Background: The process of hepatic fibrosis is common to the various etiologies of chronic liver disease such as viral hepatitis B. Objective: To evaluate hepatic fibrosis by non-invasive markers such as Aspartate-to-Platelet Ratio Index (APRI), fibrosis-4 (FIB-4), fibrotest and fibroscan. Patients and Method: This was a descriptive study during a period of 32 months. Included in our study were the records of outpatients, chronic carriers of hepatitis B virus without viral co-infection C, D or HIV, followed in the Gastroenterology unit of the Campus Teaching Hospital of Lome-Togo. Results: We retained 222 patients. Among the patients, 148 patients (66.67%) were classified in Phase 3 (inactive carrying). Only 10 patients (4.50%) had a APRI score indicating a fibrosis stage ≥ F4 (presence of cirrhosis). A FIB-4 score indicating the presence of cirrhosis was found in 12 patients (5.40%). The most represented stage at fibrotest was the F0 stage (45.45%). Cirrhosis was noted in 6.06% of cases at fibroscan. Patients with APRI score ≤ 2 (96.23%) had a FIB-4 score ≤ 3.25, (p = 0.0088). Conclusion: The evaluation of hepatic fibrosis during chronic hepatopathies is essential for patients care because it influences therapeutic decisions.
BackgroundTenofovir alafenamide fumarate has been used in late pregnancy; however, no data exist regarding its safety and effectiveness in early and middle pregnancy for mothers with hepatitis B virus infection.AimsTo design a prospective study to investigate the efficacy and safety of TAF in pregnant women with chronic HBV infection during early-middle pregnancy.MethodsPregnant women with active chronic hepatitis B who received tenofovir alafenamide fumarate during early and middle pregnancy were enrolled and followed up until 6 months postpartum. Infants received immunoprophylaxis. The primary endpoint was the safety of mothers and infants. The secondary endpoints were maternal hepatitis B virus DNA reduction at delivery and mother-to-child transmission rate.ResultsAmong 98 mothers enrolled, 31 initiated tenofovir alafenamide fumarate in early pregnancy, and 57 in middle pregnancy. The mean (± standard deviation) age was 29.00 (±3.81) years. At delivery, 100% (98/98) of the mothers achieved hepatitis B virus DNA levels <200,000 IU/L. Ninety-eight infants were born, and none had congenital defects or malformations. All infants received hepatitis B virus immunoprophylaxis. The mother-to-child transmission rate was 0%. Growth parameters including body weight, height, and head circumference were comparable to the national standards for physical development. No severe adverse effects were reported in either mothers or infants. No severe liver function damage occurred in any of the mothers.ConclusionsInitiating tenofovir alafenamide fumarate in early and middle pregnancy appears safe for both mothers and infants, and it is effective for controlling maternal disease as well as interrupting mother-to-child transmission.
Hepatitis B Virus (HBV) infection is the major risk factor for hepatocellular carcinoma (HCC) in East Asia. Here we aimed to further investigate the abundance of viral antigen and DNA within HBV-related HCC and surrounding tissues at histological level.
In addition to routine histopathology, in situ hybridization (ISH) of HBV DNA and immunohistochemistry (IHC) of HBsAg were performed in tissues from 131 HBsAg-positive HCC patients undergoing liver resection. Serum α-fetoprotein together with basic biochemical and immunological parameter was also measured.
Overall, the ISH of HBV DNA and IHC of HBsAg showed 31.3% and 92.9% positive rate respectively (p < 0.0001). The level of correlation between these two markers was much more significant in tumor (p < 0.0001) than in tumor-surrounding tissue (p = 0.01). HBsAg exhibited a much higher positive rate in tumor-adjacent tissue than in tumor tissue (86.6% versus 29.9%, p < 0.0001) with significantly different staining pattern. By contrast, the positive rate of HBV DNA ISH was comparable in tumor and surrounding tissue (17.6% versus 22.9%, p = 0.36). Yet the HBV DNA signal in tumor tissue showed predominant nuclear localization (87.0%) whereas staining pattern in adjacent tissue was mixed (43.3% nuclear localization, p = 0.0015). Finally, no significant association between intra-tumor HBV DNA/HBsAg positivity and major histological markers (microvascular invasion, tumor differentiation, etc.) or recurrence after surgery was observed.
These data confirmed the largely integrated state of HBV DNA, weaker expression and altered localization of surface antigen in tumor compared with surrounding tissue. The strikingly different prevalence and localization of HBsAg and HBV DNA reflected the complex and heterogeneous mechanisms leading to HBV-induced tumorigenesis.
Background: Hepatic jaundice results from abnormal metabolism of bilirubin in the liver. The main hepatic jaundice causes are severe damage to hepatocytes due to autoimmune diseases, infectious diseases, drugs/ medication induced, or, less commonly, hereditary genetic diseases.
Aim: The aim of this study is to determine the prevalence of hepatitis B Virus (HBV), hepatitis A virus (HAV), and hepatitis C virus (HCV), in patients with hepatic jaundice as causes of acute viral hepatitis (AVH) in Sana'a city, Yemen.
