Virological tools, including serological and molecular tools, are needed to diagnose chronic hepatitis B and C infections. They may also be useful to establish their prognosis, but they have found their principal application in guiding treatment decisions and assessing the virological responses to therapy. The goal of chronic hepatitis B therapy is to prevent progression of liver disease. This is achieved if HBV replication is durably abolished or significantly reduced. In HBeAg-positive patients, HBeAg clearance followed by the HBe seroconversion phase can be achieved. In HBeAg-negative patients, long-term antiviral suppression of viral replication is needed. The loss of HBsAg, eventually associated with an HBs seroconversion, is the most desirable endpoint of therapy but is rarely achieved. The efficacy endpoint of chronic hepatitis C treatment is the sustained virological response, defined by an undetectable HCV RNA in serum with a sensitive assay 24 weeks after the end of treatment. The HCV genotype and on-treatment viral kinetics can be used to tailor treatment dosages and duration.
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http://dx.doi.org/10.1016/j.bpg.2008.11.004 | DOI Listing |
Cureus
December 2024
Hematology and Oncology, Roger Williams Medical Center, Boston University School of Medicine, Providence, USA.
Hepatocellular carcinoma (HCC) is one of the most common forms of primary liver cancer worldwide. Herein, we present a review article that provides a broad overview of the current landscape of HCC, including the etiology, potential risk factors, and molecular pathways that can serve as potential therapeutic targets. The risk factors tend to vary depending on the geographic distribution; hepatitis B-induced cirrhosis and HCC occur more frequently in Asia and Sub-Saharan Africa, whereas metabolic disorders are the culprits in Western Europe and the Americas.
View Article and Find Full Text PDFMetabol Open
March 2025
Hepatogastroenterology and Infectious Diseases Department, Faculty of Medicine, Al-Azhar University, Cairo, Egypt.
Background: Tissue damage by viral hepatitis is a major cause of morbidity and mortality worldwide. Oxidation reactions and reactive oxygen species (ROS) transform proteins and lipids in plasma low-density lipoproteins (LDL) into the abnormal oxidized LDL (ox-LDL). Hepatitis C virus (HCV) infection induces oxidative/nitrosative stress from multiple sources, including the inducible nitric oxide synthase (iNOS), the mitochondrial electron transport chain, hepatocyte NAD(P)H oxidases (NOX enzymes), and inflammation.
View Article and Find Full Text PDFGastro Hep Adv
August 2024
Value Evidence and Outcomes, GSK, London, UK.
Background And Aims: The aim of this systematic literature review (SLR) was to examine outcomes and associated predictors following nucleos(t)ide analog (NA) treatment cessation in adult patients with chronic hepatitis B virus infection.
Methods: The SLR was conducted according to PRISMA methodology. All included studies were quality assessed using appropriate scales or checklists.
Clin Infect Dis
January 2025
Veteran Affairs Portland Health Care System, Portland, OR, USA.
Background: Chronic hepatitis C virus (HCV) infection affects >1% of the U.S. population, higher among U.
View Article and Find Full Text PDFInflammopharmacology
January 2025
Department of Clinical Pharmacy, Faculty of Pharmacy, Tanta University, El-Gharbia Government, Tanta, Egypt.
Objective: This study aimed to assess the potential antifibrotic impact of zinc sulfate in chronic Hepatitis C Virus (HCV) patients receiving direct-acting antiviral therapy.
Methods: This randomized controlled study included 50 chronic HCV-infected patients with fibrosis stage (F1 & F2). Participants were randomly assigned to two groups: Group 1 (Control group, n = 25) received standard direct-acting antiviral therapy for 3 months, while Group 2 (Zinc group, n = 25) received 50 mg/day of zinc sulfate in addition to the standard direct-acting antiviral therapy for the same duration.
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