Objective
To clarify incidence and risk factors of hepatitis B reactivation during short term (one month) in hepatitis B virus (HBV) related hepatocellular carcinoma (HCC) patients receiving partial hepatectomy.
Methods
From January 2015 to December 2015, 214 consecutive patients with HBV-related HCC who underwent partial hepatectomy were retrospectively enrolled in this study. The risk factors affecting incidence of hepatitis B reactivation were analyzed.
Results
Hepatitis B reactivation happened in 7.0% (15/214) of patients within 1 month after partial hepatectomy. By univariate analysis, the preoperative HBV-DNA negativity and hepatitis B e antigen (HBeAg) positivity were significantly correlated with the occurrence of hepatitis B reactivation (P=0.023 and P=0.001, respectively). By multivariate analysis, the preoperative HBV-DNA negativity 〔OR=9.21, 95% CI (2.40, 35.45), P=0.001〕 and HBeAg positivity 〔OR=20.51, 95% CI (5.41, 77.73), P<0.001〕 were the independent risk factors for hepatitis B reactivation.
Conclusions
Hepatitis B reactivation is common after partial hepatectomy for HBV-related HCC during short term, especially in patients whose preoperative HBV-DNA negativity and HBeAg positivity. A close monitoring of HBV-DNA during short term after partial hepatectomy is necessary, once hepatitis B is reactivated, antiviral therapy should be given.
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 evaluate the efficacy and safety of antiviral drugs for hepatitis B with YMDD motif variant. Methods We electronically searched MEDLINE (1989-April, 2004), EMBASE (1989-April, 2004), CBMdisc (expand) (1989-April, 2004), and handsearched unpublished Chinese conference proceedings. Randomized and quasi-randomized trials in patients with chronic hepatitis B with YMDD motif variant correlative to lamivudine were collected. Two reviewers extracted the data and assessed the quality of literature independently. The data were then analyzed by RevMan 4.2 software. Results Five studies involving 6 trials and 284 patients were included. According to the results of meta-analysis, antiviral therapy with adefovir plus lamivudine showed significantly better effects on the clearance of serum HBV-DNA and HBeAg and normalization of ALT than that of lamivudine alone (RR 16.61, 95%CI 2.29 to 120.71; RR 6.66, 95%CI 1.23 to 35.88 and RR 6.26, 95%CI 2.29 to 17.12 respectively); also, oxymatrine plus thymothin showed obviously better effects on the clearance of serum HBV-DNA and HBeAg (RR 2.96, 95%CI 1.26 to 6.93 and RR 2.51, 95%CI 1.05 to 5.98 respectively).But adefovir alone showed no better effects on clearance of serum HBV-DNA and HBeAg than that of lamivudine alone (RR 11.00, 95%CI 0.65 to 186.02 and RR 7.00, 95%CI 0.39 to 126.92 respectively); interferon plus lamivudine showed no better effects on the clearance of serum HBV-DNA, HBeAg and the normalization of ALT (RR 3.50, 95%CI 0.90 to 13.58; RR 4.90, 95%CI 0.70 to 35.10 and RR 2.80, 95%CI 0.91 to 8.12 respectively). Chinese herbs plus lamivudine showed no better effects on the clearance of serum HBV-DNA (RR 1.16, 95%CI 0.89 to 1.51). There were no significant side effects in the groups, except flu like symptom in the interferon group, slight kidney impairment in the adefovir group, and aggravation of rare cases in lamivudine group. Conclusions Antiviral therapy with adefovir plus lamivudine, or oxymatrine plus thymothin, shows better effects than with lamivudine alone in terms of antiviral therapy and clinical outcome improvement. However, the evidence is too weak to draw a definite conclusion in this systematic review. Larger sample size and rigorously designed randomized, double blind, placebo control trials are required for future study.
Objective
Hepatitis B virus X (HBx) protein is involved in the initiation and progression of hepatocellular carcinoma (HCC) by regulating the host protein-coding genes. Herein, we want to explore whether HBx protein can alter the expression of microRNAs (miRNAs) to promote proliferation and transformation in malignant hepatocytesin vitro.
Methods
MiRNA microarray and quantitative reverse-transcription polymerase chain reactions (qRT-PCRs) were performed to identify miRNAs that were differentially regulated by HBx protein in HCC cells. Protein and mRNA expression analyses, cell cycle and apoptosis analyses, and luciferase reporter assays were performed to delineate the consequences of miR-16 family repression in HepG2 cells.
Results
HBx protein induced widespread deregulation of miRNAs in HepG2 cells, and the downregulation of the miR-16 family was reproducible in HepG2, SK-HEP-1, and Huh7 cells. CCND1, a target gene of the miR-16 family, was derepressed by HBx protein in HepG2 cells. C-myc mediated the HBx-induced repression of miR-15a/16 in HepG2 cells. Ectopically expressed miR-15a/16 suppressed the proliferation, clonogenicity, and anchorage-independent growth of HBx-expressing HepG2 cells by arresting them in the G1 phase and inducing apoptosis, whereas reduced expression of miR-16 accelerated the growth and cell-cycle progression of HepG2 cells.
Conclusions
HBx protein altered thein vitro expression of miRNAs in host malignant hepatocytes, particularly downregulating the miR-16 family. Repression of miR-15a/16 is c-myc mediated and is required for the HBx-induced transformation of HepG2 cellsin vitro. Therefore, miR-16 family may serve as a therapeutic target for hepatitis B virus (HBV)-associated HCC.
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.
Objective To study the relationship of hepatitis B virus （HBV） to spontaneous rupture of hepatocellular carcinoma （HCC-SR） and its mechanism. Method The related literatures about theory of HCC-SR were consulted and reviewed. Results The injury of small arteries was usually followed in patients with HCC-SR， which was related to vascular autoimmune injury caused by the HBV infection. The small arteries in which immune complex deposited were readily injured， as a result HCC-SR happened while vascular load increased. Conclusion The HBV infection resulted in vascular autoimmune injury maybe a important factor in the pathogenesis of HCC-SR.
ObjectiveTo summarize the research status of the relationship between hepatitis B virus X protein (HBx), hepatitis B virus (HBV) genotypes and hepatocellular carcinoma (HCC) at home and abroad, and to prospect its clinical significance.MethodThe literatures about HBx, HBV genotypes and HCC were reviewed.ResultsThere was a close relationship between HBx and the occurrence, development, migration and metastasis of HCC. There was a certain association between HBV genotypes and HCC, but the specific mechanism had not been clarified.ConclusionsHBx and HBV genotypes play an important role in the occurrence and development of HCC. With the further study of molecular mechanism, it will promote the diagnosis and treatment of hepatitis B, liver cirrhosis and liver cancer, and provide more individualized intervention for clinical workers.
