Active clinical trials for "Liver Cirrhosis, Alcoholic"

To investigate whether simple reminders about healthy lifestyle sent via mobile phone text messages can improve the liver cirrhosis severity and prognosis (as assessed by the MELD score supported by the Child-Pugh score) among patients with liver cirrhosis that have been through a 12-week supervised and facility-based physical exercise training program and in-patient rehabilitation.

In this protocol, the investigators will determine compliance, acceptability, and patient satisfaction regarding the use of remote monitors and summarize changes in activity over time among patients with decompensated cirrhosis. This is a feasibility pilot study that will recruit 20 patients. The investigators plan to determine the feasibility of wearable devices to remotely monitor daily activity (e.g., physical activity, sedentary time, sleep), cognitive function, blood pressure, and weight in patients with decompensated cirrhosis, by assessing patient compliance. A patient is considered compliant if they wear the wristwatch at least 10 hours per day and use the Apps, body weight scale, and blood pressure monitor for at least 4 of 7 days

The main goal of this observational study is to measure the prevalence of binge eating disorder in liver transplant patients by evaluating the responses to the Bulimia Test. Secondary objectives of the study are to: Determine the prevalence of binge eating disorders in liver transplant patients following alcoholic cirrhosis, evaluated by the Bulimia Test; Study the association between the presence of eating disorder behaviours and liver damage : hepatic steatosis and fibrosis determined by Fibroscan (Transient elastography and controlled attenuation parameter) Study the association between presence of eating disorder behaviours and alcohol use disorder, measured by Alcohol Use Disorders Identification Test-Consumption

Background & Aim: Bone marrow derived mesenchymal stem cells (BM-MSCs) have capacity to differentiate into hepatocytes and anti-fibrotic effect in the experimental model. No study was done in humans with alcoholic liver cirrhosis. The researchers investigated the anti-fibrotic effect of BM-MSCs in alcoholic cirrhosis as Phase II clinical study. Methods: Eleven alcoholic cirrhosis patients (M:F = 10:1) with Child-Pugh's class B and maintenance of alcohol abstinence at least 2 months were enrolled. At baseline, all patients received liver biopsy, hepatic venous pressure gradient (HVPG) measurement and serologic tests. BM-MSCs were isolated from each patient's BM and amplified for one month and injected two times at 4, 8week through Rt. hepatic artery. 5x106cells/mL of BM-MSCs were injected in each session. Follow up biopsy, HVPG and relative expression of tissue transforming growth factor-1 (TGF-β1), α smooth muscle actin (α-SMA) and collagen-1 by real time RT PCR were measured after 12weeks from 2nd BM-MSC injection. The primary outcome was improvement in patients' histology Aim : The researchers aimed to evaluate safety and effectiveness of new therapy with bone marrow derived autologous mesenchymal stem cell for hepatic failure caused by alcoholic liver cirrhosis.

This study is to evaluate the safety and efficacy of a single dose of Cellgram™ delivered via hepatic artery in patients with decompensated alcoholic liver cirrhosis.

This is a 5-year (+30 days) long term follow up study to evaluate the safety of Livercellgram in subject who participated in and completed the Livercellgram Phase 2 trials (refer to ClinicalTrials.gov.Identifier: NCT01875081).

The purpose of this study is to determine whether losartan, an angiotensin II blocker prevents the sodium retention in patients with liver cirrhosis and by that reduces the fluid retention. Moreover is the purpose to asses whether losartan is antifibrotic.

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.

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.