ISSN: 2641-1652
Ron Hang Long Li* and Yi Kei Tse
Received:October 26, 2021 Published: November 03, 2021
*Corresponding author: Ron Hang Long Li, Department of Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China
DOI: 10.32474/CTGH.2021.03.000159
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Non-alcoholic fatty liver disease (NAFLD) encompasses a spectrum of progressive liver abnormalities from simple hepatic steatosis to non-alcoholic steatohepatitis (NASH) to advanced fibrosis, cirrhosis, and/or hepatocellular carcinoma [1]. Parallel to the rising burden of obesity and metabolic syndrome, NAFLD has emerged as the leading cause of chronic liver disease at an estimated global prevalence of 24% [2]. Besides its known clinical burden for liver-related morbidity and mortality, NAFLD is potentially linked with other extra-hepatic chronic diseases and may be considered a multisystem condition. Particularly, NAFLD increases the risk of type 2 diabetes, cardiovascular diseases, chronic kidney disease, and all-cause mortality [1]. Potential pathophysiologic mechanisms underlying the detrimental effects of NAFLD include hyperglycemia, systemic inflammation, and increased oxidative stress [3].
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