Clinical and Molecular Hepatology

"Cirrhosis"

Original Article

Transitions from Combustible to Noncombustible Tobacco Use and Liver Outcomes in Steatotic Liver Disease: Eun Seok Kang, Su Kyoung Lee, Meng Sha, Stefano Romeo, Seogsong Jeong, Won Kim; Received March 19, 2026 Accepted June 18, 2026 Published online June 25, 2026; DOI: https://doi.org/10.3350/cmh.2026.0339 [Accepted]

Abstract
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Background/Aims
In adults with steatotic liver disease (SLD), the hepatic impact of transitioning between combustible cigarettes (CCs) and noncombustible nicotine or tobacco products (NNTPs) remains unclear. We examined CC-NNTP transitions and liver-related events (LREs).
Methods
From the Korean National Health Insurance Service, 502,198 adults with SLD and at least one cardiometabolic risk factor completing health screenings during both 2012-2013 and 2019-2020 were followed through December 2023. Seven mutually exclusive groups were defined by CC status and NNTP use; the primary outcome was LRE, including hepatocellular carcinoma and liver cirrhosis. Cox proportional hazards regression, propensity-score matching (PSM), and counterfactual mediation analysis were performed.
Results
Among 502,198 participants (mean age 57.9 years; 65.6% male), 2,549 LREs occurred over a median 3.0-year follow-up. Compared with never-smokers, continuous CC smokers without NNTP use had the highest LRE risk (aHR, 1.51; 95% confidence interval (CI), 1.34-1.70), followed by CC initiators (1.45; 1.17-1.79) and CC quitters (1.28; 1.12-1.46) without NNTPs. CC quitters with NNTP use showed a lower LRE risk than continuous CC smokers without NNTP use in the full cohort (aHR, 0.65; 95% CI, 0.43-0.99), but this association was not statistically significant under PSM (aHR, 0.65; 95% CI, 0.39-1.09). Within-group PSM of NNTP versus nonuse was nonsignificant across all CC categories.
Conclusions
CC cessation was associated with lower LRE risk than continued CC smoking, even among those who transitioned to NNTPs. However, NNTP use showed no independent protective association, supporting complete tobacco/nicotine abstinence as the preferred goal.

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Special Issue

KASL clinical practice guidelines for liver cirrhosis: Ascites and related complications 2026: Do Seon Song, Jeong-Ju Yoo, Jeong Eun Song, Seong Hee Kang, Seung Kak Shin, Seul Ki Han, Sung Won Chung, Gi-Ae Kim, Moon Haeng Hur, Han Ah Lee, Yeonjung Ha, Young Chang, Jae Hyun Yoon, Jae Seung Lee, Sang Gyune Kim, Young Kul Jung, Moon Young Kim; Clin Mol Hepatol 2026;32(3):961-1028.
Published online April 28, 2026; DOI: https://doi.org/10.3350/cmh.2026.0281

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Letters to the Editor

Navigating discordant non-invasive fibrosis assessments in metabolic dysfunction-associated steatotic liver disease: Implications for generalizability, clinical decision-making, and resource allocation: Letter to the editor on “Histological severity and hepatic outcomes in patients with metabolic dysfunction-associated steatotic liver disease and discrepant FIB-4 and liver stiffness measurement”: Jiajing Zhao, Liping Liu; Clin Mol Hepatol 2026;32(3):e300-e302.
Published online February 20, 2026; DOI: https://doi.org/10.3350/cmh.2025.0157

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Clinical implications of discordant FIB-4 and LSM in MASLD: Integrating evidence and optimizing pathways: Letter to the editor on “Histological severity and hepatic outcomes in patients with metabolic dysfunction-associated steatotic liver disease and discrepant FIB-4 and liver stiffness measurement”: Deliang Huang, Jun Chen; Clin Mol Hepatol 2026;32(3):e294-e296.
Published online January 20, 2026; DOI: https://doi.org/10.3350/cmh.2026.0027

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Review

Burden of malnutrition and sarcopenia in patients with cirrhosis: pathophysiology, assessment, and management: Takao Miwa, Masahito Shimizu, Bernd Schnabl; Clin Mol Hepatol 2026;32(2):487-510.
Published online December 16, 2025; DOI: https://doi.org/10.3350/cmh.2025.1126

Abstract
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Malnutrition and sarcopenia are highly prevalent and robustly associated with reduced quality of life, disease progression, and poor outcomes, including complications and mortality, in patients with cirrhosis. Their pathophysiology is multifactorial, involving inadequate dietary intake and malabsorption, impaired liver functional reserves, altered energy, protein, and ammonia metabolism, systemic inflammation, hormonal dysregulation, and lifestyle or environmental influences. Despite extensive research, unresolved issues remain regarding optimal diagnostic criteria, as current approaches vary and lack global standardization. Regarding the diagnostic criteria for malnutrition, the usefulness of the Global Leadership Initiative on Malnutrition criteria has been proposed by international nutrition societies. However, evidence supporting their applicability in hepatology remains insufficient. For sarcopenia, differences in disease concept and diagnostic methods among societies indicate that no unified diagnostic standard exists, and clinicians should approach diagnosis with an understanding of the strengths and limitations of each method. Nutritional strategies emphasize adequate energy and protein intake, late evening snacks, and branched-chain amino acid supplementation, while deficiencies in micronutrients require tailored replacement. Nutritional therapy alone has limited effect on sarcopenia, but when combined with exercise it improves muscle mass, physical performance, and outcomes. Comprehensive approaches integrating optimized nutrition, micronutrient support, and structured exercise are essential to alleviate the burden of malnutrition and sarcopenia and to improve prognosis in patients with cirrhosis. This review addresses malnutrition and sarcopenia in cirrhosis by highlighting their prevalence, pathophysiology, clinical impact, and approaches for screening and diagnosis, and by emphasizing personalized nutritional, pharmacological, and exercise interventions to improve patient outcomes.

Citations

Citations to this article as recorded by

Letter: Amino Acid Imbalance Is an Independent Factor for Mortality in Patients With Liver Cirrhosis. Authors' reply
Yuki Utakata, Takao Miwa, Shinji Unome, Naoya Masuda, Mikita Oi, Masashi Aiba, Kenji Imai, Koji Takai, Makoto Shiraki, Naoki Katsumura, Masahito Shimizu
Alimentary Pharmacology & Therapeutics.2026; 63(9): 1329. CrossRef
Covert hepatic encephalopathy as a multi-organ syndrome: the gut–liver–muscle–brain axis, diagnosis, treatment, and multidisciplinary care
Takao Miwa, Cynthia L. Hsu, Masahito Shimizu, Patricia P. Bloom, Bernd Schnabl
Journal of Gastroenterology.2026;[Epub] CrossRef
Nutrition in cirrhosis: bridging guidelines and practice in hepatic disease
Jennifer Jin, Puneeta Tandon, Leah Gramlich
Current Opinion in Clinical Nutrition & Metabolic Care.2026;[Epub] CrossRef

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Original Article

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.

Citations

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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; 84(6): e209. CrossRef
Not just fat: muscle also matters in metabolic dysfunction-associated steatotic liver disease (MASLD)
Xinyan Zong, Grace Lai-Hung Wong
Hepatology International.2026; 20(3): 550. CrossRef

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Review

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; Clin Mol Hepatol 2026;32(2):443-463.
Published online November 25, 2025; DOI: https://doi.org/10.3350/cmh.2025.0921

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Alcohol-associated liver disease (ALD) is a leading cause of preventable cirrhosis, hepatocellular carcinoma (HCC), 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, the enhanced liver fibrosis test) 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, and 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, and epigenomics) can reveal distinct molecular signatures that predict steatohepatitis, fibrogenesis, and early HCC. Integrating these biomarkers enables phase-specific enrichment strategies, earlier intervention windows, adaptive dose-finding, and mechanismbased 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.

