Active clinical trials for "Hepatitis A"

The study is to observe the therapeutic effects and long-term follow-up after ending anti-HBV therapy with nucleos(t)ide analogs in patients with chronic hepatitis b.

This study is to investigate the long-term outcomes and prognostic risk factors in patients recovered from hepatitis B virus related acute on-chronic liver failure.

To analyze the incidence of liver cancer after entecavir administration among patients with low viral load and cirrhosis due to chronic hepatitis B infection.

Aim of the work To estimate frequency of viral HB & C infection in ITP patients who received triple therapy in comparison with another group treated with steroids only. To explore risk factors and routes of transmission of viral HB & C infection in ITP patients who received triple therapy and the another group treated with steroids . - To assess preventive measures of viral HB& C infection in the hematology ward To investigate the influence of viral HB & C infection on clinical picture, response to treatment and side effects in ITP patients who received triple therapy or steroids.

The current first-line treatment for HBV is long-term oral antiviral drugs to inhibit HBV DNA replication. First-line antiviral drugs recommended by the Chinese 2015 Hepatitis B Guidelines include ETV and TDF. This study is based on a real-world clinical cohort to retrospectively analyze the effects of ETV and TDF on the long-term (5-year) incidence of HCC in Chinese patients with chronic hepatitis B with compensated cirrhosis. The results will guide the revision of the Chinese HBV guidelines.

An observational study will be performed in subjects aged 3-65 years old to describe the dynamic changes of cellular immunity after vaccination of hepatitis B vaccine, and to find out the expression levels of Th9 cells and IL9 in subjects with different response to the primary immunization (3 single -dose injunctions).

This study aims to gain an understanding of the key components of the immune response to hepatitis B present in cord blood of HBV infected mothers.

The purpose of this study is to examine gene expression profiles by DNA microarray in patients who are responders and non-responders to interferon and ribavirin treatment for hepatitis C virus (HCV). Genes involved in inflammation and fibrosis and mediators of the Th-1 lymphocyte response will be looked for. It is hoped that genetic targets for future more effective and less toxic treatments will be identified.

The purpose of this research is to study body materials like blood proteins as well as white blood cell and liver cellular RNA in individuals with liver diseases such as chronic viral hepatitis with or without hepatoma and autoimmune liver disease. Presently it is not understood how infection with chronic viral hepatitis or autoimmune liver disease damages the liver. This research study enroll patients with either chronic viral hepatitis with or without hepatoma or autoimmune liver disease. The purpose of this study is to find the genes that are expressed in both the circulating white blood cells and the liver of patients with varying degrees of liver damage of different causes. Genes are biological messengers some of which determine how the body responds to injury. We anticipate that results from Differential Gene Expression (DGE) analysis will allow us to make predictions about likelihood of disease progression and/or response to treatment. In addition we will test the blood for markers of injury. The blood collected will be prepared differently from the liver tissue. We will use technologies to express pure proteins and then we will investigate the functions of these proteins. Nearly all drugs act on proteins, not genes, so understanding proteins is the key to really effective new medicines. Similarly the first signs of ill health appear in changes to the body's blood proteins, making them the most sensitive diagnostic indicators. The studies we plan are called proteomics. We will later correlate the patterns of gene expression in both circulating white blood cells and the liver tissue with clinical outcome and patterns of proteins measured in blood and we hope to gain an understanding of how the disease process occurs, which may in turn help us to make more precise diagnoses and develop new forms of treatment. These techniques that we use are still experimental and so we do not yet know if they will be helpful in monitoring changes which may help us to predict the potential severity of your liver disease or even if they can be used to indicate who will best respond to treatment.

A large number hepatitis B surface antigen positive individuals are HBeAg negative with normal liver tests. Historically, such patients were thought to have suppressed viral replication and were considered to be at low risk for complications. With the use of more sensitive technology, physicians are now able to identify a group of patients who are HBeAg negative, have normal liver enzymes, and detectable HBV DNA. Some of these patients develop signs of liver inflammation and fibrosis on biopsy. We intend to investigate whether normal, programmed cell death (apoptosis) plays a role in causing the silent liver injury in this group of patients. In other words the purpose of this study is to see whether apoptosis may be responsible for the silent liver death and injury that occurs in these so called inactive carriers who are HBeAg negative, have normal serum ALT values and HBV DNA > 10,000 copies/mL. In this study the liver biopsies would be routinely collected in the clinic and investigated for the evidence of inflammation and fibrosis, and special testing would be performed to detect for evidence of apoptosis. Around 30 patients from UHN would be participating in this study. This study will test the hypothesis that subjects who are HBeAg negative, have normal ALT and have HBV DNA ≥10,000 copies/mL will demonstrate an increased rate of apoptosis in liver tissue compared to healthy age-matched controls. If this hypothesis is confirmed, it will imply that the previous assumption that this group of patients has inactive disease is false and would implicate apoptosis as an important mechanism responsible for causing liver damage. If apoptotic activity is indeed elevated, further study of these pathways could potentially yield therapeutic interventions to inhibit apoptosis.