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/chemokines, 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.
To test this hypothesis, the investigators propose 2 objectives. Primary objective: To identify platelet features that correlate with liver disease progression.
Secondary objective: To study the mechanistic relationship between gut dysbiosis, metabolome composition, inflammation, and platelet activation in chronic liver disease.
age>18;
NAFLD patients according to EASL Guidelines 2016.
decompensated cirrhosis, other causes of chronic liver disease (infectious and immune-mediated); malabsorption syndromes (i.e., celiac disease, food allergy, small bowel bacterial overgrowth);
inflammatory bowel disease; previous GI surgery;
immunodeficiencies; neurological handicaps;
use of NSAIDs, antibiotics, probiotics, or anti-secretory drugs within the 2 months preceding enrollment;
Stefania Basili
Lead sponsor
University of Roma La Sapienza
Sponsor institution
University of Rome Tor Vergata
Collaborator
Catholic University of the Sacred Heart
Collaborator