Citations

Citations to this article as recorded by

Immune Determinants of MASLD Progression: From Immunometabolic Reprogramming to Fibrotic Transformation
Senping Xu, Zhaoshan Zhang, Zhongquan Zhou, Jiawei Guo
Biology.2026; 15(2): 148. CrossRef
Review Article on: AI-Driven Precision Medicine in Liver Disease: Microbiome and Nanotechnology Integration
Rahul Kumar, Amritesh Kumar, Aayush Kumar Tiwari, MD Nasiruddin Khan, Mohit Kumar, Moidul Islam Judder
Pan-African Journal of Health and Psychological Sciences.2026;[Epub] CrossRef
N-acetylcysteine for patients with alcohol use disorder, post-traumatic stress disorder, and their co-occurrence: a systematic review of placebo-controlled randomized trials
Mohamed Awad E. Ahmed, Mufreh Amin, Yomna Emad Abdalla, Amr Abdelghani, Nourhan Eid, Aya Samy, Omar Kassar, Khalid Radwan Alsaadany, Mohamed Ezzat M. Mansour
BMC Psychiatry.2026;[Epub] CrossRef

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Original Articles

Histological severity and hepatic outcomes in patients with metabolic dysfunction-associated steatotic liver disease and discrepant FIB-4 and liver stiffness measurement: Joseph Rabbat, Boyu Yang, Hye Won Lee, Huapeng Lin, Emmanuel Tsochatzis, Salvatore Petta, Elisabetta Bugianesi, Masato Yoneda, Ming-Hua Zheng, Hannes Hagström, Jérôme Boursier, José Luis Calleja, George Boon-Bee Goh, Wah-Kheong Chan, Rocio Gallego-Durán, Arun J. Sanyal, Victor de Lédinghen, Philip N Newsome, Jian-Gao Fan, Laurent Castéra, Michelle Lai, Céline Fournier-Poizat, Grace Lai-Hung Wong, Mirko Zoncape, Grazia Pennisi, Angelo Armandi, Atsushi Nakajima, Wen-Yue Liu, Ying Shang, Marc de Saint-Loup, Elba Llop, Kevin Kim Jun Teh, Carmen Lara-Romero, Amon Asgharpour, Sara Mahgoub, Mandy Sau-Wai Chan, Clemence M Canivet, Manuel Romero-Gomez, Vincent Wai-Sun Wong, Seung Up Kim, Terry Cheuk-Fung Yip; Clin Mol Hepatol 2026;32(1):289-304.
Published online November 11, 2025; DOI: https://doi.org/10.3350/cmh.2025.0888

Background/Aims
Current guidelines recommend a 2-step approach for identifying advanced fibrosis in metabolic dysfunction-associated steatotic liver disease (MASLD), using Fibrosis-4 index (FIB-4) followed by liver stiffness measurement (LSM) via vibration-controlled transient elastography (VCTE). However, some patients may exhibit discordant results. This study evaluates the histological severity and outcomes in patients with discordant FIB-4 and LSM results.
Methods
This secondary analysis of the VCTE-Prognosis study included 12,950 patients evaluated for MASLD at 16 tertiary centers, of whom 2,915 underwent liver biopsy. Patients were categorized into four groups based on established FIB-4 (1.3) and LSM (8 kPa) cutoffs.
Results
F3–F4 fibrosis was observed in 6.4%, 13.7%, 30.6%, and 62.4% in low-FIB-4-low-LSM (n=6,403), high-FIB-4-low-LSM (n=3,017), low-FIB-4-high-LSM (n=1,363), and high-FIB-4-high-LSM (n=2,167) groups, respectively. During a median follow-up of 47.4 months, 248 patients experienced hepatic decompensation, hepatocellular carcinoma, liver transplantation, or liver-related death. The incidence rates of liver-related events (LREs) were 0.67, 1.19, 2.58, and 21.30 per 1,000 person-years, respectively. Compared to low-FIB-4-low-LSM patients, those with low-FIB-4-high-LSM (adjusted subdistribution hazard ratio [aSHR] 4.12) and high-FIB-4-high-LSM (aSHR 21.38) had a significantly higher risk of LREs, while high-FIB-4-low-LSM patients did not. Similar findings were observed when hepatic decompensation and hepatocellular carcinoma were analyzed separately.
Conclusions
Approximately 30% of patients in tertiary centers exhibit discordant FIB-4 and LSM results, with LSM more likely reflecting true severity. While some patients with discordant results may have advanced fibrosis, the overall incidence of LREs remains low.

Citations

Citations to this article as recorded by

Are FIB-4 and liver stiffness measurement interchangeable for HCC risk stratification in MASLD?
Yimeng Zhou, Xue Meng
JHEP Reports.2026; : 101852. CrossRef
High Prevalence of Metabolic Dysfunction–Associated Steatohepatitis With Significant Fibrosis in Primary Care and Endocrinology Clinics
Srilaxmi Kalavalapalli, Eddison Godinez Leiva, Andrea Ortiz Rocha, Anu Sharma, Diana Barb, Nathaly Cuervo‐Pardo, Kelly Y. Chun, Toni R. Prezant, Margery A. Connelly, Jens T. Rosenberg, Joseph R. Grajo, Fernando Bril, Kenneth Cusi
Diabetes, Obesity and Metabolism.2026; 28(7): 6184. CrossRef
The Evolution of MASLD Management: From Revised Nomenclature to Disease-Modifying Therapies
Karolina Kornatowska, Szymon Kopciał, Mateusz Wiekiera, Adrianna Wiekiera, Paweł Budzik, Mateusz Tyniec, Kamal Morshed
Gastroenterology Insights.2026; 17(2): 33. CrossRef

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Evaluating treatment response thresholds for cost-effective treatment in metabolic dysfunction-associated steatotic liver disease: Eileen L. Yoon, Jeong-Yeon Cho, Huiyul Park, Mimi Kim, Ji-Hyeon Park, Hye-Lin Kim, Dae Won Jun; Clin Mol Hepatol 2026;32(1):276-288.
Published online November 3, 2025; DOI: https://doi.org/10.3350/cmh.2025.0796

Background/Aims
The first metabolic dysfunction-associated steatotic liver disease (MASLD) drug was approved with an unsatisfactorily small effect size. This study aimed to determine key factors impacting the cost-effectiveness of a new hypothetical MASLD drug as well as its treatment efficacy.
Methods
A Markov model reflecting the natural history of MASLD was developed, incorporating fibrosis progression, cardiovascular disease risk, and mortality. Treatment effect of drug X (with $20,000 of annual cost) was assumed to achieve a ≥1 stage fibrosis regression, with a 25% gap of effect size in regression rate over non-treatment in the first year. The incremental cost-effectiveness ratio (ICER) over a 20-year horizon was estimated. And sensitivity analyses were conducted to explore uncertainty and identify influential factors.
Results
In the base case analysis, drug X provided an incremental gain of 1.32 quality-adjusted life years (QALYs) and 1.20 life years compared to the non-treatment, with an ICER of $68,010/QALY–below the $100,000/QALY willingnessto- pay threshold, indicating that drug X treatment is cost-effective. Two-way sensitivity analysis further highlighted that the drug should achieve at least a 15% initial regression gap and maintain a minimum 3% sustained durability gap to remain cost-effective. In addition baseline fibrosis stage distribution also acted as an influencing factor.
Conclusions
Long-term sustained durability of the hypothetical drug, patient distribution based on baseline fibrosis stage, as well as initial treatment response rate are key factors that influence the cost-effectiveness of new MASLD drugs.

Citations

Citations to this article as recorded by

The MASLD Journey in the General Population: Linkage‐to‐Care and Patient‐Reported Uptake of Fibrosis Risk Assessment
Joo Hyun Oh, Jun‐Hyuk Lee, Sang Bong Ahn, Eunjoo Kwon, Eileen L. Yoon, Hyo Young Lee, Seon Cho, Dae Won Jun
Liver International.2026;[Epub] CrossRef

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Correspondence

Correspondence to editorial on “Human cytomegalovirus reactivation in cirrhosis patients with acute decompensation”: Changze Hong, Jinjun Chen; Clin Mol Hepatol 2026;32(3):e336-e338.
Published online September 29, 2025; DOI: https://doi.org/10.3350/cmh.2025.1063

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Editorials

Rethinking ACLF prognosis: Can machine learning outperform conventional scores?: Editorial on “Predictive machine learning model in intensive care unit patients with acute-on-chronic liver failure and two or more organ failures”: Jung Hee Kim; Clin Mol Hepatol 2026;32(3):1383-1385.
Published online September 23, 2025; DOI: https://doi.org/10.3350/cmh.2025.1053

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Human cytomegalovirus reactivation in decompensated cirrhosis: marker of immunosuppression or contributor to severity?: Editorial on “Human cytomegalovirus reactivation in cirrhosis patients with acute decompensation”: Zhujun Cao, Richard Moreau; Clin Mol Hepatol 2026;32(2):953-956.
Published online September 1, 2025; DOI: https://doi.org/10.3350/cmh.2025.0962

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Original Article

Predictive machine learning model in intensive care unit patients with acute-on-chronic liver failure and two or more organ failures: Yee Hui Yeo, Mengyi Zhang, Martin S. McCoy, Jian Zu, Yingli He, Yi Liu, Juan Li, Taotao Yan, Yuan Wang, Hirsh D. Trivedi, Ju Dong Yang, Vinay Sundaram, Xiaodan Sun, Zhujun Cao, Chun-Ying Wu, Jonel Trebicka, Fanpu Ji; Clin Mol Hepatol 2025;31(4):1355-1371.
Published online September 1, 2025; DOI: https://doi.org/10.3350/cmh.2025.0573

Background/Aims
Prediction of short-term mortality in patients with acute-on-chronic liver failure (ACLF) admitted to the intensive care unit (ICU) may enhance effective management.
Methods
To develop, explain, and validate a predictive machine learning (ML) model for short-term mortality in patients with ACLF with two or more organ failures (OFs). Utilizing a large ICU cohort with detailed clinical information, we identified ACLF patients with two or more OFs according to the EASL-CLIF and NACSELD definitions. ML model was developed for each definition to predict 30-day mortality. The Shapley value was estimated to explain the models. Validation and calibration of these models were performed.
Results
Of 5,994 patients with cirrhosis admitted to ICU, 1,511 met NACSELD criteria, and 1,692 met EASL-CLIF grade II or higher criteria. The CatBoost ACLF (CBA) model had the greatest accuracy in the NACSELD cohort (area under curve [AUC] of 0.87), while the Random Forest ACLF (RFA) model performed best in the EASL-CLIF cohort (AUC of 0.83). Both models showed robust calibration. The models were explained by SHAP score analysis, yielding a rank list, and the top twelve predictors were selected. Both simplified models demonstrated similar performance (CBA model: AUC 0.89, RFA model: AUC 0.81) and significantly outperformed contemporary scoring systems, including CLIF-C ACLF and MELD 3.0. The models were validated in both internal and external cohorts. A simple-to-use online tool was created to predict mortality rates.
Conclusions
We presented explainable, well-validated, and calibrated predictive models for ACLF patients with two or more OFs, which outperformed existing predictive scores.

