Clinical and Molecular Hepatology

"Fatty liver"

Original Articles

Outcomes of Oral Antidiabetic Drugs in Metabolic Dysfunction-Associated Steatotic Liver Disease: A Nationwide Target Trial Emulation Study: Heejoon Jang, Yeonjin Kim, Yoo Kyoung Lim, Dong Hyeon Lee, Sae Kyung Joo, Bokyung Koo, Woojoo Lee, Stefano Romeo, Won Kim, Innovative Target Exploration of NAFLD (ITEN) consortium; Received September 5, 2025 Accepted December 30, 2025 Published online January 6, 2026; DOI: https://doi.org/10.3350/cmh.2025.1006 [Accepted]

Abstract
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Background/Aims
Patients with concurrent type 2 diabetes mellitus (T2DM) and metabolic dysfunction-associated steatotic liver disease (MASLD) face elevated cardiovascular risks. However, optimal oral antidiabetic drug (OAD) selection for this population remains unclear.
Methods
Using the Korean National Health Information Database, we conducted a target trial emulation comparing cardiovascular outcomes among patients with T2DM and MASLD (defined by fatty liver index ≥30) who initiated sodium-glucose cotransporter 2 (SGLT2) inhibitors, thiazolidinediones, dipeptidyl peptidase-4 (DPP-4) inhibitors, or sulfonylureas with metformin. The primary outcome was major adverse cardiovascular events (MACE), including cardiovascular mortality, nonfatal myocardial infarction, and nonfatal stroke.
Results
Among 71,071 patients (331,726 person-years), SGLT2 inhibitor users experienced a significantly lower MACE risk compared to sulfonylurea users (adjusted subdistribution hazard ratio [aSHR], 0.44; 95% CI, 0.31–0.62). SGLT2 inhibitors also demonstrated a lower MACE risk compared to thiazolidinediones (aSHR, 0.61; 95% CI, 0.39–0.96) and DPP-4 inhibitors (aSHR, 0.59; 95% CI, 0.42–0.96). Cardiovascular mortality risk was notably reduced with SGLT2 inhibitors compared to sulfonylureas (aSHR, 0.13; 95% CI, 0.03-0.50), thiazolidinediones (aSHR, 0.19; 95% CI, 0.04-0.86), and DPP-4 inhibitors (aSHR, 0.22; 95% CI, 0.06-0.84). Mediation analysis revealed that MASLD regression accounted for 8.7% of the total cardiovascular benefit when comparing SGLT2 inhibitors to sulfonylureas.
Conclusions
In patients with concurrent T2DM and MASLD, SGLT2 inhibitors demonstrated better cardiovascular outcomes compared to other OADs. These findings suggest that SGLT2 inhibitors may be the preferred OAD choice for cardiovascular risk reduction in this high-risk population.

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Hypothyroidism and the risk of liver-related events in patients with metabolic dysfunction-associated steatotic liver disease: Xinrui Jin, Sherlot Juan Song, Jimmy Che-To Lai, Grace Lai-Hung Wong, Alice Pik-Shan Kong, Nana Peng, Xiang Xiao, Vincent Wai-Sun Wong, Terry Cheuk-Fung Yip; Clin Mol Hepatol 2026;32(1):353-367.
Published online December 1, 2025; DOI: https://doi.org/10.3350/cmh.2025.0860

Background/Aims
Previous studies suggest that hypothyroidism is associated with metabolic dysfunction-associated steatotic liver disease (MASLD) and its histological severity, but clinical outcome data are largely lacking. We aimed to study the impact of hypothyroidism on liver-related events (LREs).
Methods
Patients with MASLD were identified from a territory-wide registry in Hong Kong during 2000–2024. Thyroid status was determined using diagnosis codes and thyroid function tests. The primary outcome, LRE, was defined as a composite of hepatic decompensation, hepatocellular carcinoma, liver transplantation, and liver-related death.
Results
A total of 20,478 patients with MASLD were included in the final analysis (mean age 56.4±13.2 years; 43.9% male). At baseline, 18,178 (88.8%) patients were euthyroid, 598 (2.9%) were hyperthyroid, and 1,702 (8.3%) were hypothyroid. Compared with euthyroid patients, both hyperthyroidism and overt hypothyroidism were associated with cirrhosis. At a median follow-up of 4.8 years, 179 patients developed LREs, and 26 died from liver disease. Compared with patients with normal serum thyroid-stimulating hormone (TSH) levels of 0.4–4 mIU/L, those with subclinical (4–10 mIU/L; adjusted time-dependent cause-specific hazard ratio [aCSHR], 2.49; 95% CI, 1.51–4.13) and overt hypothyroidism (>10 mIU/L; aCSHR, 4.91; 95% CI, 1.56–15.47) had an increased risk of LREs. Time-dependent, but not baseline, TSH and thyroid status were associated with LRE risk.
Conclusions
Subclinical and overt hypothyroidism are associated with an increased risk of LREs in a dose-dependent manner. The association with time-dependent but not baseline thyroid status underscores the importance of thyroid monitoring and suggests that correction of hypothyroidism may mitigate LRE risk.

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Review Article

Novel Biomarkers for Alcohol-Associated Liver Disease and Their Implications Across Clinical Settings: Kaanthi Rama, Vinay Jahagirdar, Francisco Idalsoaga, Hanna Blaney, S. Fisher Rhoads, Luis Antonio Díaz, Marco Arrese, Juan Pablo Arab; Received August 15, 2025 Accepted November 17, 2025 Published online November 25, 2025; DOI: https://doi.org/10.3350/cmh.2025.0921 [Accepted]

Abstract
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Alcohol-associated liver disease (ALD) is a leading cause of preventable cirrhosis, hepatocellular carcinoma, and liver-related mortality, yet current laboratory and imaging tools detect only late-stage disease. This narrative review synthesizes emerging evidence on novel biomarkers that capture the multidimensional pathophysiology of ALD and discusses their utility for routine clinical practice. Traditional serum-based liver fibrosis markers (e.g., cytokeratin-18 fragments, Pro-C3, or the Enhanced Liver Fibrosis) improve non-invasive staging risk beyond aminotransferases, while elastography techniques, such as vibration-controlled transient elastography and magnetic resonance elastography, can also quantify liver stiffness with high precision. Among novel mechanistic biomarkers, genetic polymorphisms in PNPLA3, TM6SF2, MBOAT7, HSD17B13, and polygenic risk scores define lifetime risk, whereas sex-specific hormonal milieus also modify susceptibility and progression. Moreover, gut dysbiosis signatures, including reduced Faecalibacterium prausnitzii, Akkermansia muciniphila, and a lower Firmicutes/Bacteroidetes ratio, and their metabolites (short-chain fatty acids, bile acids, trimethylamine N-oxide) correlate with liver inflammation and fibrosis. Endocrine imbalances of cortisol, testosterone, and thyroid hormones further stratify metabolic vulnerability. Ultimately, multi-omics platforms (i.e., transcriptomics, lipidomics, proteomics, metabolomics, epigenomics) can reveal distinct molecular signatures that predict steatohepatitis, fibrogenesis, and early hepatocellular carcinoma. Integrating these biomarkers enables phase-specific enrichment strategies, earlier intervention windows, adaptive dose-finding, and mechanism-based endpoints in ALD trials. Remaining challenges include assay standardization, validation across diverse cohorts, and incorporation into regulatory frameworks. Future work could evaluate cost-effectiveness and feasibility in routine clinical practice. Widespread adoption promises earlier diagnosis, personalized risk reduction, and more efficient drug development for this globally prevalent disorder.

