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"Liver diseases"

Original Article

Hepatic fibro-inflammation measured by magnetic resonance imaging iron-corrected T1 predicts extrahepatic cancer risk: a UK Biobank study
Hye Yeon Chon, Seok-Jae Heo, SungA Bae, Tae Seop Lim, Ja Kyung Kim
Clin Mol Hepatol 2026;32(3):1349-1363.
Published online June 9, 2026
DOI: https://doi.org/10.3350/cmh.2025.1372
Background/Aims
Iron-corrected T1 (cT1) is a magnetic resonance imaging (MRI)-derived biomarker of hepatic fibro-inflammation. This study aimed to investigate whether high cT1 values are associated with an increased risk of extrahepatic malignancy in a large prospective cohort.
Methods
We included 24,003 cancer-free participants from the United Kingdom (UK) Biobank with liver MRI and complete covariate data. Incident extrahepatic malignancy was assessed over a median follow-up of 4.28 years. Multivariable Fine–Gray subdistribution hazard models were used to evaluate the association between cT1 and extrahepatic cancer risk, accounting for competing risks and adjusting for demographic, metabolic, and liver-related factors.
Results
During follow-up, 1,144 participants developed extrahepatic malignancies. In the multivariable analysis, higher cT1 was independently associated with increased extrahepatic cancer risk (hazard ratio [HR] 1.116; 95% confidence interval [CI] 1.033–1.205; per standard deviation increase; P=0.005). Older age (HR 1.512; 95% CI 1.402–1.631) and male sex (HR 1.388; 95% CI 1.220–1.578) were also significant predictors (P<0.001). The fibrosis-4 score showed a modest positive association (HR 1.032; 95% CI 1.004–1.062; P=0.026), whereas MRI-proton density fat fraction demonstrated an inverse association (HR 0.906; 95% CI 0.832–0.987; P=0.024). When dichotomized at 771 ms, elevated cT1 was associated with a higher cumulative incidence of extrahepatic malignancy (6.1% vs. 4.6%, P=0.002).
Conclusions
Elevated cT1 is independently associated with an increased risk of future extrahepatic malignancy, suggesting that it may reflect systemic disease processes related to cancer risk. These findings highlight the potential relevance of cT1 beyond liver-specific outcomes; however, further validation is required before clinical implementation.
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  • 91 Download

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
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  Crossref logo
  • 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
  • 5,101 View
  • 355 Download
  • 3 Web of Science
  • Crossref

Editorial

Mechanistic insights into a noncanonical RAB25-GCN1 axis in ALD: Editorial on “RAB25/GCN1 signaling promotes endoplasmic reticulum stress to mediate alcohol-associated liver disease progression”
Seol Hee Park, Wonhyo Seo
Clin Mol Hepatol 2026;32(3):1390-1393.
Published online December 8, 2025
DOI: https://doi.org/10.3350/cmh.2025.1346

Citations

Citations to this article as recorded by  Crossref logo
  • Correspondence to editorial on “RAB25/GCN1 signaling promotes endoplasmic reticulum stress to mediate alcohol-associated liver disease progression”
    Xue-Wen Liu, Zi-Bin Zhan, Yu Gong, Ze-Hua Li, Kun-Hao Bai, Jun Weng
    Clinical and Molecular Hepatology.2026; 32(3): e349.     CrossRef
  • Reply to correspondence on “RAB25/GCN1 signaling promotes endoplasmic reticulum stress to mediate alcohol-associated liver disease progression”
    Seol Hee Park, Wonhyo Seo
    Clinical and Molecular Hepatology.2026; 32(3): e432.     CrossRef
  • 786 View
  • 39 Download
  • 1 Web of Science
  • Crossref

Reviews

Pediatric metabolic dysfunction–associated steatotic liver disease and the gut microbiome: from research landscape to targeted modulation
Lu Jiang, Lan-Duoduo Du, Jing Zeng, Hui-Kuan Chu, Zhong Peng, Jian-Gao Fan
Clin Mol Hepatol 2026;32(1):53-68.
Published online August 19, 2025
DOI: https://doi.org/10.3350/cmh.2025.0718
Metabolic dysfunction–associated steatotic liver disease (MASLD), formerly known as non-alcoholic fatty liver disease, has become the most common form of chronic liver disease in children. The spectrum of pediatric MASLD ranges from simple steatosis to steatohepatitis, fibrosis, cirrhosis, and in rare cases, hepatocellular carcinoma. Its pathogenesis involves a complex interplay among genetic, epigenetic, and environmental factors, along with alterations in the gut microbiota and its associated metabolites. Given the staggering prevalence and the distinct etiopathogenesis of pediatric MASLD, characterization of the gut microbiota and microbial products could facilitate the development of diagnostic tools and inform targeted therapeutic strategies. Current research on the gut microbiome in the context of pediatric MASLD is limited by small sample size, inadequate use of liver biopsy, methodological inconsistencies in sequencing, and confounding effects from metabolic comorbidities. In this review, we summarize clinical studies on alterations in the gut microbiota and microbial products (short-chain fatty acids, bile acids, and ethanol) that impact the pathogenesis of pediatric MASLD. We discuss the therapeutic potential of dietary modification, pharmacological treatments, and probiotics in improving disease progression by summarizing current clinical studies. Enhancing our understanding of the gut-liver axis may aid in the development of effective therapeutic strategies for pediatric MASLD.