Citations

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Unbiased clustering of acute-on-chronic liver failure patients using machine learning in a real-world ICU cohort
Mengyi Zhang, Fanpu Ji, Jian Zu, Yingli He, Tao Chen, Yi Liu, Hirsh D. Trivedi, Ju Dong Yang, Vinay Sundaram, Yuan Wang, Xiaodan Sun, Zhujun Cao, Chun-Ying Wu, Yee Hui Yeo, Rajiv Jalan
Nature Communications.2026;[Epub] CrossRef
Systematic evaluation of machine learning models for clinical risk prediction on real-world hospital datasets
Qingwen Wu, Ziyou Qi, Qingwei Li, Cuiping Hao, Sujuan Tang
iScience.2026; 29(5): 115654. CrossRef
Navigating the therapeutic tightrope: Precision use of plasmapheresis and continuous renal replacement therapy in liver failure
Manish Manrai, Aditya V Pachisia, Saurabh Dawra, Siddharth Shukla, Atul A Jha
World Journal of Hepatology.2026;[Epub] CrossRef
Beyond the Tipping Point: Advances in the Diagnosis and Management of Acute-on-Chronic Liver Failure and End-Stage Liver Disease
Jonathan Soldera
Diagnostics.2026; 16(10): 1548. CrossRef
Gut–Liver Axis Failure in Critical Alcohol‐Associated Liver Disease: From ICU Secondary Hits to Microbiome‐Targeted Therapy
Yuting Zhang, Yiyu Wang, Yong Yang, Hong Mei, Xinxin Liu, Yuanxiu He, Song Qin, Banghai Feng, Ranjitsinh V. Devkar
Mediators of Inflammation.2026;[Epub] CrossRef
A machine learning model for 90-day mortality prediction in hepatitis B virus-related acute-on-chronic liver failure: the pivotal role of CALLY index
Yijun Zhang, Chunyan Li, Shaohui Su, Jilin Huang, Siyu Fu, Yong Zhang, Shanhong Tang
Frontiers in Medicine.2026;[Epub] CrossRef

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Letter to the Editor

Sex‑specific trends and demographic vs. epidemiologic drivers of alcohol‑related cirrhosis in United States, 2021–2040: Letter to the editor on "Sex disparities in alcohol-associated liver disease and subtype differences in alcohol-attributable cancers in the United States": Kui Wang, Yunqing Zeng; Clin Mol Hepatol 2026;32(2):e155-e157.
Published online August 25, 2025; DOI: https://doi.org/10.3350/cmh.2025.0790

Citations

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Evaluation methods of hepatic steatosis: From conventional techniques to emerging biomarkers
Kengo Moriyama
World Journal of Hepatology.2026;[Epub] CrossRef
Divergent trajectories of inflammatory bowel disease in East, South, South-East and Central Asia: A comprehensive GBD 2021 analysis
Kui Wang, Yunqing Zeng, Shanshan Zhang, Yanqing Li
Journal of Translational Autoimmunity.2025; 11: 100325. CrossRef

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Correspondence

Correspondence to letter to the editor 2 on “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, Mindie H. Nguyen; Clin Mol Hepatol 2026;32(2):e249-e250.
Published online August 19, 2025; DOI: https://doi.org/10.3350/cmh.2025.0884

Citations

Citations to this article as recorded by

Reply to correspondence on “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”
Xingyu Yao
Clinical and Molecular Hepatology.2026; 32(2): e267. CrossRef

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Editorial

Call for preemptive treatment of cytomegalovirus in patients with cirrhosis and acute decompensation: Editorial on “Human cytomegalovirus reactivation in cirrhosis patients with acute decompensation”: Norihiro Imai; Clin Mol Hepatol 2026;32(2):949-952.
Published online August 6, 2025; DOI: https://doi.org/10.3350/cmh.2025.0840

Citations

Citations to this article as recorded by

Correspondence to editorial on “Human cytomegalovirus reactivation in cirrhosis patients with acute decompensation”
Changze Hong, Jinjun Chen
Clinical and Molecular Hepatology.2026; 32(2): e227. CrossRef

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Snapshot

Decoding platelet function in liver cirrhosis: A shift from quantity to quality: Vibhuti Jakhmola, Sukriti Baweja, Chhagan Bihari; Clin Mol Hepatol 2025;31(4):1384-1386.
Published online July 29, 2025; DOI: https://doi.org/10.3350/cmh.2025.0809

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Original Article

Human cytomegalovirus reactivation in cirrhosis patients with acute decompensation: Changze Hong, Zuxiong Huang, Yingli He, Rongqi Wang, Jiaying Lin, Yushan Liu, Baicheng Liu, Xiaoqin Lan, Qinjun He, Wenfan Luo, Qintao Lai, Ling Zhou, Tingting Qi, Yali Ji, Miaoxia Liu, Qiaoping Wu, Yichen Yao, Weihao Liang, Xianbo Wang, Guohong Deng, Yanhang Gao, Yan Huang, Feng Liu, Xiaobo Lu, Zhongji Meng, Yuemin Nan, Hai Li, Beiling Li, Rajiv Jalan, Jinjun Chen; Clin Mol Hepatol 2025;31(4):1316-1332.
Published online July 4, 2025; DOI: https://doi.org/10.3350/cmh.2025.0332

Background/Aims
The role of reactivation of human cytomegalovirus (HCMV) in determining outcomes of cirrhotic patients with acute decompensation (AD) is unknown. We aimed to investigate HCMV incidence and potential correlation with hepatic outcomes in AD patients.
Methods
Two prospective multicentre cohorts with AD patients were investigated. Patients in cohort 1 were recruited from 4 centres, while patients in cohort 2 were randomly selected from a second multicentre cohort. HCMV reactivation was established with quantitative real-time polymerase chain reaction assay in seropositive patients.
Results
HCMV reactivation was found in 35 patients from cohort 1 (n=722) and 14 from cohort 2 (n=291), with an incidence of 4.8% in both cohorts. Bacterial infection and liver failure were independently correlated with HCMV reactivation. HCMV reactivation was an independent predictor of 90-day mortality. Among bacterial infection populations in these two cohorts, patients with HCMV reactivation had worse prognosis compared to those without. Incidence of acute-on-chronic liver failure (ACLF) was higher in patients with HCMV reactivation compared to those without and was also independently correlated with development of ACLF. In a total of 49 HCMV reactivation cases, 8 patients were treated with ganciclovir, in whom a significantly lower 90-day mortality compared with those not treated was observed. All 3 patients who underwent liver transplantation with reactivation of HCMV died.
Conclusions
In AD patients, HCMV reactivation was common, especially in those with bacterial infection or liver failure, and they were more prone to having ACLF and 90‑day mortality. The data propose the need for active surveillance for HCMV infection in AD patients.

Citations

Citations to this article as recorded by

Human cytomegalovirus reactivation in decompensated cirrhosis: marker of immunosuppression or contributor to severity?: Editorial on “Human cytomegalovirus reactivation in cirrhosis patients with acute decompensation”
Zhujun Cao, Richard Moreau
Clinical and Molecular Hepatology.2026; 32(2): 953. CrossRef
Correspondence to editorial on “Human cytomegalovirus reactivation in cirrhosis patients with acute decompensation”
Changze Hong, Jinjun Chen
Clinical and Molecular Hepatology.2026; 32(2): e227. CrossRef
Call for preemptive treatment of cytomegalovirus in patients with cirrhosis and acute decompensation: Editorial on “Human cytomegalovirus reactivation in cirrhosis patients with acute decompensation”
Norihiro Imai
Clinical and Molecular Hepatology.2026; 32(2): 949. CrossRef

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Review

Update in the treatment of cirrhotic patients with portal vein thrombosis: Jialin Wu, Xinyi Deng, Junyang Luo, Zaibo Jiang, Fuda Xie, Bonan Chen, Hoi Wing Leung, Ge Zhang, Ka Fai To, Wei Kang; Clin Mol Hepatol 2025;31(4):1139-1166.
Published online June 24, 2025; DOI: https://doi.org/10.3350/cmh.2025.0411

Abstract
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Portal vein thrombosis (PVT) is characterized by the formation of a thrombus (blood clot) within the portal vein system, including main portal vein and its intrahepatic portal vein branches, and may extend to the superior mesenteric vein or splenic vein. The emergence of PVT is linked to diverse risk factors, encompassing liver conditions with cirrhosis, abdominal infections, previous abdominal surgeries, malignancies, inherited or acquired thrombophilias, and systemic hypercoagulable conditions. Recent studies revealed a possible connection between the occurrence of PVT and either contracting corona virus disease 2019 (COVID-19) or receiving a COVID-19 vaccination. Current treatment strategies were primarily based on symptom management, extent, and progression of thrombosis, but their efficacy was inconsistent and suboptimal. Untimely or inadequate treatment can lead to the progression of the thrombus and increase the risk of complications, such as portal hypertension, variceal bleeding, and hepatic decompensation, posing a significant risk to the patient’s life. Thus, early and appropriate initiation of pharmacologic and interventional treatments, as well as more aggressive strategies, is crucial for the management and prevention of PVT progression and recurrence. This review focuses on the literature on the recent advancements in the treatment of PVT using various therapeutic modalities, including anticoagulant therapy, thrombolysis, thrombectomy, interventional therapy and liver transplant in cirrhotic patients. In addition, we discuss pearls and pitfalls of these strategies for PVT, highlighting recent progress, identifying knowledge gaps, and proposing avenues towards precision management.