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Original Articles

Aspirin and hepatocellular carcinoma risk in metabolic dysfunction-associated steatotic liver disease: nationwide cohort study with genetic risk analysis: Juhee Ahn, Moon Haeng Hur, Hyunjae Shin, Min Kyung Park, Sungho Won, Jeayeon Park, Yunmi Ko, Youngsu Park, Yun Bin Lee, Eun Ju Cho, Jeong-Hoon Lee, Su Jong Yu, Jung-Hwan Yoon, Yoon Jun Kim; Clin Mol Hepatol 2026;32(1):339-352.
Published online November 25, 2025; DOI: https://doi.org/10.3350/cmh.2025.0528

Background/Aims
The association between aspirin use and hepatocellular carcinoma (HCC) risk in patients with metabolic dysfunction-associated steatotic liver disease (MASLD) remains unclear. This study evaluated the effect of aspirin on HCC development in MASLD patients using Korean National Health Insurance Service (NHIS) and UK Biobank (UKB) databases.
Methods
A retrospective cohort analysis was conducted using the NHIS database with a 3-year landmark design. Baseline characteristics were balanced using inverse probability of treatment weighting (IPTW) and 1:3 propensity score matching (PSM). Additionally, Mendelian randomization analysis was performed in the UKB cohort using a genomic risk score (GRS) for salicylic acid, based on genetic variants related to aspirin metabolism, as a proxy for aspirin use.
Results
In the NHIS cohort, 6,584,155 eligible patients were included, of whom 1,723,435 had MASLD. After PSM, aspirin use was associated with a significantly lower risk of HCC compared to no aspirin use, in both the overall population (adjusted subdistribution hazard ratio [ASHR]=0.86; 95% confidence interval [CI] 0.78–0.95; P=0.002) and MASLD group (ASHR=0.86; 95% CI 0.75–0.99; P=0.036). Similar results were reproduced in the IPTW population and several sensitivity and subgroup analyses. In the UKB cohort, individuals in the top 95% of GRS had a significantly lower risk of HCC compared to those in the bottom 5%, in both the overall population (ASHR=0.61; 95% CI 0.39–0.95; P=0.028) and MASLD group (ASHR=0.47; 95% CI 0.29–0.76; P=0.002).
Conclusions
Findings from both population-based and genetic analyses suggest a possible protective association between aspirin use and HCC in patients with MASLD, which warrants further validation.

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Comparative risk of fibrosis progression with sodium-glucose cotransporter-2 vs. dipeptidyl peptidase-4 inhibitors in metabolic dysfunction-associated steatotic liver disease and type 2 diabetes mellitus with low-to-intermediate fibrosis: Jonggi Choi, Daniel Fulop, Vy H. Nguyen, Eric Przybyszewski, Jiunn Song, Allison Carroll, Megan Michta, Erik Almazan, Tracey G. Simon, Raymond T. Chung; Clin Mol Hepatol 2026;32(1):305-317.
Published online November 11, 2025; DOI: https://doi.org/10.3350/cmh.2025.0825

Background/Aims
Metabolic dysfunction-associated steatotic liver disease (MASLD) is a growing cause of cirrhosis and its complications. Given its close association with type 2 diabetes mellitus (T2DM), evaluating whether sodium-glucose cotransporter-2 inhibitors (SGLT2is) can mitigate the progression of liver fibrosis is clinically important. We examined the association between SGLT2i use and liver fibrosis progression in patients diagnosed with MASLD and T2DM.
Methods
We conducted a target trial emulation study using a retrospective, active comparator new-user design among adults with MASLD, T2DM, and low-to-intermediate Fibrosis-4 (FIB-4≤2.67) scores who initiated treatment with either SGLT2is or dipeptidyl peptidase-4 inhibitors (DPP-4is) at Mass General Brigham or Asan Medical Center from 2013 to 2023. The primary outcome was the progression to advanced fibrosis (FIB-4>2.67), confirmed on ≥2 occasions within 1 year. The secondary outcome was the development of major adverse liver outcomes (MALO), including incident cirrhosis, decompensation events, hepatocellular carcinoma, or liver transplantation.
Results
Among 16,901 eligible patients, 2,571 propensity score-matched pairs were identified with balanced baseline characteristics. During follow-up (median, 3.7 years), fibrosis progression occurred at a rate of 3.46/100 personyears in SGLT2i users and 4.44 in DPP4i users. SGLT2i use was associated with a lower risk of fibrosis progression (HR 0.78, 95% CI 0.67–0.89; P<0.001). No significant difference in MALO incidence was observed. Subgroup analyses showed a consistent association among users of metformin, statins, and aspirin.
Conclusions
SGLT2i use was associated with reduced risk of fibrotic progression compared to DPP4i use in adults with MASLD and T2DM.

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Correspondence

Correspondence to editorial on “Risk stratification by noninvasive tests in patients with metabolic dysfunction-associated steatotic liver disease”: Hye Won Lee, Seung Up Kim; Clin Mol Hepatol 2026;32(1):e87-e89.
Published online May 8, 2025; DOI: https://doi.org/10.3350/cmh.2025.0477

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Original Article

Glucagon-like peptide 1 receptor agonist and reduced liver and non-liver complications in adults with type 2 diabetes and metabolic dysfunction-associated steatotic liver disease: a target trial emulation study: Xianhua Mao, Xinrong Zhang, Rongtao Lai, Ka-Shing Cheung, Man-Fung Yuen, Ramsey Cheung, Wai-Kay Seto, Mindie H. Nguyen; Clin Mol Hepatol 2025;31(3):1084-1099.
Published online April 23, 2025; DOI: https://doi.org/10.3350/cmh.2024.1096

Background/Aims
Information about the association of glucagon-like peptide-1 receptor (GLP-1RA) with liver and non-liver complications is insufficient in patients with type 2 diabetes (T2D) and metabolic dysfunction-associated steatotic liver disease (MASLD). We conducted a target trial emulation study to evaluate whether GLP-1RA decreases the risk of liver and non-liver outcomes.
Methods
Patients with T2D and MASLD initiating GLP-1RA or dipeptidyl peptidase-4 inhibitor (DPP-4i) were included from 2013 to 2022 in Merative™ Marketscan^® Research Databases. Primary outcomes included incidences of (1) hepatocellular carcinoma (HCC) and cirrhosis, and (2) cardiovascular disease (CVD), chronic kidney disease (CKD), and non-liver cancer. Inverse probability of treatment weighting was applied to balance baseline characteristics and Cox regression models were conducted to estimate hazard ratio (HR) and 95% confidence interval (CI).
Results
In the intention-to-treat design, GLP-1RA, compared with DPP-4i, had a significantly lower incidence (per 1,000 person-years) of HCC (0.8 vs. 1.7; HR 0.53, 95% CI 0.39–0.71), of cirrhosis (29.3 vs. 32.9; HR 0.91, 95% CI 0.86–0.96), of CVD (57.2 vs. 73.9; HR 0.90, 95% CI 0.86–0.95), of CKD (4.5 vs. 6.8; HR 0.73, 95% CI 0.64–0.84), and of non-liver cancer (16.9 vs. 22.9; HR 0.82, 95% CI 0.77–0.89). In the per-protocol design, significant inverse associations for these study outcomes still were observed, with HR 0.60–0.77.
Conclusions
In this emulated target trial of nationwide patients with T2D and MASLD, GLP-1RA use, when compared with DPP-4i, was associated with a significantly lower risk of liver and non-liver complications.