Citations

Citations to this article as recorded by  Crossref logo
  • Obesity, Metabolic Syndrome and MASLD in Children: Inflammation as the Missing Link—A Short Narrative Review
    Mihaela-Andreea Podeanu, Claudiu Marinel Ionele, Raluca Elena Sandu, Ion Rogoveanu, Mioara Desdemona Stepan, Carmen Elena Niculescu, Sergiu-Marian Cazacu, Ștefănița Bianca Vintilescu
    Life.2026; 16(2): 310.     CrossRef
  • Artificial intelligence for metabolic dysfunction-associated steatotic liver disease diagnosis: A systematic review
    Ruijuan Wang, Chang Liu, Mei Xue, Jun Qian, Yue Hu
    Computers in Biology and Medicine.2026; 208: 111619.     CrossRef
  • Effects of metabolic syndrome on pulmonary infection in pediatric bronchial asthma: a narrative review
    Li He, Yang Ye
    Frontiers in Pediatrics.2026;[Epub]     CrossRef
  • Microbial metabolites at the nexus of gut-brain communication and neurodevelopmental disorders
    Yupeng Lai, Ming Zhang, Dandan Lang, Enfu Tao
    Frontiers in Nutrition.2026;[Epub]     CrossRef
  • Targeting the Human Gut Microbiota—Between Conventional Therapy and Precision Genetic Engineering
    Naomi-Adina Ciurea, Laura Mahdi, Annarita Graziani, Agostino Di Ciaula, Piero Portincasa, Mohamad Khalil
    Nutrients.2026; 18(12): 1958.     CrossRef
  • 9,485 View
  • 336 Download
  • 4 Web of Science
  • Crossref
Prospects of Mendelian randomization in hepatology: a comprehensive literature review with practice guidance
Lanlan Chen, Qi Rao, Menghan Gao, Guoyue Lv, Frank Tacke
Clin Mol Hepatol 2025;31(4):1115-1138.
Published online June 9, 2025
DOI: https://doi.org/10.3350/cmh.2025.0541
Mendelian randomization (MR), a powerful statistical tool for causal inference, has been widely applied in various fields of medical research, even extending to economics and psychology. In hepatology, MR has been utilized to identify risk factors and potential therapeutic targets for liver diseases, including metabolic dysfunction-associated steatotic liver disease, cholestatic and autoimmune liver diseases, and hepatobiliary cancer. MR can provide evidence of causation via associations between genetic variants, modifiable exposures and liver disease occurrence or outcomes, using large existing datasets. However, results from MR studies are sometimes scattered, biologically not plausible or even controversial between analyses, potentially reflecting a trend of inappropriate application of this method (e.g., inappropriate selection of genetic instruments, insufficient assessment of horizontal pleiotropy, compromised statistical power, and neglected genetic diversity among different populations), and thus hinder the translation of MR findings from bench to bedside. Assessing these critical issues and pinpointing bona fide evidence are essential but quite challenging for clinicians. In this review, we aim to introduce the MR method to hepatologists and provide a comprehensive overview of the current MR findings that are relevant for hepatologists. Furthermore, we will discuss how to evaluate the quality of MR publications, interpret MR findings, and illustrate good practice of using MR studies in hepatology.

Citations

Citations to this article as recorded by  Crossref logo
  • Childhood Obesity and Age‐Related Diseases: A Systematic Review and Meta‐Analysis of Mendelian Randomization Evidence
    Haoxue Zhu, Xinghao Yi, Mengyu He, Siyi Wu, Ming Li, Shan Gao
    Pediatric Obesity.2026;[Epub]     CrossRef
  • Association of genetically instrumented HMGCR inhibition with the therapeutic role of prostate cancer: a Mendelian randomization study and supporting in vitro experiments
    Xiaojie Hao, Jingjun Mu
    Frontiers in Pharmacology.2026;[Epub]     CrossRef
  • 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
    Clinical and Molecular Hepatology.2026; 32(1): 339.     CrossRef
  • Integrative Mendelian randomization and experimental validation unveil novel druggable targets in primary biliary cholangitis
    Yinling Li, Huanhuan Xie, Zhenjie Zhuang, Xin Fang, Wenjun Yang, Yan Luo, Jiangyi Hu, Wei Wang, Haitao Wang, Xiaobing Dou, Junping Shi, Jin Yang
    European Journal of Pharmacology.2026; 1020: 178775.     CrossRef
  • Integrated Plasma Proteomics and Functional Analyses Reveal Hepatic CDHR2 as a Potential Therapeutic Target in MASLD
    Yuanping Shi, Qi Huang, Yingning Liu, Xinlei Zhang, Feng Liu, Huiying Rao, Xueyao Han, Linong Ji, Xiantong Zou
    Diabetes, Obesity and Metabolism.2026; 28(5): 4303.     CrossRef
  • Metabolic Dysfunction‐Associated Steatotic Liver Disease and Obesity: Pathogenesis, Diagnostics, Risk Stratification, and Therapeutic Approach
    Beom Kyung Kim
    The Kaohsiung Journal of Medical Sciences.2026;[Epub]     CrossRef
  • Liver Aging Index: A Noninvasive Score for Liver Biological Aging and Liver‐Related Outcomes in Multicohorts
    Zhiyu Wu, Shanshan Wu, Shuyao Song, Yating Huang, Canqing Yu, Dianjianyi Sun, Pei Pei, Ling Yang, Yiping Chen, Huaidong Du, Robin Walters, Iona Millwood, Hao Xu, Xiaoming Yang, Junshi Chen, Seung Up Kim, Salvatore Petta, Atsushi Nakajima, Emmanuel Tsochat
    Aging Cell.2026;[Epub]     CrossRef
  • Correspondence to editorial 2 on “Aspirin and hepatocellular carcinoma risk in metabolic dysfunction-associated steatotic liver disease: nationwide cohort study with genetic risk analysis”
    Hyunjae Shin, Moon Haeng Hur, Yoon Jun Kim
    Clinical and Molecular Hepatology.2026; 32(3): e381.     CrossRef
  • Helicobacter pylori, peptic ulcer disease, and colorectal cancer: a prospective study with genome-wide interaction analysis and Mendelian randomization
    Ziqi Wan, Jiarui Mi, Xiaoyin Bai, Dong Wu, Sunny Hei Wong
    Infectious Agents and Cancer.2025;[Epub]     CrossRef
  • 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
  • Integrative genome-wide analysis unveils the genetic landscape of gallstone disease and highlights novel loci with therapeutic potential
    Haotian Chen, Zhengye Liu, Hanze Du, Mixue Zheng, Ziqi Wan, Nan Zhao, Guanqiao Li, Xiaoyin Bai, Dong Wu, Jiarui Mi
    BMJ Open Gastroenterology.2025; 12(1): e001976.     CrossRef
  • 7,671 View
  • 275 Download
  • 9 Web of Science
  • Crossref

Research Letters

Lipidomic analysis of alcohol use disorder patients revealed the biomarkers for alcohol-related liver disease susceptibility
Dongyao Wang, Hongwei Zhang, Yuxiao Tang
Clin Mol Hepatol 2025;31(3):e259-e262.
Published online April 2, 2025
DOI: https://doi.org/10.3350/cmh.2025.0227

