1.Burden of alcohol use disorder, alcohol-related liver disease, and alcohol-related liver cancer: Editorial on “Global epidemiology of alcohol-related liver disease, liver cancer, and alcohol use disorder, 2000–2021
Youxin WANG ; Noriko OZA ; Jazleen LEO ; Ashok CHOUDHURY ; Daniel Q. HUANG
Clinical and Molecular Hepatology 2025;31(2):654-657
2.Vibration-controlled transient elastography in shaping the epidemiology and management of steatotic liver disease: Editorial on “Current burden of steatotic liver disease and fibrosis among adults in the United States, 2017–2023”
Xiao-Dong ZHOU ; Terry Cheuk-Fung YIP ; Daniel Q HUANG ; Mark Dhinesh MUTHIAH ; Mazen NOUREDDIN ; Ming-Hua ZHENG
Clinical and Molecular Hepatology 2025;31(2):620-624
3.Burden of alcohol use disorder, alcohol-related liver disease, and alcohol-related liver cancer: Editorial on “Global epidemiology of alcohol-related liver disease, liver cancer, and alcohol use disorder, 2000–2021
Youxin WANG ; Noriko OZA ; Jazleen LEO ; Ashok CHOUDHURY ; Daniel Q. HUANG
Clinical and Molecular Hepatology 2025;31(2):654-657
4.Vibration-controlled transient elastography in shaping the epidemiology and management of steatotic liver disease: Editorial on “Current burden of steatotic liver disease and fibrosis among adults in the United States, 2017–2023”
Xiao-Dong ZHOU ; Terry Cheuk-Fung YIP ; Daniel Q HUANG ; Mark Dhinesh MUTHIAH ; Mazen NOUREDDIN ; Ming-Hua ZHENG
Clinical and Molecular Hepatology 2025;31(2):620-624
5.Burden of alcohol use disorder, alcohol-related liver disease, and alcohol-related liver cancer: Editorial on “Global epidemiology of alcohol-related liver disease, liver cancer, and alcohol use disorder, 2000–2021
Youxin WANG ; Noriko OZA ; Jazleen LEO ; Ashok CHOUDHURY ; Daniel Q. HUANG
Clinical and Molecular Hepatology 2025;31(2):654-657
6.Vibration-controlled transient elastography in shaping the epidemiology and management of steatotic liver disease: Editorial on “Current burden of steatotic liver disease and fibrosis among adults in the United States, 2017–2023”
Xiao-Dong ZHOU ; Terry Cheuk-Fung YIP ; Daniel Q HUANG ; Mark Dhinesh MUTHIAH ; Mazen NOUREDDIN ; Ming-Hua ZHENG
Clinical and Molecular Hepatology 2025;31(2):620-624
8.Global incidence and prevalence of nonalcoholic fatty liver disease
Margaret LP TENG ; Cheng Han NG ; Daniel Q. HUANG ; Kai En CHAN ; Darren JH TAN ; Wen Hui LIM ; Ju Dong YANG ; Eunice TAN ; Mark D. MUTHIAH
Clinical and Molecular Hepatology 2023;29(Suppl):S32-S42
Nonalcoholic fatty liver disease (NAFLD) is a leading cause of liver disease worldwide. The estimated global incidence of NAFLD is 47 cases per 1,000 population and is higher among males than females. The estimated global prevalence of NAFLD among adults is 32% and is higher among males (40%) compared to females (26%). The global prevalence of NAFLD has increased over time, from 26% in studies from 2005 or earlier to 38% in studies from 2016 or beyond. The prevalence of NAFLD varies substantially by world region, contributed by differing rates of obesity, and genetic and socioeconomic factors. The prevalence of NAFLD exceeds 40% in the Americas and South-East Asia. The prevalence of NAFLD is projected to increase significantly in multiple world regions by 2030 if current trends are left unchecked. In this review, we discuss trends in the global incidence and prevalence of NAFLD and discuss future projections.
9.Diabetes and Risk of Hepatocellular Carcinoma in Cirrhosis Patients with Nonalcoholic Fatty Liver Disease
Pai-Chi TENG ; Daniel Q. HUANG ; Ting-Yi LIN ; Mazen NOUREDDIN ; Ju Dong YANG
Gut and Liver 2023;17(1):24-33
Nonalcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease in the world. NAFLD is a hepatic manifestation of insulin resistance, the core pathophysiology of diabetes. Multiple clinical studies show that diabetes increases the risk of liver disease progression and cirrhosis development in patients with NAFLD. Diabetes has causal associations with many different cancers, including hepatocellular carcinoma (HCC). More recent studies demonstrate that diabetes increases the risk of HCC in patients with underlying NAFLD cirrhosis, confirming the direct hepatocarcinogenic effect of diabetes among cirrhosis patients. Diabetes promotes hepatocarcinogenesis via the activation of inflammatory cascades producing reactive oxygen species and proinflammatory cytokines, leading to genomic instability, cellular proliferation, and inhibition of apoptosis. Given the global increase in the burden of NAFLD and HCC, high-risk patients such as older diabetic individuals should be carefully monitored for HCC development. Future larger studies should explore whether the effect of diabetes on HCC risk in NAFLD cirrhosis is modifiable by the type of antidiabetic medication and the effectiveness of diabetes control.

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