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Gastroenterology, Hepatology and Endoscopy Practice.2026; 6(3): 101. CrossRef
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Prediction of bowel resection due to bowel necrosis in recent portal vein thrombosis based on CT presentations and clinical data
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Thrombosis Journal.2025;[Epub] CrossRef

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Letter to the Editor

Letter to the editor on “Baveno VI-SSM stratifies the risk of portal hypertension-related events in patients with HBV-related cirrhosis”: Bo Zheng, Lizhou Wang; Clin Mol Hepatol 2026;32(2):e141-e143.
Published online June 4, 2025; DOI: https://doi.org/10.3350/cmh.2025.0521

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Correspondence to letter to the editor on “Baveno VI-SSM stratifies the risk of portal hypertension-related events in patients with HBV-related cirrhosis”
Haiyu Wang, Jinjun Chen
Clinical and Molecular Hepatology.2026; 32(2): e238. CrossRef

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Original Article

Distinct inflammatory imprint in non-cirrhotic and cirrhotic patients before and after direct-acting antiviral therapy: Moana Witte, Carlos Oltmanns, Jan Tauwaldt, Hagen Schmaus, Jasmin Mischke, Gordon Grabert, Mara Bretthauer, Lennart M. Roesner, Thomas Werfel, Katja Deterding, Benjamin Maasoumy, Heiner Wedemeyer, Tim Kacprowski, Anke R.M. Kraft, Markus Cornberg; Clin Mol Hepatol 2025;31(4):1269-1284.
Published online June 4, 2025; DOI: https://doi.org/10.3350/cmh.2025.0292

Background/Aims
Hepatitis C virus (HCV) infection remains a global health challenge, leading to chronic liver disease, cirrhosis, and hepatocellular carcinoma (HCC). Despite the high efficacy of direct-acting antiviral therapy in achieving sustained virologic response (SVR), concerns persist regarding long-term immune alterations and residual risks, particularly in cirrhotic patients.
Methods
This study investigates 75 soluble immune mediator (SIM) profiles in 102 chronic HCV patients, stratified by cirrhosis status, at therapy initiation, end of treatment, and long-term follow-up (median 96 weeks). Findings were compared with 51 matched healthy controls and validated in an independent cohort of 47 cirrhotic patients, 17 of whom developed HCC.
Results
We observed significant SIM alterations at baseline, with cirrhotic patients displaying a more profoundly dysregulated inflammatory milieu. Despite an overall decline in inflammatory markers following SVR, persistent alterations were evident, particularly in cirrhotic patients. Notably, those with liver stiffness exceeding 14 kPa exhibited sustained inflammatory dysregulation, correlating with liver elastography values. Key SIM such as interleukin (IL)-6, IL-8, urokinase plasminogen activator, and hepatocellular growth factor remained elevated and were associated with HCC development. Network analysis highlighted their roles in liver fibrosis, regeneration, and carcinogenesis.
Conclusions
These findings underscore the importance of early antiviral intervention to prevent cirrhosis-related sequelae. Future studies should explore the mechanistic pathways linking chronic inflammation, fibrosis, and oncogenesis to identify predictive biomarkers and novel therapeutic targets. Addressing persistent immune alterations post-HCV clearance may improve long-term outcomes, particularly in patients with advanced liver disease.

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Yasser Fouad, Ming-Lung Yu, Saeed Hamid, Robert G. Gish, Mohammed Eslam
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Clinical implications of residual changes following HCV clearance: Editorial on “Distinct inflammatory imprint in non-cirrhotic and cirrhotic patients before and after direct-acting antiviral therapy”
So-Young Kim, Eui-Cheol Shin
Clinical and Molecular Hepatology.2026; 32(2): 935. CrossRef
HBV Dominance Is Associated With a Distinct Inflammatory Milieu in HBV/HCV Coinfection
Carlos Oltmanns, Moana Witte, Anika Wranke, Katja Deterding, Heiner Wedemeyer, Christine S. Falk, Anke R. M. Kraft, Steffen B. Wiegand, Markus Cornberg
Journal of Viral Hepatitis.2025;[Epub] CrossRef
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Journal of Translational Medicine.2025;[Epub] CrossRef

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Reply to Correspondence

Reply to correspondence on “Baveno VI-SSM stratifies the risk of portal hypertension-related events in patients with HBV-related cirrhosis”: Mathias Jachs, Mattias Mandorfer; Clin Mol Hepatol 2026;32(1):e106-e108.
Published online April 16, 2025; DOI: https://doi.org/10.3350/cmh.2025.0391

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Editorials

vibraA non-invasive risk stratification tool for hepatitis B-related liver cirrhosis: The Baveno VI-SSM combined model: Editorial on “Baveno VI-SSM stratifies the risk of portal hypertension-related events in patients with HBV-related cirrhosis”: Ruiling He, Bingtian Dong, Xiaolong Qi; Clin Mol Hepatol 2026;32(1):395-399.
Published online March 19, 2025; DOI: https://doi.org/10.3350/cmh.2025.0281

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Global analysis of incidence trends and projections of liver cirrhosis among women of childbearing age: An observational study based on the Global Burden of Disease data
Pengfei Cheng, Yueyi Sun, Yuanming Qiang, Jushan Wu, Binwei Duan, Guangming Li
Medicine.2026; 105(23): e48955. CrossRef
Revisiting the role of liver cirrhosis in surgical treatment for hepatocellular carcinoma
Qi Ke, Bujiangcun Luo, Zunyi Zhang, Zhiyong Huang, Erlei Zhang
Medicine Plus.2025; 2(3): 100096. CrossRef

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Predicting decompensation risk in compensated HBV cirrhosis: Eternal sunshine for a spotless mind?: Editorial on “Baveno VI-SSM stratifies the risk of portal hypertension-related events in patients with HBV-related cirrhosis”: Mathias Jachs, Mattias Mandorfer; Clin Mol Hepatol 2026;32(1):390-394.
Published online March 19, 2025; DOI: https://doi.org/10.3350/cmh.2025.0280

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Correspondence to editorial 1 on “Baveno VI-SSM stratifies the risk of portal hypertension-related events in patients with HBV-related cirrhosis”
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Reply to correspondence on “Baveno VI-SSM stratifies the risk of portal hypertension-related events in patients with HBV-related cirrhosis”
Mathias Jachs, Mattias Mandorfer
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Correspondence to letter to the editor on “Baveno VI-SSM stratifies the risk of portal hypertension-related events in patients with HBV-related cirrhosis”
Haiyu Wang, Jinjun Chen
Clinical and Molecular Hepatology.2026; 32(2): e238. 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”: Weixiong Zhu, Xuefan Zeng, Zengxi Yang, Yusheng Cheng, Wence Zhou; Clin Mol Hepatol 2025;31(3):e252-e253.
Published online February 26, 2025; DOI: https://doi.org/10.3350/cmh.2025.0189

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Reply to Correspondence

Liver fibrosis, cirrhosis, and portal hypertension

Decreasing systemic inflammation after TIPS: Still hope for the liver: Reply to correspondence on “Insertion of a transjugular intrahepatic portosystemic shunt leads to sustained reversal of systemic inflammation in patients with decompensated liver cirrhosis”: Georg Semmler, Lorenz Balcar, Mattias Mandorfer; Clin Mol Hepatol 2025;31(2):e224-e225.
Published online February 17, 2025; DOI: https://doi.org/10.3350/cmh.2025.0149

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Annals of Medicine.2025;[Epub] CrossRef

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Editorial

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 steatotic liver disease”: Michael Kwan-Lung Ko, Loey Lung-Yi Mak; Clin Mol Hepatol 2026;32(1):371-373.
Published online February 11, 2025; DOI: https://doi.org/10.3350/cmh.2025.0118

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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
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Correspondence to editorial 1 on “Baveno VI-SSM stratifies the risk of portal hypertension-related events in patients with HBV-related cirrhosis”
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Editorial: Residual HCC Risk After Hepatitis C Cure—Can Polygenic Risk Scores Refine Surveillance?
Heechul Nam, Sung Won Lee
Alimentary Pharmacology & Therapeutics.2026; 63(10): 1427. CrossRef

