[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"health-studies-list:{\"conditionNormalized\":\"steatosis\",\"overallStatus\":[\"RECRUITING\",\"AVAILABLE\",\"NOT_YET_RECRUITING\"],\"orderBy\":\"LastUpdateSubmitDate:desc\",\"size\":25,\"offset\":0}":3,"health-study-condition:steatosis":27},{"pageToken":4,"total":5,"offset":6,"count":5,"results":7},null,2,0,[8,42],{"id":9,"slug":10,"hasResults":11,"nctId":12,"briefTitle":13,"officialTitle":14,"acronym":15,"eligibilityCriteria":16,"healthyVolunteers":11,"sex":17,"minAge":18,"maxAge":4,"enrollmentInfo":19,"targetDuration":4,"studyType":22,"phases":4,"briefSummary":23,"conditions":24,"keywords":4,"overallStatus":29,"whyStopped":4,"lastUpdateSubmitDate":30,"lastUpdatePostDateStruct":31,"startDateStruct":34,"completionDateStruct":36,"leadSponsor":38,"locationsCount":41},"100578692","prevalence-of-non-alcoholic-fatty-liver-disease-in-inflammatory-bowel-disease-patients-100578692",false,"NCT06814600","Prevalence of Non-Alcoholic Fatty Liver Disease in Inflammatory Bowel Disease Patients","Prevalence of Non-Alcoholic Fatty Liver Disease in Inflammatory Bowel Disease Patients: A Prospective Monocentric Study","PONI","Inclusion Criteria:\n\n* Diagnosis of IBD based on clinical, endoscopic, and histological gounds according to the latest ECCO guidelines\n* Willingness to provide informed consent for study participation\n\nExclusion Criteria:\n\n* Presence of established liver disease (including autoimmune hepatitis, primary biliary cholangitis, primary biliary cirrhosis, hemochromatosis, Wilson's disease, positive serology for viral hepatitis B or C)\n* History of hepatocellular carcinoma or liver transplantation\n* History of excessive alcohol consumption defined as \\>3 units per day for women and \\> 5 units per day for men\n* Pregnancy at the time of recruitment\n* Failure to perform an elastography mesure or missing elastography data","ALL","18 Years",{"count":20,"type":21},150,"ESTIMATED","OBSERVATIONAL","Non-alcoholic Fatty Liver Disease (NAFLD) refers to a spectrum of disease characterized by the presence of more than 5% of steatosis in hepatocytes of individuals who consume little or no alcohol. It ranges from simple steatosis without evidence of inflammation, to the association of steatosis and inflammation with cellular necrosis, the so-called non-alcoholic steatohepatitis (NASH). NAFLD has become increasingly common in developed countries affecting up to 38% of the population. It is mostly but not exclusively associated with metabolic syndrome including obesity, insulin resistance, and hypertension. There is growing evidence of a close interaction between the gut and the liver \"Gut-liver axis\", particularly in the pathogenesis of NAFLD. The pathophysiological mechanism behind this association is not well understood but involves small intestinal bacterial overgrowth (SIBO), intestinal wall inflammation and increased permeability, all leading to systemic translocation of microbial metabolites including endotoxins and pro-inflammatory markers called Pathogen Associated Molecular Pattern (PAMPs). Thus, the gut-liver interaction, mediated by cytokines and inflammatory proteins seem to be the cornerstone of this complex liver disease.\n\nRecent studies underlined the increased prevalence of NAFLD in the Inflammatory Bowel Disease (IBD) population, accounting for almost 32% of hepatic extra-intestinal manifestations of the disease. Several hypotheses have been proposed to explain the pathophysiology behind this association, encompassing chronic intestinal wall inflammation, increased intestinal permeability and altered gut microbiota or dysbiosis. To our knowledge, no studies have been conducted so far to investigate the correlation between intestinal disease activity (IBD flare versus remission state) and NAFLD incidence and behavior (progression versus regression of steato-fibrosis). We therefore aim to conduct a prospective paired study, on IBD patients followed at Saint-Pierre University Hospital, aiming to explore this correlation.\n\nIn this paired study design, patients will be their own controls over the course of their disease: An evaluation of NAFLD will be done for all patients during both phases of their inflammatory bowel disease: In the active phase and in remission phase. Our primary outcome is to assess NAFLD prevalence in the IBD population followed at our institution. Secondary outcomes will be to explore NAFLD prevalence and behavior (progression versus regression of steato-fibrosis) according to IBD activity, IBD type, IBD duration and types of IBD treatments.",[25,26,27,28],"NAFLD","Inflammatory Bowel Diseases","Steatosis","Fibrosis, Liver","RECRUITING","2025-02-05",{"date":32,"type":33},"2025-02-07","ACTUAL",{"date":35,"type":33},"2024-11-01",{"date":37,"type":21},"2025-12-01",{"name":39,"class":40},"Centre Hospitalier Universitaire Saint Pierre","OTHER",1,{"id":43,"slug":44,"hasResults":11,"nctId":45,"briefTitle":46,"officialTitle":46,"acronym":4,"eligibilityCriteria":47,"healthyVolunteers":11,"sex":17,"minAge":18,"maxAge":4,"enrollmentInfo":48,"targetDuration":4,"studyType":50,"phases":51,"briefSummary":53,"conditions":54,"keywords":4,"overallStatus":56,"whyStopped":4,"lastUpdateSubmitDate":57,"lastUpdatePostDateStruct":58,"startDateStruct":60,"completionDateStruct":61,"leadSponsor":63,"locationsCount":4},"100569220","phase-3-obeticholic-acid-among-chronic-hbv-patients-with-hepatic-steatosis--clinical-and-portal-doppler-outcomes-100569220","NCT06691412","Obeticholic Acid Among Chronic HBV Patients with Hepatic Steatosis : Clinical and Portal Doppler Outcomes","Inclusion Criteria:\n\n* Patients 18 years of age or older who had diagnosed as chronic HBV on treatment with with Controlled Attenuation Parameter (CAP) value more than 238 dB\u002Fm .\n\nExclusion Criteria:\n\n* patients under the age of 18.\n* patients with other viral hepatitis infection .\n* Hepatocellular carcinoma .\n* portal vein thrombosis.\n* Subjects with risk of 2nd hepatic steatosis liver disease (excessive alcohol consumption and medications).\n* history of liver disease such as (α-1 antitrypsin deficiency, autoimmune hepatitis, drug-induced liver injury, 1ry biliary cirrhosis, 1ry sclerosing cholangitis).\n* Body Mass Index (BMI) \\> 35 (to avoid the possibility of Fibroscan failure).\n* Patient with end organ disease.",{"count":49,"type":21},100,"INTERVENTIONAL",[52],"PHASE3","In this study, the investigators aimed to evaluate the hepatoprotective effect of OCA against HBV-induced liver injury by comparing patients demographic , laboratory date ( liver function , viremia ) , degree of hepatic steatosis and fibrosis and portal doppler at the beginning and after six months .",[55,27],"Hepatitis B Virus","NOT_YET_RECRUITING","2024-11-14",{"date":59,"type":33},"2024-11-15",{"date":59,"type":21},{"date":62,"type":21},"2026-03-01",{"name":64,"class":40},"Assiut University"]