[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"health-studies-list:{\"overallStatus\":[\"RECRUITING\",\"AVAILABLE\",\"NOT_YET_RECRUITING\"],\"leadSponsorName\":\"Stefania Basili\",\"orderBy\":\"LastUpdateSubmitDate:desc\",\"size\":25,\"offset\":0}":3,"health-study-condition:":45},{"pageToken":4,"total":5,"offset":6,"count":5,"results":7},null,1,0,[8],{"id":9,"slug":10,"hasResults":11,"nctId":12,"briefTitle":13,"officialTitle":13,"acronym":4,"eligibilityCriteria":14,"healthyVolunteers":15,"sex":16,"minAge":17,"maxAge":4,"enrollmentInfo":18,"targetDuration":4,"studyType":21,"phases":4,"briefSummary":22,"conditions":23,"keywords":28,"overallStatus":33,"whyStopped":4,"lastUpdateSubmitDate":34,"lastUpdatePostDateStruct":35,"startDateStruct":38,"completionDateStruct":40,"leadSponsor":42,"locationsCount":4},"100563970","integrated-phenotyping-of-the-gut-platelet-liver-axis-in-the-progression-of-chronic-liver-disease-igal-axis-100563970",false,"NCT06623084","Integrated Phenotyping of the Gut-plAtelet-Liver AXIS in the Progression of Chronic Liver Disease (iGAL-AXIS)","Inclusion Criteria:\n\n* age\\>18;\n* NAFLD patients according to EASL Guidelines 2016.\n\nExclusion Criteria:\n\n* decompensated cirrhosis, other causes of chronic liver disease (infectious and immune-mediated); malabsorption syndromes (i.e., celiac disease, food allergy, small bowel bacterial overgrowth);\n* inflammatory bowel disease; previous GI surgery;\n* immunodeficiencies; neurological handicaps;\n* use of NSAIDs, antibiotics, probiotics, or anti-secretory drugs within the 2 months preceding enrollment;\n* abnormality of hemostasis and thrombosis; malignancies.",true,"ALL","18 Years",{"count":19,"type":20},132,"ESTIMATED","OBSERVATIONAL","Objective of the study Our working hypothesis is that platelets activated by gut-derived metabolites dock in the liver of NAFLD patients and amplify the inflammatory state by releasing pro-inflammatory cytokines\u002Fchemokines, which in turn recruit and activate leukocytes in the liver sinusoids. Combined stimuli from leukocytes and platelets would then lead to metabolic reprogramming of hepatocytes, progression to NASH and eventually cirrhosis.\n\nTo test this hypothesis, the investigators propose 2 objectives. Primary objective: To identify platelet features that correlate with liver disease progression.\n\nSecondary objective: To study the mechanistic relationship between gut dysbiosis, metabolome composition, inflammation, and platelet activation in chronic liver disease.",[24,25,26,27],"Non-alcoholic Fatty Liver Disease (NAFLD)","NASH - Nonalcoholic Steatohepatitis","Cirrhosis","Control Condition",[29,30,31,32],"Platelets","Liver","Metabolomics","Microbiota","NOT_YET_RECRUITING","2024-10-02",{"date":36,"type":37},"2024-10-04","ACTUAL",{"date":39,"type":20},"2024-09-30",{"date":41,"type":20},"2025-12-24",{"name":43,"class":44},"Stefania Basili","OTHER",""]