Objectives: To study the relationship between liver pathology and clinical characters of chronic HBV carriers.
Methods: Analyze the age, sex, grade of liver inflammation and stage of liver fibrosis among patients with chronic HBV carriers (n = 58) and non-active HBsAg carriers (n = 32), and compare the grade of liver inflammation and stage of liver fibrosis in different groups according to age, ALT levels and with/without HBeAg. The data was processed by using t test or Chi-square test for statistical analysis, respectively.
Results: (1) No differences existed in gender composition ratio between chronic HBV carriers and non-active HBsAg carriers. However, the ages of non-active HBsAg carriers group (35.2+/-7.6) were much older than that of the HBV carriers group (24.7+/-4.8) (t = 2.576, P = 0.017). (2) The stage of liver fibrosis in non-active HBsAg carriers group was more aggravated than that of the chronic HBV carriers group (Chi-square = 23.231, P less than 0.01), whereas no significant differences existed between these 2 groups (Chi-square = 0.058, P = 0.972). (3) As to the grade of liver inflammation and the stage of liver fibrosis, significant differences existed between the groups with higher level of serum ALT (20-40 U/L) and lower level ( is less than or equal to 20 U/L) (Chi-square = 7.827, P = 0.008; Chi-square = 14.303, P = 0.001), and similar results also existed between elder group (more than 40) and younger group (is less than or equal to 40) (Chi-square = 10.949, P = 0.001; Chi-square = 21.271, P less than 0.01); (4) Among the chronic HBV carriers, significant differences existed in grade of liver inflammation between groups with HBeAg positive and negative patients (Chi-square = 10.275, P = 0.002), and the latter was more aggravated; however, there was no difference in stage of liver fibrosis between them (Chi-square test = 3.457, P = 0.178).
Conclusion: Liver histopathology can be recommended to guide the clinical diagnosis and treatment, especially for the chronic HBV carriers, with elder age, ALT close to normal and HBeAg negative.
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http://dx.doi.org/10.3760/cma.j.issn.1007-3418.2010.06.009 | DOI Listing |
J Glob Infect Dis
December 2024
Department of Basic Medical Sciences, College of Medicine, King Saud Bin Abdulaziz University for Health Sciences, Jeddah, Saudi Arabia.
Introduction: Hepatitis B and C are viral infections causing chronic liver inflammation and, when left untreated, lead to cirrhosis and a risk for hepatocellular carcinoma, the most common type of primary liver cancer with high mortality. The hepatitis B virus-hepatitis C virus (HBV-HCV) coinfection leads to a faster progression to advanced liver diseases and higher hepatocellular carcinoma (HCC) risk than monoinfection. Unlike the relative risk for HCC due to either HBV or HCV, no recent analysis of the risk for HBV-HCV coinfection exists.
View Article and Find Full Text PDFBMC Infect Dis
January 2025
School of Medicine, College of Medicine and Health Sciences, Wachemo University, Hossana, Ethiopia.
Background: Human hepatitis is an inflammation of the liver brought on by the DNA virus known as the hepatitis B virus (HBV). Around the world, 240 million people are thought to have HBV in a chronic state. The prevalence of viral hepatitis is extremely high in Africa.
View Article and Find Full Text PDFPLoS Pathog
January 2025
Department of Infectious Diseases, Shanghai Institute of Infectious Diseases and Biosecurity, Shanghai Key Laboratory of Infectious Diseases and Biosafety Emergency Response, National Medical Center for Infectious Diseases, Huashan Hospital, Fudan University, Shanghai, China.
Hepatitis B virus (HBV) X protein (HBx) is a key factor for regulating viral transcription and replication. We recently characterized homeobox protein MSX-1 (MSX1) as a host restriction factor that inhibits HBV gene expression and genome replication by directly binding to HBV enhancer II/core promoter (EnII/Cp) and suppressing its promoter and enhancer activities. Notably, HBx expression was observed to be repressed more drastically by MSX1 compared to other viral antigens.
View Article and Find Full Text PDFFront Immunol
January 2025
Univ. Grenoble Alpes, Inserm U 1209, CNRS UMR 5309, Institute for Advanced Biosciences, Grenoble, France.
Background: Patients with chronic hepatitis B virus (HBV) infection are characterized by impaired immune response that fails to eliminate HBV. Immune checkpoint molecules (ICMs) control the amplitude of the activation and function of immune cells, which makes them the key regulators of immune response.
Methods: We performed a multiparametric flow cytometry analysis of ICMs and determined their expression on intrahepatic lymphocyte subsets in untreated and treated patients with HBV in comparison with non-pathological liver tissue.
J Viral Hepat
March 2025
Department of Infectious Diseases, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Current guidelines to prevent hepatocellular carcinoma (HCC) by chronic hepatitis B virus (HBV) infection are based on risk assessments that include age, sex, and virological and biochemical parameters. The study aim was to investigate the impact of predictive markers on long-term outcomes. The clinical outcomes of 100 patients with chronic hepatitis B were investigated 30 years after a baseline assessment that included liver biopsy.
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