Changing incidence of reported viral hepatitis in China from 2004 to 2016: an observational study.

OBJECTIVE: China's national hepatitis burden is high. This study aims to provide a detailed national-level description of the reported incidence of viral hepatitis in China during 2004-2016. DESIGN: Observational study. SETTING: Data were obtained from China's National Notifiable Disease Reporting System, and changing trends were estimated by joinpoint regression analysis. PARTICIPANTS: In this system, 16 927 233 reported viral hepatitis cases occurring during 2004-2016 were identified. PRIMARY OUTCOME MEASURE: Incidence rates per 100 000 person-years and changing trends were calculated. RESULTS: There were 16 927 233 new cases of viral hepatitis reported in China from 2004 to 2016. Hepatitis B (HBV) (n=13 543 137, 80.00%) and hepatitis C (HCV) (n=1 844 882, 10.90%) accounted for >90% of the cases. The overall annual percent change (APC) in reported cases of viral hepatitis and HBV were 0.3%(95% CI -2.0 to 0.8, p=0.6) and -0.2% (95% CI -1.6 to 1.2, p=0.8), respectively, showing a stable trend. HBV rates were highest in the 20-29 year old age group and lowest in younger individuals, likely resulting from the universal HBV vaccination. The reported incidence of HCV and hepatitis E (HEV) showed increasing trends; the APCs were 14.5% (95% CI 13.1 to 15.9, p<0.05) and 4.7% (95% CI 2.8 to 6.7, p<0.05), respectively. The hepatitis A (HAV) reporting incidence decreased, and the APC was -13.1% (95% CI -15.1 to -11.0, p<0.05). There were marked differences in the reporting of hepatitis among provinces. CONCLUSIONS: HBV continues to constitute the majority of viral hepatitis cases in China. Over the entire study period, the HBV reporting incidence was stable, the HCV and HEV incidence increased and the HAV incidence decreased. There were significant interprovincial disparities in the burden of viral hepatitis, with higher rates in economically less-developed areas. Vaccination is important for viral hepatitis prevention and control.

IL28B Is Associated with Outcomes of Chronic HBV Infection

PURPOSE: The role of IL28B gene variants and expression in hepatitis B virus (HBV) infections are not well understood. Here, we evaluated whether IL28B gene expression and rs12979860 variations are associated with HBV outcomes. MATERIALS AND METHODS: IL28B genetic variations (rs12979860) were genotyped by pyrosequencing of DNA samples from 137 individuals with chronic HBV infection [50 inactive carriers (IC), 34 chronic hepatitis B (CHB), 27 cirrhosis, 26 hepatocellular carcinoma (HCC)], and 19 healthy controls. IL28A/B mRNA expression in peripheral blood mononuclear cells was determined by qRT-PCR, and serum IL28B protein was measured by ELISA. RESULTS: Patients with IL28B C/C genotype had greater IL28A/B mRNA expression and higher IL28B protein levels than C/T patients. Within the various disease stages, compared to IC and healthy controls, IL28B expression was reduced in the CHB, cirrhosis, and HCC cohorts (CHB vs. IC, p=0.02; cirrhosis vs. IC, p=0.01; HCC vs. IC, p=0.001; CHB vs. controls, p<0.01; cirrhosis vs. controls, p<0.01; HCC vs. controls, p<0.01). When stratified with respect to serum HBV markers in the IC and CHB cohorts, IL28B mRNA and protein levels were higher in HBeAg-positive than negative individuals (p=0.01). Logistic regression analysis revealed that factors associated with high IL28B protein levels were C/C versus C/T genotype [p=0.016, odds ratio (OR)=0.25, 95% confidence interval (CI)=0.08-0.78], high alanine aminotransferase values (p<0.001, OR=8.02, 95% CI=2.64-24.4), and the IC stage of HBV infection (p<0.001). CONCLUSION: Our data suggest that IL28B genetic variations may play an important role in long-term development of disease in chronic HBV infections.

Predicting Hepatocellular Carcinoma Recurrence and Survival.

BACKGROUND/AIMS: Beta blockers can inhibit tumor growth and metastases, while necroinflammation can enhance these tumor properties. The aim of this study was to determine whether beta blockers and necroinflammatory disease predict tumor recurrence and/or overall survival following potentially curative therapeutic interventions for patients with hepatocellular carcinoma (HCC). METHODOLOGY: The medical records of 36 adults with non-metastatic HCC who had undergone surgical resections and/or radiofrequency ablation (RFA) were retrospectively reviewed. In addition to post-intervention beta blocker usage and serum alanine aminotransferase levels greater than 2xULN, other variables commonly associated with recurrences such as number and size of tumors, state of differentiation and vascular invasion were included in univariate and multivariate analyses for recurrence and survival. RESULTS: Vascular invasion (OR 29.3, 95% CI 2.6-33.6) and surgical resection (OR 0.19, 95% CI 0.04-0.90) emerged from univariate (p = 0.003 and 0.03 respectively) and multivariate (p = 0.005 and 0.048 respectively) regression as predictors of tumor recurrence whereas beta blocker usage (OR 0.03, 95% CL 0.04-0.9, p = 0.03) and tumor recurrence (OR 6.7, 95% CI 1.6-28.1, p = 0.026) correlated with overall mortality. CONCLUSIONS: Neither beta blocker usage nor serum ALT levels predict HCC recurrences, but beta blocker usage is associated with improved overall survival following potentially curative therapeutic interventions for HCC in adults.

Apoptotic and survival signals in hepatic stellate cells / 中南大学学报(医学版)

Hepatic stellate cells (HSCs) play an important role in hepatic fibrogenesis.In response to liver injury, HSCs undergo a process called activation, which involves 2 stepsinitiation from quiescent phenotype to myofibroblast-like phenotype, and perpetuation that maintains the activated phenotype of HSCs. The fate of the activated HSCs depends on the apoptotic and survival signals that they receive. The apoptosis of HSCs results from a series of complex and interrelated signaling events. Apoptotic signals for the activated HSCs include proteins from membrane receptors, such as death receptors, nerve growth factor receptor and peripheral-type benzodiazepine receptor, as well as proteins from cytoplasm such as Bcl-2 family members. The survival signals for the activated HSCs are induced by some kinases and cytokines including tissue inhibitors of metalloproteinase-1, Rho/Rho kinase, platelet-derived growth factor, transforming growth factor beta-l, and insulin-like growth factor-1. Approaches that specifically initiate HSC apoptosis are promising to be direct and effective strategies to treat liver fibrosis. Although it remains unclear whether the activated HSCs could be reversed back to the quiescent phenotype,the different expression and sensitivity of pro-apoptotic and survival molecules between quiescent and activated HSCs provide a prospect to develop therapeutic approaches that specifically targets apoptosis of the activated HSCs. These therapeutic strategies to induce HSC apoptosis are current research hotspot and the future for the patients with liver fibrosis and cirrhosis.