Active clinical trials for "Non-alcoholic Fatty Liver Disease"

The purpose of this study is is to use non-invasive diagnostic tests, Fibroscan and a simple blood test, to diagnose NASH in patients who undergo liver transplantation. Liver transplantation is a life-saving procedure for people with cirrhosis. Fatty liver is a common reason for liver transplantation due to obesity and diabetes. Fatty liver can happen again to the new transplanted liver and it is often due to metabolic risk factors (including diabetes, rapid weight gain, and immunosuppressive therapy, which are used to avoid rejection of the new liver). Some patients with fatty liver after liver transplant have non-alcoholic steatohepatitis (NASH) injury to liver the tissue (inflammation) and damage which is caused by a build-up of fat in the liver. This is a serious problem and can lead to cirrhosis and loss of the transplanted liver. There has been no detailed study into the recurrence of NASH. One reason for this is one of the only ways to detect fatty liver and NASH is to have a liver biopsy, which can be painful and have complications. Recently, a new technology (Fibroscan) and a simple blood test (cytokeratin 18) have been developed which can tell doctors how much a liver is damaged and how much fat it contains without pain or complications. This is a year long study involving one screening visit and 3 study visits, 3 months apart.

The rise in high fructose corn syrup (HFCS) consumption over the past 40 years since its introduction as a popular sweetener in the United States has led to much concern regarding its contribution to the rise in obesity (1), diabetes (2) and related cardiometabolic disorders (3).Unlike sucrose which contains equal proportions of fructose and glucose bound by an α-glycosidic bond, HFCS contains 42-55% of fructose to glucose in a free (unbound) form (4). Despite these differences in composition, both sugars possess identical energy contribution on a gram to gram basis (4). However, the higher ratio of fructose to glucose in HFCS has led to the hypothesis that HFCS may uniquely contribute to cardiometabolic risk, more so than sucrose, through proposed differences in fructose metabolism, endocrine and hedonic properties (5). We will conduct a series of systematic reviews and meta-analyses to assess the role of HFCS versus sucrose under energy matched (isocaloric) conditions on cardiometabolic risk.

The aim of the project is to investigate the metabolic regulation of the hepatic urea nitrogen handling and various cognitive functions measured by psychometric and neurophysiological tests before and after bariatric surgery in patients with non-alcoholic fatty liver disease (NAFLD).

NAFLD is a common comordidity in patients with IMID, including inflammatory bowel disease and psoriasis. Nevertheless, the prevalence of NAFLD and NASH in the IMID population is not clear, and the risk factors are not completely understood. Interestingly, NASH and most of IMIDs share main molecular and immunological mechanisms of disease, as the inflammatory pathways depending on TNFa or imbalance in T cell subtypes like Th17/Treg. This common pathogenesis may explain, at least in a subset of patients, the development of NASH in the absence of classic metabolic risk factor. Thus, our main hypothesis is that in the NASH assciated to IMIDs two different phenotypes co-exist. First, a predominantly inflammatory phenotype, and not associated to the metabolic syndrome ande second, a predominantly metabolic phenptype, strongly associated to he metabolic syndrome. In this way, we believe that in a particular subset of NAFLD patients, NASH could be considered as an IMID, as most of the definiting features of IMIDs are present. To demonstrate our hypothesis, we consider a two-stage study. First, we will determine the NAFLD and NASH prevalence in a cohort of well-characterized IMID patients and controls. Second, we will adress the molecular and immunophenotype characterization in liver biopsies of NASH patients with and without the co-existence of IMIDs.

The aim of the present study is to assess, by using a simple algorithm combining FIB-4 and Fibroscan, the prevalence of NASH with advanced fibrosis in outpatients followed in various hospital specialty clinics other than hepato/gastroenterology and to examine risk factors associated with this condition. The prevalence of NASH will be investigated among 6 cohorts of outpatients followed in different hospital specialty clinics at Hôpitaux Universitaires de Strasbourg.

Early detection of renal impairment in patients with non-alcoholic fatty liver disease and its correlation with serum Adiponectin level.

The investigators intend to assess the role of several biomarkers in the prediction of relapse in IBD. Clinical, laboratory and endoscopic data will be gathered and a predictive score will be derived in order to assess the relapse risk at 1 year.

• Main objectives and outcome measures. Establish prevalence of and factors contributing to fatty liver disease and liver fibrosis in patients with psoriasis. Fatty liver disease diagnosed via ultrasound. Liver fibrosis diagnosed by liver biopsy or non-invasive tests of fibrosis including transient elastography, ultrasound, serum markers of fibrosis including procollagen-3-N-terminal peptide (P3NP). Evaluate non-invasive markers of liver fibrosis in the psoriasis population. Namely transient elastography, standard liver function tests and P3NP. Evaluate the impact of psoriasis disease severity and comorbidities including metabolic syndrome on response to treatment in patients with psoriasis. Data on co-morbid disease collected through questionnaires and review of medical records. Response to treatment assessed using psoriasis area and severity index (PASI) physician global assessment (PGA) and dermatology life quality index (DLQI). Study population: 380 patients with moderate to severe psoriasis will be prospectively recruited to the study. Chief investigator: Professor Jonathan Barker. Co-investigator: Professor Catherine Smith Sponsor/funding organization: Pfizer and Biomedical Research Centre (BRC) at Guys and St Thomas Hospitals Trust

The true incidence and prevalence of NAFLD in Hong Kong has not been determined. The natural history of NAFLD is not well defined partly because of differences in the exclusion limit of alcohol and the required histological criteria between studies. NAFLD is previously believed to be a benign non-progressive condition, but it has since been determined that a subset of patients can progress to cirrhosis and even hepatocellular carcinoma. In fact in a recent histological review of NAFLD, fibrosis or liver cirrhosis was present in 15-50% of patients at index liver biopsy. The presence of obesity or type 2 diabetes mellitus are the strongest predictors of fibrosis. These same risk factors are also more common in patients with cryptogenic cirrhosis. Further evidence of the link between diabetes, obesity and NAFLD are mainly from the field of liver transplantation. In patients who underwent liver transplantation for cryptogenic liver cirrhosis, NAFLD recuured in a quarter of the hepatic allografts. The patients with recurrent NAFLD were more likely to be diabetic and had a higher body mass index (BMI) at the time of recurrent NAFLD. This suggests that NAFLD may have a significant role in the pathogenesis of crytogenic cirrhosis. Although NAFLD was initially described as a slowly progressive disease, there are emerging data which shows that it can progress rapidly. Liver failure has even been described in patients with NAFLD after bariatric surgery, and a recent report described 5 cases of subacute liver failure in obese middle aged females with NAFLD related cirrhosis. NAFLD can also affect the progression of other diseases as well. Hepatic steatosis related to visceral obesity is a major independent risk factor for fibrogenesis related to chronic HCV hepatitis. However, the prevalence of NAFLD and its interaction with chronic HBV, if any, is uncertain. This study aims to determine the prevalence of NAFLD in patients with unknown cause of hepatitis and to determine the histological fibrosis and inflammation in chronic HBV patients with NAFLD.

The aim of our study is: The early detection of NAFLD in CKD patients with different stages (stage I to IV) to avoid progression to liver fibrosis. Evaluation of the relationship between the severity of fatty liver in NAFLD assessed by liver enzymes, biochemical markers, ultrasonography and grades of Fibroscan with CKD staging, eGFR and proteinuria.