Citations

Citations to this article as recorded by

Evaluating causal protective effect of dual GLP-1R/GIPR agonists on MASLD: A Mendelian randomization and colocalization study
Yangke Cai, Siyuan Xie, Liyi Xu, Jiamin Chen, Jianting Cai
European Journal of Pharmacology.2025; 1005: 178088. CrossRef
Impaired Thyroid Hormone Sensitivity is Associated with Increased Risk of Liver Fibrosis in Euthyroid Population: A Cross-Sectional Analysis of NHANES
Xingyu Yao, Kaiwen Xiao, Hein Ko Oo
Hormone and Metabolic Research.2025; 57(09): 511. CrossRef

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Reply to Correspondence

Steatotic liver disease

Reply to correspondence on “Current burden of steatotic liver disease and fibrosis among adults in the United States, 2017-2023”: Jeayeon Park, Su Jong Yu; Clin Mol Hepatol 2025;31(2):e221-e223.
Published online March 4, 2025; DOI: https://doi.org/10.3350/cmh.2025.0226

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Special Issue

Steatotic liver disease

KASL clinical practice guidelines for the management of metabolic dysfunction-associated steatotic liver disease 2025: Won Sohn, Young-Sun Lee, Soon Sun Kim, Jung Hee Kim, Young-Joo Jin, Gi-Ae Kim, Pil Soo Sung, Jeong-Ju Yoo, Young Chang, Eun Joo Lee, Hye Won Lee, Miyoung Choi, Su Jong Yu, Young Kul Jung, Byoung Kuk Jang, on behalf of The Korean Association for the Study of the Liver (KASL); Clin Mol Hepatol 2025;31(Suppl):S1-S31.
Published online February 19, 2025; DOI: https://doi.org/10.3350/cmh.2025.0045

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Eun Ji Jang, Ho Joong Choi, Young Kyoung You, Deok Hwa Seo, Mi Hyun Kwon, Keungmo Yang, Jaejun Lee, Jeong Won Jang, Seung Kew Yoon, Ji Won Han, Pil Soo Sung
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Metabolic Dysfunction-Associated Steatotic Liver Disease, Recent Revision of Terminology and Its Implications
Hyo Young Lee, Eileen L. Yoon
The Korean Journal of Gastroenterology.2025; 85(2): 126. CrossRef
Advances in identifying risk factors of metabolic dysfunction-associated alcohol-related liver disease
Rui-Qi Ye, Yi-Fan Chen, Chang Ma, Xi Cheng, Wei Guo, Sha Li
Biomedicine & Pharmacotherapy.2025; 188: 118191. CrossRef
A Case Report of Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) with Improved Cardiometabolic Risk Factors Following Treatment with Saenggangunbi-tang
Eun Kyung Lee, Min Jeong Park, Youngchul Kim, Jang-Hoon Lee
The Journal of Internal Korean Medicine.2025; 46(2): 303. CrossRef
Food Nutrients and Bioactive Compounds for Managing Metabolic Dysfunction-Associated Steatotic Liver Disease: A Comprehensive Review
Erdenetsogt Dungubat, Kohei Fujikura, Masahiko Kuroda, Toshio Fukusato, Yoshihisa Takahashi
Nutrients.2025; 17(13): 2211. CrossRef
Associations between steatotic liver disease subtypes and incident atrial fibrillation in young adults: a nationwide cohort study
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Second-line antidiabetic drugs: friend or foe of the liver
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Journal of Liver Cancer.2025; 25(2): 187. CrossRef
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The Journal of Korean Diabetes.2025; 26(3): 172. CrossRef
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Letter to the Editor

Letter to the editor on “Bariatric surgery reduces long-term mortality in patients with metabolic dysfunction-associated steatotic liver disease and cirrhosis”: Chi-Kuei Hsu, Po-Yu Huang, Chih-Cheng Lai; Clin Mol Hepatol 2025;31(3):e247-e248.
Published online February 6, 2025; DOI: https://doi.org/10.3350/cmh.2025.0073

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Snapshot

Interventions targeting the gut-liver axis: A potential treatment strategy for metabolic dysfunction-associated steatotic liver disease: Pingping Jin, Xinyi Lu, Daozhen Chen, Yu Chen; Clin Mol Hepatol 2025;31(3):1100-1102.
Published online February 6, 2025; DOI: https://doi.org/10.3350/cmh.2024.1090

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Phytochemistry.2026; 243: 114720. CrossRef
Hypertension and Long-Term Adverse Clinical Outcomes in MASLD: Sensitivity Analyses for Unmeasured or Uncontrolled Confounding
Guiying Gao, Xiuhong Wang, Ruizhe Huang, Jing Cao
Journal of Hepatology.2026;[Epub] CrossRef
Extracellular Vesicles: Orchestrators of Intrahepatic and Systemic Crosstalk in Metabolic Dysfunction-Associated Steatotic Liver Disease
Yu Lei, Mei Liu, Xiang Tao
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Probiotic-Derived Strain-Specific Metabolites Ameliorate Metabolic Dysfunction–Associated Steatotic Liver Disease through Modulation of the Gut-Liver Axis
Sang Jun Yoon, Jieun Choi, Sung-Min Won, Jeong Seok Yu, Hee Young Kim, Hyun Chae Joung, In Gyu Park, Jung A Eom, Sang Hak Han, Do Yup Lee, Ki Tae Suk
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From liver to gut: the hidden gastrointestinal impact of pediatric metabolic dysfunction-associated steatotic liver disease
Gianmario Forcina, Vittoria Frattolillo, Maria De Cesare, Assunta Floriano, Rosamaria Palma, Federica Casamassima, Mario Bartiromo, Pierluigi Marzuillo, Emanuele Miraglia del Giudice, Anna Di Sessa
Expert Review of Gastroenterology & Hepatology.2025; 19(12): 1329. CrossRef

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Editorial

Steatotic liver disease

Revealing the importance of a multidisciplinary approach to reducing the global burden of SLD through the COVID-19 pandemic: Editorial on “Current burden of steatotic liver disease and fibrosis among adults in the United States, 2017–2023”: Jeayeon Park, Su Jong Yu; Clin Mol Hepatol 2025;31(2):625-627.
Published online January 16, 2025; DOI: https://doi.org/10.3350/cmh.2025.0019

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The burden of steatotic liver disease before and during the COVID-19 pandemic: Correspondence to editorial on “Current burden of steatotic liver disease and fibrosis among adults in the United States, 2017-2023”
Donghee Kim, Pojsakorn Danpanichkul, Karn Wijarnpreecha, George Cholankeril, Rohit Loomba, Aijaz Ahmed
Clinical and Molecular Hepatology.2025; 31(2): e183. CrossRef
Reply to correspondence on “Current burden of steatotic liver disease and fibrosis among adults in the United States, 2017-2023”
Jeayeon Park, Su Jong Yu
Clinical and Molecular Hepatology.2025; 31(2): e221. CrossRef

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Correspondences

Steatotic liver disease

Correspondence to letter to the editor 2 on “Evolutionary changes in metabolic dysfunction-associated steatotic liver disease and risk of hepatocellular carcinoma: A nationwide cohort study”: Seogsong Jeong, Won Kim, Sang Min Park; Clin Mol Hepatol 2025;31(2):e210-e211.
Published online January 6, 2025; DOI: https://doi.org/10.3350/cmh.2024.1175

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Steatotic liver disease

Correspondence to letter to the editor 1 on “Evolutionary changes in metabolic dysfunction-associated steatotic liver disease and risk of hepatocellular carcinoma: A nationwide cohort study”: Seogsong Jeong, Won Kim, Sang Min Park; Clin Mol Hepatol 2025;31(2):e208-e209.
Published online January 6, 2025; DOI: https://doi.org/10.3350/cmh.2024.1171

