Table of Content

25 October 2019, Volume 24 Issue 10

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Original Articles

Incidence and predictors of HBV relapse in patients with chronic hepatitis B after discontinuation of tenofovir therapy

PAN Chen-en, MENG Xian-min, YAO Xiao-ying

2019, 24(10):  1112-1115. 

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Objective To investigate the incidence and predictive factors of hepatitis B virus (HBV) relapse in patients with chronic hepatitis B (CHB) after discontinuation of tenofovir (TDF). Methods A total of 197 patients with CHB admitted to our hospital from January 2015 to June 2017 were selected as the study subjects. The Cox model was used to analyze the factors affecting viral relapse at week 96. The best cut-off value was calculated by the receiver operating characteristic (ROC) curve. Results There were correlations between the age, HBV deoxyribonucleic acid, HBV genotype, baseline hepatitis B surface antigen (HBsAg), treatment time, HBsAg level at 12 months of treatment and HBsAg level at the end of treatment in CHB patients (P<0.05). There was no significant difference in sex, baseline ALT level and total bilirubin level between the hepatitis B envelope antigen (HBeAg) positive and negative CHB patients (P>0.05). The viral relapse rates of HBeAg positive patients at week 12, 24, 48, 72 and 96 were 26.23% (16/61), 45.90% (28/61), 55.74% (34/61), 57.38% (35/61) and 72.13 (44/61), respectively, and the clinical relapse rates were 13.11% (8/61), 27.87% (17/61), 40.98% (25/61), 44.26% (27/61) and 57.38% (35/61), respectively. The viral relapse rates of HBeAg negative patients at week 12, 24, 48, 72 and 96 were 18.38% (25/136), 43.38% (59/136), 61.03% (83/136), 67.65% (92/136) and 72.06% (98/136), respectively, and the clinical relapse rates were 11.03% (15/136), 27.94% (38/136), 40.44% (55/136), 53.68% (73/136) and 58.09% (79/136), respectively. Besides, the multivariate analysis showed that HBsAg level at the end of treatment was an independent risk factor for viral relapse within 96 weeks after TDF withdrawal for both HBeAg positive and negative CHB patients. ROC curve showed that the best cut-off value of HBsAg at the end of treatment was 92 IU/mL for HBeAg negative patients. Conclusion The relapse rate of CHB patients within 48 weeks after termination of TDF treatment is high. The level of HBsAg at the end of treatment is related to the relapse rate, which may be an effective factor for predicting the relapse in CHB patients after discontinuation of TDF treatment.

Prognostic risk factors in patients with cirrhosis and cerebral hemorrhage

WANG Dan, MU Jin-song, HU Zhi-jun, YAN Bing-bing, KUANG Zhi-dan

2019, 24(10):  1116-1118. 

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Objective To analyze the clinical characteristics of patients with cirrhosis and cerebral hemorrhage, to study the prognosis and mortality of these patients, and to investigate the risk factors affecting prognosis. Methods Clinical data of 51 patients with cirrhosis and cerebral hemorrhage in our hospital from December 2008 to July 2018 were collected. The patients were divided into the death and the improvement groups according to discharge conditions. The clinical characteristics of the 2 groups and the risk factors for prognosis were analyzed and discussed. Results Thirty-one patients died when they were discharged from hospital, and the case fatality rate was 61%. Univariate analysis showed that the volumes of hematoma in the death and improvement groups were (57±28) ml and (25±11) ml, platelet counts were (31±27)×10⁹/L and (62±21)×10⁹/L. Numbers of cases with severe disturbance of consciousness were 25 and 5, with Child-Pugh C status was 26 and 8, the differences were statistically significant (P<0.05). Multivariate analysis showed that platelet count was an independent risk factor for prognosis of patients with cirrhosis and cerebral hemorrhage (P<0.05). The cut-off value was 30.5×10⁹/L. The area under receiver operator characteristic curve was 0.894 (0.803-0.986), the sensitivity and specificity were 100% and 77.4%, respectively, and the maximum of Youden’s index was 0.774. Conclusion Platelet count is an independent risk factor for prognosis of patients with cirrhosis complicated with cerebral hemorrhage. The etiology of cirrhosis is related to the occurrence of cerebral hemorrhage, but has no relationship with prognosis.

Meta analysis of low-fat and low-carbohydrate diet for the treatment of non-alcoholic fatty liver disease

ZHANG Yu-ting, HUANG Yi-qin, CHEN Jie, BAO Zhi-jun

2019, 24(10):  1119-1124. 

