View clinical trials related to Hepatitis A.
Filter by:Interleukin 29 (IL-29) is a substance that is produced in the body to help fight viral infections. The purpose of this study is to test the safety and antiviral effects of PEG-rIL-29 (a man-made form of IL-29) when it is given either by itself at different doses or in combination with the approved dose of ribavirin (an antiviral drug) to subjects with hepatitis C infection who have received no prior treatment for this disease or who have relapsed following previous treatment with PEGylated interferon alpha (PEG-IFN-α), or other form of IFN-α, and ribavirin.
The aim of the study was to verify the influence of Agaricus blazei (Murrill) ss. Heinemann (A. blazei) on the evolution of nutritional state and liver function in hepatitis C patients.
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.
The purpose of this study is to investigate how efficient TMC435350 will work against the Hepatitis C virus genotype 1 (genotypes refer to the genetic constitution of the virus) and what the concentrations of TMC435350 in the blood are with or without pegylated interferon alpha-2a (PegIFNa-2a) or PegIFNa-2a plus ribavirin.
The purpose of this study is to assess the effect of telaprevir on early hepatitis (inflammation of the liver) C virus (HCV) viral kinetics in treatment-naive participants who are chronically (lasting a long time) infected with genotype 2 or 3 HCV.
Insulin resistance is known to adversely effect viral response to treatment in hepatitis C patients We are aiming to study the effect of an insulin sensitizer, metformin, in viral response of hepatitis C to treatment with pegylated interferon and ribavirin in a double blind randomized controlled trial
A multi-center and open study to compare the safety and effectiveness of switching treatment from lamivudine to clevudine for 24 weeks.
The primary objective of this study is to evaluate the effectiveness of TCM-700C as an add-on treatment to the combination drug therapy (Peginterferon α-2b plus Ribavirin) for patients with genotype 1 chronic hepatitis C infections. This will be demonstrated by a higher sustained virologic response rate, defined as the absence of detectable HCV RNA 24 weeks after the termination of combinational drug treatment, compared with the placebo add-on.
Hypothesis: A regimen of low dose of peginterferon alfa-2a plus ribavirin may be as effective as currently recommended regimen for chronic hepatitis C in HIV-coinfected patients. Objective: To evaluate the efficacy of lower dose of pegylated interferon-α 2a (135 µg weekly) plus ribavirin and a shorter duration of treatment (20 weeks after achieving an undetectable plasmatic HCV-RNA)than the current recommended in patients with chronic hepatitis or compensated cirrhosis by hepatitis C virus, genotypes 2 or 3, in HIV-coinfected patients in real use conditions. Method: Phase IV, postautorization, open labelled multicenter trial with a planned duration of 118 weeks in which 71 patients from several hospitals of the Servicio Andaluz de Salud will be enrolled. The usual clinical and analytical follow up will be performed but additional blood samples will be obtained for determination of interferon and ribavirin plasma levels. The primary end point wall be a sustained virologic response (defined as an undetectable serum HCV-RNA after 24 weeks after the cessation of treatment). Likewise, rapid virological response (at 4 weeks of treatment), early virological response (at 12 weeks), and end of treatment response rates will be evaluated as well as their relationships with the plasma interferon an ribavirin concentrations determined by ELISA and HPLC, respectively. The safety and tolerability of the studied medications will be evaluated by means of clinical adverse events, physical examination and laboratory results.
The primary purpose of this study is to evaluate the safety profile and tolerability of single oral doses of daclatasvir in subjects with chronic hepatitis C infection