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Original Article

High Steatosis-Associated Fibrosis Estimator scores predict hepatocellular carcinoma in viral and non-viral hepatitis and metabolic dysfunction-associated steatotic liver disease: Tung-Hung Su, Sheng-Shun Yang, Mei-Hsuan Lee, Wei-Yu Kao, Shang-Chin Huang, Fen-Fang Chen, Francis SK Poon, Lung-Wen Tsai, Yi-Ting Chen, Che Lin, Weichung Wang, W Ray Kim, Jia-Horng Kao; Clin Mol Hepatol 2025;31(3):796-809.
Published online January 6, 2025; DOI: https://doi.org/10.3350/cmh.2024.0822

Background/Aims
There are no hepatocellular carcinoma (HCC) surveillance recommendations for non-viral chronic liver diseases (CLD), such as metabolic dysfunction-associated steatotic liver disease (MASLD). We explored the Steatosis-Associated Fibrosis Estimator (SAFE) score to predict HCC in MASLD and other CLD etiologies.
Methods
Patients with various CLDs were included from medical centers in Taiwan. The SAFE score, consisting of age, body mass index, diabetes, and laboratory data, was calculated at baseline, and patients were traced for new development of HCC. The predictability of the SAFE score for HCC was analyzed using the sub-distribution hazard model with adjustments for competing risks.
Results
Among 12,963 CLD patients with a median follow-up of 4 years, 258 developed HCC. The SAFE score classifies 1-, 3-, and 5-year HCC risk regardless of CLD etiologies. High (≥100) and intermediate (0–100) SAFE scores increased 11 and 2 folds HCC risks compared to low (<0) SAFE scores. Combining two lower risk tiers (SAFE<100), a high SAFE score (≥100) was associated with a 7.5-fold risk of HCC (adjusted sub-distributional hazard ratio [aSHR] 7.54; 95% confidence interval (CI) 5.38–10.60). A high SAFE score increased the risks of HCC in subgroups of viral hepatitis, non-viral hepatitis (aSHR 11.10; 95% CI 3.97–31.30) and MASLD (aSHR 4.23; 95% CI 1.43–12.50). A hospital cohort (n=8,103) and a community MASLD cohort (n=120,166) validated the high SAFE score (≥100) for HCC risk prediction.
Conclusions
The SAFE score stratifies high risks for HCC in CLD patients regardless of etiologies and helps to select at-risk candidates for HCC surveillance.

Citations

Citations to this article as recorded by

HCC predictors in routine practice for patients with chronic liver diseases: Correspondence to editorial on “High SAFE scores predict hepatocellular carcinoma in viral and non-viral hepatitis and metabolic dysfunction associated steatotic liver disease”
Tung-Hung Su, Jia-Horng Kao
Clinical and Molecular Hepatology.2026; 32(1): e52. CrossRef
Can SAFE score be utilized as a universal hepatocellular carcinoma prediction score?: Editorial on “High Steatosis-Associated Fibrosis Estimator scores predict hepatocellular carcinoma in viral and non-viral hepatitis and metabolic dysfunction-associated
Michael Kwan-Lung Ko, Loey Lung-Yi Mak
Clinical and Molecular Hepatology.2026; 32(1): 371. CrossRef
Risk stratification for hepatocellular carcinoma in metabolic dysfunction-associated steatotic liver disease: Editorial on “High Steatosis-Associated Fibrosis Estimator scores predict hepatocellular carcinoma in viral and non-viral hepatitis and metabolic
Ho Soo Chun, Minjong Lee
Clinical and Molecular Hepatology.2026; 32(1): 368. CrossRef

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Editorial

Steatotic liver disease

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; Clin Mol Hepatol 2025;31(2):620-624.
Published online December 26, 2024; DOI: https://doi.org/10.3350/cmh.2024.1131

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Liver Fibrosis and the Risk of Coronary Artery Disease, Stent Thrombosis, Restenosis and Adverse Clinical Outcomes
Na Tian, Tie Xiao, Tianyi Xia, Hai‐Yang Yuan, Michael D. Shapiro, Gregory Y. H. Lip, Cheng‐Han Fanren, Li‐You Lian, Chen‐Xiao Huang, Yi‐Xuan Wei, Giovanni Targher, Christopher D. Byrne, Cheng‐Lv Hong, Shenghong Ju, Ming‐Hua Zheng
Alimentary Pharmacology & Therapeutics.2026; 63(1): 70. CrossRef
Editorial: Does Metabolic Dysfunction‐Associated Steatotic Liver Disease With Advanced Fibrosis Also Equate to Risk of Advanced Coronary Artery Disease? Authors' Reply
Xiao‐Dong Zhou, Yusuf Yilmaz, Ming‐Hua Zheng
Alimentary Pharmacology & Therapeutics.2026; 63(1): 155. CrossRef
Statins in MASLD: Challenges and Future
Xiao-Dong Zhou, Mark D. Muthiah, Ming-Hua Zheng
JHEP Reports.2025; : 101372. CrossRef
Addressing the burden of steatotic liver disease: The role of transient elastography: Correspondence to editorial on “Current burden of steatotic liver disease and fibrosis among adults in the United States, 2017-2023”
Donghee Kim, Pojsakorn Danpanichkul, Karn Wijarnpreecha, George Cholankeril, Rohit Loomba, Aijaz Ahmed
Clinical and Molecular Hepatology.2025; 31(2): e180. CrossRef
The association of advanced lung cancer inflammation index with non-alcoholic fatty liver disease in NHANES 2017–2020
Lin Cheng, Shumeng Li, Hui Li, Jiafeng You, Mingwei Yu, Guowang Yang
Frontiers in Medicine.2025;[Epub] CrossRef
Long-Term Glycemic Control and the Risk of Liver Stiffness Progression and Liver-Related Events in MASLD
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Clinical Gastroenterology and Hepatology.2025;[Epub] CrossRef

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Reviews

Steatotic liver disease

Microbiome-centered therapies for the management of metabolic dysfunction-associated steatotic liver disease: Huma Saeed, Luis Antonio Díaz, Antonio Gil-Gómez, Jeremy Burton, Jasmohan S. Bajaj, Manuel Romero-Gomez, Marco Arrese, Juan Pablo Arab, Mohammad Qasim Khan; Clin Mol Hepatol 2025;31(Suppl):S94-S111.
Published online November 28, 2024; DOI: https://doi.org/10.3350/cmh.2024.0811

Abstract
PDF

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a significant global health issue, affecting over 30% of the population worldwide due to the rising prevalence of metabolic risk factors such as obesity and type 2 diabetes mellitus. This spectrum of liver disease ranges from isolated steatosis to more severe forms such as steatohepatitis, fibrosis, and cirrhosis. Recent studies highlight the role of gut microbiota in MASLD pathogenesis, showing that dysbiosis significantly impacts metabolic health and the progression of liver disease. This review critically evaluates current microbiome-centered therapies in MASLD management, including prebiotics, probiotics, synbiotics, fecal microbiota transplantation, and emerging therapies such as engineered bacteria and bacteriophage therapy. We explore the scientific rationale, clinical evidence, and potential mechanisms by which these interventions influence MASLD. The gut-liver axis is crucial in MASLD, with notable changes in microbiome composition linked to disease progression. For instance, specific microbial profiles and reduced alpha diversity are associated with MASLD severity. Therapeutic strategies targeting the microbiome could modulate disease progression by improving gut permeability, reducing endotoxin-producing bacteria, and altering bile acid metabolism. Although promising, these therapies require further research to fully understand their mechanisms and optimize their efficacy. This review integrates findings from clinical trials and experimental studies, providing a comprehensive overview of microbiome-centered therapies’ potential in managing MASLD. Future research should focus on personalized strategies, utilizing microbiome features, blood metabolites, and customized dietary interventions to enhance the effectiveness of these therapies.

