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Table of Content

    30 June 2019, Volume 24 Issue 6
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    Original Articles
    Efficacy of different anti-viral therapy regimens for HBV related hepatocellular carcinoma receiving radiotherapy
    HE Ya-jing, ZHANG Zhi-ming, HE Wei-meng, HOU Jin-lin
    2019, 24(6):  622-627. 
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    Objective To investigate the effect of entecavir (ETV) and other antiviral therapies on hepatitis B virus (HBV) quantification and liver function in HBV related hepatocellular carcinoma (HCC) patients receiving radiotherapy and factors influencing, and to evaluate overall survival time.Methods Clinical data of 128 HBV related HCC patients in our hospital from January 2011 to June 2016 were retrospectively analyzed. All the patients received 3-dimensional conformal radiotherapy for liver cancer. Patients were divided into ETV group (87 cases) and non-ETV group (41 cases) according to the antiviral therapy regimen before radiotherapy. After 4-8 weeks of radiotherapy, the liver function, HBV DNA load and other parameters were tested. The 1-, 2-, 3-year survival rate and survival time were also recorded. The reactivation rates of hepatitis B, hepatotoxicity rates and survival rates were compared between 2 groups. Results After radiotherapy, only 1 case (1.15%) had HBV reactivation in ETV group, while 12 cases (29.27%) in non-ETV group. There was a significant difference between 2 groups (P=0.000). A total of 51 patients had hepatotoxicity, 26 (29.89%) in ETV group and 25 (60.89%) in non-ETV group. The difference was significant between 2 groups (P=0.008). The median survival time was 19.27±2.53 months (95% confidence interval: 14.305-24.235) and 11.43±5.29 months (95% confidence interval: 1.059-21.801) in ETV group and non-ETV group, respectively. There was no significant difference in the 3-year survival rate between 2 groups (P=0.167).Conclusion In the HBV related HCC patients receiving radiotherapy, ETV works better than other antiviral therapy in the prevention of HBV reactivation and hepatotoxicity. However, there is no difference in the long-term survival benefits of patients with different antiviral treatment.
    Clinical Study of transient ALT elevation in patients with chronic hepatitis B in the early stage of entecavir treatment
    ZHAO Jing-jing, HAN Fang-zheng
    2019, 24(6):  628-630. 
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    Objective To investigate the difference in the efficacy of entecavir between treatment-na?ve hepatitis B envelope antigen (HBeAg)-positive chronic hepatitis B (CHB) patients with and without alanine aminotransferase (ALT) elevation in the early treatment.Methods Eighty-six CHB patients initially treated with entecavir in our hospital from January 2015 to October 2016 were selected. Among them, 28 patients with ALT elevation were in group A, and 58 patients without ALT elevation were in group B, The ALT normalization rate, hepatitis B virus deoxyribonucleic acid (HBV DNA) negative conversion rate, hepatitis B surface antigen (HBsAg) decline and HBeAg negative conversion rate were compared between the 2 groups at week 24,48 and 96 of antiviral therapy. Results At week 24 of treatment, in group A and B, the HBV DNA conversion rates were 75.0% and 51.7%, the HBsAg declines were 0.47 lg IU/mL (0.19-0.52 lg IU/mL) and 0.25 lg IU/mL (0.07-0.41 lg IU/mL), the differences were both statistically significant (P<0.05). At week 48, in group A and B, the HBV DNA conversion rates were 89.3% and 67.2%, the HBsAg declines were 0.62 lg IU/mL (0.27-0.74 lg IU/mL) and 0.32 lg IU/mL (0.11-0.47 lg IU/mL), the differences were both statistically significant (P<0.05). At week 96, in group A and B, the HBsAg declines were 0.69 lg IU/mL (0.30-0.99 lg IU/mL) and 0.36 lg IU/mL (0.20-0.60 lg IU/mL), the level of HBsAg were 3.30 ± 0.29 lg IU/mL and 3.48 ± 0.44 lg IU/mL, the differences were both statistically significant (P<0.05). While, there was no statistical difference in other indicators in other time periods between the 2 groups. Moreover, within the group, the indicators in both groups were significantly ameliorated.Conclusion ALT transient elevation in early entecavir treatment may accelerate HBV DNA clearance and HBsAg decline.
    The correlation between serum interleukin-33 and liver injury in systemic lupus erythematosus
    Zhong Yuchai, Chen Zhanling, Mo Weiping, Zhang Bashan, Hu Keding
    2019, 24(6):  631-634. 
