View clinical trials related to Alcoholic Cirrhosis.
Filter by:The study is aimed to evaluate the additional role of ciprofloxacin therapy in severe alcoholic hepatitis combined to prednisolone therapy in an open-label placebo controlled manner.
The purpose of this study is to determine if zinc therapy: (1) strengthens your intestine's defensive barrier preventing damaging substances from reaching your liver, (2) decreases liver injury (inflammation, oxidative stress, cell death) and scarring, and (3) improves your liver-related health. Based on our preliminary animal data and other published reports, we expect zinc therapy to achieve all of these goals. Zinc is affordable, available over the counter or by prescription, and has an excellent safety profile. Positive results from this study will show that zinc is a significant therapy for millions of Americans with alcoholic liver disease.
The purpose of this study is to validate a strategy of identification of patients for early liver transplantation in severe alcoholic hepatitis. In this setting, short-term survival is very low (approx. 25% at 6 months) and a pilot study has suggested (mathurin et al. N Engl J Med 2011) that liver transplantation may be an option in very carefully selected patients who did not respond to medical treatment. This selection process deserves to be confirmed in a population of greater size. We hypothesized that patients selected with this process would have a same alcohol relapse rate after liver transplantation than patients transplanted for alcoholic cirrhosis and selected using a 6-month sobriety period
The main objective of the study is to assess in patients with compensated alcoholic cirrhosis and hepatic iron overload (HIO), as assessed by MRI, the effect of phlebotomy in order to lower and maintain serum ferritin below 50 µg / l on the risk of hepatocellular carcinoma (HCC) occurrence. The effect of bloodletting will be jointly evaluated on 1) episodes of hepatic decompensation, 2) non HCC liver-related mortality 3) changes in HIO during follow-up.
Hepatocellular carcinoma (HCC) is a major public health problem, whose incidence is increasing in developed countries and is the leading cause of death in patients with cirrhosis. The diagnosis and the early management are key issues that could improve the prognosis. In France, alcoholic cirrhosis is the leading cause of HCC, while the aetiology of underlying chronic liver disease is mainly hepatitis C (HCV) in Southern Europe and Japan, and hepatitis B (HBV) in Asia and Africa. In the next years, due to the improved results of anti-viral therapies, this trend should be reinforced with a decreasing proportion of HCC related to viral cirrhosis and an increasing proportion of HCC related to alcoholic cirrhosis. However, natural history of alcoholic cirrhosis remains poorly understood, most studies being retrospective and including a small number of patients. This project is filed by the consortium CIRRAL including French Academic hospitals centers currently involved and referees in the field of alcoholic liver disease and HCC (8 at the moment, and more in the next months). It is a national multicenter prospective study that will include 1200 patients with alcoholic cirrhosis histologically proven over 3 years. The main goal of this cohort is to describe the natural history of a large number of patients with alcoholic cirrhosis prospectively followed, and to identify predictors of the occurrence of HCC.
Hepatocellular carcinoma (HCC) is a frequent complication of cirrhosis. Occurrence of HCC could be linked with multiple functional region of genome. The determining of a genomic mapping of " single nucleotide polymorphisms " (SNPs) permit to perform some genetic link studies with pathologies without clear hereditary disposition. In this study, the investigators will identify predictives genetic polymorphism of HCC.
The aim of the investigators' study is to elucidate the relationship between a functional liver test (e.g., ICG) and the PREOPERATIVE value of portal hypertension in the patients with impaired liver function from alcoholic and non-alcoholic aetiologies. Alcoholic and viral cirrhosis present important differences in terms of cellular mechanisms responsible for the disease progression with a distinct and unique gene expression pattern that regulates the type of inflammatory response. These differences probably influence the hepatic functional reserve and the onset of portal hypertension at a comparable clinical and biological level of derangement and the investigators may expect significant differences in the recovery from hepatectomy. The investigators' hypothesis is that at a comparable ICGR-15 rate non-viral cirrhotic liver presents higher portal pressure values and the investigators also argue that alcoholic cirrhotic patients would tolerate a larger hepatic resection than would viral cirrhotic do.
The histological characteristics of alcoholic liver disease (ALD) and non-alcoholic steatohepatitis (NASH) related to overweight and obesity suggest the presence of partly common physiopathological mechanisms. We reported that the ponderal overload was an independent risk factor of alcoholic cirrhosis. The adipose tissue was considered for a long time as a simple place of storage of fat. However, it is now recognized that the adipose tissue can secrete cytokines called ADIPOKINES. The adipose tissue can secrete others cytokines such as TNF-alpha, IL6, IL10 and IL1-Ra. Increase in the production of the leptin and TNF-alpha by the adipose tissue after alcohol administration in the rat, as well as the role of leptin in inflammation and liver fibrogenesis in the murine model of chemical hepatotoxicity strongly suggest that activation of adipocytes by alcohol can explain the strong correlation observed between the body mass index (BMI) and the severity of ethanol-induced liver injury. Conversely, it was suggested in a murine model that the reduction in adiponectin production would sensitize the liver with the toxicity of alcohol. The PPAR alpha and gamma are the receptors which play a role both in inflammation and glucide and lipid metabolism. Taking into account the inhibiting role of PPAR alpha on the proliferation of the hepatic stellate cells, responsible for the fibrosis, the PPAR could also be implied in the relation between the overweight and the hepatic fibrosis in the alcoholic.
The aim of this study was assesment of splanchnic and systemic hemodynamic effects of chronic administration (2 month) of spironolactone or propranolol, alone or in association in alcoholic cirrhotic patients. The patients were randomized in 4 groups (aldactone 150 mg/day, propranolol 160 mg/day, aldactone 150 mg/day + propranolol 160 mg/day, placebo). Systemic and splanchnic hemodynamic effect were evaluated by hepatic venous pressure gradient measurements before and after 2 month of treatment.