Active clinical trials for "Liver Diseases"

The main objective of this study is to analyze the pathophysiological implications of glucagon and the incretin hormones in patients with liver disease (Non alcoholic fatty liver disease (NAFLD) or cirrhosis) with and without diabetes compared with healthy controls. The present study will contribute significantly to the understanding of the pathophysiology of liver disease and glucose metabolism. The final goal is that the results could pave the way for new treatment modalities for patients with liver disease.

Specific urine proteases or groups of these enzymes can be reliable biomarkers and an effective gauge of response to therapy in patients with hepatocellular carcinoma.

The pathogenesis of nonalcoholic fatty liver disease has not been fully elucidated. The most widely supported theory implicates insulin resistance as the key mechanism leading to hepatic steatosis, and perhaps also to steatohepatitis. Selenoprotein P(SeP) is a secretory protein primarily produced by the liver. Previous studies demonstrated that SeP, a liver-derived secretory protein, causes insulin resistance. Therefore, the purpose of this study is to determine the different Sep levels between healthy normal group and NAFLD group.

The study is designed to assess the feasibility of evaluating YSPSL for the amelioration of ischemia reperfusion injury following liver transplantation by administering YSPSL into the liver graft directly ex vivo via the portal vein and to the recipient intravenously prior to reperfusion. Recently, P-selectin expression has been associated in liver grafts with prolonged cold storage times and rejection. By examining biomarkers of IRI including P-selectin by immunohistochemistry and/or quantitative PCR, liver histology and hepatic blood flow using established techniques, the goal of this study is to evaluate the feasibility of using these modalities for future studies of safety and efficacy.

Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in affluent countries. It may progress to cirrhosis and liver cancer. At present, there is no approved drug for NAFLD. Although healthy diet and exercise is often recommended, there is little supportive evidence. Therefore, the investigators plan to conduct a randomized controlled trial comparing a low glycemic index dietary intervention program and simple lifestyle advice in NAFLD patients. The primary endpoint is resolution of NAFLD. Non-invasive tests will be used to assess the study subjects. Proton-magnetic resonance spectroscopy is used to quantify hepatic triglyceride content, and transient elastography is used to quantify liver fibrosis.

In patients with NAFLD/NASH, changes in liver lipid composition and function tests following a short dietary intervention are associated with changes in gut microbiota

The main objective of this study was to evaluate the 5-day kinetics of plasma paracetamol levels in postoperative major hepatic surgery (resection greater than or equal to three hepatic segments) compared with less extensive liver resection and hepatic re-intervention. The clearance of indocyanine green is a marker of hepatic perfusion but also of the proper hepatocyte functioning, if hemodynamic conditions are stable. Some patients may be operated on up to four or five times in the liver. Moreover, these patients probably present an increased risk of postoperative hepatocellular insufficiency due to a quantitative and qualitative decrease in their hepatic parenchyma. It is therefore interesting to evaluate the use of paracetamol in this situation.

To assess the pharmacokinetics of MCI-186 after a single intravenous infusion of 30mg/hour in subjects with mild or moderate Hepatic impairment compared to subjects with normal hepatic function

Non-alcoholic fatty liver disease (NAFLD) covers a spectrum from reversible hepatic steatosis to inflammation and fibrosis termed steatohepatitis (NASH) and cirrhosis. New evidence indicates that NAFLD is associated with development of heart failure, abnormal ventricular glucose and fatty acid (FA) utilisation and cardiosteatosis. The mechanisms behind cardiac involvement and the progression from NAFL to NASH are poorly understood but must include altered cardiac and intrahepatic lipid handling. In collaboration with renowned research groups from Oxford, Mayo Clinic and Copenhagen we plan comprehensive kinetic studies of heart and liver FA uptake and oxidation, ventricular function and substrate utilisation, and hepatic triglyceride (TG) secretion in order to assess mechanisms governing cardiac and hepatic lipid and glucose trafficking in subjects with NAFL and NASH and the relationship with heart function. In addition, we will assess skeletal muscle and adipose tissue enzyme activities, gene expression and protein concentrations in these subjects to define mechanisms involved in the cross-talk between heart, liver, muscle and adipose tissues. We will address these questions using innovative tracer techniques (11Cpalmitate, 11C acetate, 18FDG glucose PET tracers and TG tracers) in combination with hepatic vein catherisation to study cardiac and liver substrate trafficking, as well as NMR spectroscopy, echocardiography, muscle and fat biopsies in combination with state-of-the art muscle and adipose tissue enzyme kinetics, gene- and protein expression. Effects of acute exercise as well as GLP-1 agonist and SGLT-2 inhibitor treatment (alone and in combination) will be assessed. The overarching goals are to define abnormalities and differences between NAFLD and NASH in hepatic lipid (FA and TG) metabolism and to assess hepatic, adipose and skeletal muscle lipid and substrate utilisation.

Previous reports have suggested that ALT-immunoglobulin complex was increased according to the severity of the liver disease, and high concentration of mAST and this might indicate a severely damaged liver. Immunoassay might be useful as a screening method in the differ-ential diagnosis of liver fibrosis according to patients. In this study, the efficacy of immunoas-say in the prediction of liver fibrosis in patients with chronic hepatitis B (CHB) was evaluated.