Loading...

Table of Content

    15 October 2017, Volume 22 Issue 10
    Original Articles
    Analysis of recurrence in HBeAg-negative chronic hepatitis B patients with entecavir withdrawal
    ZHOU Zhao-hui.
    2017, 22(10):  882-884. 
    Asbtract ( 255 )   PDF (682KB) ( 266 )  
    References | Related Articles | Metrics
    Objective To evaluate the off-treatment efficacy of entecavir (ETV) therapy and to investigate the treatment and withdrawal standard of antiviral therapy for hepatitis B e antigen (HBeAg)-negative chronic hepatitis B (CHB) patients.Methods In the retrospective analysis, 121 HBeAg-negative CHB patients with ETV withdrawal for more than 6 months from January 2006 to December 2015 in our hospital were enrolled. Hepatitis B virus (HBV) DNA levels, liver function and HBV markers at month 6 and 12 after ETV withdrawal were measured.Results After ETV withdrawal, HBV DNA load was increased (>5×102 copies/mL) in 33% and 45.5% patients at month 6 and 12, respectively, and alanine aminotransferase (ALT) was elevated in 19.8% and 30.6% patients. Patients with more than 5-year ETV administration had the lowest recurrence rate. In addition, HBV DNA load <2×105 copies/mL at baseline showed a lower recurrence rate at both month 6 and 12 after ETV withdrawal than the HBV DNA load >107 copies/ml at baseline.Conclusion The recurrence rate was negatively correlated with ETV treatment course in HBeAg-negative CHB patients, and positively correlated with the HBV DNA load at baseline.
    Clinical characteristics and associated factors in patients with statins induced liver injury
    CHEN Bu-kuan
    2017, 22(10):  885-887. 
    Asbtract ( 346 )   PDF (676KB) ( 407 )  
    References | Related Articles | Metrics
    Objective To investigate the characteristics of patients with statins-induced liver injury.Methods Twenty-six patients with statins-induced liver injury were enrolled, and age, sex, liver disease history, clinical manifestations, laboratory index, drugs, treatments, etc. were retrospectively analyzed.Results Among all the patients, 19 were female and 7 were male. Clinical manifestations included poor appetite, fatigue, yellow urine and so on. Hepatocellular type was the predominant type in these cases. Five kinds of drugs were involved, mainly including simvastatin, atorvastatin, and rosuvastatin.Conclusion Patients with statins-induced liver injury had various clinical manifestations with comparatively good prognosis.
    Distribution and drug resistance of pathogens in patients with biliary tract infection
    LV Gui-fang, CHENG Zhao-xia, ZHU Yue-wen, TeNiGeEr, HOU Wei, SUN Jian-wen
    2017, 22(10):  888-890. 
    Asbtract ( 213 )   PDF (675KB) ( 407 )  
    References | Related Articles | Metrics
    Objective To investigate the distribution and drug resistance of pathogen in patients with biliary tract infection, and to guild clinical application of antibiotics.Methods The cases of biliary tract infection with positive bile pathogen culture in our hospital from September 2014 to August 2016 were retrospectively analyzed, and the distribution and drug resistance of 143 strains of pathogen from those cases were statistically analyzed using WHONET 5.4.Results Among the 143 strains of pathogen, there were 77 (53.8%) gram-negative bacilli, 63 (44.1%) gram-positive coccus and 3 (2.1%) fungal strains. The most common pathogenic bacteria in biliary tract infection were Enterococcus faecalis (12.6%, 18/143), Enterococcus faecium (11.9%, 17/143), Klebsiella pneumoniae (11.2%, 16/143), Escherichia coli (9.1%, 13/143) and Pseudomonas aeruginosa (8.9%, 12/143). The susceptibility tests revealed that resistant rates of gram-negative bacilli against amikacin and doripenem were fairly low, and of gram-positive coccus against linezolid, daptomycin and vancomycin were also fairly low.Conclusion In biliary tract infection, the infectious rate of gram-positive coccus increased year by year, though the rate of gram-negative bacilli took the lead invariably. Clinical selection of antibiotics should be more reasonable and specific, as the pathogen developed resistance to the most common antibiotics obviously.
    The effect of lipophagy on hepatitis C virus core protein-induced hepatic steatosis via down-regulation of silent information regulator 1 in mice
    SUN Li-jie, SHI Yu-guang, ZHANG Xiao-yu, SHU Meng-ni, CHEN Mo-yang, YU Jian-wu
    2017, 22(10):  891-893. 
