ObjectiveTo explore the association between viral hepatitis and extrahepatic cholangiocarcinoma (ECC). MethodsDatabase of Medline, Embase, PubMed, CNKI, and Wanfang were searched for the articles which were related to the relationship between viral hepatitis and ECC. After the quality evaluation and the data extraction of the literatures, statistical software of RevMan 5.0 was used to perform Meta analysis. ResultsAccording to the inclusion criteria and exclusion criteria, 9 articles were enrolled, 8 articles of them were related to hepatitis B virus(HBV) and 6 articles of them were related to hepatitis C virus(HCV). Meta analysis results showed that the HBV infection may be the risk factor for ECC(OR=1.69, 95% CI:1.32-2.17, P<0.000 1). In the United States, HCV infection may be the risk factor for ECC(OR=5.53, 95% CI:2.21-13.82, P=0.000 3), but the relationship was not found in China(OR=0.82, 95% CI:0.44-1.52, P=0.520 0). ConclusionsThe present studies suggest that HBV infection may be a high risk factor for ECC. HCV in the United States can increase the incidence of ECC, but the situation can not be found in China.
ObjectiveTo analyze hepatitis B virus (HBV) genotype distribution and drug-resistant mutations in West China Hospital of Sichuan University, providing basis for hepatitis B individualized treatment.MethodsA total of 786 chronic hepatitis B patients admitted to West China Hospital of Sichuan University from January 2016 to December 2018 were enrolled in the study. Genotype and drug-resistant mutations were analyzed by Sanger sequencing, and statistical analysis was conducted by χ2 test.ResultsThree genotypes (B, C and D) were identified in 786 samples, 489 (62.2%) in genotype B, 291 (37.0%) in genotype C , and 6 (0.8%) in genotype D. The distribution differences of B and C genotypes in age and ethnic groups were statistically significant (P<0.05). Among them, 627 cases had drug-resistant mutations, with a drug-resistant mutation rate of 79.8%. A total of 262 cases (33.3%) were resistant to lamivudine and tibivudine, 102 cases (13.0%) were resistant to lamivudine, tibivudine and entecavir; 83 cases (10.6%) were resistant to adefovir dipivoxil. No tenofovir resistant strains were detected in 786 samples. There were statistically significant differences in drug resistance between B and C genotypes (χ2=14.356, P<0.01). The most common single mutation was M204I [179 cases (22.8%)], followed by 46 cases (5.9%) of A181V/T associated with adefovir dipivoxil resistance. The most common mixed mutation was L180M+M204V/I in 83 cases (10.6%), and another 102 cases (13.0%) showed M250V and/or V173L and/or T184A/G/S/I and/or S202G/I with L180M+M204V/I.ConclusionsHBV genotypes in West China Hospital of Sichuan University are mainly B and C, and the situation of drug resistance is severe and the mutation pattern is complex. Therefore, detecting HBV genotype and drug resistance mutation is necessary, which may develop better clinical treatments.
Drugs may induce hepatitis B virus (HBV) reactivation (HBV-R). Here we have reviewed the definition and harm of HBV-R, the risk drugs and their underlying mechanism, the influence factors, as well as the early intervention measures. It is shown that multiple drugs, including chemotherapy drugs, immunotherapy drugs, directly acting antivirals, cell therapy, etc., can induce HBV-R by affecting host immunity or directly activating HBV transcription factors. HBV-R could cause severe liver damage, even interruption of treatment of original diseases, affecting the prognosis of patients. Through precisely identifying risk drugs, monitoring the influence factors, and prescribing preventive anti-HBV regimen if necessary, the incidence of HBV-R can be significantly reduced. It is also suggested that clinical physicians should not only pay attention to the early identification and intervention of HBV-R, but also further study the mechanism of HBV-R in depth, especially the underlying mechanism between host, HBV and risk factors. This will help to promote the discovery of more valuable markers for risk prediction and targets for early intervention, and to further reduce the risk of HBV-R and improve the prognosis of patients.