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Correspondence

Liver fibrosis, cirrhosis, and portal hypertension

TIPS insertion and systemic inflammation: Is it ever too late to lower portal pressure? Correspondence to editorial on “Insertion of a transjugular intrahepatic portosystemic shunt leads to sustained reversal of systemic inflammation in patients with decompensated liver cirrhosis”: Anja Tiede, Benjamin Maasoumy; Clin Mol Hepatol 2025;31(2):e176-e179.
Published online February 10, 2025; DOI: https://doi.org/10.3350/cmh.2025.0135

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Decreasing systemic inflammation after TIPS: Still hope for the liver: Reply to correspondence on “Insertion of a transjugular intrahepatic portosystemic shunt leads to sustained reversal of systemic inflammation in patients with decompensated liver cirrh
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Clinical and Molecular Hepatology.2025; 31(2): e224. CrossRef
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Thomas Reiberger, Benjamin Maasoumy
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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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Original Article

Baveno VI-SSM stratifies the risk of portal hypertension-related events in patients with HBV-related cirrhosis: Haiyu Wang, Weihao Liang, Ling Zhou, Jiankang Song, Biao Wen, Qiaoping Wu, Yuanjian Zhang, Xiaofeng Zhang, Haoran Ke, Yujun Tang, Fuyuan Zhou, Youfu Zhu, Weiqun Wen, Zhihua Liu, Yali Ji, Qintao Lai, Qinjun He, Wenfan Luo, Tingting Qi, Miaoxia Liu, Xiaoqin Lan, Yongpeng Chen, Ranran Xi, Junting Wan, Lin Dai, Yuan Li, Jinjun Chen; Clin Mol Hepatol 2025;31(3):866-880.
Published online February 5, 2025; DOI: https://doi.org/10.3350/cmh.2024.0609

Background/Aims
Cirrhotic patients with liver stiffness measurement (LSM) <20 kPa and platelet count ≥150×10⁹/L (Baveno VI criteria), otherwise spleen stiffness measurement (SSM) ≤40 kPa (Baveno VI-SSM criteria) can avoid endoscopy screening; however, no prospective data for their hepatic outcomes.
Methods
Compensated cirrhosis with HBV were prospectively enrolled from April 2019 to April 2022 and followed until July 2023. All patients underwent LSM, SSM and esophagogastroduodenoscopy assessment.
Results
Among 1,224 patients enrolled with median follow-up of 30 months (interquartile range, 21–42), the incidence of decompensation was greater in 560 patients with unfavored Baveno VI criteria (0.5 vs. 20.4 per 1,000 person-years, P=0.0004) than that in 664 patients with favored Baveno VI-SSM criteria. The Baveno VI-SSM model identified more patients (54.2%) as low-risk for decompensation than Baveno VII-SSM model (single cutoff) (48.4%, P=0.004) and than Baveno VI criteria (34.6%, P<0.0001) did. Patients with high-risk varices diagnosed via endoscopy following Baveno VI-SSM model assessment had greater probability of decompensation compared to those identified by the Baveno VII-SSM model (single cutoff) (42.8 vs. 21.1 per 1,000 person-years, P=0.0088). Additionally, among the 493 patients who underwent endoscopic re-assessment, 242 patients with favored Baveno VI-SSM criteria had much lower incidence of EV progression (2.6 vs. 99.5 per 1,000 person-years, P=0.0004) and lower risk of decompensation compared to 140 patients with unfavored Baveno VI-SSM model (0 vs. 34.2 per 1,000 person-years, P=0.0256).
Conclusions
Baveno VI-SSM model could identify HBV-related cirrhosis patients at low risk of decompensation, which was greatly improved upon Baveno VI-SSM reassessment.

Citations

Citations to this article as recorded by

Correspondence to editorial 1 on “Baveno VI-SSM stratifies the risk of portal hypertension-related events in patients with HBV-related cirrhosis”
Haiyu Wang, Jinjun Chen
Clinical and Molecular Hepatology.2026; 32(1): e58. CrossRef
Correspondence to editorial 2 on “Baveno VI-SSM stratifies the risk of portal hypertension-related events in patients with HBV-related cirrhosis”
Haiyu Wang, Jinjun Chen
Clinical and Molecular Hepatology.2026; 32(1): e62. CrossRef
Correspondence to editorial 3 on “Baveno VI-SSM stratifies the risk of portal hypertension-related events in patients with HBV-related cirrhosis”
Haiyu Wang, Jinjun Chen
Clinical and Molecular Hepatology.2026; 32(1): e65. CrossRef
Reply to correspondence on “Baveno VI-SSM stratifies the risk of portal hypertension-related events in patients with HBV-related cirrhosis”
Mathias Jachs, Mattias Mandorfer
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Noninvasive Tests for Predicting Decompensation in Compensated Advanced Chronic Liver Disease: A Comprehensive Review
Audrey Payancé, Pierre‐Emmanuel Rautou, Jérôme Boursier, Laurent Castera, Dominique Valla, Laure Elkrief
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JGH Open.2025;[Epub] CrossRef

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Reply to Correspondence

Steatotic liver disease

Reply to correspondence on “Bariatric surgery reduces long-term mortality in patients with metabolic dysfunction-associated steatotic liver disease and cirrhosis”: Jing Zeng, Jian-Gao Fan; Clin Mol Hepatol 2025;31(2):e218-e220.
Published online February 3, 2025; DOI: https://doi.org/10.3350/cmh.2025.0070

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33 Download

Correspondence

Correspondence to editorial on “Bariatric surgery reduces long-term mortality in patients with metabolic dysfunction-associated steatotic liver disease and cirrhosis”: Nicholas A. Rouillard, Linda Henry, Mindie H. Nguyen; Clin Mol Hepatol 2025;31(2):e173-e175.
Published online January 9, 2025; DOI: https://doi.org/10.3350/cmh.2025.0001

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Reply to correspondence on “Bariatric surgery reduces long-term mortality in patients with metabolic dysfunction-associated steatotic liver disease and cirrhosis”
Jing Zeng, Jian-Gao Fan
Clinical and Molecular Hepatology.2025; 31(2): e218. CrossRef

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Original Articles

Alcohol-related liver disease

Global epidemiology of alcohol-related liver disease, liver cancer, and alcohol use disorder, 2000–2021: Pojsakorn Danpanichkul, Luis Antonio Díaz, Kanokphong Suparan, Primrose Tothanarungroj, Supapitch Sirimangklanurak, Thanida Auttapracha, Hanna L. Blaney, Banthoon Sukphutanan, Yanfang Pang, Siwanart Kongarin, Francisco Idalsoaga, Eduardo Fuentes-López, Lorenzo Leggio, Mazen Noureddin, Trenton M. White, Alexandre Louvet, Philippe Mathurin, Rohit Loomba, Patrick S. Kamath, Jürgen Rehm, Jeffrey V. Lazarus, Karn Wijarnpreecha, Juan Pablo Arab; Clin Mol Hepatol 2025;31(2):525-547.
Published online January 9, 2025; DOI: https://doi.org/10.3350/cmh.2024.0835

Background/Aims
Alcohol represents a leading burden of disease worldwide, including alcohol use disorder (AUD) and alcohol-related liver disease (ALD). We aim to assess the global burden of AUD, ALD, and alcohol-attributable primary liver cancer between 2000–2021.
Methods
We registered the global and regional trends of AUD, ALD, and alcohol-related liver cancer using data from the Global Burden of Disease 2021 Study, the largest and most up-to-date global epidemiology database. We estimated the annual percent change (APC) and its 95% confidence interval (CI) to assess changes in age-standardized rates over time.
Results
In 2021, there were 111.12 million cases of AUD, 3.02 million cases of ALD, and 132,030 cases of alcohol-attributable primary liver cancer. Between 2000 and 2021, there was a 14.66% increase in AUD, a 38.68% increase in ALD, and a 94.12% increase in alcohol-attributable primary liver cancer prevalence. While the age-standardized prevalence rate for liver cancer from alcohol increased (APC 0.59%; 95% confidence interval [CI] 0.52 to 0.67%) over these years, it decreased for ALD (APC –0.71%; 95% CI –0.75 to –0.67%) and AUD (APC –0.90%; 95% CI –0.94 to –0.86%). There was significant variation by region, socioeconomic development level, and sex. During the last years (2019–2021), the prevalence, incidence, and death of ALD increased to a greater extent in females.
Conclusions
Given the high burden of AUD, ALD, and alcohol-attributable primary liver cancer, urgent measures are needed to prevent them at both global and national levels.

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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.

