View clinical trials related to Liver Cirrhosis.
Filter by:Study Design: Double-blind randomized placebo-controlled clinical trial Study Duration: 2 years Study Center: Single center Hospital de la Santa Creu i Sant Pau, Barcelona Objectives: To assess the effect of Vivomixx® on neuroinflammation and systemic inflammatory response in patients with cirrhosis
Exocrine pancreatic insufficiency (EPI) is the inability of the pancreas to perform a normal digestive function. The prevalence of IPE in patients with decompensated hepatic cirrhosis (HC) is unknown and most published series are short, old and use a single diagnostic technique with potential risk of false positives and negatives. Demonstrating IPE in a patient with HC can change their vital prognosis with the indication of pancreatic enzymes that can improve their nutritional status and help control their decompensations. Objectives: To assess the prevalence of IPE in patients with decompensated CH. To establish correlation between fecal elastase and 13C triolein breath test. Methodology: Unicentric, transversal study that will be carried out during hospitalization. Patients with HC who enter for decompensation and requiere hospitalization will be included consecutively. Exclusion criteria will include prior diagnosis of IPE, suspicion of biliary obstruction, more than 5 dep / d induced by laxatives or liquid stools. The diagnosis of IPE will be made with the combination of two techniques (13C triolein breath test and fecal elastase). Demographic, epidemiological data, clinical data as well as anthropometric parameters will be collected. A blood test will also be done to assess nutritional status and associated deficits. A multivariate analysis will be performed to assess the predictive factors of IPE
This study will evaluate the efficacy and safety of glecaprevir/pibrentasvir (ABT-493/ABT-530) in chronic hepatitis C virus (HCV) genotype (GT)1 to GT6-infected Asian participants with compensated cirrhosis with or without human immunodeficiency virus (HIV) co-infection who are HCV treatment-naïve or treatment-experienced with interferon (IFN) (alpha, beta or pegylated interferon [pegIFN]) with or without ribavirin (RBV) OR sofosbuvir with RBV with or without IFN.
Detection of Volatile Organic Compounds (VOC) directly from tissue by headspace analysis (skin, surgery material, other tissue) and exhaled breath is feasible using affordable user-friendly novel nano-chemo sensors that can accurately be used for screening and monitoring purpose
To determine the rate and mechanisms of skeletal muscle protein synthesis and breakdown in cirrhotic patients by using multiple tracers and single muscle biopsies.
This is a multi-center, open-label trial of Elbasvir/ Grazoprevir 50/100 mg fixed dose combination 12 week treatment aimed to evaluate SVR12 in treatment naïve patients with chronic hepatitis C (genotype 1b) infection, associated with of metabolic syndrome. The study to be conducted in conformance with Good Clinical Practices. A total of 60 subjects will be studied at 2 sites in the Republic of Kazakhstan. Males and Females treatment naïve patients with CHC genotype 1b infection associated with metabolic syndrome (MS), 18-70 years of age, with or without severe fibrosis / compensated cirrhosis will be enrolled. SVR 12 (primary endpoint) will be evaluated. Patients will be stratified by fibrosis stage and presence of metabolic syndrome components. Interim Analysis will be performed in order to estimate viral kinetics, applicability of SVR4 and durability of SVR12 by evaluation of virologic response at week 4 and 8 of treatment and follow-up at week 4 (SVR 4) and 24 will be performed - this will be a descriptive summary only without hypothesis testing. The main hypothesis is that 12-week therapy with MK-5172 in combination with MK-8742 for treatment-naïve patients with HCV genotype 1b with metabolic syndrome is not notably worse than the same course for treatment-naïve patients with HCV genotype 1b without metabolic syndrome.
Hepatocellular Carcinoma (HCC) is a major health concern in the United States, particularly among people with liver cirrhosis. Out of every 100 patients with liver cancer, only 18 will survive 5 years or more. While locoregional therapies are utilized in an effort to combat this disease, the recurrence rate of HCC after these therapies are high. Statins are widely used drugs that lower cholesterol levels. Some studies have suggested that statins lower risk of HCC recurrence, but this possibility has not been studied thoroughly in a clinical trial. This study will examine the effects of pravastatin, a type of statin, on time to HCC recurrence in patients with early stage HCC. It is possible that pravastatin in combination with locoregional therapies may delay or protect against HCC recurrence.
There has been great interest in recent years to take advantage of stem cells to treat liver cirrhosis. Mesenchymal stem cells (MSC) has been shown to be safe and effective for liver diseases in some studies. Randomization controlled studies are needed to confirm the long term effect of MSC treatment for liver cirrhosis. This study aimed to investigate the safety and efficacy of mesenchymal stem cells in hepatitis B and C related liver cirrhosis patients. This study is an open-label multicenter randomized control study. Patients with with decompensated cirrhosis will be randomly assigned to receive MSC treatment plus standard medical care(treatment）or standard medical care (control). Three times of MSC infusion (1x10E6 cells/kg body weight) via peripheral vein will be given to the experimental group (once in 4 weeks). The primary outcome is absolute change in liver function indexes and and scores. Secondary outcomes are cirrhosis-related complications, symptoms, life quality, and survival.
Loss of skeletal muscle mass or sarcopenia is the most common and potentially reversible complication in cirrhosis that increases morbidity and mortality before, during and after liver transplantation. No proven treatments exist for the prevention or reversal of sarcopenia in cirrhosis, primarily because the mechanisms responsible for this are unknown. Based on compelling preliminary studies and those of the co investigator, investigators hypothesize that the mechanism of reduced skeletal muscle mass in cirrhosis is due to a myostatin mediated impaired mTOR (mechanistic target of rapamycin) signaling resulting in reduced protein synthesis and increased autophagy. Investigators further postulate that leucine, a direct stimulant of mTOR, will reverse the impaired mTOR phosphorylation in the skeletal muscle of cirrhotics. The consequent increase in protein synthesis reduced autophagy will result in an increase in skeletal muscle mass. Investigators will test these hypotheses by quantifying the response to acute and long term (3 month) administration of leucine enriched essential amino acid (EAA/LEU) compared with an isonitrogenous isocaloric non-essential balanced amino acid mixture (does not stimulate protein synthesis) in cirrhotic patients. Fractional protein synthesis rate (FSR) in skeletal muscle, responses of the molecular regulatory pathways of skeletal muscle protein synthesis, and autophagy flux will be quantified in the acute and long term protocols. Tracer studies using L-[D5]-phenylalanine (Phe) as a primed constant infusion (prime 2µmol.kg-1.hr-1; constant 0.05 µmol.kg-1.hr-1) with and L [ring-D2] tyrosine, forearm plethysmography, and sequential skeletal muscle biopsies (total of 3 per study subject) will be used to quantify these outcomes. Anthropometric, clinical and body composition measures will be additional outcome measures for the long term intervention. Expression of regulatory signaling proteins, myostatin, IGF-1 (insulin like growth factor) , phospho-Akt, phospho-AMPK (activated protein kinase), phospho-mTOR and phospho-p70s6k will be quantified by Western immunoblots. Autophagy flux will be measured by quantifying expression of the autophagosome proteins.
This is a multicenter, double-blind, randomized, placebo-controlled study to evaluate the safety and efficacy of emricasan in improving event-free survival based on a composite clinical endpoint (where all-cause mortality, new decompensation events, and MELD score progression are events) in subjects with decompensated NASH cirrhosis.