Objective To analyze the clinical characteristics of individuals with high hepatitis B virus (HBV) pregenomic RNA (pgRNA), and further explore the value of pgRNA in the management of patients with chronic hepatitis B. Methods From December 1st, 2020 to April 1st, 2022, chronic hepatitis B patients who had been treated with nucleotide analogues for a long time and followed up in the Hepatitis Clinic of the Center of Infectious Diseases, West China Hospital, Sichuan University were included, and the clinical characteristics of chronic hepatitis B patients with high pgRNA were analyzed and summarized. Results A total of 107 patients were included. Male patients accounted for 66.4%, with an average age of 44.02 years. There were no statistically significant differences in gender, age, aspartate transaminase, alanine transaminase, γ-glutamyl transferase, HBV surface antigen, proportion of patients with HBV e antigen ≥0.1 U/mL, HBV DNA, and alpha fetoprotein between the high and low pgRNA groups (P>0.05). The proportion of patients with HBV surface antigen<100 U/mL in the high pgRNA group was lower than that in the low pgRNA group (4.4% vs. 22.6%, P<0.05). Conclusion The proportion of chronic hepatitis B patients with high pgRNA whose HBV surface antigen≥100 U/mL is higher.
ObjectiveTo study the value of hepatitis B virus surface antigen (HBsAg) in the evaluation of antiviral efficacy and its influencing factors under a complex population background resulting from various nationalities in Xinjiang. MethodsWe retrospectively analyzed patients with chronic hepatitis B (CHB) admitted and administrated with nucleot(s)ide analogues (NAs) for the first time in Traditional Chinese Medical Hospital of Xinjiang Uygur Autonomous Region from January 2012 to August 2013. The biological, virological, and serological responses were analyzed as well as the possible factors related to HBsAg levels and its reduction levels. ResultsThere were 63 CHB patients enrolled. After 48 weeks' treatment, all patients achieved biological response, and 59 of them achieved complete virological response in spite of 4 patients with partial response. In all the 30 hepatitis B virus e antigen (HBeAg) positive patients, 5 achieved HBeAg seroconversion. After correlation and regression analysis, it turned out that the history (P=0.033) and HBeAg levels at week 48 (P<0.001) were independent impact factors for HBsAg level at week 48. And the reduction degree of HBsAg at week 48 was influenced by HBsAg at week 48. In 21 patients counting to week 72 maintaining biological response, 18 achieved complete virological response. Unfortunately, all 8 HBeAg positive patients encountered no HBeAg loss or seroconversion. After correlation and regression analysis, it turned out that HBsAg level at week 72 was influenced by HBsAg at week 48 (r=0.700, P<0.001). And the decline degree of HBsAg at week 72 was related to baseline HBsAg level. ConclusionSatisfactory efficacy can be achieved via NAs treatment in CHB patients. But when HBsAg is used separately as an indicator for therapeutic efficacy, we should be aware that intrahepatic covalently closed circular DNA (cccDNA) is not only the impact factor of HBsAg variation, the history, the variations of HBeAg and HBsAg itself during the treatment should also be considered.
ObjectiveTo explore the relationship between liver transplantation procedure with or without preservation of retrohepatic vena cava and postoperative reinfection of hepatitis B virus.MethodsHepatitis B virus makers of 15 retrohepatic vena cava samples from hepatitis B virus active replicating recipients was detected using immunohistochemistry stain LSAB and HBV DNA hybridization in situ. Hepatitis B virus reinfection rate and survival rate after transplantation in classic group (20 cases) and piggyback group (7 cases) was analyzed retrospectively. ResultsHepatitis B virus makers including HBsAg and HBcAg and HBV DNA of all 15 retrohepatic vena cava samples, 10 from classic group and 5 from piggyback group, was negative. In classic group, 20 recipients were followedup 6-30 months, mean 18 months, only one case of hepatitis B recurrence was confirmed 22 months after operation; In piggyback group,7 recipients were followedup 5-12 months, mean 8 months, none of hepatitis B virus reinfection was encountered. Recurrence rate in classic group and piggyback group was 5.0%(1/20) and 0(0/7), respectively.ConclusionThis preliminary study indicated that the retrohepatic vena cava of hepatitis B virus active replicating recipients don’t have the residence and replication of hepatitis B virus particle. Orthotopic liver transplantation procedure with preservation of retrohepatic vena cava appears not to increase the hepatitis B virus reinfection rate in hepatitis B virus active replicating recipients after transplantation.
Long non-coding RNA (lncRNA) is a type of nucleic acid sequence that exceeds 200 nucleotides in length and cannot encode any complete protein. In recent years, its important regulatory role in various pathophysiological processes has been gradually clarified, however, few studies have reported its role in carcinogenic virus infection. This article summarizes the currently known lncRNAs abnormally expressed in hepatitis B virus-induced hepatocellular carcinoma, and focuses on the mechanisms of lncRNAs regulating the occurrence and development of hepatitis B virus-related hepatocellular carcinoma such as controlling virus replication and host immunity, cell cycle and proliferation, invasion and metastasis, autophagy and apoptosis of liver cancer cells, hoping to provide a theoretical basis for the molecular targeted therapy of hepatocellular carcinoma.
