Triglyceride-Glucose Index is an Independent Risk Factor for Hepatocellular Carcinoma Development in Patients with HBV-Related Liver Cirrhosis.

Aim: This study aimed to explore the effects of the triglyceride-glucose (TyG) index on hepatocellular carcinoma (HCC) development in patients with hepatitis B virus (HBV)-related liver cirrhosis (LC). Methods: A total of 242 patients with HBV-related LC were enrolled and followed-up. Logistic regression analysis was performed to investigate risk factors for HCC. Results: The median follow-up time was 37 months (range: 6-123 months). At the end of the follow-up, 11 (11.3%) patients with compensated cirrhosis (CC) and 45 (31.0%) with decompensated cirrhosis (DC) developed HCC. The TyG index was higher in the HCC group than in the non-HCC group (P=0.05). Univariate analysis showed that age (P<0.01), DC (P<0.01), TyG index (P=0.08), albumin (ALB) level (P=0.05), platelet (PLT) count (P<0.01), and HBV DNA positivity (P<0.01) were associated with HCC development. Multivariate analysis revealed that age, DC, TyG index, PLT count, and HBV DNA positivity were independent risk factors for HCC development (P=0.01, 0.01, <0.01, 0.05, and <0.01, respectively). For patients with DC, multivariate logistic regression analysis revealed that age, TyG index, and HBV DNA positivity were independent risk factors for HCC development (all P<0.05). A new model encompassing age, DC, TyG, PLT, and positive HBV DNA had optimal predictive accuracy in patients with DC or CC, with a cutoff value of 0.197. The areas under the receiver operating characteristic curves (AUROCs) of the model for predicting HCC development in patients with LC, DC, and CC were 0.778, 0.721, and 0.783, respectively. Conclusion: TyG index was identified as an independent risk factor for HCC development in patients with LC.

A new model predicts hepatocellular carcinoma in patients with HBV-related decompensated liver cirrhosis and long-term antiviral therapy: a prospective study.

Background: We aimed to evaluate the prediction values of non-invasive models for hepatocellular carcinoma (HCC) development in patients with HBV-related liver cirrhosis (LC) and long-term NA treatment. Methods: Patients with compensated or decompensated cirrhosis (DC), who achieved long-term virological response, were enrolled. DC and its stages were defined by the complications including ascites, encephalopathy, variceal bleeding, or renal failure. Prediction accuracy of several risk scores, including ALBI, CAMD, PAGE-B, mPAGE-B and aMAP, was compared. Results: The median follow-up duration was 37 (28-66) months. Among the 229 patients, 9 (9.57%) patients in the compensated LC group and 39 (28.89%) patients in the DC group developed HCC. The incidence of HCC was higher in the DC group ( X 2 = 12.478, P < 0.01). The AUROC of ALBI, aMAP, CAMD, PAGE-B and mPAGE-B scores were 0.512, 0.667, 0.638, 0.663, 0.679, respectively. There was no significant difference in AUROC between CAMD, aMAP, PAGE-B and mPAGE-B (all P > 0.05). Univariable analysis showed that age, DC status and platelet were associated with HCC development, and multivariable analysis showed that age and DC status (both P < 0.01) were independent risk factors for HCC development, then Model (Age_DC) was developed and its AUROC was 0.718. Another model, Model (Age_DC_PLT_TBil) consisting of age, DC stage, PLT, TBil was also developed, and its AUROC was larger than that of Model (Age_DC) (0.760 vs. 0.718). Moreover, AUROC of Model (Age_DC_PLT_TBil) was larger than the other five models (all P < 0.05). With an optimal cut-off value of 0.236, Model (Age_DC_PLT_TBil) achieved 70.83% sensitivity, 76.24% specificity. Conclusion: There is a lack of non-invasive risk scores for HCC development in HBV-related DC, and a new model consisting of age, DC stage, PLT, TBil may be an alternative.

Incident hepatocellular carcinoma developing during tenofovir alafenamide treatment as a rescue therapy for multi-drug resistant hepatitis B virus infection: A case report and review of the literature.

Tenofovir disoproxil fumarate (TDF) is a potent nucleotide analogue with high barrier to resistance, which is recommended for multi-drug resistant hepatitis B virus (HBV) infection. However, nephrotoxicity has been reported during TDF treatment, and tenofovir alafenamide (TAF), which has comparable efficacy to TDF and improves bone and renal safety, can be used as a replacement strategy. Herein, we describe a clinical case concerning a 60-year-old individual suffering liver cirrhosis and renal dysfunction, and being infected with multidrug-resistant HBV. When failing treatment with TDF, he received TAF as a rescue therapy. TAF effectively inhibited HBV replication without worsening renal function or serum phosphorus abnormality. Furthermore, hepatocellular carcinoma (HCC) occurred during TAF treatment despite controlling the viral load. The risk of HCC could not be eliminated and should be monitored during TAF treatment.

Asialoglycoprotein receptor interacts with the preS1 domain of hepatitis B virus in vivo and in vitro.

BACKGROUND: The preS1 domain of the large envelope protein has been identified as an essential viral structure involved in hepatitis B virus (HBV) attachment. However, the cellular receptor(s) for HBV has not yet been identified. AIMS: To identify a cell-surface receptor for HBV, which could elucidate the molecular mechanism of HBV infection. METHODS: A novel yeast two-hybrid system was used to screen proteins interacting with the preS1 region of HBV. Their interaction was verified by yeast cotransformation, coimmunoprecipitation and mammalian two-hybrid assay, while their intracellular and tissue localization was analyzed by confocal microscopy and immunohistochemistry, respectively. RESULTS: Asialoglycoprotein receptor (ASGPR) interacted specifically and directly with the preS1 domain of HBV in vivo and in vitro. The levels of expression of preS1 and ASGPR in the liver were similar and correlated with each other. CONCLUSIONS: ASGPR is a candidate receptor for HBV that mediates further steps of HBV entry.