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Objective To evaluate the curative effect of the low-fat diet (LFD) and low-carbohydrate diet (LCD) on non-alcoholic fatty liver disease (NAFLD). Methods Databases including PubMed, Embase, Medline, Cochrane library, Web of Science, China National Knowledge Infrastructure and Wanfang Data were searched from inception to January 2019 for the randomized controlled trials on LFD or LCD in NAFLD therapy. Patients in studies included were divided into the very low-carbohydrate diet (VLCD) group, the LCD group, the medium-carbohydrate diet (MCD) group and the high-carbohydrate diet (HCD) group. And Stata11.0 was used to process the data. Results A total of 11 studies were included, comprising 420 NAFLD patients. There was no statistical difference in the body weight loss, total cholesterol (TC), triglyceride (TG), high density lipoprotein (HDL), low density lipoprotein (LDL), alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutamyltranspeptidase (GGT) and intrahepatic fat in patients with NAFLD between VLCD and LCD groups (P>0.05). Compared with the LFD group, the MCD group had lower TG in NAFLD patients (mean difference [MD] =-32.141, 95% confidence interval [CI] -58.280 ~ -6.001, P=0.016), while there were no significant differences in the body weight loss, TC, HDL, LDL, ALT, AST, GGT and intrahepatic fat (P>0.05). The HCD group had lower TC in patients with NAFLD (MD=-0.59, 95%CI -0.979 ~ -0.201, P=0.003), while there were no statistical differences in the body weight loss, TG, HDL, LDL, ALT, AST, GGT and intrahepatic fat (P>0.05). Conclusion There is still a lack of evidence for the superiority of LCD or LFD in the treatment of NAFLD. More evidence-based studies should be conducted to evaluate the long-term effects and stability of LCD.

Protective effect and mechanism of histone acetyltransferase inhibitor DCH36_06 on mice with acute liver injury

PENG Jin-jin, HUANG He-ming, LIU Yan-jun, SHI Cui-cui, FAN Jian-gao, ZHANG Yuan-yuan, LUO Cheng, LI Guang-ming

2019, 24(10):  1125-1128. 

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Objective To investigate the protective effect of histone acetyltransferase inhibitor DCH36_06 on mice with lipopolysaccharide (LPS)/D-galactose (D-Gal)-induced acute liver injury (ALI) and its mechanism. Methods A total of 75 C57BL/6 mice were randomly divided into 4 groups, 20 in normal control group, 20 in LPS/D-Gal-induced ALI group, 20 in DCH36_06 treatment group and 15 in DCH36_06 control group, injected intraperitoneally with normal saline, LPS/D-Gal, LPS/D-Gal + DCH36_06 and DCH36_06, respectively. After 4 hours of LPS/D-Gal injection, 5 mice in each of the first 3 groups were sacrificed. The peripheral serum and liver tissues of the mice were harvest to detect biochemical indexes, to evaluate liver tissue pathological changes and hepatocyte apoptosis by hematine-eosin and terminal deoxynucleotidyl transferase mediated biotinylated deoxyuridine triphosphate nick end labelling staining, and to detect the expression of pro-inflammatory cytokines in liver tissues by real-time polymerase chain reaction and enzyme-linked immunosorbent assay. The remaining mice were kept for 24 hours to test the 24-hour survival rate of each group. Results The 24-hour survival rate in the ALI group was only 40% (6/15), which reached 86.6% (13/15) in DCH36_06 treatment group (P<0.05). The necroinflammation and hepatocyte apoptosis of liver tissue were ameliorated in DCH36_06 treatment group compared with those in the ALI group. The serum levels of aspartate aminotransferase, alanine aminotransferase and total bilirubin in the treatment group were significantly lower than those in the ALI group (281.4±48.1 U/L vs 1151.0±111.1 U/L, 175.2±32.5 U/L vs 921.5±47.9 U/L, and 9.8±0.7 μmol/L vs 21.0±0.4 μmol/L, P<0.05). Additionally, the mRNA and protein levels in liver tissues of tumor necrosis factor alpha, interleukin 1β and interleukin 6 in the treatment group (72.0±9.3, 91.4±4.6, 175.5±19.6, 25.9±2.3 pg/mL, 816.5±60.8 pg/mL and 305.6±20.1 pg/mL) were significantly lower than those in the ALI group (15.4±0.2, 6.0±1.6, 21.5±0.9, 7.9±1.2 pg/mL, 211.4±22.4 pg/mL and 53.2±7.3 pg/mL) (P<0.05). Conclusion DCH36_06 can protect mice from LPS/D-Gal-induced ALI, and the mechanism might be related to the inhibition of crucial pro-inflammatory cytokines expression and liver inflammatory injury, indicating the epigenetic regulation could be a promising target for the treatment of ALI.