Citations

Citations to this article as recorded by  Crossref logo
  • Discovery of Bufalin as a Molecular Glue Degrader of NCAPG to Inhibit the Proliferation of Hepatoma Cells
    Chenghua Wu, Xiaobin Zhuo, Jianxin Yang, Yuxiao Tang, Weili Wang, Mengpu Wu, Gen Miao, Chenqi Li, Hui Shen, Jianxin Qian, Dongyao Wang
    Drug Development Research.2026;[Epub]     CrossRef
  • Dihydroberberine in metabolic disorders: Bioavailability, molecular mechanisms, toxicology, and future perspectives
    Dongyao Wang, Yuxiao Tang
    Food and Chemical Toxicology.2026; 216: 116267.     CrossRef
  • Targeting Annexin A2 to reactivate tumor-associated antigens presentation and relieve immune tolerance in liver cancer
    Yuxiao Tang, Jianxin Yang, Qicong Shen, Zelong Gao, Mengpu Wu, Chenghua Wu, Jicong Du, Min Li, Changquan Ling, Feng Lu, Yifeng Chai, Xin Dong, Jianxin Qian, Chenqi Li, Feng Xie, Zhenhong Guo, Hui Shen, Dongyao Wang
    Journal for ImmunoTherapy of Cancer.2025; 13(6): e011716.     CrossRef
  • 9,777 View
  • 116 Download
  • 4 Web of Science
  • Crossref
Mendelian randomization does not support the effects of G CSF on decompensated liver disease
Liling Li, Hui Wang, Hong Wang, Jinchang Huang
Clin Mol Hepatol 2025;31(3):e254-e258.
Published online March 4, 2025
DOI: https://doi.org/10.3350/cmh.2025.0172
  • 9,383 View
  • 74 Download

Special Review

Liver disease trends in the Asia-Pacific region for the next 50 years
Shuichiro Shiina, Javkhlan Maikhuu, Qing Deng, Terguunbileg Batsaikhan, Lariza Marie Canseco, Maki Tobari, Hitoshi Maruyama, Hiroaki Nagamatsu, Diana Alcantara-Payawal, Rino Gani, Yi-Hsiang Huang, Tawesak Tanwandee, Giovanni Galati, Yoon Jun Kim
Clin Mol Hepatol 2025;31(3):671-684.
Published online March 4, 2025
DOI: https://doi.org/10.3350/cmh.2025.0043
Liver disease has emerged as a critical and escalating public health concern worldwide, with the Asia-Pacific region at the forefront of this challenge due to its vast population and diverse socioeconomic landscape. Over the coming five decades, this region will experience profound changes in liver disease patterns, shaped by rapid urbanization, lifestyle modifications, advancements in medical technologies, and evolving public health strategies. This article offers an in-depth analysis of six transformative areas defining the trajectory of liver disease in the region. First, it highlights the alarming rise of metabolic dysfunction-associated fatty liver disease and metabolic dysfunction-associated steatohepatitis, diseases driven by modern lifestyle factors and inherent metabolic susceptibilities. Concurrently, it celebrates the declining burden of viral hepatitis, underscoring the success of sustained public health interventions. However, new challenges are emerging, such as the growing impact of environmental and occupational exposures on liver health. Breakthroughs in genomic and epigenetic research promise to advance precision medicine, offering targeted therapeutic solutions. Additionally, the integration of artificial intelligence, big data, and telemedicine is poised to revolutionize liver disease management, improving accessibility and personalized care. Finally, the article emphasizes the critical role of robust health policies, preventive strategies, and cross-border collaboration in shaping a healthier future. By synthesizing these insights, the study aims to guide innovative and effective responses to the evolving liver disease landscape in the Asia-Pacific region.

Citations

Citations to this article as recorded by  Crossref logo
  • Digital divide and healthcare service utilization among older adults with chronic liver disease in China: a nationwide cross-sectional study
    Yang Feng, Ke Pu, Chang Liu
    Scientific Reports.2026;[Epub]     CrossRef
  • Association Between Sarcopenic Obesity–Related Scores and Liver Fibrosis in Patients with Steatotic Liver Disease: A Cross-Sectional Study
    Tatsuki Ichikawa, Satoshi Miuma, Mio Yamashima, Shinobu Yamamichi, Makiko Koike, Yusuke Nakano, Hiroyuki Yajima, Osamu Miyazaki, Tomonari Ikeda, Takuma Okamura, Naohiro Komatsu, Mayuko Kakizoe, Ryusei Tanaka, Hisamitsu Miyaaki
    Diagnostics.2026; 16(2): 324.     CrossRef
  • The role and possible mechanism of intestinal fungi in the progression of chronic liver diseases
    Yirui Hu, Ye Yang, Shuyan Wang, Huikuan Chu
    npj Biofilms and Microbiomes.2026;[Epub]     CrossRef
  • Liver Transplantation Following Immune Checkpoint Inhibitor Therapy: What Do We Need to Know from Clinical and Immunological Perspective?
    Hee Sun Cho, Soon Kyu Lee
    International Journal of Molecular Sciences.2026; 27(6): 2680.     CrossRef
  • 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
  • Targeting the AMPK/ACC pathway with luteolin suppresses de novo lipogenesis and limits tumor burden in a MASH-HCC mouse model
    Gaoxuan Shao, Chenceng Sun, Chenhao Ye, Ying Liu, Jiashu Pan, Yujing Liu, Lu Lu, Lei Wang, Zemin Lin, Fan Yang, Guang Ji, Hanchen Xu
    Life Sciences.2026; 397: 124440.     CrossRef
  • Global trends in metabolic-associated hepatocellular carcinoma: genetic and socio-demographic drivers
    Na Wu, Xinying Xiong, Xinyue Wang, Shuang Wei, Xinyu Shi, Yilin Chen, Wenjun Zhou, Jianying Wang, Lei Zhang, Baocheng Liu, Hualing Song, Huiting Yu, Guang Ji
    Hepatology International.2026;[Epub]     CrossRef
  • Predictors of Discordance Between Controlled Attenuation Parameter and Magnetic Resonance-Proton Density Fat Fraction in Hepatic Steatosis
    Dong Yun Kim, Hyung-Jin Rhee, Beom Kyung Kim
    Clinical and Translational Gastroenterology.2026; 17(7): e01042.     CrossRef
  • Antiviral Therapy and Post‐Resection Outcomes in Patients With Hepatitis B Virus‐Related Hepatocellular Carcinoma
    Jaehong Jeong, Jung Pyo Hong, Dong Yun Kim, Jae Seung Lee, Mi Na Kim, Seung Up Kim, Beom Kyung Kim, Jun Yong Park, Do Young Kim, Sang Hoon Ahn, Hye Won Lee
    Alimentary Pharmacology & Therapeutics.2026;[Epub]     CrossRef
  • Trends and future projections of liver cancer attributable to metabolic dysfunction-associated steatohepatitis in China from 1990 to 2050
    Jincheng Tang, Renyi Yang, Kexiong Li, Wei Peng, Zuomei He, Wenhui Gao, Puhua Zeng
    Scientific Reports.2025;[Epub]     CrossRef
  • Bridging the Gap in Elimination of Hepatitis C Virus among People Who Use Drugs in South Korea
    Beom Kyung Kim
    Gut and Liver.2025; 19(5): 635.     CrossRef
  • Precision prevention of liver cancer based on risk factors
    Jian-Guo Chen
    Exploration of Digestive Diseases.2025;[Epub]     CrossRef
  • MAFLD in Vietnam: a neglected public health challenge requiring urgent policy action
    Thong Duy Vo, Huong Tu Lam
    Frontiers in Clinical Diabetes and Healthcare.2025;[Epub]     CrossRef
  • 13,435 View
  • 254 Download
  • 12 Web of Science
  • Crossref

