Genomic change in hepatitis B virus associated with development of hepatocellular carcinoma

AIM: To determine the genomic changes in hepatitis B virus(HBV) and evaluate their role in the development of hepatocellular carcinoma(HCC) in patients chronically infected with genotype C HBV.METHODS: Two hundred and forty chronic hepatitis B(CHB) patients were subjected and followed for a median of 105 mo. HCC was diagnosed in accordance with AASLD guidelines. The whole X, S, basal core promoter(BCP), and precore regions of HBV were sequenced using the direct sequencing method.RESULTS: All of the subjects were infected with genotype C HBV. Out of 240 CHB patients, 25(10%) had C1653 T and 33(14%) had T1753 V mutation in X region; 157(65%) had A1762T/G1764 A mutations in BCP region, 50(21%) had G1896 A mutation in precore region and 67(28%) had pre-S deletions. HCC occurred in 6 patients(3%). The prevalence of T1753 V mutation was significantly higher in patients who developed HCC than in those without HCC. The cumulative occurrence rates of HCC were 5% and 19% at 10 and 15 years, respectively, in patients with T1753 V mutant, which were significantly higher than 1% and 1% in those with wild type HBV(P < 0.001).CONCLUSION: The presence of T1753 V mutation in HBV X-gene significantly increases the risk of HCC development in patients chronically infected with genotype C HBV.

Predictors of poor outcomes in patients with wild mushroom-induced acute liver injury

To identify early predictive markers of poor outcomes in patients with acute liver injury from wild mushroom intoxication.METHODSThis observational, retrospective record review involved adults aged ≥ 18 years admitted to emergency department with mushroom intoxication from January 2005 to December 2015. The diagnosis of mushroom intoxication was based on the following: (1) a positive history of recent wild mushroom intake (either raw or cooked); (2) the onset of gastrointestinal symptoms, such as watery diarrhea, vomiting, and/or abdominal pain, after ingestion; and (3) the exclusion of other possible causes of acute liver injury. Acute liver injury was defined by a > 5-fold elevation of liver enzymes or moderate coagulopathy [international normalized ratio (INR) > 2.0]. Clinical and laboratory findings were compared in survivors and non-survivors.RESULTSOf 93 patients with mushroom intoxication, 23, 11 men (47.8%) and 12 women (52.2%), of median age 61 years, developed acute liver injury. The overall in-hospital mortality rate was 43.5% (10/23). Among the laboratory variables, mean serum alkaline phosphatase (73.38 ± 10.89 mg/dL vs 180.40 ± 65.39 mg/dL, P < 0.01), total bilirubin (2.312 ± 1.16 mg/dL vs 7.16 ± 2.94 mg/dL, P < 0.01) concentrations and indirect/direct bilirubin (2.45 ± 1.39 mg/dL vs 0.99 ± 0.45 mg/dL, P < 0.01) ratio as well as prothrombin time (1.88 ± 0.83 mg/dL vs 10.43 ± 4.81 mg/dL, P < 0.01), and activated partial thromboplastin time (aPTT; 32.48 ± 7.64 s vs 72.58 ± 41.29 s, P = 0.01), were significantly higher in non-survivors than in survivors. Logistic regression analysis showed that total bilirubin concentration (OR = 3.58, 95%CI: 1.25-10.22), indirect/direct bilirubin ratio (OR = 0.14, 95%CI: 0.02-0.94) and aPTT (OR = 1.30, 95%CI: 1.04-1.63) were significantly associated with mortality. All patients with total bilirubin > 5 mg/dL or aPTT > 50 s on day 3 died.CONCLUSIONMonitoring of bilirubin concentrations and aPTT may help in predicting clinical outcomes in patients with acute liver injury from wild mushroom intoxication.

A case with acute-on-chronic liver failure receiving liver transplantation during daclatasvir and asunaprevir therapy in chronic hepatitis C patient

We report a case with hepatitis C virus genotype 1 b liver cirrhosis who received liver transplantation because of acute-onchronic liver failure during daclatasvir(DSV)and asunaprevir(ASV)combination therapy.To our knowledge,this is the first case received liver transplantation during DSVtASV therapy.Therefore,clinicians should pay particular attention to the possibility of acute liver failure during DSV and ASV combination therapy.