View clinical trials related to Hepatitis, Alcoholic.
Filter by:Loss of total mass of muscles (catabolism) is a serious clinical problem in patients with alcoholic hepatitis. The liver might play an important role in this stress-catabolism by increasing the production of urea during the inflammatory process. The purpose of this study is to examine the regulation of urea synthesis in patients with alcoholic hepatitis and to study the effect of the anti-inflammatory drugs prednisolone and pentoxifylline on this regulation.
The treatment of severe forms of alcoholic hepatitis (AH) constitutes a major challenge for clinicians involved in the management of severe alcoholic liver disease. In patients with Maddrey function higher than 32, compelling evidence from data has shown that corticosteroids improve short-term survival. However, novel strategies or molecules are required in light of the fact that approximately 40 % of patients continue to die at 6 months. A double-blinded randomized controlled trial of 101 patients has showed that Pentoxifylline improves survival of patients with severe AH, as compared to placebo. In terms of mechanisms, the effect of pentoxifylline is related to prevention of hepatorenal function whereas corticosteroids induce an early improvement in liver function. When considering these differences of mechanisms, many clinicians suggest that the addition of pentoxyfilline to corticosteroids is an attractive option that needs to be tested in patients with severe AH.
The purpose of this study is to investigate the role of endotoxins and the endotoxin mediated immune activation pathway in patients with alcoholic hepatitis. Also, to determine the effect of Liver assist (liver dialyses) intervention on these parameters in patients with severe alcoholic hepatitis.
Acute alcoholic hepatitis (AAH) is the most severe form of alcoholic liver disease (ALD) and is associated with a high risk of dying in the short term. Corticosteroids are generally recommended in patients with severe AAH, but its use is still controverted and contraindicated in case of active infection or gastrointestinal bleeding. Therefore, alternative therapeutic options are needed.Ethanol consumption results in the depletion of endogenous antioxidant capabilities and patients with ALD have evidence of antioxidant deficiencies.Due to its effects on glutathion stores restoration and as such the limitation of the oxidative stress and its good tolerance and safety profile, N-acetylcysteine (NAC) is an attractive agent for the treatment of AAH.In this context, we hypothesized that NAC might be beneficial in severe AAH.
Background: - Liver cancer is the third most deadly and fifth most common cancer worldwide. Hepatocellular carcinoma (HCC) is the most frequent primary liver cancer, and it has grown more prevalent in the United States. - More information is needed about the causes and effects of liver cancer, and further research into individuals who are at high risk for developing liver cancer is needed for early diagnosis and prevention. Objectives: - To identify genetic factors that may help to explain the aggressiveness of liver cancer. - To determine if HCC biomarkers exist in blood, urine, and tissue samples. Eligibility: - Patients between the ages of 18 and 90 who have been diagnosed with HCC or have a high risk for developing HCC because of fatty liver disease (alcohol-related or non-alcohol-related) or chronic hepatitis B or C. - Participants will reside in Baltimore City and the surrounding areas. Design: - Participants will complete a questionnaire and provide blood and urine samples for testing: - The questionnaire will include questions about individual and family medical history, tobacco use, and exposure to known factors for liver cancer. - Blood and urine samples will be collected from all participants after the questionnaire. - Tumor tissue and healthy tissue will be collected from selected participants if they undergo surgery for their cancer or disease. - No specific treatment will be offered as part of this protocol, but participants have the option to be treated under different protocols.
35% of Acute Alcoholic Hepatitis patients (AAH) do not respond to corticoids and died after 6 months. Chronic alcohol abuse depletes glutathione in the hepatocytes and makes the latter more sensitive to excessive TNFα levels. Re-establishment of a stock of antioxidants by administration of a precursor (N-acetyl cysteine, NAC) in combination with corticoids (C) could make the hepatocytes more resistant and improve survival. The investigators' study's primary endpoint was improvement of survival at 6 months. The secondary endpoints were survival at 1 and 3 months, tolerance of NAC and a drop in blood bilirubin levels at D7
Background: Alcoholic liver disease is one of the most important causes of chronic liver disease in this country. There is currently no treatment for chronic alcoholic liver disease other than abstinence. Hepatic methionine metabolism is abnormal in these patients and one of the consequences is depletion of S-adenosylmethionine (SAMe) levels, which can affect numerous important cellular processes. SAMe has been increasingly utilized for the treatment of liver diseases although the protective mechanisms remain unclear. A recent randomized double-blind trial using SAMe in patients with alcoholic liver disease and found improvement in 2-year survival in those with less advanced liver disease. However, important changes in methionine metabolism and histological changes were not included in the study. Aim: The goal of this study is to determine the effect of SAMe administration on key metabolic abnormalities of the methionine cycle and on the recovery from alcoholic liver disease.
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 goal of this study is to demonstrate the effectiveness of pentoxifylline compared to placebo in AAH while studying putative mechanisms that are plausible and testable. The main hypothesis is that pentoxifylline reduces the 90-day mortality of AAH.
The purpose of this study is to test the effectiveness of the amino acid arginine in reducing liver injury in individuals with alcohol-related hepatitis.