Review

Liver fibrosis, cirrhosis, and portal hypertension

Prediction and prevention of post-procedural bleedings in patients with cirrhosis
Alix Riescher-Tuczkiewicz, Pierre-Emmanuel Rautou
Clin Mol Hepatol 2025;31(Suppl):S205-S227.
Published online February 18, 2025
DOI: https://doi.org/10.3350/cmh.2024.0928
Although post-procedural bleedings are infrequent in patients with cirrhosis, they are associated with significant morbidity and mortality. Therefore, predicting and preventing such bleedings is important. Established predictors of post-procedural bleeding include high-bleeding risk procedure, severe cirrhosis and high body mass index; prognostic value of anemia, acute kidney injury and bacterial infection is more uncertain. While prothrombin time and international normalized ratio do not predict post-procedural bleeding, some evidence suggests that platelet count, whole blood thrombin generation assay and viscoelastic tests may be helpful in this context. Prevention of postprocedural bleeding involves careful management of antithrombotic drugs during the periprocedural period. Patients with cirrhosis present unique challenges due to altered pharmacokinetics and pharmacodynamics of antithrombotic drugs, but there is a lack of dedicated studies specifically focused on this patient population. Guidelines for periprocedural management of antithrombotic drugs developed for patients without liver disease are thus applied to those with cirrhosis. Some technical aspects may decrease the risk of post-procedural bleeding, namely ultrasoundguidance, opting for transjugular route rather than percutaneous route, and the level of expertise of the operator. The effectiveness of platelet transfusions or thrombopoietin-receptor agonists remains uncertain. Transfusion of fresh-frozen plasma, of fibrinogen, and administration of tranexamic acid are not recommended for reducing post-procedural bleeding in patients with cirrhosis. In conclusion, prediction of post-procedural requires a global approach taking into account the patients characteristics, the risk of the procedure, and the platelet count. There is little data to support prophylactic correction of hemostasis, and dedicated studies are needed.

Citations

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  • Liver biopsy quality criteria to exclude cirrhosis in case of suspicion of porto-sinusoidal vascular disorder
    Chloé de Broucker, Valérie Paradis, Maria Luisa Botero, Miguel Albuquerque, Audrey Payancé, Aurélie Plessier, Laure Elkrief, François Durand, Sophie Hillaire, Paul-Emile Zafar, Juan Carlos Garcia Pagan, Pierre-Emmanuel Rautou
    JHEP Reports.2026; 8(1): 101670.     CrossRef
  • Acute Changes in Liver and Spleen Stiffness Following Endoscopic Variceal Ligation in Advanced Liver Disease—A Pilot Study
    Esra Görgülü, Eva Herrmann, Jonel Trebicka, Alexander Queck, Georg Dultz, Vitali Koch, Stefan Zeuzem, Jörg Bojunga, Viola Knop, Florian Alexander Michael, Mireen Friedrich Rust
    Journal of Clinical Medicine.2026; 15(2): 816.     CrossRef
  • Tranexamic acid in the management of post-procedural bleeding in bronchoscopy: A comprehensive review
    Anthony Christanto, Ngakan Putu Parsama Putra, Christian Surya Eka Putra
    Lung India.2026; 43(2): 185.     CrossRef
  • Thrombosis and anticoagulation in patients with Cirrhosis. An overview
    Dominique-Charles Valla
    Digestive and Liver Disease.2026; 58(7): 871.     CrossRef
  • Real-world efficacy and safety of avatrombopag in Japanese patients with chronic liver disease and severe thrombocytopenia
    Yosuke Otsuka, Naoki Morimoto, Satoru Kakizaki, Tadashi Ikegami, Shunji Watanabe, Yuichi Majima, Hirotaka Arai, Takeharu Asano, Yoshihito Uchida, Toshiro Kamoshida, Takeshi Hatanaka, Satoshi Takakusagi, Takeshi Nihei, Atsuko Soeda, Yuichi Yamazaki, Naoyuk
    Journal of Gastroenterology.2026;[Epub]     CrossRef
  • 10,334 View
  • 215 Download
  • 5 Web of Science
  • Crossref

