View clinical trials related to Hepatitis B.
Filter by:The new formulation administered as a 4th consecutive dose will be compared to the current formulation of the vaccine in this partially double blind study. The study will be double-blind with respect to the two DTPa-HBV-IPV/Hib groups. The study will be open with respect to the DTPa-HBV-IPV group.
This protocol posting describes the booster phase of the study. The objectives & outcome measures of the primary phase are presented in a separate protocol posting (NCT number = NCT00289731).
Cirrhosis is a diffuse lesion characterized by architectural distortion of the liver because of collagen deposition and development of nodules of regenerating hepatocytes. It is an irreversible change that results from diseases characterized by chronic liver injury (Fujimoto, 2000). Cirrhosis alters the pattern of blood flow through the liver and results in impaired perfusion of hepatic lobules with intrahepatic and extrahepatic shunting of blood. This deprives hepatocytes of uniform perfusion by arterial and portal venous blood resulting in both portal hypertension and other consequences of cirrhosis including impaired protein synthesis and altered drug metabolism. The histologic diagnosis of cirrhosis requires the presence of regenerative nodules or pseudolobules completely encircled by fibrosis such as congenital hepatic fibrosis can result in portal hypertension in the absence of cirrhosis (Anthony et al., 1977). The events leading to the development of cirrhosis are generally those of chronic injury with hepatocyte destruction. Acute severe liver injury as in fulminant viral hepatitis does not result in cirrhosis and the liver generally returns to normal after recovery. Cirrhosis can be classified by macroscopic appearance, by cause, and by histologic appearance and location of liver damage. Micronodular cirrhosis is composed of uniform nodules less than 3 mm in diameter, whereas macronodular cirrhosis has varying size nodules greater than 3 mm diameter. Mixed nodular cirrhosis has nodules of both sizes. Some liver diseases such as alcoholic liver disease may present as micronodular cirrhosis and develop larger nodules with subsequent regeneration of hepatocytes. For this reason, many prefer etiologic classification (e.g., alcoholic cirrhosis). The designation of cirrhosis as post necrotic, biliary and portal are still commonly used and imply predominant histologic location of fibrosis. Cirrhosis is an irreversible disease, and attempts should be made to stabilize the patient and to control the cause. Factors that indicate a poor outcome include an elevated prothrombin time that does not correct itself with parenteral vitamin K, upper gastrointestinal bleeding caused by varices, ascites refractory to therapy, increased age of the patient, sever malnutrition, spontaneous bacterial peritonitis, a pronounced increase of serum bilirubin in the absence of haemolysis, and heptocellular carcinoma (Yeh et al., 2003). In general, all causes of upper GI bleeding are associated with an increased mortality in patients with cirrhosis. For those with alcoholic cirrhosis who lack portal hypertension, survival is similar to an age-matched cohort if alcohol intake is stopped (Nakamura et al., 1991). If ethanol consumption continues, mortality is higher. Cirrhosis can be present without clinically significant complications and be identified only at autopsy or during evaluation of abnormal liver tests (Mendez et al., 2003). However, for many patients the disease is slowly progressive resulting in one or more complications. The clinical manifestations of cirrhosis are a result of altered hepatic blood flow through the liver with intrahepatic shunting causing impaired perfusion of hepatocytes or portal hypertension with shunting of blood around the liver though portosystemic communications. The major complications of portal hypertension include oesophageal or gastric varices, ascites, portosystemic encephalopathy, and hepatorenal-syndrome (Menon & Kamath, 2000). With impairment of hepatocyte perfusion or reduction of hepatocyte number, altered synthetic function can result in hypoalbuminemia, hypoprothrombinemia, and changes in drug metabolism. Vitalliver is a Chinese medicine which is administered in the form of a suppository, which is uncommon for most Chinese medicines. Medications released from the suppositories are absorbed directly from the circulation around the rectum and then reach the liver via the portal vein. Basic pharmacological studies have shown that Vitalliver has good immunomodulating functions, increases the activities of T-cells, B-cells and NK cells, therefore this formulation may have special values in treating liver diseases.
A open-labeled phase lV study with 96 weeks of treatment period. The purpose of this study is to investigate safety and efficacy of clevudine in patients chronically infected with hepatitis B virus, HBeAg positive or negative.
A multi-center and open study to compare the safety and effectiveness of switching treatment from lamivudine to clevudine for 24 weeks.
This study is to evaluate the antiviral efficacy of add-on adefovir to telbivudine in non-responders to telbivudine monotherapy after 24 and 36 initial weeks. Antiviral efficacy is assessed by hepatitis B virus (HBV) DNA non-detectability (PCR <300 copies/ml) by week 104 with CHB.
The purpose of this study is to determine if DNA vaccination of chronic HBV patients under treatment with NRTI can restore T-cell responsiveness and delay virologic reactivation after treatment discontinuation.
The purpose of this study is to determine the efficacy and safety of two dosages of PegIntron for treating hepatitis B e antigen (HBeAg) positive chronic hepatitis B compared with the approved dosage, which is PegIntron 1.0 microgram (mcg)/kg given once a week for 24 weeks. This study compares dosages of (1) 1.5 mcg/kg once a week for 24 weeks and (2) 1.5 mcg/kg once a week for 48 weeks with the approved dosage. All subjects are followed for 24 weeks after their treatment ends.
The present trial is a follow-up of AL203 study (NCT00343889). Primary Objectives: To describe the antibody persistence at 15 to 18 months of age and the booster effect of a dose of DTaP-HB-PRP~T or Tritanrix-HepB/Hib™ (given concomitantly with Oral Polio Vaccine [OPV]). Secondary Objective: To describe the safety profile of a booster dose of DTaP-HB-PRP~T or Tritanrix-HepB/Hib™ when administered concomitantly with OPV in each vaccine group.
Antiviral resistance mutations limit the efficacy of therapy for chronic hepatitis B. At year 2, resistance to adefovir may occur as high as 25% in patients with history of lamivudine resistance. Resistance to entecavir is reported to be 10% in lamivudine refractory patients during the same period. However, combination of lamivudine and adefovir decreased the adefovir resistance rate as low as 0% in the recent studies. By overcoming the antiviral resistance, the efficacy of therapy will be maximized. This study is intended to compare the efficacy of two strategies, combination of lamivudine and adefovir vs. entecavir monotherapy in patients with lamivudine resistance.