Background And Aims: Non-alcoholic fatty liver disease is recognized not only as part of the metabolic syndrome but also as an independent predictor of cardiovascular disease.
Methods: In this study, NMR spectroscopy method, together with perfusion techniques, was used to detect subclinical brain vascular damage in subjects with NAFLD without overt atherosclerosis risk factors (i.e. hypertension, diabetes, hypercholesterolemia, obesity).
Results: The results suggest that subjects with histologically proven NAFLD have a reduced cerebral perfusion (CBFr) confined to limited brain areas, i.e., left semioval center and posterior cingulate cortex. No statistically significant differences in CBFr values were found, dividing the NAFLD cohort into subgroups, considering NAS score, presence/absence of NASH/fibrosis, and degree of steatosis.
Conclusions: Our data suggest that NAFLD per se may be involved in cerebral atherosclerotic disease. It will be interesting to draw longitudinal studies to determine whether these changes could evolve in more serious cerebral injury.
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http://dx.doi.org/10.1016/j.atherosclerosis.2017.11.012 | DOI Listing |
Diabetes Metab Syndr
September 2024
Department of Endocrinology, Key Laboratory of Endocrinology of National Health Commission, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100730, China. Electronic address:
Objective: This investigation aimed to evaluate the efficacy and safety of rosuvastatin in treating moderate to severe metabolic associated fatty liver disease (MAFLD).
Methods: This prospective, open-label, randomized study included non-diabetic participants with metabolic syndrome and intrahepatocellular lipid (IHCL) levels >10 %, as determined by proton magnetic resonance spectroscopy (H-MRS). The primary objective was the effect of a 52-week rosuvastatin treatment (10 mg/day) on IHCL content.
J Clin Endocrinol Metab
September 2024
Department of Clinical Therapeutics, Alexandra Hospital, National and Kapodistrian University of Athens Medical School, Athens, Greece.
Aims: Non-alcoholic fatty liver disease (NAFLD) with advanced liver fibrosis is associated with cardiovascular disease (CVD). To examine if markers of vascular injury mediate the link between liver fibrosis non-invasive tests (LFNITs) and CVD events, and to compare the incremental predictive value of LFNITs over established CVD risk scores.
Methods: Consecutively recruited individuals (n=1,692) with or without clinically overt coronary artery disease (CAD) from the Athens Cardiometabolic Cohort, were analysed.
Am J Gastroenterol
July 2024
Division of Gastroenterology and Hepatology, Virginia Commonwealth University and Richmond VA Medical Center, Richmond, Virginia, USA.
Introduction: One of the primary goals of the Liver Cirrhosis Network (LCN) is to develop a cohort study to better understand and predict the risk of hepatic decompensation and other clinical and patient-reported outcomes among patients with Child A cirrhosis.
Methods: The LCN consists of a Scientific Data Coordinating Center and 10 clinical centers whose investigators populate multiple committees. The LCN Definitions and Measurements Committee developed preliminary definitions of cirrhosis and its complications by literature review, expert opinion, and reviewing definition documents developed by other organizations.
Gut
August 2024
Metabolic Diseases Research Unit, IRCCS Sacro Cuore - Don Calabria Hospital, Negrar di Valpolicella (VR), Italy
Cureus
April 2024
Internal Medicine, University of Central Florida College of Medicine, Gainesville, USA.
Hepatic encephalopathy is typically seen in advanced liver disease and in patients with a transjugular intrahepatic portosystemic shunt. Common triggers include infections, gastrointestinal bleeding, electrolyte disturbances, dehydration, and drug/toxin use such as benzodiazepines and alcohol. In rare instances, other metabolic abnormalities such as hypothyroidism may also exacerbate hyperammonemia in patients with underlying liver disease due to hypothyroidism-induced myopathy, which increases urea production and decreases clearance through reduced glutamine synthetase activity.
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