Original Article

Modulation of phosphatase of regenerating liver-1 within placental mesenchymal stem cells instigates the transition between epithelial-to-mesenchymal transition and mesenchymal-to-epithelial transition subsequent to hepatic fibrosis
Jae Yeon Kim, Hyeri Park, Soo Young Park, Se Ho Kim, Ja Yun Lim, Ki Seog Lee, Si Hyun Bae, Gi Jin Kim
Clin Mol Hepatol 2025;31(3):823-840.
Published online January 22, 2025
DOI: https://doi.org/10.3350/cmh.2024.0741
Background/Aims
Epithelial-to-mesenchymal transition (EMT) plays a crucial role in hepatic fibrogenesis and liver repair in chronic liver disease. Our research highlights the antifibrotic potential of placenta-derived mesenchymal stem cells (PD-MSCs) and the role of phosphatase of regenerating liver-1 (PRL-1) in promoting liver regeneration.
Methods
We evaluated the efficacy of PD-MSCs overexpressing PRL-1 (PD-MSCsPRL-1) in a bile duct ligationinduced rat injury model, focusing on their ability to regulate EMT.
Results
PD-MSCsPRL-1 significantly reduced mesenchymal markers by downregulating TGFB1/SMAD2, outperforming naïve PD-MSCs. The transplantation of PD-MSCsPRL-1 enhanced BMP7/SMAD1/5 expression, promoting epithelial marker expression and stimulating BMP7 within hepatocytes, modulating downstream SMAD signaling. Importantly, further validation confirmed that PRL-1 directly interacts with BMP7 in hepatocytes.
Conclusions
PRL-1 expression in PD-MSCsPRL-1 restores TGFB1/BMP7 balance, promoting hepatic regeneration through mesenchymal-to-epithelial transition. These findings highlight the therapeutic potential of engineered MSCs for liver disease and suggest innovative strategies for future stem cell therapies.

Citations

Citations to this article as recorded by  Crossref logo
  • Modulation of PRL-1 in placental MSCs: A novel therapeutic strategy for hepatic fibrosis: Editorial on “Modulation of phosphatase of regenerating liver-1 within placental mesenchymal stem cells instigates the transition between epithelial-to-mesenchymal t
    Lihai Jiang, Wenjie Zheng
    Clinical and Molecular Hepatology.2026; 32(1): 377.     CrossRef
  • 3D-cultured hUC-MSC-derived exosomes as macrophage mediators to suppress cholestatic fibrosis in mice via miR-1291–mediated multi-targeted pathways
    Yu Liu, Senyi Gong, Xingyu Luo, Yuwen Hu, Qinbiao Yan, Zhe Yang, Ali Mohsin, Shusen Zheng, Meijin Guo
    Chemical Engineering Journal.2026; 532: 174376.     CrossRef
  • BMP7 in kidney development and disease: a multilayer regulatory network integrating inflammation, fibrosis, and regeneration
    Heng Wang, Yaling Li, Guoping Zheng
    Cell Signaling, Inflammation & Disease.2026;[Epub]     CrossRef
  • Link between Metabolic Dysfunction-Associated Steatotic Liver Disease and Cardiovascular Diseases
    Daifei Shen, Runji Chen, Shu Ye
    Research.2026;[Epub]     CrossRef
  • Advances in Biliary Disease Organoid Research: From Model Construction to Clinical Applications
    Boming Peng, Min Huang, Jianquan Zhang, Yang Xiang
    Advanced Healthcare Materials.2025;[Epub]     CrossRef
  • Mechanisms, efficacy, and future perspectives of cellular-based therapies for liver fibrosis/cirrhosis: focusing on mesenchymal stromal cells
    Xuan Pan, Tianyun Gao, Bin Wang
    Cell & Bioscience.2025;[Epub]     CrossRef
  • 15,345 View
  • 939 Download
  • 5 Web of Science
  • Crossref

Correspondence

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
  • 7,488 View
  • 39 Download

Reviews

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
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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Steatotic liver disease

Immunological mechanisms in steatotic liver diseases: An overview and clinical perspectives
Mengyao Yan, Shuli Man, Long Ma, Lanping Guo, Luqi Huang, Wenyuan Gao
Clin Mol Hepatol 2024;30(4):620-648.
Published online July 11, 2024
DOI: https://doi.org/10.3350/cmh.2024.0315
Steatotic liver diseases (SLD) are the principal worldwide cause of cirrhosis and end-stage liver cancer, affecting nearly a quarter of the global population. SLD includes metabolic dysfunction-associated alcoholic liver disease (MetALD) and metabolic dysfunction-associated steatotic liver disease (MASLD), resulting in asymptomatic liver steatosis, fibrosis, cirrhosis and associated complications. The immune processes include gut dysbiosis, adiposeliver organ crosstalk, hepatocyte death and immune cell-mediated inflammatory processes. Notably, various immune cells such as B cells, plasma cells, dendritic cells, conventional CD4+ and CD8+ T cells, innate-like T cells, platelets, neutrophils and macrophages play vital roles in the development of MetALD and MASLD. Immunological modulations targeting hepatocyte death, inflammatory reactions and gut microbiome include N-acetylcysteine, selonsertib, F-652, prednisone, pentoxifylline, anakinra, JKB-121, HA35, obeticholic acid, probiotics, prebiotics, antibiotics and fecal microbiota transplantation. Understanding the immunological mechanisms underlying SLD is crucial for advancing clinical therapeutic strategies.

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Acute liver injury and Acute liver failure

Current status and perspective on molecular targets and therapeutic intervention strategy in hepatic ischemia-reperfusion injury
Jia Liu, Ranyi Luo, Yinhao Zhang, Xiaojiaoyang Li
Clin Mol Hepatol 2024;30(4):585-619.
Published online July 1, 2024
DOI: https://doi.org/10.3350/cmh.2024.0222
Hepatic ischemia‒reperfusion injury (HIRI) is a common and inevitable complication of hepatic trauma, liver resection, or liver transplantation. It contributes to postoperative organ failure or tissue rejection, eventually affecting patient prognosis and overall survival. The pathological mechanism of HIRI is highly complex and has not yet been fully elucidated. The proposed underlying mechanisms include mitochondrial damage, oxidative stress imbalance, abnormal cell death, immune cell hyperactivation, intracellular inflammatory disorders and other complex events. In addition to serious clinical limitations, available antagonistic drugs and specific treatment regimens are still lacking. Therefore, there is an urgent need to not only clarify the exact etiology of HIRI but also reveal the possible reactions and bottlenecks of existing drugs, helping to reduce morbidity and shorten hospitalizations. We analyzed the possible underlying mechanism of HIRI, discussed various outcomes among different animal models and explored neglected potential therapeutic strategies for HIRI treatment. By thoroughly reviewing and analyzing the literature on HIRI, we gained a comprehensive understanding of the current research status in related fields and identified valuable references for future clinical and scientific investigations.

