRNAs) are important posttranscriptional regulators of gene expression, and the dysregulation of miRNAs is involved in various biological processes in the liver, including lipid homeostasis, inflammation, apoptosis, and cell proliferation. This study aimed at suggesting the miRNAs may be a biomarker of the fat accumulation and inflammation in NAFLD. Methods We use male mice of 6- to 8-week old had fed normal diet or 60% high fat diet for 3 months and 6 months. The accumulation of lipid in liver was examined by hematoxylin and eosin stain (H&E stain). We used human liver cell lines loaded with free fatty acids. And we performed quantitative real-time reverse transcriptase polymerase chain reaction and Western blotting for the validation of miRNAs and lipid droplets formation markers. Results miRNAs levels were identified in NAFLD in vivo and in vitro model. In the high fat diet group, liver index and body weigh were increased. H&E stain results show that high fat diet groups had accumulated lots of fat. And in the high fat diet group, lipid droplets formation markers and inflammation markers were increased. In NAFLD in vitro model, lipid droplets formation markers and inflammation markers were increased. miRNA level of miR-26a, miR-26b, let-7f and miR-22 was increased in the NAFLD in vivo and in vitro model. But, level of miR-101 was decreased in the NAFLD in vivo ad in vitro model. Conclusions In this study we evaluated the level of miRNAs on lipid metabolism using the in vitro and in vivo NAFLD model. Our results demonstrate that miRNAs may be a biomarker in NAFLD. [ABSTRACT FROM AUTHOR]