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Viral hepatitis

Mechanisms of hepatocellular carcinoma and cirrhosis development in concurrent steatotic liver disease and chronic hepatitis B: Saisai Zhang, Lung-Yi Mak, Man-Fung Yuen, Wai-Kay Seto; Clin Mol Hepatol 2025;31(Suppl):S182-S195.
Published online November 21, 2024; DOI: https://doi.org/10.3350/cmh.2024.0837

Abstract
PDF

Chronic hepatitis B (CHB) poses a major global public health challenge and is a leading cause of cirrhosis and liver cancer. Hepatic steatosis is common in individuals with CHB compared to the non-CHB population and is particularly prevalent in hepatitis B virus (HBV)-endemic regions, affecting about one-third of CHB patients. The interaction between hepatic steatosis and CHB-related disease progression is complex and still under debate. Evidence demonstrates that co-existing steatosis may worsen liver fibrosis while paradoxically increasing the likelihood of achieving better HBV control. In particular, despite the association of steatotic liver disease (SLD) with lower HBV viral loads and higher rates of HBsAg seroclearance, the coexistence of CHB and SLD can potentially accelerate liver disease progression. Factors such as fat deposition, lipotoxicity, oxidative stress, and chronic inflammation in SLD may foster a pro-fibrotic and pro-carcinogenic environment, accelerating the disease progression. Additionally, loss of global DNA methylation, changes in the immune microenvironment, and genetic susceptibility further contribute to the development of CHB-related cirrhosis and hepatocellular carcinoma (HCC). This review examines the mechanisms driving liver disease progression and the heightened risk of cirrhosis and HCC in patients with concurrent CHB and steatotic liver disease, underscoring the importance of prioritizing antiviral therapy for CHB in addition to addressing SLD.

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Correspondences

Liver fibrosis, cirrhosis, and portal hypertension

Correspondence to editorial on “Optimal cut-offs of vibration-controlled transient elastography and magnetic resonance elastography in diagnosing advanced liver fibrosis in patients with nonalcoholic fatty liver disease: a systematic review and meta-analysis”: Young Eun Chon, Jung Hwan Yu, Seung Up Kim; Clin Mol Hepatol 2025;31(1):e61-e63.
Published online October 15, 2024; DOI: https://doi.org/10.3350/cmh.2024.0878

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Steatotic liver disease

Correspondence to editorial on “Optimal cutoffs of vibration-controlled transient elastography and magnetic resonance elastography in diagnosing advanced liver fibrosis in patients with nonalcoholic fatty liver disease: A systematic review and meta-analysis”: Jung Hwan Yu, Seung Up Kim; Clin Mol Hepatol 2025;31(1):e52-e54.
Published online September 24, 2024; DOI: https://doi.org/10.3350/cmh.2024.0815

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Letter to the Editor

Steatotic liver disease

Letter to the editor on “Bariatric intervention improves metabolic dysfunction-associated steatohepatitis in patients with obesity: A systematic review and meta-analysis”: Xiao-Song Li, Xi-Ping Shen, Hang Li; Clin Mol Hepatol 2025;31(1):e15-e16.
Published online September 12, 2024; DOI: https://doi.org/10.3350/cmh.2024.0784

Citations

Citations to this article as recorded by

Correspondence to letter to the editor on “Bariatric intervention improves metabolic dysfunction-associated steatohepatitis in patients with obesity: A systematic review and meta-analysis”
Yuri Cho, Dae Won Jun
Clinical and Molecular Hepatology.2025; 31(1): e103. CrossRef

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Correspondence

Steatotic liver disease

Correspondence to editorial on “Comparison of glucagon-like peptide-1 receptor agonists and thiazolidinediones on treating nonalcoholic fatty liver disease: a network meta-analysis”: Hayeon Kim, Min Jeong Park, Myeong Gyu Kim, Kyungim Kim; Clin Mol Hepatol 2024;30(4):989-991.
Published online August 27, 2024; DOI: https://doi.org/10.3350/cmh.2024.0705

Citations

Citations to this article as recorded by

Reply to correspondence on “Comparison of glucagon-like peptide-1 receptor agonists and thiazolidinediones on treating nonalcoholic fatty liver disease: a network meta-analysis”
Tian-Yi Ren, Mohammed Eslam, Jian-Gao Fan
Clinical and Molecular Hepatology.2024; 30(4): 1039. CrossRef

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Original Article

Steatotic liver disease

Optimal cut-offs of vibration-controlled transient elastography and magnetic resonance elastography in diagnosing advanced liver fibrosis in patients with nonalcoholic fatty liver disease: A systematic review and meta-analysis: Young Eun Chon, Young-Joo Jin, Jihyun An, Hee Yeon Kim, Miyoung Choi, Dae Won Jun, Mi Na Kim, Ji Won Han, Han Ah Lee, Jung Hwan Yu, Seung Up Kim; Clin Mol Hepatol 2024;30(Suppl):S117-S133.
Published online August 21, 2024; DOI: https://doi.org/10.3350/cmh.2024.0392

Background/aims
Opinions differ regarding vibration-controlled transient elastography and magnetic resonance elastography (VCTE/MRE) cut-offs for diagnosing advanced fibrosis (AF) in patients with non-alcoholic fatty liver disease (NAFLD). We investigated the diagnostic performance and optimal cut-off values of VCTE and MRE for diagnosing AF.
Methods
Literature databases, including Medline, EMBASE, Cochrane Library, and KoreaMed, were used to identify relevant studies published up to June 13, 2023. We selected studies evaluating VCTE and MRE regarding the degree of liver fibrosis using liver biopsy as the reference. The sensitivity, specificity, and area under receiver operating characteristics curves (AUCs) of the pooled data for VCTE and MRE for each fibrosis stage and optimal cut-offs for AF were investigated.
Results
A total of 19,199 patients from 63 studies using VCTE showed diagnostic AUC of 0.83 (95% confidence interval: 0.80–0.86), 0.83 (0.80–0.86), 0.87 (0.84–0.90), and 0.94 (0.91–0.96) for ≥F1, ≥F2, ≥F3, and F4 stages, respectively. Similarly, 1,484 patients from 14 studies using MRE showed diagnostic AUC of 0.89 (0.86–0.92), 0.92 (0.89–0.94), 0.89 (0.86–0.92), and 0.94 (0.91–0.96) for ≥F1, ≥F2, ≥F3, and F4 stages, respectively. The diagnostic AUC for AF using VCTE was highest at 0.90 with a cut-off of 7.1–7.9 kPa, and that of MRE was highest at 0.94 with a cut-off of 3.62–3.8 kPa.
Conclusions
VCTE (7.1–7.9 kPa) and MRE (3.62–3.8 kPa) with the suggested cut-offs showed favorable accuracy for diagnosing AF in patients with NAFLD. This result will serve as a basis for clinical guidelines for non-invasive tests and differential diagnosis of AF.

