Hepatitis Monthly
Volume:19 Issue: 1, Jan 2019

We conducted a meta-analysis to evaluate the role of the vitamin D receptor (VDR) polymorphism in the risk of hepatocellular carcinoma (HCC) in patients infected with hepatitis B virus (HBV). To develop new preventions, mechanisms, and therapies for HCC, it is important to investigate the underlying causes of HCC. Recently, there has been increasing attention to the relationship between VDR polymorphism and the risk of HBV-related HCC, but no specific conclusion has been made. PubMed/Medline, EMBASE, Cochrane Library, Chinese National Knowledge Infrastructure, VIP Database for Chinese Technical Periodicals, Wanfang Data, and SINOMED databases were searched until August 2018. Studies reporting VDR polymorphism and HBV-related HCC risks were included and the quality was assessed by Newcastle-Ottawa scale (NOS). Odds ratio (OR) and 95% confidence interval (CI) were calculated to compare the pooled data between HCC risks and different genotypes, such as FF, Ff, F, f, and ff, with each other. Three case-control studies with totally 728 HBV-related HCC cases and 920 HBV controls were included. When comparing HBV-related HCC cases with HBV controls, our data showed that all genotypes of Fok I polymorphism significantly increased the risk of HCC in the overall population (ff vs. FF: OR = 1.816, 95% CI = 1.161 - 2.841, P = 0.0009; Ff vs. FF: OR = 1.315, 95% CI = 1.037 - 1.667, P = 0.024; ff/Ff vs. FF, OR = 1.504, 95% CI = 1.206 - 1.876, P < 0.001; ff vs. FF/Ff: OR = 1.591, 95% CI = 1.270 - 1.992, P < 0.001; ff vs. Ff: OR = 1.435, 95% CI = 1.127 - 1.827, P = 0.003; f vs. F: OR = 1.375, 95% CI = 1.075 - 1.759). The results of our analysis suggest the “f” allele of Fok I polymorphism might be a risk factor for HCC in HBV-infected patients and it could be a predictive factor to screen HCC in HBV-infected patients. However, more accurate analyses and larger studies are needed.

The effect of bariatric surgery on non-alcoholic fatty liver disease is still controversial. In most cases, bariatric surgery results in hepatic improvement, but sometimes it can lead to impairment. We systematically reviewed the English literature for reports of stunting or deterioration of hepatic histology following bariatric surgeries through sequential liver biopsies to show the possibility of this negative occurrence by gathering all the reports regarding this event until March 2018. Underlying mechanisms, patient characteristics, possible risk factors, preventative strategies, presenting signs and symptoms, and available management options are discussed. This paper concludes that although rare, hepatic decompensation following bariatric surgeries can occur. Therefore, bariatric surgeons should be aware of the ways to prevent, monitor, and manage hepatic impacts.

Reports on HBV genotype I in Vietnam, Laos, northeastern India, and China are limited and thus, no studies have examined HBV genotype I quasi species with coexistence of HBsAg and anti-HBs. The current study reports on an HBV genotype I quasi species isolated from a male patient (A02) showing coexistence of HBsAg and anti-HBs. The researchers identified a HBV strain isolated from a CHB patient from Zhaotong city, Yunnan province, China, who was infected with HBV genotype I and presented HBsAg and anti-HBs coexistence. In an effort to elucidate the mechanism underlying the coexistence of HBsAg and anti-HBs in this patient, the researchers performed full-length genome amplification, and the HBV strain was cloned to conduct a comprehensive analysis of mutations and to analyze quasi species variation in relation to the coexistence of HBsAg and anti-HBs. The analysis indicated that the pre-core/core had the highest diversity, and HBsAg and MHBsAg accumulated more nonsynonymous mutations than synonymous mutations. Phylogenetic analyses and genotype identification suggest that A02 was infected with a putative genotype I strain. Unusual deletions of PreS (11 of 16 clones (69%) in PreS1) and amino acid variants of HBsAg (11 of 16 clones; 69%) were observed in the A02 quasi species that were associated with the coexistence of HBsAg and anti-HBs and other clinical features, thus conferring resistance to current antiviral therapies. Further functional studies are needed to assess the correlation between these variants and the coexistence of HBsAg and anti-HBs. The propensity for PreS1 deletions and the complexity of HBsAg variants in HBV isolates from a single patient infected with HBV genotype I could explain the coexistence of HBsAg and anti-HBs and the resistance to current antiviral therapies.

Patients undergoing dialysis treatment and hemodialysis are at risk of viral infections due to inadequate cellular immunity. The aim of the study was to determine the prevalence of hepatitis B virus (HBV), hepatitis C virus (HCV), and human immunodeficiency virus (HIV) in hemodialysis (HD) centers in North Cyprus. The present study reviewed the health records of 140 patients in two dialysis units that represented all HD units in North Cyprus. Serological markers for HBV, HCV, and HIV were determined by the immunoenzymatic assay using commercial diagnostic kits (Architect i2000 SR, Abbott, USA). HCV RNA, HBV DNA, and HIV RNA were determined quantitatively using polymerase chain reaction (PCR). One hundred forty HD patients were included in the study, consisting of 39.3% (n = 55) female and 60.7% (n = 85) male patients. Five (3.6%) patients were anti-HCV positive, one (0.7%) patient was HBsAg positive, and one (0.7%) was anti-HIV positive. Anti-HCV and HBsAg were negative in all of the patients according to the PCR results. There were no significant differences between males (1.2%) and females (7.3%) in terms of anti-HCV positivity (P = 0.078), HBsAg seropositivity (P = 0.607), and anti-HIV seropositivity (P = 0.607). The prevalence of HBV, HCV, and HIV infection in hemodialysis patients in North Cyprus is moderate to low. The main reason for the significantly lower rates compared to other areas could be effective protective measures and national vaccination.

The study aimed to investigate the role of miR-125b as a non-invasive biomarker in chronic hepatitis C. An observational study was conducted on 94 treatment-naïve HCV-infected patients (mean age 49.8 ± 11.5 years, 59.6% females). Liver fibrosis was assessed by transient elastography (TE) and the expression of miR-125b in plasma was quantified by real-time PCR. All patients were infected with HCV genotype 1b and had active viral replication, 42.6% had significant cytolysis, and 73.4% had increased serum gamma-glutamyl transferase (GGT) values. Significant fibrosis (liver stiffness measured by TE of > 7.1 kPa) was present in 61.7% of the patients. No significant associations were found between miR-125b expression and baseline HCV viral load (P = 0.56), IL28B polymorphisms (P = 0.5), alpha-fetoprotein levels (P = 0.27), and patients’ gender (P = 0.13) or age (P = 0.5). In a univariate analysis, the miR-125b expression level was significantly correlated with ALT (P = 0.001) and GGT levels (P < 0.0001). An up-regulated expression of miR-125b was found in plasma samples from patients with advanced liver fibrosis as compared to those with mild/moderate fibrosis [mean miR-125b value = 0.002 versus 0.001 (P = 0.02)]. In a multiple regression analysis, an upregulated miR-125b expression level remained independently in association only with significant fibrosis and increased GGT level (P = 0.026; R2 = 0.242). An up-regulated miR-125b expression might be an indicator of severe liver fibrosis in patients with chronic hepatitis C, independent of the viral replication level.