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Reply to Correspondence

Artificial intelligence, epidemiology, methodology, or others

Reply to correspondence on “Protein-centric omics analysis reveals circulating complements linked to non-viral liver diseases as potential therapeutic targets”
Mohammad Saeid Rezaee-Zavareh, Naomy Kim, Ju Dong Yang
Clin Mol Hepatol 2024;30(4):1037-1038.
Published online May 2, 2024
DOI: https://doi.org/10.3350/cmh.2024.0320
  • 6,126 View
  • 57 Download

Correspondence

Artificial intelligence, epidemiology, methodology, or others

Correspondence to editorial on “Protein-centric omics analysis reveals circulating complements linked to non-viral liver diseases as potential therapeutic targets”
Yingzhou Shi, Guandou Yuan, Xiude Fan, Chao Xu
Clin Mol Hepatol 2024;30(4):987-988.
Published online April 19, 2024
DOI: https://doi.org/10.3350/cmh.2024.0266
  • 6,553 View
  • 53 Download

Editorial

Artificial intelligence, epidemiology, methodology, or others

Starting the journey: Understanding the roles of complement proteins in liver diseases through mendelian randomization
Mohammad Saeid Rezaee-Zavareh, Naomy Kim, Ju Dong Yang
Clin Mol Hepatol 2024;30(2):150-153.
Published online February 22, 2024
DOI: https://doi.org/10.3350/cmh.2024.0116

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  • Reply to correspondence on “Protein-centric omics analysis reveals circulating complements linked to non-viral liver diseases as potential therapeutic targets”
    Mohammad Saeid Rezaee-Zavareh, Naomy Kim, Ju Dong Yang
    Clinical and Molecular Hepatology.2024; 30(4): 1037.     CrossRef
  • Correspondence to editorial on “Protein-centric omics analysis reveals circulating complements linked to non-viral liver diseases as potential therapeutic targets”
    Yingzhou Shi, Guandou Yuan, Xiude Fan, Chao Xu
    Clinical and Molecular Hepatology.2024; 30(4): 987.     CrossRef
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Original Article

Artificial intelligence, epidemiology, methodology, or others

Protein-centric omics analysis reveals circulating complements linked to non-viral liver diseases as potential therapeutic targets
Yingzhou Shi, Hang Dong, Shiwei Sun, Xiaoqin Wu, Jiansong Fang, Jianbo Zhao, Junming Han, Zongyue Li, Huixiao Wu, Luna Liu, Wanhong Wu, Yang Tian, Guandou Yuan, Xiude Fan, Chao Xu
Clin Mol Hepatol 2024;30(1):80-97.
Published online December 7, 2023
DOI: https://doi.org/10.3350/cmh.2023.0343
Background/Aims
To evaluate the causal correlation between complement components and non-viral liver diseases and their potential use as druggable targets.
Methods
We conducted Mendelian randomization (MR) to assess the causal role of circulating complements in the risk of non-viral liver diseases. A complement-centric protein interaction network was constructed to explore biological functions and identify potential therapeutic options.
Results
In the MR analysis, genetically predicted levels of complement C1q C chain (C1QC) were positively associated with the risk of autoimmune hepatitis (odds ratio 1.125, 95% confidence interval 1.018–1.244), while complement factor H-related protein 5 (CFHR5) was positively associated with the risk of primary sclerosing cholangitis (PSC;1.193, 1.048– 1.357). On the other hand, CFHR1 (0.621, 0.497–0.776) and CFHR2 (0.824, 0.703–0.965) were inversely associated with the risk of alcohol-related cirrhosis. There were also significant inverse associations between C8 gamma chain (C8G) and PSC (0.832, 0.707–0.979), as well as the risk of metabolic dysfunction-associated steatotic liver disease (1.167, 1.036–1.314). Additionally, C1S (0.111, 0.018–0.672), C7 (1.631, 1.190–2.236), and CFHR2 (1.279, 1.059–1.546) were significantly associated with the risk of hepatocellular carcinoma. Proteins from the complement regulatory networks and various liver diseaserelated proteins share common biological processes. Furthermore, potential therapeutic drugs for various liver diseases were identified through drug repurposing based on the complement regulatory network.
Conclusions
Our study suggests that certain complement components, including C1S, C1QC, CFHR1, CFHR2, CFHR5, C7, and C8G, might play a role in non-viral liver diseases and could be potential targets for drug development.

Citations

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Reviews

Artificial intelligence, epidemiology, methodology, or others

A decade of liver organoids: Advances in disease modeling
Yue Liu, Jian-Ying Sheng, Chun-Fang Yang, Junjun Ding, Yun-Shen Chan
Clin Mol Hepatol 2023;29(3):643-669.
Published online March 6, 2023
DOI: https://doi.org/10.3350/cmh.2022.0428
Liver organoids are three-dimensional cellular tissue models in which cells interact to form unique structures in culture. During the past 10 years, liver organoids with various cellular compositions, structural features, and functional properties have been described. Methods to create these advanced human cell models range from simple tissue culture techniques to complex bioengineering approaches. Liver organoid culture platforms have been used in various research fields, from modeling liver diseases to regenerative therapy. This review discusses how liver organoids are used to model disease, including hereditary liver diseases, primary liver cancer, viral hepatitis, and nonalcoholic fatty liver disease. Specifically, we focus on studies that used either of two widely adopted approaches: differentiation from pluripotent stem cells or epithelial organoids cultured from patient tissues. These approaches have enabled the generation of advanced human liver models and, more importantly, the establishment of patient-tailored models for evaluating disease phenotypes and therapeutic responses at the individual level.