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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
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Clinical and Molecular Hepatology.2026; 32(1): 368. CrossRef
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Clinical and Translational Gastroenterology.2026;[Epub] 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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Alimentary Pharmacology & Therapeutics.2026; 63(1): 70. CrossRef
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Review

Hepatic neoplasm

Hepatocellular carcinoma: updates on epidemiology, surveillance, diagnosis and treatment: Soo Young Hwang, Pojsakorn Danpanichkul, Vatche Agopian, Neil Mehta, Neehar D. Parikh, Ghassan K. Abou-Alfa, Amit G. Singal, Ju Dong Yang; Clin Mol Hepatol 2025;31(Suppl):S228-S254.
Published online December 26, 2024; DOI: https://doi.org/10.3350/cmh.2024.0824

Abstract
PDF

Hepatocellular carcinoma (HCC) is a major global burden, ranking as the third leading cause of cancer-related mortality. HCC due to chronic hepatitis B virus (HBV) or C virus (HCV) infection has decreased due to universal vaccination for HBV and effective antiviral therapy for both HBV and HCV, but HCC related to metabolic dysfunction-associated steatotic liver disease and alcohol-associated liver disease is increasing. Biannual liver ultrasonography and serum α-fetoprotein are the primary surveillance tools for early HCC detection among high-risk patients (e.g., cirrhosis, chronic HBV). Alternative surveillance tools such as blood-based biomarker panels and abbreviated magnetic resonance imaging (MRI) are being investigated. Multiphasic computed tomography or MRI is the standard for HCC diagnosis, but histological confirmation should be considered, especially when inconclusive findings are seen on cross-sectional imaging. Staging and treatment decisions are complex and should be made in multidisciplinary settings, incorporating multiple factors including tumor burden, degree of liver dysfunction, patient performance status, available expertise, and patient preferences. Early-stage HCC is best treated with curative options such as resection, ablation, or transplantation. For intermediate-stage disease, locoregional therapies are primarily recommended although systemic therapies may be preferred for patients with large intrahepatic tumor burden. In advanced-stage disease, immune checkpoint inhibitor-based therapy is the preferred treatment regimen. In this review article, we discuss the recent global epidemiology, risk factors, and HCC care continuum encompassing surveillance, diagnosis, staging, and treatments.

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G2E3 Suppresses the Tumor‐Killing Function of CD8+ T Cells in Hepatocellular Carcinoma by Boosting CLCN2 Ubiquitination
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Original Article

Viral hepatitis

Longitudinal profile of plasma pregenomic RNA in patients with chronic hepatitis B infection on long-term nucleoside analogues and its interaction with clinical parameters: Lung-Yi Mak, Mark Anderson, Michael Stec, Matthew Shing-Hin Chung, Danny Ka-Ho Wong, Rex Wan-Hin Hui, Wai-Kay Seto, Gavin Cloherty, Man-Fung Yuen; Clin Mol Hepatol 2025;31(2):460-473.
Published online December 26, 2024; DOI: https://doi.org/10.3350/cmh.2024.0724

Backgrounds/Aims
Plasma pregenomic hepatitis B virus RNA (pgRNA) is a novel biomarker in chronic hepatitis B infection (CHB). We aimed to describe the longitudinal profile of pgRNA and factors influencing its levels in CHB patients on nucleoside analogue (NUC).
Methods
Serial plasma samples from 1,354 CHB patients started on first-line NUC were evaluated. Time of NUC initiation was taken as baseline (year 0), followed by 1-year, 3-year and 5-year of NUC therapy. pgRNA was measured by Research Use Only RealTime HBV RNA v2.0 (0.2 mL) (Abbott Diagnostics) with lower limit of detection of 0.8 log U/mL (~20 copies/mL).
Results
Among 1,354 subjects (median age at baseline 49.8 [interquartile range, IQR 40.2–57.3]) years, 65.2% male, 16.1% hepatitis B e antigen (HBeAg)-positive, 28.6% cirrhotic), baseline median HBV RNA was 3.68 (IQR 2.42–5.19) log U/mL. Upon NUC therapy, median pgRNA levels were 2.45 (IQR 1.82–3.62), 2.23 (IQR 1.67–3.05) and 2.14 (IQR 1.48–2.86) log U/mL at 1, 3 and 5 years, respectively, with the corresponding log U/mL reductions of 0.82, 1.20 and 1.54. Undetectable/ unquantifiable pgRNA was achieved in 13.5%, 15.9% and 20.1% of patients at 1, 3 and 5 years, respectively. Older age, male sex, HBeAg-negativity and high PAGE-B score were associated with lower pgRNA.
Conclusions
Plasma pgRNA declines are modest under NUC therapy, with only 16.3% achieving RNA undetectability after 5 years of first-line NUC indicating cccDNA silencing has not been achieved in the majority of patients. Clinical characteristics should be taken into consideration when interpreting the plasma pgRNA level.

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Reconsidering the role of plasma pgRNA in NUC-treated CHB: Stratified biomarker interpretation and the limits of current assays: Letter to the editor on “Longitudinal profile of plasma pregenomic RNA in patients with chronic hepatitis B infection on long-
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Editorial

Steatotic liver disease

A leap in the dark: Bariatric surgery for treatment of metabolic dysfunction-associated steatotic liver disease related cirrhosis: Editorial on “Bariatric surgery reduces long-term mortality in patients with metabolic dysfunction-associated steatotic liver disease and cirrhosis”: Jing Zeng, Jian-Gao Fan; Clin Mol Hepatol 2025;31(2):610-614.
Published online December 17, 2024; DOI: https://doi.org/10.3350/cmh.2024.1099

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Correspondence to editorial on “Bariatric surgery reduces long-term mortality in patients with metabolic dysfunction-associated steatotic liver disease and cirrhosis”
Nicholas A. Rouillard, Linda Henry, Mindie H. Nguyen
Clinical and Molecular Hepatology.2025; 31(2): e173. CrossRef
Reply to correspondence on “Bariatric surgery reduces long-term mortality in patients with metabolic dysfunction-associated steatotic liver disease and cirrhosis”
Jing Zeng, Jian-Gao Fan
Clinical and Molecular Hepatology.2025; 31(2): e218. CrossRef

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Review

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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Original Articles

Liver fibrosis, cirrhosis, and portal hypertension

Insertion of a transjugular intrahepatic portosystemic shunt leads to sustained reversal of systemic inflammation in patients with decompensated liver cirrhosis: Anja Tiede, Lena Stockhoff, Zhaoli Liu, Hannah Rieland, Jim B. Mauz, Valerie Ohlendorf, Birgit Bremer, Jennifer Witt, Anke Kraft, Markus Cornberg, Jan B. Hinrichs, Bernhard C. Meyer, Heiner Wedemeyer, Cheng-Jian Xu, Christine S. Falk, Benjamin Maasoumy; Clin Mol Hepatol 2025;31(1):240-255.
Published online November 21, 2024; DOI: https://doi.org/10.3350/cmh.2024.0587

Background/Aims
Systemic Inflammation (SI) is considered a key mechanism in disease progression and development of complications in decompensated liver cirrhosis. SI is mainly driven by portal hypertension and bacterial translocation. Transjugular intrahepatic portosystemic shunt (TIPS) insertion represents an effective treatment for portal hypertension. This study aims to investigate the impact of TIPS insertion on SI and bacterial translocation.
Methods
We prospectively included 59 cirrhotic patients undergoing TIPS insertion. Blood samples were collected at TIPS insertion and follow-up (FU) 1, 3, 6, and 12 months thereafter. At all time points, we performed a comprehensive analysis of SI including 43 soluble inflammatory markers (SIMs), and surrogates of bacterial translocation (sCD14, sCD163). To investigate long-term kinetics of SI, C-reactive protein (CRP) and white blood cells (WBC) were retrospectively analyzed in a cohort of 177 patients up to 3 years after TIPS insertion.
Results
At TIPS insertion, 30/43 SIMs, sCD14, and sCD163 measured significantly higher in cirrhotic patients compared to healthy controls. By FU6 25 SIMs and sCD14 measured at significantly lower levels compared to baseline. Interestingly, in patients with TIPS indication of refractory ascites, IL-6 decreased to levels documented in earlier stages of cirrhosis. In long-term follow-up, CRP levels significantly decreased after TIPS insertion, which translated into lower mortality in Cox regression analysis (HR 0.968, p=0.042). Notably, patients with residual ascites post-TIPS showed significantly higher CRP and IL-6 levels across all follow-ups compared to patients with resolved ascites.
Conclusions
Decreasing portal hypertension via TIPS insertion leads to a significant attenuation of SI and bacterial translocation over time.