Subjects and Methods: Data of patients with hepatic jaundice tested for hepatitis B surface antigen, total anti-HCV antibody, and anti-HAV immunoglobulin M (IgM) by enzyme-linked immunosorbent assay were collected from Class I Viral Diagnostic Laboratories in Sana'a for 3 years. Then the statistical analysis of the data was used where the descriptive analysis was calculated: frequency and percentage, as well as the association of infection with sex and age group by means of detection odds ratio, 95% CI and X2 more than 3.9 and P<0.05 were considered statistically significant.
Results: The study included 644 males (43.8%) and 826 females (56.2%), while most patients were less than 21 years old. The rate of Hepatitis viruses positive was 27.6% positive. Hepatitis A virus infection was the most common virus diagnosed accounting for 259 cases (17.6% of the total), while HBV was less common with 104 (7.1%) and HCV only 42 cases (2.9%). The highest incidence of hepatitis B was in 11-20 years patients (18.2%), with an associated OR 9.3 (p < 0.0001). The highest incidence of hepatitis C was in 31-40 years patients (7.3%), with an associated OR 3.3 (p<0.0001).
Conclusion: Alarmingly changing the epidemiology and dynamics of hepatitis A-C viruses in Yemen, a detailed study is required to understand the definite disease problem caused by these viruses. It is noticeable in this study the high prevalence of hepatitis A virus and hepatitis B virus in the Yemeni population with hepatic jaundice. Also, to our knowledge, this study is the first to report epidemiological transformation of hepatitis A virus in Sana'a, Yemen.
Peer Review History:
Received: 13 November 2021; Revised: 11 December; Accepted: 30 December, Available online: 15 January 2022
Academic Editor: Dr. Nuray Arı, Ankara University, Turkiye, [email protected]
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Received file: Reviewer's Comments:
Average Peer review marks at initial stage: 5.5/10
Average Peer review marks at publication stage: 7.0/10
Dr. Gulam Mohammed Husain,, National Research Institute of Unani Medicine for Skin Disorders, Hyderabad, India, [email protected]
Dr. Salfarina Ramli, Department of Pharmacology and Pharmaceutical Chemistry, Faculty of Pharmacy, Universiti Teknologi MARA, 42300 Puncak Alam, Selangor, Malaysia. [email protected]
PREVALENCE OF DIFFERENT HEPATITIS B VIRUS GENOTYPES AND RISK FACTORS ASSOCIATED AMONG SELECTED YEMENI PATIENTS WITH CHRONIC HEPATITIS B INFECTION
SERO-EPIDEMIOLOGICAL STUDY OF HEPATITIS B, C, HIV AND TREPONEMA PALLIDUM AMONG BLOOD DONORS IN HODEIDA CITY- YEMEN
EXPLOSION OF HEPATITIS B AND C VIRUSES AMONG HEMODIALYSIS PATIENTS AS A RESULT OF HEMODIALYSIS CRISIS IN YEMEN
The hepatitis B virus (HBV) core protein (HBc) functions in multiple steps of the viral life cycle. Heteroaryldihydropyrimidine compounds (HAPs) such as Bay41-4109 are capsid protein allosteric modulators that accelerate HBc degradation and inhibit the virion secretion of HBV, specifically by misleading HBc assembly into aberrant non-capsid polymers. However, the subsequent cellular fates of these HAP-induced aberrant non-capsid polymers are not well understood. Here, we discovered that that the chaperone-binding E3 ubiquitin ligase protein STUB1 is required for the removal of Bay41-4109-induced aberrant non-capsid polymers from HepAD38 cells. Specifically, STUB1 recruits BAG3 to transport Bay41-4109-induced aberrant non-capsid polymers to the perinuclear region of cells, thereby initiating p62-mediated macroautophagy and lysosomal degradation. We also demonstrate that elevating the STUB1 level enhances the inhibitory effect of Bay41-4109 on the production of HBeAg and HBV virions in HepAD38 cells, in HBV-infected HepG2-NTCP cells, and in HBV transgenic mice. STUB1 overexpression also facilitates the inhibition of Bay41-4109 on the cccDNA formation in de novo infection of HBV. Understanding these molecular details paves the way for applying HAPs as a potentially curative regimen (or a component of a combination treatment) for eradicating HBV from hepatocytes of chronic infection patients.
Hepatitis B virus (HBV) reactivation associated with various therapeutic interventions is an important cause of morbidity and mortality in patients with current or resolved HBV infection. Because no curative treatment for HBV infection is yet available, there are many individuals at risk for HBV reactivation in the general population. Populations at risk for HBV reactivation include patients who are currently infected with HBV or who have been exposed to HBV in the past. HBV reactivation and its potential consequences is a concern when these populations are exposed to anti-cancer chemotherapy, immunosuppressive or immunomodulatory therapies for the management of various malignancies, rheumatologic diseases, inflammatory bowel disease, or solid-organ or hematologic stem cell transplantation. Accordingly, it has become important to understand the basics of HBV reactivation and the mechanisms by which certain therapies are more susceptible to HBV reactivation. This review aims to raise the awareness of HBV reactivation and to understand the mechanisms and the risks of HBV reactivation in various clinical settings.