    Asbtract ( 154 )   PDF (764KB) ( 340 )  
    References | Related Articles | Metrics
    Objective To investigate the effect of lipophagy on hepatitis C virus (HCV) core protein-induced hepatic steatosis via down-regulating silent information regulator 1 (SIRT1) in mice.Methods Mice were randomized into HCV group and control group (n=10 in both groups), with injection of HCV core recombinant expression vectors or sterile phosphate buffered solution (PBS) through the tail vein, respectively. All mice were sacrificed in 1 month after the injection. Liver function and serum adiponectin were collected. Total triacylglycerol (TG) were measured in both serum and liver tissues. Levels of SIRT1 protein, adiponectin receptor 2 (AdipoR2) protein, light chain 3-Ⅱ (LC3-Ⅱ) protein, adipose differentiation related protein (ADRP), tail interacting protein 47KD (TIP-47) and P62 protein in liver were measured using western blot. Quantitative data was analyzed using t-test.Results In HCV group, histopathological examinations revealed hepatic steatosis, and the hepatic TG content ( 80.9±20.1 vs 45.8±10.5 μg/mg, t=4.964, P<0.01) and levels of LC3-Ⅱ protein (0.8±0.2 vs 0.4±0.1, t=5.656, P<0.01), TIP-47 protein (0.9±0.3 vs 0.4±0.1, t=5.000, P<0.01) and ADRP protein (0.8±0.3 vs 0.4±0.1, t=4.000, P<0.01) were all increased than those in the control group. However, serum adiponectin (1.05±0.25 vs 1.41±0.45 ng/ml, t=2.211, P<0.05 ), SIRT1 protein (0.4±0.1 vs 0.9±0.2, t=7.071, P<0.01) and AdipoR2 protein (0.4±0.1 vs 0.8±0.2, t=5.656, P<0.01) were decreased in HCV mice group compared with those in control group. Expression of P62 protein (0.7±0.2 vs 0.8±0.3, t=0.877, P>0.05) showed no significant difference between the two groups.Conclusion HCV core protein might cause hepatic steatosis via inducing incomplete lipophagy through down-regulating the expression of SIRT1, adiponectin and AdipoR2.
    Establishment and preliminary evaluation of HBsAg mutated hepatitis B transfected mice model via hydrodynamic injection
    ZHANG Yi, CHEN Jie-liang, FANG Zhong, XU Guo-guang, LI Jun.
    2017, 22(10):  894-898. 
    Asbtract ( 179 )   PDF (1159KB) ( 371 )  
    References | Related Articles | Metrics
    Objective To investigate the role of hepatitis B surface antigen (HBsAg) in chronicity of hepatitis B virus (HBV) and regulation of host immune responses in vivo.Methods Site-directed mutagenesis was used to establish HBsAg mutated HBV mice model, based on transfection of plasmid adeno-associated virus (pAAV)-HBV through hydrodynamic injection. Then the serum HBsAg, hepatitis B e antigen (HBeAg) and HBV DNA were measured to evaluate the infection in both mice models. In addition, hematoxylin-eosin (HE) staining was performed to analyze pathological changes and infiltration of immune cells in liver.Results HBsAg mutated HBV mice model was successfully established. HBeAg levels in HBV mice model and HBsAg mutated HBV mice model were both 4 COI/ml with no difference. HBsAg and HBV DNA were undetected in HBsAg mutated HBV mice model, while HBsAg was > 102 COI/ml and HBV DNA was 103 ~ 106 copies/ml in HBV mice model. Dynamic monitor showed that percentage of HBeAg positive rate gradually declined in both mice models, which was more obvious in HBsAg mutated HBV model. At week 8, HBeAg positive rate was 20% in HBsAg mutated HBV model compared to 60% in HBV model. Compared with HBV model, there was less infiltration of immune cells but more ground-glass hepatocytes were in the liver of HBsAg mutated HBV mice model with HBsAg deficiency. Conclusion HBsAg mutated HBV mice model was successfully established. HBsAg might have an important role in pathologic process and infiltration of immune cells in liver. It lays a foundation for further study on the role of HBsAg in HBV replication and immunologic escape.
    Identification of synergistic effect of microRNA-A6 on transiently transfected-HepG2 replication system of HEV in vitro
    ZHANG Wei, YOU Shao-li, LIU Hong-ling, ZHU Bing, ZANG Hong, XIN Shao-jie, RONG Yi-hui
    2017, 22(10):  899-903. 
    Asbtract ( 189 )   PDF (745KB) ( 428 )  
    References | Related Articles | Metrics
    Objective To investigate the synergistic effect of hepatitis E virus (HEV)-encoded microRNA-A6 (miR-A6) on viral replication in full-length HEV transiently transfected-human hepatocellular carcinoma cell line (HepG2).Methods miR-A6 was synthesized according to the reported sequence. Technologies of recombinant polymerase chain reaction (PCR), gene cloning and in vitro transcription were used to obtain a high concentration of HEV RNA. Proportional mixed HEV RNA and miR-A6 were transiently transfected into HepG2 using pulse current. Immunoglobulin G (IgG) secretion and HEV RNA load in supernatants of cultured HepG2 were measured at hour 24, 48 and 96 after transfection, respectively. Replication of HEV was compared between HepG2 cells with and without miR-A6 transfection. Moreover, anti-A6 was further used to confirm the effect of miR-A6 on the replication of HEV.Results Compared with that in HepG2 transfected with HEV RNA alone, lg HEV RNA increased by 1.57 and 2.44 at hour 48 after co-transfection of miR-A6 and HEV RNA with mass ratio of 0.5∶1 and 1∶1, respectively. Detection of IgG in supernatants was prior to HEV RNA. There was no obvious difference of replication in vitro between HEV type Ⅰ and type Ⅳ, in which HEV RNA replication both peaked up at hour 48 after transfection. The expression of HEV-IgG and HEV RNA were inhibited by 47.12% and 43.3% after addition of anti-A6.Conclusion miR-A6 could significantly increase the replication ability of HEV RNA in full-length HEV transiently transfected HepG2 in vitro, which may lay a foundation for further research on HEV molecular virology and phenotype resistance.