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Valerie Ohlendorf, Laura Buttler, Benjamin Maasoumy
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Timing of Transjugular Intrahepatic Portosystemic Shunts for Acute Esophagogastric Variceal Bleeding in Liver Cirrhosis
Wentun Yao, Chunxiu Tan, Houqiang Su, Juan Xie, Liya Huang
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Wen Wang, Ying Wen
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Post‐TIPS Dynamics of von Willebrand Factor for Risk Stratification After TIPS Placement
Marlene Hintersteininger, Simon Johannes Gairing, Katrin Kirsch, Theresa Müllner‐Bucsics, Susanna Riegler, Lukas Reider, Mathias Jachs, Lorenz Balcar, Eva M. Schleicher, Jasmin Söhngen, Lukas Müller, Michael B. Pitton, Julia Weinmann‐Menke, Christian M. L
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Triple Parallel TIPSs for Porto-sinusoidal Vascular Disorder with Refractory Hemorrhage: Portal Hypertension, But Not as We Know It
Jing Li, Bohan Luo, Na Zhang, Ana Gao, Guohong Han
Journal of Hepatology.2026;[Epub] CrossRef
Post-TIPS Anticoagulation Avoidable with Viatorr Stent in Cirrhotic Patients
Jiamin Xu, Chenrui Zhang, Rongfang Tu, Qinnian Li, Weimin Bao, Yingmei Tang
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Jie Cheng, Xiaobing Wang, Lihua Zhou, Xiaojia Chen, Nuer Tang, Feng Zhou, Feng Ding, Yuan Yang, Jun Lin, Liping Chen
Annals of Medicine.2025;[Epub] CrossRef
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Thomas Reiberger, Benjamin Maasoumy
Journal of Hepatology.2025; 83(3): 615. CrossRef
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Na Han, Xulong Yuan, Zhengcai Liu, Yuanping Xu, Shuqiang Yue, Yongquan Shi, Jun Tie
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Lucie Simonis, Lorenz Balcar, Anna Schedlbauer, Marta Tonon, Nikolaj Torp, Valeria Santori, Katharina Stopfer, Jan Embacher, Christian Sebesta, Leonie Hafner, Benedikt Silvester Hofer, Nina Dominik, Georg Kramer, Paul Thöne, Michael Trauner, Aleksander Kr
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Anja Tiede, Benjamin Maasoumy
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JHEP Reports.2024; : 101308. CrossRef

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Steatotic liver disease

Bariatric surgery reduces long-term mortality in patients with metabolic dysfunction-associated steatotic liver disease and cirrhosis: Nicholas A. Rouillard, Scott D. Barnett, Xinrong Zhang, Leslie Kam, Richie Manikat, Ramsey Cheung, Mindie H. Nguyen; Clin Mol Hepatol 2025;31(1):227-239.
Published online November 14, 2024; DOI: https://doi.org/10.3350/cmh.2024.0564

Background/Aims
With the obesity pandemic, metabolic dysfunction-associated steatotic liver disease (MASLD) is the most common liver disease and a leading cause of end-stage liver disease and liver-related deaths in the USA. Therefore, we aimed to compare the long-term outcomes of patients with MASLD and cirrhosis with and without bariatric surgery.
Methods
Patients were retrospectively identified from the California Department of Healthcare Access and Information database, 2005 to 2019, for a population-based cohort study. Propensity score matching (PSM) was used to balance background risks between patients with cirrhosis who underwent bariatric surgery and those who did not. Overall, liver-related and non-liver-related mortality were analyzed.
Results
Of 91,708 eligible patients with MASLD and cirrhosis, PSM yielded 2,107 patients who underwent bariatric surgery and 8,428 non-bariatric controls. Compared to matched controls, patients who underwent bariatric surgery had lower 5-year overall (24.9% vs. 37.1%; p<0.0001), liver-related (3.3% vs. 14%; p<0.0001), and non-liver-related mortality (22.3% vs. 26.9%; p=0.046). In multivariable analysis, bariatric surgery was associated with decreased overall mortality (adjusted hazard ratio [aHR]=0.63; p<0.0001), liver-related (aHR=0.24; p<0.0001), and non-liverrelated (aHR=0.81; p=0.0026) mortality. However, only laparoscopic surgeries were associated with lower overall mortality (aHR=0.39; p<0.0001) whereas open surgeries were associated with higher overall mortality (aHR=1.24; p=0.022).
Conclusions
Patients with MASLD and cirrhosis who underwent bariatric surgery, specifically laparoscopic approaches, had significantly lower mortality risk than non-surgical counterparts.

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Clinical and Molecular Hepatology.2025; 31(2): 610. CrossRef
Letter to the editor on “Bariatric surgery reduces long-term mortality in patients with metabolic dysfunction-associated steatotic liver disease and cirrhosis”
Wei Wang, Yating Xie, Ailei Xu
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Nicholas A. Rouillard, Linda Henry, Mindie H. Nguyen
Clinical and Molecular Hepatology.2025; 31(2): e173. CrossRef
Reply to correspondence on “Bariatric surgery reduces long-term mortality in patients with metabolic dysfunction-associated steatotic liver disease and cirrhosis”
Jing Zeng, Jian-Gao Fan
Clinical and Molecular Hepatology.2025; 31(2): e218. CrossRef
Letter to the editor on “Bariatric surgery reduces long-term mortality in patients with metabolic dysfunction-associated steatotic liver disease and cirrhosis”
Weixiong Zhu, Xuefan Zeng, Zengxi Yang, Yusheng Cheng, Wence Zhou
Clinical and Molecular Hepatology.2025; 31(3): e252. CrossRef
Association between body roundness index and risks of all-cause and cardiovascular mortality in adults with metabolic dysfunction-associated steatotic liver disease: NHANES 1999–2018
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Chi-Kuei Hsu, Po-Yu Huang, Chih-Cheng Lai
Clinical and Molecular Hepatology.2025; 31(3): e247. CrossRef
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Janna Vanessa Diaz Torres, Vanessa Rocío Villanueva Guerrero, Jennifer Patricia Vargas Gómez, Fredy Javier Pacheco Miranda, Lorena Rocío Orozco Álvarez, Joseph David León Insignares, Marian Mares, Héctor Mario Rodríguez Ortiz, Evelyn Mendoza-Torres
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Endoscopic Bariatric Therapies for Metabolic Dysfunction-Associated Steatotic Liver Disease: Mechanistic Insights and Metabolic Implications
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Biomedicines.2025; 13(10): 2437. CrossRef

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Review

Hepatitis E as a trigger for acute-on-chronic liver failure: Maria Buti, Juan Carlos Ruiz-Cobo, Rafael Esteban, Mar Riveiro-Barciela; Clin Mol Hepatol 2025;31(Suppl):S196-S204.
Published online November 11, 2024; DOI: https://doi.org/10.3350/cmh.2024.0758

Abstract
PDF

Acute hepatitis E virus (HEV) infection is typically self-limiting and has a favourable prognosis. However, certain populations such as patients with pre-existing chronic liver disease may experience severe manifestations, including progression to acute-on-chronic liver failure (ACLF). Among viral hepatitis types, hepatitis A, E, and B are major causes of ACLF. Active screening and early diagnosis of HEV infection in patients with cirrhosis, especially those who develop ACLF, can improve management and enable timely antiviral therapy. Preventive measures, including HEV vaccination for high-risk groups, could reduce the morbidity and mortality associated with hepatitis E.

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Editorial

Steatotic liver disease

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 fibrosis in patients with nonalcoholic fatty liver disease: A systematic review and meta-analysis”: Won Sohn; Clin Mol Hepatol 2025;31(1):277-280.
Published online October 11, 2024; DOI: https://doi.org/10.3350/cmh.2024.0823

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Young Eun Chon, Jung Hwan Yu, Seung Up Kim
Clinical and Molecular Hepatology.2025; 31(1): e61. CrossRef
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Review

Artificial intelligence, epidemiology, methodology, or others

Roles of X-box binding protein 1 in liver pathogenesis: Jihoon Tak, Yun Seok Kim, Sang Geon Kim; Clin Mol Hepatol 2025;31(1):1-31.
Published online October 2, 2024; DOI: https://doi.org/10.3350/cmh.2024.0441

Abstract
PDF

The prevalence of drug-induced liver injury (DILI) and viral liver infections presents significant challenges in modern healthcare and contributes to considerable morbidity and mortality worldwide. Concurrently, metabolic dysfunctionassociated steatotic liver disease (MASLD) has emerged as a major public health concern, reflecting the increasing rates of obesity and leading to more severe complications such as fibrosis and hepatocellular carcinoma. X-box binding protein 1 (XBP1) is a distinct transcription factor with a basic-region leucine zipper structure, whose activity is regulated by alternative splicing in response to disruptions in endoplasmic reticulum (ER) homeostasis and the unfolded protein response (UPR) activation. XBP1 interacts with a key signaling component of the highly conserved UPR and is critical in determining cell fate when responding to ER stress in liver diseases. This review aims to elucidate the emerging roles and molecular mechanisms of XBP1 in liver pathogenesis, focusing on its involvement in DILI, viral liver infections, MASLD, fibrosis/cirrhosis, and liver cancer. Understanding the multifaceted functions of XBP1 in these liver diseases offers insights into potential therapeutic strategies to restore ER homeostasis and mitigate liver damage.