Hepatitis B virus related acute-on-chronic liver failure (HBV-ACLF) has the characteristics of rapid progress and high mortality. Artificial liver support system (ALSS) is far superior to standard drug therapy in the treatment of such patients, and is widely used in emergency. ALSS is the use of external mechanical or biological devices to replace a part of the damaged liver function, divided into bioartificial, non-bioartificial liver and a combination of the two. At present, there is no unified sensitive prognostic index and recognized prognostic model for HBV-ACLF in artificial liver treatment. This paper reviews the research progress of prognosis evaluation of ALSS in the treatment of HBV-ACLF, in order to provide reference for clinicians and researchers
ObjectiveTo investigate the correlation of spontaneous YMDD mutation in different hepatitis B virus (HBV) genotypes with HBV-related hepatocellular carcinoma (HCC). MethodFrom May 2010 to May 2012, 110 HBV-related hepatocellular cancer patients not treated by anti-virus drugs and 1 079 chronic HBV infectors (including asymptomatic HBV carriers, chronic hepatitis B patients, and HBV-related liver cirrhosis patients) were included in our study. HBV YMDD mutation was detected by fluorescence hybridization bioprobe polymerase chain reaction (PCR) and melting curve assay using Diagnosis Kit for HBV YMDD Mutation (Qiagen Biotechnology). Serum HBV genotype was detected by real time PCR using genotype specific TaqMan probe. According to data type, t-test, χ2-test and unconditional logistic regression were used for statistical analysis. ResultsIn the HCC group, genotype C virus, spontaneous YMDD mutation and genotype C virus with YMDD mutation were detected in 39 patients (35.5%), 16 patients (14.5%) and 14 patients (12.7%), respectively. In the chronic HBV infection group, HBV genotype C virus, spontaneous YMDD mutation and genotype C virus with YMDD mutation were detected in 153 patients (14.2%), 46 patients (4.3%) and 17 patients (1.6%), respectively. The difference between the two groups were statistically significant (χ2=33.368, P<0.001; χ2=21.353, P<0.001; χ2=48.889, P<0.001). Unconditional logistic regression analysis suggested that infection of genotype C virus and genotype C virus with spontaneous YMDD mutation might be important risk factors for the development of HCC[OR=2.943, 95%CI (1.778, 4.872), P<0.001; OR=5.989, 95%CI (2.394, 14.980), P<0.001]. ConclusionsInfection of genotype C virus with spontaneous YMDD mutation is tightly related with the occurrence of HCC and has important value for earlier warning of HCC.
ObjectiveTo explore the influence of paternal serum HBV-DNA load levels and pregnant women's HBsAb on vertical transmission of hepatitis B virus (HBV) from HBsAg positive fathers to infants in order to provide effective methods for paternal-fetal ventrical transmission of HBV prevention. MethodsUsing HBsAg and HBV-DNA as indicators to screen pregnant women and their husbands after gained consent, 121 families with HBVM negative or only HBsAb positive and HBV-DNA negative pregnant women, HBsAg positive husbands and their newborns were selected. In this case-control study, according to neonatal cord blood HBV-DNA detection, 23 newborns with cord blood HBV-DNA positive were selected as cases, 98 newborns as controls. ResultsThe positive rate of neonatal cord blood HBV-DNA was 19.0% (23/121); and there was dose-response relationship between paternal serum HBV-DNA load levels and neonatal cord blood HBV-DNA positive (trend χ2=60.108, P=0.000). The analysis of ROC curve showed that paternal serum HBV-DNA load level (106 copies/mL) is a better demarcation point to forecast the occurrence of vertical transmission of HBV from HBsAg positive fathers to infants, because there was a better sensitivity and specificity during forecast; and HBsAb negative pregnant women's were statistically significant (χ2=12.399, P=0.000). There was no significant difference at the positive rate of neonatal cord blood HBV-DNA between the case group and control group when paternal serum HBV-DNA load levels exceed 107 copies/mL (P > 0.05). ConclusionPaternal serum HBV-DNA load levels and HBsAb negative pregnant women are the risk factors of vertical transmission of HBV from HBsAg positive father to infants. Paternal serum HBV-DNA load level (106 copies/mL) is an appropriate index of the occurrence of vertical transmission.