Citations

Citations to this article as recorded by

Correspondence to editorial on “Optimal cut-offs of vibration-controlled transient elastography and magnetic resonance elastography in diagnosing advanced liver fibrosis in patients with nonalcoholic fatty liver disease: a systematic review and meta-analy
Young Eun Chon, Jung Hwan Yu, Seung Up Kim
Clinical and Molecular Hepatology.2025; 31(1): e61. CrossRef
Essential tools for assessing advanced fibrosis in metabolic dysfunction-associated steatotic liver disease: Editorial on “Optimal cut-offs of vibration-controlled transient elastography and magnetic resonance elastography in diagnosing advanced liver fib
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Correspondence to editorial on “Optimal cutoffs of vibration-controlled transient elastography and magnetic resonance elastography in diagnosing advanced liver fibrosis in patients with nonalcoholic fatty liver disease: A systematic review and meta-analys
Jung Hwan Yu, Seung Up Kim
Clinical and Molecular Hepatology.2025; 31(1): e52. CrossRef
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Reply to Correspondence

Steatotic liver disease

Reply to correspondence on “Differences in liver and mortality outcomes of non-alcoholic fatty liver disease by race and ethnicity: A longitudinal real-world study”: Jae Hyun Bae; Clin Mol Hepatol 2024;30(4):1047-1049.
Published online August 19, 2024; DOI: https://doi.org/10.3350/cmh.2024.0666

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Editorials

Viral hepatitis

MASLD after hepatitis C virus eradication: Do not overlook the cardiometabolic risk factors: Editorial on “Dynamic change of metabolic dysfunction-associated steatotic liver disease in chronic hepatitis C patients after viral eradication: A nationwide registry study in Taiwan”: Rex Wan-Hin Hui, Lung-Yi Mak; Clin Mol Hepatol 2025;31(1):290-292.
Published online August 7, 2024; DOI: https://doi.org/10.3350/cmh.2024.0630

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Journal of the Formosan Medical Association.2025;[Epub] CrossRef

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Steatotic liver disease

Racial and ethnic disparities in metabolic dysfunction-associated steatotic liver disease outcomes: A call for culturally sensitive interventions: Editorial on “Differences in liver and mortality outcomes of non-alcoholic fatty liver disease by race and ethnicity: A longitudinal real-world study”: Jae Hyun Bae; Clin Mol Hepatol 2024;30(4):665-668.
Published online July 29, 2024; DOI: https://doi.org/10.3350/cmh.2024.0562

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Correspondence to editorial on “Differences in liver and mortality outcomes of non-alcoholic fatty liver disease by race and ethnicity: A longitudinal real-world study”
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Clinical and Molecular Hepatology.2024; 30(4): 1000. CrossRef
Reply to correspondence on “Differences in liver and mortality outcomes of non-alcoholic fatty liver disease by race and ethnicity: A longitudinal real-world study”
Jae Hyun Bae
Clinical and Molecular Hepatology.2024; 30(4): 1047. CrossRef

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Correspondence

Steatotic liver disease

The role of SPP1 in MASLD pathogenesis: Therapeutic insights into ursolic acid’s mechanisms of action: Correspondence to editorial on “Ursolic acid targets secreted phosphoprotein 1 to regulate Th17 cells against metabolic dysfunction-associated steatotic liver disease”: Yiyuan Zheng, Zhekun Xiong, Lina Zhao, Chaoyuan Huang, Qiuhong Yong, Dan Fang, Fengbin Liu, Yong Li; Clin Mol Hepatol 2024;30(4):1019-1022.
Published online July 8, 2024; DOI: https://doi.org/10.3350/cmh.2024.0471

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Letter to the Editor

Steatotic liver disease

Metabolic-associated fatty liver disease is less effective in predicting mortality than non-alcoholic fatty liver disease and metabolic dysfunction-associated steatotic liver disease: Letter to the editor on “Prognosis of biopsy-confirmed metabolic dysfunction-associated steatotic liver disease: A sub-analysis of the CLIONE study”: Yixuan Zhu, Xiaoyan Ma, Wenjing Ni, Yee Hui Yeo, Junping Shi, Jie Li; Clin Mol Hepatol 2024;30(4):974-977.
Published online July 4, 2024; DOI: https://doi.org/10.3350/cmh.2024.0417

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MAFLD or MASLD: Which better represents the prognosis of the steatotic liver population: Letter to the editor on “Evolutionary changes in metabolic dysfunction-associated steatotic liver disease and risk of hepatocellular carcinoma: A nationwide cohort st
Ying Wang, Shengfeng Wang, Xiude Fan, Jiajun Zhao, Yongfeng Song
Clinical and Molecular Hepatology.2025; 31(2): e128. CrossRef

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Review

Steatotic liver disease

Role of noninvasive tests in the prognostication of metabolic dysfunction-associated steatotic liver disease: Yue Wang, Sherlot Juan Song, Yichong Jiang, Jimmy Che-To Lai, Grace Lai-Hung Wong, Vincent Wai-Sun Wong, Terry Cheuk-Fung Yip; Clin Mol Hepatol 2025;31(Suppl):S51-S75.
Published online June 27, 2024; DOI: https://doi.org/10.3350/cmh.2024.0246

Abstract
PDF

In managing metabolic dysfunction-associated steatotic liver disease, which affects over 30% of the general population, effective noninvasive biomarkers for assessing disease severity, monitoring disease progression, predicting the development of liver-related complications, and assessing treatment response are crucial. The advantage of simple fibrosis scores lies in their widespread accessibility through routinely performed blood tests and extensive validation in different clinical settings. They have shown reasonable accuracy in diagnosing advanced fibrosis and good performance in excluding the majority of patients with a low risk of liver-related complications. Among patients with elevated serum fibrosis scores, a more specific fibrosis and imaging biomarker has proved useful to accurately identify patients at risk of liver-related complications. Among specific fibrosis blood biomarkers, enhanced liver fibrosis is the most widely utilized and has been approved in the United States as a prognostic biomarker. For imaging biomarkers, the availability of vibration-controlled transient elastography has been largely improved over the past years, enabling the use of liver stiffness measurement (LSM) for accurate assessment of significant and advanced fibrosis, and cirrhosis. Combining LSM with other routinely available blood tests enhances the ability to diagnose at-risk metabolic dysfunction-associated steatohepatitis and predict liver-related complications, some reaching an accuracy comparable to that of liver biopsy. Magnetic resonance imaging-based modalities provide the most accurate quantification of liver fibrosis, though the current utilization is limited to research settings. Expanding their future use in clinical practice depends on factors such as cost and facility availability.

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Editorials

Steatotic liver disease

Macrophage ATG16L1: Potential candidate for metabolic dysfunction-associated steatohepatitis treatment: Editorial on “Macrophage ATG16L1 expression suppresses metabolic dysfunction-associated steatohepatitis progression by promoting lipophagy”: Junjie Yu; Clin Mol Hepatol 2024;30(4):721-723.
Published online June 18, 2024; DOI: https://doi.org/10.3350/cmh.2024.0443

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Steatotic liver disease

Metabolic dysfunction-associated fatty liver disease is a ubiquitous latent cofactor in viral- and alcoholic-related hepatocellular carcinoma: Editorial on “Global prevalence of metabolic dysfunction-associated fatty liver disease-related hepatocellular carcinoma: A systematic review and meta-analysis”: Toru Nakamura, Masahito Nakano, Tsubasa Tsutsumi, Keisuke Amano, Takumi Kawaguchi; Clin Mol Hepatol 2024;30(4):705-708.
Published online May 20, 2024; DOI: https://doi.org/10.3350/cmh.2024.0372

