Category Ranking

98%

Total Visits

921

Avg Visit Duration

2 minutes

Citations

20

Article Abstract

Objective: To evaluate the relationship between mortality and HBVDNA and HBeAg expression of severe hepatitis B patients.

Methods: The mortality rates of different types of severe hepatitis patients in our hospital during the last five years were analysed. HBV DNA was detected using the fluorescence quantitative PCR method and the HBeAg expression of severe hepatitis B was studied using a microparticle method.

Results: (1) Hepatitis B morbidity was 83.5% in each type of severe hepatitis, and severe chronic hepatitis B morbidity was 96.77% in each type of severe chronic hepatitis. (2) The mortality rate of those with HBV DNA more than 1 x 10(5) copies/ml was 53.25% and the mortality of those with HBV DNA less than 1 x 10(5) copies/ml was 34.50% (P less than 0.01). The HBeAg expression had no influence on the death rate. (3) The death rate descended to 30.38% from 54.64% (HBV DNA more than 1 x 10(5) copies/ml) when treated with Lamivudine (P less than 0.01).

Conclusion: In severe hepatitis the quantity of virus carried in the patient is one of the key factors of mortality; antivirus treatment can lower mortality.

Download full-text PDF

Source

Publication Analysis

Top Keywords

severe hepatitis
24
hbv dna
20
hbeag expression
16
dna 105
12
105 copies/ml
12
hepatitis
9
severe
8
expression severe
8
hepatitis morbidity
8
type severe
8

Similar Publications

Portopulmonary hypertension (POPH), a subtype of pulmonary arterial hypertension (PAH), develops with portal hypertension and may persist after liver transplantation. While there have been successes using balloon-occluded retrograde transvenous obliteration (BRTO) for POPH, no reports exist on long-term follow-up. A 60-year-old man with hepatitis C cirrhosis developed POPH.

View Article and Find Full Text PDF

Background: Cytomegalovirus (CMV) viremia is a critical concern and known by the presence of the virus DNA in the blood, which poses sever risks and develops many complications in immuno-compromised patients. When CMV is untreated, it can cause pneumonitis, colitis, hepatitis, and encephalitis. Current diagnosis relies on molecular methods with qPCR as the preferred method.

View Article and Find Full Text PDF

The Proteomic Profiling of Circulating Extracellular Vesicles of Western Diet and Chemical-Induced Murine MASH Model.

Kaohsiung J Med Sci

September 2025

Hepatitis Research Center, College of Medicine; Center for Metabolic Disorders and Obesity; Center for Liquid Biopsy and Cohort Research, Kaohsiung Medical University, Kaohsiung, Taiwan.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is an increasingly prevalent chronic liver condition that can progress to severe complications such as metabolic dysfunction-associated steatohepatitis (MASH). Despite its growing burden, there are no reliable non-invasive biomarkers for tracking disease progression. In this study, we established a murine MASLD/MASH model using a high-fat diet and chemical (CCl) induction.

View Article and Find Full Text PDF

Objectives: To describe a rare case of transplantation-mediated alloimmune thrombocytopenia (TMAT) following liver transplantation from a donor with immune thrombocytopenia (ITP), and to contextualize findings within the literature.

Methods: We reviewed the clinical course of a 63-year-old man with hepatitis C cirrhosis and hepatocellular carcinoma who underwent orthotopic liver transplantation from a donor with severe thrombocytopenia consistent with ITP. Clinical, laboratory, and bone marrow findings were analyzed, and alternative causes of thrombocytopenia were excluded.

View Article and Find Full Text PDF

High morbidity and mortality associated with human β-coronavirus (CoV) infection highlight the need to determine host responses to infection and develop anti-viral therapies. Gap junction intercellular communication (GJIC), particularly involving Connexin43 (Cx43), is vital for maintaining central nervous system (CNS) homeostasis, and disruption of GJIC is a well-documented pathogenic mechanism among β-coronaviruses. Specifically, murine β-coronavirus, mouse hepatitis virus (MHV-A59) inoculation in the mouse brain causes acute-stage CNS viral spread and chronic neuroinflammatory demyelination while causing pronounced downregulation of Cx43 at the acute stage, reflecting a critical role in CNS pathology.

View Article and Find Full Text PDF