Hepatitis Monthly
Volume:21 Issue: 1, Jan 2021

Angiogenesis is closely related to the development and progression of hepatocellular carcinoma (HCC). Angiogenic factors have been confirmed to be overexpressed in HCC. The hepatitis B virus preS2 domain is a transactivator that plays an important role in hepatitis B virus (HBV)-related HCC. Here, we aimed to investigate the potential of the preS2 domain in inducing angiogenesis in HCC. A total of 25 cases of pathologically confirmed HCC were screened. The levels of preS2, CD34, and vascular endothelial growth factor A (VEGFA) in HCC samples were evaluated by immunohistochemistry (IHC). The proliferation of vascular endothelial cells was detected by CCK-8. Besides, VEGFA was analyzed by Western blot in HCC cells. The effect of preS2 on the VEGFA promoter was measured by dual-luciferase reporter assays. We found that preS2 domain-positive HCCs had significantly higher microvessel density (MVD) and VEGFA expression than preS2 domain-negative HCCs. Overexpression of preS2 upregulated VEGFA expression in HepG2 and activated vascular endothelial cell proliferation. However, blocking preS2 expression reduced VEGFA expression in HepG2.2.15 and inhibited the proliferation of vascular endothelial cells. In addition, a dual-luciferase assay indicated that the preS2 domain could activate VEGFA promoter activity. In conclusion, we showed that the expression of the preS2 domain promotes angiogenesis by transactivating the VEGFA promoter in HCC.

 To assess the association between hepatic venous pressure gradient (HVPG) baseline and the response rate of cirrhotic in patients who received carvedilol treatment.

 In total 48 cirrhotic patients with a basic HVPG value greater than 12 mmHg were included (from July 2011 to October 2014). All patients received carvedilol treatment and underwent the second HVPG measurement 7 days later. In the following, all participants received an endoscopic variceal ligation (EVL) treatment.

 HVPG was significantly reduced from 16.04 ± 3.10 to 12.76 ± 5.26 mmHg following carvedilol treatment. The response rate was about 58.33% (28/48). The response rate of the HVPG < 16 mmHg group (71.4%) was significantly higher than that of the HVPG ≥ 16 mmHg group (40%) (P < 0.05). Patients were followed up for a median of 26 months, ranged from 6 to 33 months. During the follow-up period (two years), the rebleeding rate was 9.97% and 49.56% in HVPG < 16 and HVPG ≥ 16 mmHg groups, respectively, with a statistically significant difference (P = 0.004). Also, the mortality rate (at 2 years) was 5.26% and 21.05%, respectively, which was significant (P = 0.035).

 This study demonstrated that the response rate of carvedilol on portal hypertension may be affected by the HVPG baseline, and the carvedilol was effective in reducing HVPG, especially for those with a HVPG < 16 mmHg.

 Glecaprevir/pibrentasvir (GLE/PIB) is the latest approved pan-genotypic direct-acting antiviral agent (DAA) for the treatment of chronic hepatitis C virus (HCV) infection. However, real-world data of GLE/PIB in European patient cohorts are limited.

 A single-center cohort of 100 unselected HCV patients seen at the Outpatient Clinic of the University Medical Center Hamburg-Eppendorf from October 2017 until September 2019 was retrospectively analyzed by chart review with a special focus on demographic clinical and virologic aspects as well as treatment compliance outcome.

 A total of 99 patients with chronic HCV infection (genotype (GT) 1 - 6), who started antiviral treatment with GLE/PIB, were included. Treatment duration lasted from 4 to 16 weeks. The primary endpoint was a sustained virological response at week 12 (SVR12) after the end of treatment (EoT). Only three patients (3/100; 3%) were diagnosed with liver cirrhosis by non-invasive measures. Ten patients (10/100; 10%) were pre-treated with Interferon (IFN) containing regiments. Most patients received 8 weeks of treatment (96/100; 96%). One patient discontinued treatment after four weeks due to poor compliance (1/100; 1%). A high number of patients were lost to follow-up (22/100; 22%). All patients who were regularly seen to follow-up visits (76/100; 76%) achieved SVR12 (76/76; 100%). Virological relapse occurred in none of the patients. Adverse events (AEs) were rarely reported (4 patients) (4/100; 4%), and none of these patients discontinued treatment.

 This study demonstrated that initial and re-treatment with GLE/PIB were effective and safe in a German cohort with chronic HCV infection in real-life settings, regardless of GT.

 Behcet's disease (BD) is a chronic multisystem vasculitis with an unknown etiology. During the past years, several reports are published on the occult hepatitis B infection (OBI), the presence of hepatitis B virus (HBV) DNA in the absence of HBsAg, in rheumatic diseases.

 The current study aimed to, firstly, investigate the prevalence of OBI in patients with BD, and, secondly, its potential association with the clinical and therapeutic status of BD.

 HBV serological markers and HBV DNA were evaluated in 220 consecutive BD patients to detect OBI. Demographic and clinical data of OBI positive and negative groups were compared.

 The mean age of patients was 39.24 (± 10.57), and 134 (62.9%) were male. The mean disease duration was 14.13 (± 8.63) years. No HBsAg positive case was found, but HBV DNA was found in 19 (8.6%) patients. The median viral load value was 475.84 copy/mL. We compared clinical data of 10 OBI positive and 156 OBI negative BD patients with complete and accessible data. There was no difference between the two groups concerning demographic characteristics (age, sex, and disease duration), different clinical manifestations, or types of medications (immunomodulatory, cytotoxic, and corticosteroids).

 This is the first study showing a rather high prevalence of OBI among BD patients. We did not find any correlation between OBI positivity and different clinical manifestations, medications, or HLA-B51. Further studies are needed on a larger group of patients and by molecular HBV evaluation (as well as serologic) regarding this possible association.
 

About 5% of cases with chronic hepatitis B virus (HBV) are co-infected with hepatitis D virus (HDV), and this co-infection possesses a high risk for hepatocellular carcinoma (HCC) and cirrhosis. We aimed to evaluate the epidemiological and histopathological characteristics ‎and response to treatment in patients with HBV and HDV co-infection in a hepatitis clinic in Tehran, Iran. In this study, 80 patients were enrolled and evaluated for age, sex, degree of liver fibrosis, virologic status, and response rate. The incidence of co-infection of hepatitis B and D was 4.9% (80/1,631 HBV-infected cases) in our clinic. Thirty-seven (46.25%) patients had liver cirrhosis, and four (5%) patients had HCC. Besides, HDV Ribonucleic Acid (RNA) polymerase chain reaction (PCR) was positive for 31 (38.75 %) patients. Among 30 patients, 14 (46.6%) completed interferon therapy (for equal to or more than 48 weeks) and had a response with undetectable HDV RNA PCR after treatment. According to our results, for cirrhotic patients in HBV/HDV co-infection that was about 46%, it seems that the early detection of HDV antibody (Ab) plays a significant role in the prevention of progressive liver failure, and treatment with interferon can help these patients by improving the prognosis.