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Letters to the Editor

Steatotic liver disease

Equivalent prevalence and progression of chronic kidney disease in non-alcoholic fatty liver disease and metabolic dysfunction-associated steatotic liver disease: Hiroyuki Suzuki, Tsubasa Tsutsumi, Machiko Kawaguchi, Keisuke Amano, Takumi Kawaguchi; Clin Mol Hepatol 2024;30(4):962-964.
Published online May 20, 2024; DOI: https://doi.org/10.3350/cmh.2024.0264

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Original Articles

Steatotic liver disease

Evolutionary changes in metabolic dysfunction-associated steatotic liver disease and risk of hepatocellular carcinoma: A nationwide cohort study: Seogsong Jeong, Yun Hwan Oh, Joseph C Ahn, Seulggie Choi, Sun Jae Park, Hye Jun Kim, Gyeongsil Lee, Joung Sik Son, Heejoon Jang, Dong Hyeon Lee, Meng Sha, Lei Chen, Won Kim, Sang Min Park; Clin Mol Hepatol 2024;30(3):487-499.
Published online May 7, 2024; DOI: https://doi.org/10.3350/cmh.2024.0145

Background/Aims
To determine the association between evolutionary changes in metabolic dysfunction-associated steatotic liver disease (MASLD) status and the risk of hepatocellular carcinoma (HCC) in a nationwide population-based cohort.
Methods
Information on study participants was derived from the Korea National Health Insurance Service database. The study population consisted of 5,080,410 participants who underwent two consecutive biennial health screenings between 2009 and 2012. All participants were followed up until HCC, death, or 31 December 2020. The association of evolutionary changes in MASLD status, as assessed by the fatty liver index and cardiometabolic risk factors, including persistent non-MASLD, resolved MASLD, incident MASLD, and persistent MASLD, with HCC risk was evaluated using multivariable-adjusted Cox proportional hazards regression.
Results
Among the 5,080,410 participants with 39,910,331 person-years of follow-up, 4,801 participants developed HCC. The incidence of HCC in participants with resolved, incident, and persistent MASLD was approximately 2.2-, 2.3-, and 4.7-fold higher, respectively, than that in those with persistent non-MASLD among the Korean adult population. When stratifying the participants according to the evolutionary change in MASLD status, persistent (adjusted hazard ratio [aHR], 2.94; 95% confidence interval [CI], 2.68–3.21; P<0.001), incident (aHR, 1.85; 95% CI, 1.63–2.10; P<0.001), and resolved MASLD (aHR, 1.33; 95% CI, 1.18–1.50; P<0.001) had an increased risk of HCC compared to persistent non-MASLD.
Conclusions
The evolutionary changes in MASLD were associated with the differential risk of HCC independent of metabolic risk factors and concomitant medications, providing additional information on the risk of HCC stratification in patients with MASLD.

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Steatotic liver disease

Global prevalence of metabolic dysfunction-associated fatty liver disease-related hepatocellular carcinoma: A systematic review and meta-analysis: Harry Crane, Guy D. Eslick, Cameron Gofton, Anjiya Shaikh, George Cholankeril, Mark Cheah, Jian-Hong Zhong, Gianluca Svegliati-Baroni, Alessandro Vitale, Beom Kyung Kim, Sang Hoon Ahn, Mi Na Kim, Simone I Strasser, Jacob George; Clin Mol Hepatol 2024;30(3):436-448.
Published online April 16, 2024; DOI: https://doi.org/10.3350/cmh.2024.0109

Background/Aims
The global proportion of hepatocellular carcinoma (HCC) attributable to metabolic dysfunction-associated fatty liver disease (MAFLD) is unclear. The MAFLD diagnostic criteria allows
objective
diagnosis in the presence of steatosis plus defined markers of metabolic dysfunction, irrespective of concurrent liver disease. We aimed to determine the total global prevalence of MAFLD in HCC cohorts (total-MAFLD), including the proportion with MAFLD as their sole liver disease (single-MAFLD), and the proportion of those with concurrent liver disease where MAFLD was a contributary factor (mixed-MAFLD).
Methods
This systematic review and meta-analysis included studies systematically ascertaining MAFLD in HCC cohorts, defined using international expert panel criteria including ethnicity-specific BMI cut-offs. A comparison of clinical and tumour characteristics was performed between single-MAFLD, mixed-MAFLD, and non-MAFLD HCC.
Results
22 studies (56,565 individuals with HCC) were included. Total and single-MAFLD HCC prevalence was 48.7% (95% confidence interval [CI] 34.5–63.0%) and 12.4% (95% CI 8.3–17.3%), respectively. In HCC due to chronic hepatitis B, C, and alcohol-related liver disease, mixed-MAFLD prevalence was 40.0% (95% CI 30.2–50.3%), 54.1% (95% CI 40.4–67.6%) and 64.3% (95% CI 52.7–75.0%), respectively. Mixed-MAFLD HCC had significantly higher likelihood of cirrhosis and lower likelihood of metastatic spread compared to single-MAFLD HCC, and a higher platelet count and lower likelihood of macrovascular invasion compared to non-MAFLD HCC.
Conclusions
MAFLD is common as a sole aetiology, but more so as a co-factor in mixed-aetiology HCC, supporting the use of positive diagnostic criteria.

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Letter to the Editor

Steatotic liver disease

Changing from NAFLD to MASLD: Prevalence and progression of ASCVD risk are similar between NAFLD and MASLD in Asia: Hiroyuki Suzuki, Tsubasa Tsutsumi, Machiko Kawaguchi, Keisuke Amano, Takumi Kawaguchi; Clin Mol Hepatol 2024;30(3):577-579.
Published online March 6, 2024; DOI: https://doi.org/10.3350/cmh.2024.0157

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Steatotic liver disease: Know your enemies: Lung-Yi Mak; Clin Mol Hepatol 2024;30(2):171-173.
Published online February 2, 2024; DOI: https://doi.org/10.3350/cmh.2024.0078

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Correspondence

Steatotic liver disease

Correspondence on Letter regarding “Waiting for the changes after the adoption of steatotic liver disease”: Eileen L. Yoon, Dae Won Jun; Clin Mol Hepatol 2024;30(1):126-128.
Published online November 28, 2023; DOI: https://doi.org/10.3350/cmh.2023.0500

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Letter to the Editor

Steatotic liver disease

Letter regarding “Waiting for the changes after the adoption of steatotic liver disease”: Kuo Chao Yew, Sunny H. Wong, Vincent Wai-Sun Wong, Hazel H. Oon; Clin Mol Hepatol 2024;30(1):118-120.
Published online November 14, 2023; DOI: https://doi.org/10.3350/cmh.2023.0472

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Correspondence

Artificial intelligence, epidemiology, methodology, or others

Correspondence on Letter regarding “Assessing the performance of ChatGPT in answering questions regarding cirrhosis and hepatocellular carcinoma”: Yee Hui Yeo, Ju Dong Yang; Clin Mol Hepatol 2024;30(1):124-125.
Published online November 14, 2023; DOI: https://doi.org/10.3350/cmh.2023.0470

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Letter to the Editor

Artificial intelligence, epidemiology, methodology, or others

Letter 2 regarding “Assessing the performance of ChatGPT in answering questions regarding cirrhosis and hepatocellular carcinoma”: Yiwen Zhang, Liwei Wu, Zepeng Mu, Linlin Ren, Ying Chen, Hanyun Liu, Lili Xu, Yangang Wang, Yaxing Wang, Susan Cheng, Yih Chung Tham, Bin Sheng, Tien Yin Wong, Hongwei Ji; Clin Mol Hepatol 2024;30(1):113-117.
Published online November 10, 2023; DOI: https://doi.org/10.3350/cmh.2023.0440