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Artificial intelligence, epidemiology, methodology, or others

Wnt signaling in liver regeneration, disease, and cancer
Gengyi Zou, Jae-Il Park
Clin Mol Hepatol 2023;29(1):33-50.
Published online July 4, 2022
DOI: https://doi.org/10.3350/cmh.2022.0058
The liver exhibits the highest recovery rate from acute injuries. However, in chronic liver disease, the long-term loss of hepatocytes often leads to adverse consequences such as fibrosis, cirrhosis, and liver cancer. The Wnt signaling plays a pivotal role in both liver regeneration and tumorigenesis. Therefore, manipulating the Wnt signaling has become an attractive approach to treating liver disease, including cancer. Nonetheless, given the crucial roles of Wnt signaling in physiological processes, blocking Wnt signaling can also cause several adverse effects. Recent studies have identified cancer-specific regulators of Wnt signaling, which would overcome the limitation of Wnt signaling target approaches. In this review, we discussed the role of Wnt signaling in liver regeneration, precancerous lesion, and liver cancer. Furthermore, we summarized the basic and clinical approaches of Wnt signaling blockade and proposed the therapeutic prospects of cancer-specific Wnt signaling blockade for liver cancer treatment.

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Alcohol-related liver disease

Subclinical versus advanced forms of alcohol-related liver disease: Need for early detection
Concepción Gómez-Medina, Luma Melo, David Martí-Aguado, Ramón Bataller
Clin Mol Hepatol 2023;29(1):1-15.
Published online April 15, 2022
DOI: https://doi.org/10.3350/cmh.2022.0017
Alcohol-related liver disease (ALD) consists of a wide spectrum of clinical manifestations and pathological features, ranging from asymptomatic patients to decompensated cirrhosis and hepatocellular carcinoma. Patients with heavy alcohol intake and advanced fibrosis often develop a subacute form of liver failure called alcohol-induced hepatitis (AH). Globally, most patients with ALD are identified at late stages of the disease, limiting therapeutic interventions. Thus, there is a need for early detection of ALD patients, which is lacking in most countries. The identification of alcohol misuse is hampered by the existence of alcohol underreporting by many patients. There are useful biomarkers that can detect recent alcohol use. Moreover, there are several non-invasive techniques to assess the presence of advanced fibrosis among patients with alcohol misuse, which could identify patients at high risk of liver related events or early death. In this review, we discuss differences between early stages of ALD and AH as the cornerstone of advanced forms. A global overview of epidemiological, anthropometric, clinical, analytical, histological, and molecular differences is summarized in this article. We propose that campaigns aimed at identifying patients with subclinical forms can prevent the development of life-threatening forms.

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Letter to the Editor

Autoimmune liver disease

The major diagnostic role of autoantibodies in the diagnosis of autoimmune hepatitis, a disease of all ages
Linda Beenet
Clin Mol Hepatol 2021;27(3):510-511.
Published online March 22, 2021
DOI: https://doi.org/10.3350/cmh.2021.0058

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  • Working Algorithms and Detection Methods of Autoantibodies in Autoimmune Liver Disease: A Nationwide Study
    Guillermo Muñoz-Sánchez, Albert Pérez-Isidro, Iñaki Ortiz de Landazuri, Antonio López-Gómez, Luz Yadira Bravo-Gallego, Milagros Garcia-Ormaechea, Maria Rosa Julià, Odette Viñas, Estíbaliz Ruiz-Ortiz
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Original Article

Steatotic liver disease

Loss-of-function HSD17B13 variants, non-alcoholic steatohepatitis and adverse liver outcomes: Results from a multi-ethnic Asian cohort
Yi-Wen Ting, Amanda Shen-Yee Kong, Shamsul Mohd Zain, Wah-Kheong Chan, Hwa-Li Tan, Zahurin Mohamed, Yuh-Fen Pung, Rosmawati Mohamed
Clin Mol Hepatol 2021;27(3):486-498.
Published online February 23, 2021
DOI: https://doi.org/10.3350/cmh.2020.0162
Background/Aims
17β-hydroxysteroid dehydrogenase 13 (HSD17B13) variants were recently reported to have significantly lower odds of non-alcoholic fatty liver disease (NAFLD). This is a two-part study that aimed to evaluate the association of HSD17B13 variants with NAFLD and its histological severity, and to identify the association of the variants with clinical outcomes in a cohort of biopsy-proven NAFLD patients.
Methods
Consecutive biopsy-proven NAFLD patients and controls without fatty liver were recruited for this study between 2009 and 2014. Genotyping for HSD17B13 variants was performed using rhAmp assays. A total of 165 patients with NAFLD were monitored up until August 2019. Clinical outcomes were recorded.
Results
HSD17B13 rs72613567 TA allele and rs6834314 G allele were associated with lower odds of non-alcoholic steatohepatitis (NASH) in the overall cohort and among ethnic Chinese, but not among ethnic Malays or Indians (P<0.05). During a mean follow-up of 89 months, 32 patients (19.4%) experienced at least one clinical outcome (cardiovascular events, n=22; liver-related complications, n=6; extra-hepatic malignancy, n=5; and mortality, n=6). The rs72613567 homozygous TA allele and the rs6834314 homozygous G allele were independently associated with a lower incidence of liver-related complications (hazard ratio [HR], 0.004; 95% confidence interval [CI], 0.00–0.64; P=0.033 and HR, 0.01; 95% CI, 0.00–0.97; P=0.048, respectively) and were associated with lower grade of hepatocyte ballooning among the ethnic Chinese.
Conclusion
HSD17B13 rs72613567 and rs6834314 variants were inversely associated with NAFLD and NASH, and were associated with lower incidence of adverse liver outcomes in a cohort of multi-ethnic Asian patients with NAFLD.

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Special topic: Alcoholic liver diseases
The 14th International Symposium on Alcoholic Liver and Pancreatic Diseases and Cirrhosis (ISALPDC)

Alcohol-related liver disease

Liver-lung axes in alcohol-related liver disease
Gavin E. Arteel
Clin Mol Hepatol 2020;26(4):670-676.
Published online October 1, 2020
DOI: https://doi.org/10.3350/cmh.2020.0174
Alcohol-related liver disease (ALD) and alcohol-related susceptibility to acute lung injury are the leading causes of morbidity and mortality due to chronic alcohol abuse. Most commonly, alcohol-induced injury to both organs are evaluated independently, although they share many parallel mechanisms of injury. Moreover, recent studies indicate that there is a potential liver lung axis that may contribute to organ pathology. This mini-review explores established and potential mechanisms of organ-organ crosstalk in ALD and alcohol-related lung injury.