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    Objective To investigate the correlation between serum interleukin-33 (IL-33) and liver injury in systemic lupus erythematosus (SLE).Methods A total of 213 SLE patients admitted to our hospital from November 2016 to November 2018 were enrolled in the study, and retrospective analysis was carried out. The clinical data of SLE patients were collected and the incidence of liver injury was analyzed. The independent influencing factors of hepatic injury in SLE patients were analyzed by multivariate logistic regression analysis, and the correlation between IL-33 and hepatic injury in SLE patients was analyzed. Results Among 213 SLE patients, 42 (19.72%) had liver injury, 171 (80.28%) did not have liver injury. In the liver injury group, the incidence rates of infection, neuropsychiatric system damage and blood system damage, the positive rate of anti-U1-nuclear ribonucleoprotein (anti-U1-nRNP) antibody, erythrocyte sedimentation rate, Systemic Lupus Erythematosus Disease Activity Index score, and levels of immunoglobulin G and serum IL-33 were higher than those in the non-liver injury group (P<0.05). The ROC curve showed that serum IL-33 had certain predictive value for liver injury in SLE. The area under the curve was 0.816. The best cut-off value in predicting the liver injury in SLE was 939.475 pg/ml, with sensitivity and specificity was 0.760 and 0.810 respectively. Multivariate logistic regression analysis showed that besides less than 3-month duration of the disease odd ratio (OR) = 3.394, 95% confidence interval (CI) = 1.156 ~ 9.952), neuropsychiatric system damage (OR=4.116, 95% CI=1.638 ~ 10.336), blood system damage (OR=4.118, 95% CI=1.118 ~ 4.980), and anti-U1-nRNP antibody (OR=2.061, 95% CI=1.055 ~ 4.017), serum IL-33 (OR=1.189, 95% CI=1.012 ~ 2.779) was also an independent risk factor for liver injury in SLE(P<0.05).Conclusion Serum IL-33 participates in the pathological process of SLE, and is significantly correlated to liver injury in SLE. Therefore, it should be paid enough attention to clinically.
    Perinatal outcomes of early- and late-onset intrahepatic cholestasis of pregnancy
    LI Ya-nan, WEI Juan-bing
    2019, 24(6):  635-637. 
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    Objective To study the perinatal outcomes of early- and late-onset intrahepatic cholestasis of pregnancy.Methods A total of 170 patients with intrahepatic cholestasis of pregnancy admitted to our hospital from December 2016 to December 2018 were divided into observation group (early-onset type, < 28 gestational weeks, 68 cases) and control group (late-onset type, ≥ 28 gestational weeks, 102 cases). The occurrences of mild and severe intrahepatic cholestasis of pregnancy in 2 groups were counted. The biochemical indexes including serum total bile acid, glycocholic acid, alanine aminotransferase, aspartate transaminase, alkaline phosphatase, total cholesterol, triglycerides, fasting blood glucose, glycosylated hemoglobin were tested. Labor gestational age, birth weight, Apgar score, postpartum blood loss and perinatal outcome were recorded. Results In the observation group, the incidence of severe intrahepatic cholestasis of pregnancy and the serum total bile acid, glycocholic acid, total cholesterol, triglyceride and fasting blood sugar were significantly higher than that in the control group (P<0.05), inversely, the alanine aminotransferase, aspartate transferase and alkaline phosphatase were significantly lower than those in the control group (P<0.05). In the observation group, the gestational weeks of delivery were significantly shorter than those in the control group (P<0.05), the neonatal weight was significantly lower than that in the control group (P<0.05), and the Apgar score was significantly higher than that in the control group (P<0.05). Moreover, the incidences of cesarean section, neonatal asphyxia, grade II to III amniotic fluid pollution and premature delivery in the observation group were significantly higher than those in the control group (P<0.05).Conclusion Compared with late-onset intrahepatic cholestasis of pregnancy patients, early-onset patients have worse perinatal outcomes. Therefore, they should be paid more attention to clinically.
    Establishment and evaluation of a fructose-induced hepatic steatosis cell model
    He Wenxi, Yang Jinyu, Xu Yanjiao, Lan Lulu, Zhang Chengliang, Liu Dong
    2019, 24(6):  638-642. 
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    Objective To establish a L02 cell model of hepatic steatosis induced by fructose, and to study the lipid synthesis of the model.Methods L02 cells were cultured in vitro and treated with different concentrations of fructose for 24 hours to induce steatosis. Cell viability was detected by cell-counting kit-8 to assess the effects of fructose. Levels of alanine aminotransferase and aspartate aminotransferase in the medium were detected to assess the damage of fructose on hepatocytes. Oil red O staining was used to observe the intracellular lipid droplet deposition. The intracellular triglyceride (TG) content was measured to determine the optimal modeling concentration. Meanwhile, the protein levels of carbohydrate responsive element binding protein (ChREBP), sterol regulatory element binding protein-1c (SREBP-1c), acetyl-CoA carboxylase 1 (ACC1) and stearoyl-CoA desaturase 1 (SCD1) in L02 cells treated with fructose were detected and compared with those in cells treated with free fatty acid (FFA). Results There was no significant difference between the viability of L02 cells under the intervention of 0?32 mmol/L fructose, and no significant cell injury was observed. When the fructose concentration was 4 mmol/L, a large amount of lipid droplets were formed in the L02 hepatocytes, the intracellular TG content was significantly higher, which was 1.5 times than that of the normal control, and the intracellular protein levels of ChREBP, SREBP-1 and ACC1 were significantly higher than those of FFA-treated cells.Conclusion The L02 cell steatosis can be successfully induced by 4 mmol/L fructose. This model is suitable for investigating the de novo lipogenesis in non-alcoholic fatty liver disease induced by high fructose diet.