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Snapshot

Steatotic liver disease

Recent updates on pharmacologic therapy in non-alcoholic fatty liver disease: Young Chang, Soung Won Jeong, Jae Young Jang; Clin Mol Hepatol 2024;30(1):129-133.
Published online October 13, 2023; DOI: https://doi.org/10.3350/cmh.2023.0356

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Editorial

Steatotic liver disease

Adding to the confusion in more than just the name: Jacob George; Clin Mol Hepatol 2023;29(4):973-976.
Published online September 18, 2023; DOI: https://doi.org/10.3350/cmh.2023.0367

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Special Review

Steatotic liver disease

Waiting for the changes after the adoption of steatotic liver disease: Eileen L. Yoon, Dae Won Jun; Clin Mol Hepatol 2023;29(4):844-850.
Published online September 6, 2023; DOI: https://doi.org/10.3350/cmh.2023.0291

Abstract
PDF

Steatotic liver disease was suggested as an overarching term encompassing various etiologies of hepatic steatosis. Experts from multinational liver societies went through the Delphi process, including four rounds of surveys, and consented to adopt a new nomenclature and definition instead of the conventional nonalcoholic fatty liver disease (NAFLD). This was to improve the understanding of the patients and primary care physicians, with an explanation of the pathophysiology in the name of the disease. Also, it could minimize the stigmatization of patients by using the histological neutral term “steatosis” instead of “fatty”. Herein, we will discuss the changes and continuity between the two nomenclatures, metabolic dysfunction-associated steatotic liver disease (MASLD) and NAFLD, as well as the challenges to MASLD which need to be addressed in future.

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Correspondence

Steatotic liver disease

Correspondence on Letter regarding “Risk factors in nonalcoholic fatty liver disease”: Eileen L. Yoon, Dae Won Jun; Clin Mol Hepatol 2023;29(4):1050-1051.
Published online August 29, 2023; DOI: https://doi.org/10.3350/cmh.2023.0310

Citations

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Reply to correspondence on “Prognosis of biopsy-confirmed metabolic dysfunction-associated steatotic liver disease: A sub-analysis of the CLIONE study”
Eileen Laurel Yoon, Dae Won Jun
Clinical and Molecular Hepatology.2024; 30(4): 1033. CrossRef

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Special Review

Steatotic liver disease

Critical appraisal of metabolic dysfunction-associated steatotic liver disease: Implication of Janus-faced modernity: Gi-Ae Kim, Joon Ho Moon, Won Kim; Clin Mol Hepatol 2023;29(4):831-843.
Published online August 25, 2023; DOI: https://doi.org/10.3350/cmh.2023.0277

Abstract
PDF

The existing term non-alcoholic fatty liver disease (NAFLD) has raised substantial concerns due to its inherent disadvantages of using exclusionary diagnostic criteria and the stigmatizing word ‘fatty.’ Three pan-national liver associations set out to explore a new nomenclature to replace both NAFLD and its suggested alternative, metabolic (dysfunction)-associated fatty liver disease (MAFLD). They surveyed if a change in nomenclature and/or definition is favored and which nomenclature best communicates disease characteristics and increases awareness. In lieu of NAFLD/MAFLD, metabolic dysfunction-associated steatotic liver disease (MASLD) has been chosen, and an umbrella term, steatotic liver disease (SLD), encompassing the whole spectrum of liver disease, has been proposed. It has been suggested that cardiometabolic risk factors should be considered when categorizing SLD patients. Furthermore, a new subcategory, MASLD with increased alcohol intake (MetALD), casts light on a neglected group of patients with moderate or more alcohol consumption. The importance of metabolic dysfunction was acknowledged in this new nomenclature, but the precise contribution of metabolic dysfunction and alcohol consumption to the development and progression of SLD remains unclear. Herein, we review hepatologists’ and endocrinologists’ perspectives on the new nomenclature, along with its possible impact on clinical practice. Although it is premature to predict the settlement of the new nomenclature, this review may help build more evidence for a soft landing of it in the future.

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Clinical and Molecular Hepatology.2024; 30(Suppl): S214. CrossRef
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Clinical and Molecular Hepatology.2024; 30(4): 962. CrossRef
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Antioxidants.2024; 13(11): 1389. CrossRef
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The Ewha Medical Journal.2024;[Epub] CrossRef
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Jacob George
Clinical and Molecular Hepatology.2023; 29(4): 973. CrossRef
From nonalcoholic steatohepatitis, metabolic dysfunction-associated fatty liver disease, to steatotic liver disease: Updates of nomenclature and impact on clinical trials
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Editorial

Steatotic liver disease

Lean or Non-obese Nonalcoholic Fatty Liver Disease Patients: Are They Really Lean?: Eugene Han, Yong-ho Lee; Clin Mol Hepatol 2023;29(4):980-983.
Published online August 16, 2023; DOI: https://doi.org/10.3350/cmh.2023.0250

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7,294 View
127 Download
3 Web of Science
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Original Article

Steatotic liver disease

Association of Visceral Fat Obesity, Sarcopenia, and Myosteatosis with Non-Alcoholic Fatty Liver Disease without Obesity: Hong-Kyu Kim, Sung-Jin Bae, Min Jung Lee, Eun Hee Kim, Hana Park, Hwi Seung Kim, Yun Kyung Cho, Chang Hee Jung, Woo Je Lee, Jaewon Choe; Clin Mol Hepatol 2023;29(4):987-1001.
Published online July 5, 2023; DOI: https://doi.org/10.3350/cmh.2023.0035

Background/Aims
To investigate whether non-alcoholic fatty liver disease (NAFLD) in individuals without generalized obesity is associated with visceral fat obesity (VFO), sarcopenia, and/or myosteatosis.
Methods
This cross-sectional analysis included 14,400 individuals (7,470 men) who underwent abdominal computed tomography scans during routine health examinations. The total abdominal muscle area (TAMA) and skeletal muscle area (SMA) at the 3^rd lumbar vertebral level were measured. The SMA was divided into the normal attenuation muscle area (NAMA) and low attenuation muscle area, and the NAMA/TAMA index was calculated. VFO was defined by visceral to subcutaneous fat ratio, sarcopenia by body mass index-adjusted SMA, and myosteatosis by the NAMA/TAMA index. NAFLD was diagnosed with ultrasonography.
Results
Of the 14,400 individuals, 4,748 (33.0%) had NAFLD, and the prevalence of NAFLD among non-obese individuals was 21.4%. In regression analysis, both sarcopenia (men: odds ratio [OR] 1.41, 95% confidence interval [CI] 1.19–1.67, P<0.001; women: OR=1.59, 95% CI 1.40–1.90, P<0.001) and myosteatosis (men: OR=1.24, 95% CI 1.02–1.50, P=0,028; women: OR=1.23, 95% CI 1.04–1.46, P=0.017) were significantly associated with non-obese NAFLD after considering for VFO and other various risk factors, whereas VFO (men: OR=3.97, 95% CI 3.43–4.59 [adjusted for sarcopenia], OR 3.98, 95% CI 3.44–4.60 [adjusted for myosteatosis]; women: OR=5.42, 95% CI 4.53–6.42 [adjusted for sarcopenia], OR=5.33, 95% CI 4.51–6.31 [adjusted for myosteatosis]; all P<0.001) was strongly associated with non-obese NAFLD after adjustment with various known risk factors.
Conclusions
In addition to VFO, sarcopenia and/or myosteatosis were significantly associated with non-obese NAFLD.

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