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Editorials

Liver fibrosis, cirrhosis, and portal hypertension

Unveiling the distinctive gut microbiota and metabolites in liver cirrhosis and its complications: Novel diagnostic biomarkers: Editorial on “Gut microbiome and metabolome signatures in liver cirrhosis-related complications”: Soon Kyu Lee, Jong Young Choi; Clin Mol Hepatol 2025;31(1):301-303.
Published online August 30, 2024; DOI: https://doi.org/10.3350/cmh.2024.0716

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Chao Cui, Shuai Gao, Jingfei Shi, Kai Wang
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Liver fibrosis, cirrhosis, and portal hypertension

From invasive to intuitive: The emerging role of non-invasive models in hepatic decompensation: Editorial on “Carvedilol to prevent hepatic decompensation of cirrhosis in patients with clinically significant portal hypertension stratified by new non-invasive model (CHESS2306)”: Akhil Deshmukh, Rakhi Maiwall; Clin Mol Hepatol 2025;31(2):577-580.
Published online August 19, 2024; DOI: https://doi.org/10.3350/cmh.2024.0661

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Correspondence to editorial on “Carvedilol to prevent hepatic decompensation of cirrhosis in patients with clinically significant portal hypertension stratified by new non-invasive model (CHESS2306)”
Chuan Liu, Ling Yang, Hong You, Gao-Jun Teng, Xiaolong Qi
Clinical and Molecular Hepatology.2025; 31(2): e155. CrossRef

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Original Articles

Microbiome

Gut microbiome and metabolome signatures in liver cirrhosis-related complications: Satya Priya Sharma, Haripriya Gupta, Goo-Hyun Kwon, Sang Yoon Lee, Seol Hee Song, Jeoung Su Kim, Jeong Ha Park, Min Ju Kim, Dong-Hoon Yang, Hyunjoon Park, Sung-Min Won, Jin-Ju Jeong, Ki-Kwang Oh, Jung A Eom, Kyeong Jin Lee, Sang Jun Yoon, Young Lim Ham, Gwang Ho Baik, Dong Joon Kim, Ki Tae Suk; Clin Mol Hepatol 2024;30(4):845-862.
Published online July 25, 2024; DOI: https://doi.org/10.3350/cmh.2024.0349

Background/Aims
Shifts in the gut microbiota and metabolites are interrelated with liver cirrhosis progression and complications. However, causal relationships have not been evaluated comprehensively. Here, we identified complication-dependent gut microbiota and metabolic signatures in patients with liver cirrhosis.
Methods
Microbiome taxonomic profiling was performed on 194 stool samples (52 controls and 142 cirrhosis patients) via V3-V4 16S rRNA sequencing. Next, 51 samples (17 controls and 34 cirrhosis patients) were selected for fecal metabolite profiling via gas chromatography mass spectrometry and liquid chromatography coupled to time-of-flight mass spectrometry. Correlation analyses were performed targeting the gut-microbiota, metabolites, clinical parameters, and presence of complications (varices, ascites, peritonitis, encephalopathy, hepatorenal syndrome, hepatocellular carcinoma, and deceased).
Results
Veillonella bacteria, Ruminococcus gnavus, and Streptococcus pneumoniae are cirrhosis-related microbiotas compared with control group. Bacteroides ovatus, Clostridium symbiosum, Emergencia timonensis, Fusobacterium varium, and Hungatella_uc were associated with complications in the cirrhosis group. The areas under the receiver operating characteristic curve (AUROCs) for the diagnosis of cirrhosis, encephalopathy, hepatorenal syndrome, and deceased were 0.863, 0.733, 0.71, and 0.69, respectively. The AUROCs of mixed microbial species for the diagnosis of cirrhosis and complication were 0.808 and 0.847, respectively. According to the metabolic profile, 5 increased fecal metabolites in patients with cirrhosis were biomarkers (AUROC >0.880) for the diagnosis of cirrhosis and complications. Clinical markers were significantly correlated with the gut microbiota and metabolites.
Conclusions
Cirrhosis-dependent gut microbiota and metabolites present unique signatures that can be used as noninvasive biomarkers for the diagnosis of cirrhosis and its complications.

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Liver fibrosis, cirrhosis, and portal hypertension

Carvedilol to prevent hepatic decompensation of cirrhosis in patients with clinically significant portal hypertension stratified by new non-invasive model (CHESS2306): Chuan Liu, Hong You, Qing-Lei Zeng, Yu Jun Wong, Bingqiong Wang, Ivica Grgurevic, Chenghai Liu, Hyung Joon Yim, Wei Gou, Bingtian Dong, Shenghong Ju, Yanan Guo, Qian Yu, Masashi Hirooka, Hirayuki Enomoto, Amr Shaaban Hanafy, Zhujun Cao, Xiemin Dong, Jing LV, Tae Hyung Kim, Yohei Koizumi, Yoichi Hiasa, Takashi Nishimura, Hiroko Iijima, Chuanjun Xu, Erhei Dai, Xiaoling Lan, Changxiang Lai, Shirong Liu, Fang Wang, Ying Guo, Jiaojian Lv, Liting Zhang, Yuqing Wang, Qing Xie, Chuxiao Shao, Zhensheng Liu, Federico Ravaioli, Antonio Colecchia, Jie Li, Gao-Jun Teng, Xiaolong Qi; Clin Mol Hepatol 2025;31(1):105-118.
Published online July 11, 2024; DOI: https://doi.org/10.3350/cmh.2024.0198

Backgrounds/Aims
Non-invasive models stratifying clinically significant portal hypertension (CSPH) are limited. Herein, we developed a new non-invasive model for predicting CSPH in patients with compensated cirrhosis and investigated whether carvedilol can prevent hepatic decompensation in patients with high-risk CSPH stratified using the new model.
Methods
Non-invasive risk factors of CSPH were identified via systematic review and meta-analysis of studies involving patients with hepatic venous pressure gradient (HVPG). A new non-invasive model was validated for various performance aspects in three cohorts, i.e., a multicenter HVPG cohort, a follow-up cohort, and a carvediloltreating cohort.
Results
In the meta-analysis with six studies (n=819), liver stiffness measurement and platelet count were identified as independent risk factors for CSPH and were used to develop the new “CSPH risk” model. In the HVPG cohort (n=151), the new model accurately predicted CSPH with cutoff values of 0 and –0.68 for ruling in and out CSPH, respectively. In the follow-up cohort (n=1,102), the cumulative incidences of decompensation events significantly differed using the cutoff values of <–0.68 (low-risk), –0.68 to 0 (medium-risk), and >0 (high-risk). In the carvediloltreated cohort, patients with high-risk CSPH treated with carvedilol (n=81) had lower rates of decompensation events than non-selective beta-blockers untreated patients with high-risk CSPH (n=613 before propensity score matching [PSM], n=162 after PSM).
Conclusions
Treatment with carvedilol significantly reduces the risk of hepatic decompensation in patients with high-risk CSPH stratified by the new model.

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Machine learning-based prediction models for liver-related events in patients with hepatitis B-related cirrhosis and clinically significant portal hypertension
Yan-Qiu Li, Zhuo-Jun Li, Yong-Qi Li, Ying Feng, Xian-Bo Wang
World Journal of Gastroenterology.2026;[Epub] CrossRef
Carvedilol Versus Endoscopic Variceal Ligation for Prophylaxis of Esophageal Variceal Bleeding in Patients With Liver Cirrhosis
Luiz G.S. Almeida, Ocílio R. Gonçalves, Thiago H.F. de Oliveira, João V. Andrade Fernandes, Hildel F.L. Filho, Maria J.G. Siqueira, Paweł Łajczak, Wagner Rios-Garcia, Jefferson H. Marques Fontes, Lucas L. Mendes, Marcos de Vasconcelos Carneiro
Journal of Clinical Gastroenterology.2026; 60(7): 569. CrossRef
Endoscopic variceal ligation combined with carvedilol versus endoscopic variceal ligation combined with propranolol for the treatment of oesophageal variceal bleeding in cirrhosis: study protocol for a multicentre, randomised controlled trial
Yiling Li, Li Du, Shuairan Zhang, Chuan Liu, Chao Ma, Xiaochao Liu, Huanhai Xu, Zhixu Fan, Shengjuan Hu, Jing Wang, Lichun Shao, Lijun Peng, Huiling Xiang, Xuan Liang, Wenhui Zhang, Hongyun Zhao, Pengyuan He, Jingyi Xu, Qianlong Li, Ling Yang, Yunhai Wu,
BMJ Open.2025; 15(4): e093866. CrossRef
Relative change rate of liver stiffness measurements predicts the risk of liver decompensation in compensated advanced chronic liver disease
Yanqiu Li, Zihang Qiao, Jinze Li, Bingbing Zhu, Yu Lu, Ying Feng, Xianbo Wang
Clinical and Experimental Medicine.2025;[Epub] CrossRef
Revolutionising portal hypertension diagnosis: the rise of non-invasive techniques in liver cirrhosis
Bocheng Gao, Yumeng Lin, Huimin Zhang, Yulin Li, Shuhua Gou, Peiling Ma, Xueni Zhao, Yue Zhou, Qian Chen, Lan Yuan, Zhongyu Han, Chang Yu
Frontiers in Medicine.2025;[Epub] CrossRef
Editorial: Non‐selective beta‐blockers: A lifesaving shield for critically ill patients with acute decompensation of cirrhosis?
Ling Yang, Chuan Liu, Jimmy Che‐To Lai, Xiaolong Qi
Alimentary Pharmacology & Therapeutics.2024; 60(7): 965. 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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Preface
Seung Up Kim
Clinical and Molecular Hepatology.2024; 30(Suppl): S3. CrossRef

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Editorial

Acute liver injury and Acute liver failure

Modified quick-SOFA score: Can it enhance prognostic assessment for hospitalized patients with chronic liver diseases?: Editorial on “Dynamic analysis of acute deterioration in chronic liver disease patients using modified quick sequential organ failure assessment”: Simone Incicco, Salvatore Piano; Clin Mol Hepatol 2024;30(4):695-697.
Published online June 3, 2024; DOI: https://doi.org/10.3350/cmh.2024.0409

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