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Long non-coding RNAs in liver diseases: Focusing on nonalcoholic fatty liver disease, alcohol-related liver disease, and cholestatic liver disease
Sen Han, Ting Zhang, Praveen Kusumanchi, Nazmul Huda, Yanchao Jiang, Zhihong Yang, Suthat Liangpunsakul
Clin Mol Hepatol 2020;26(4):705-714.
Published online October 1, 2020
DOI: https://doi.org/10.3350/cmh.2020.0166
Long non-coding RNAs (lncRNAs), a class of transcribed RNA molecules with the lengths exceeding 200 nucleotides, are not translated into protein. They can modulate protein-coding genes by controlling transcriptional and posttranscriptional processes. The dysregulation of lncRNAs has been related to various pathological disorders. In this review, we summarized the current knowledge of lncRNAs and their implications in the pathogenesis of three common liver diseases: nonalcoholic fatty liver disease, alcohol-related liver disease, and cholestatic liver disease. Future studies to further define the role of lncRNAs and their mechanisms in various types of liver diseases should be explored. An improved understanding from these studies will provide us a useful perspective leading to mechanism-based intervention by targeting specific lncRNAs for the treatment of liver diseases.

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Original Article

COVID-19

Clinical outcomes of coronavirus disease 2019 in patients with pre-existing liver diseases: A multicenter study in South Korea
Yu Rim Lee, Min Kyu Kang, Jeong Eun Song, Hyun Jung Kim, Young Oh Kweon, Won Young Tak, Se Young Jang, Jung Gil Park, Changhyeong Lee, Jae Seok Hwang, Byoung Kuk Jang, Jeong Ill Suh, Woo Jin Chung, Byung Seok Kim, Soo Young Park
Clin Mol Hepatol 2020;26(4):562-576.
Published online October 1, 2020
DOI: https://doi.org/10.3350/cmh.2020.0126
Background/Aims
Although coronavirus disease 2019 (COVID-19) has spread rapidly worldwide, the implication of pre-existing liver disease on the outcome of COVID-19 remains unresolved.

Methods
A total of 1,005 patients who were admitted to five tertiary hospitals in South Korea with laboratory-confirmed COVID-19 were included in this study. Clinical outcomes in COVID-19 patients with coexisting liver disease as well as the predictors of disease severity and mortality of COVID-19 were assessed.

Results
Of the 47 patients (4.7%) who had liver-related comorbidities, 14 patients (1.4%) had liver cirrhosis. Liver cirrhosis was more common in COVID-19 patients with severe pneumonia than in those with non-severe pneumonia (4.5% vs. 0.9%, P=0.006). Compared to patients without liver cirrhosis, a higher proportion of patients with liver cirrhosis required oxygen therapy; were admitted to the intensive care unit; had septic shock, acute respiratory distress syndrome, or acute kidney injury; and died (P<0.05). The overall survival rate was significantly lower in patients with liver cirrhosis than in those without liver cirrhosis (log-rank test, P=0.003). Along with old age and diabetes, the presence of liver cirrhosis was found to be an independent predictor of severe disease (odds ratio, 4.52; 95% confidence interval [CI], 1.20–17.02;P=0.026) and death (hazard ratio, 2.86; 95% CI, 1.04–9.30; P=0.042) in COVID-19 patients.

Conclusions
This study suggests liver cirrhosis is a significant risk factor for COVID-19. Stronger personal protection and more intensive treatment for COVID-19 are recommended in these patients.

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Special topic: Alcoholic liver diseases
The 14th International Symposium on Alcoholic Liver and Pancreatic Diseases and Cirrhosis (ISALPDC)

Alcohol-related liver disease

Roles of the complement system in alcohol-induced liver disease
Yi Zhou, Guandou Yuan, Fudi Zhong, Songqing He
Clin Mol Hepatol 2020;26(4):677-685.
Published online October 1, 2020
DOI: https://doi.org/10.3350/cmh.2020.0094
Alcohol-induced liver disease (ALD) is a complex disorder, with a disease spectrum ranging from steatosis to steatohepatitis, cirrhosis, and hepatocellular carcinoma. Although the pathogenesis of ALD is incompletely understood and currently no effective drugs are available for ALD, several lines of evidence suggest that complement activation and oxidative stress play crucial roles in the pathogenesis of ALD. Complement activation can regulate the production of ROS and influence oxidative stress in ALD. Precise regulation of the complement system in ALD may be a rational and novel avenue to postpone and even reverse the progression of disease and simultaneously promote the repair of liver injury. In this mini-review, we briefly summarize the recent research progress, especially focusing on the role of complement and oxidative stress-induced transfer RNA-derived fragments, which might help us to better understand the pathogenesis of ALD and provide aid in the development of novel therapeutic strategies for ALD.

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Alcohol-related liver disease

Programmed cell death in alcohol-associated liver disease
Tatsunori Miyata, Laura E. Nagy
Clin Mol Hepatol 2020;26(4):618-625.
Published online September 21, 2020
DOI: https://doi.org/10.3350/cmh.2020.0142
Alcohol-associated liver disease (ALD), which ranges from mild disease to alcohol-associated hepatitis and cirrhosis, is the most prevalent type of chronic liver disease and a leading cause of morbidity and mortality worldwide. Accumulating evidence reveals that programmed cell death (PCD) plays a crucial role in progression of ALD involving crosstalk between hepatocytes and immune cells. Multiple pathways of PCD, including apoptosis, necroptosis, autophagy, pyroptosis and ferroptosis, are reported in ALD. Interestingly, PCD pathways are intimately linked and interdependent, making it difficult to therapeutically target a single pathway. This review clarifies the multiple types of PCD occurring in liver and focuses on crosstalk between hepatocytes and innate immune cells in ALD.

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Reviews

Microbiome

Fecal microbiota transplantation in alcohol related liver diseases
Saggere Muralikrishna Shasthry
Clin Mol Hepatol 2020;26(3):294-301.
Published online June 23, 2020
DOI: https://doi.org/10.3350/cmh.2020.0057
The current standard of care for severe alcoholic hepatitis (SAH) has several limitations in that only up to one-third of patients are eligible for steroid therapy. Additionally, steroids have their own issues: a portion of patients do not respond, while there is doubtful long-term benefit in those who do and a large proportion are ineligible to receive steroids entirely and hence have no definitive options for treatment. As such, there is a large gap between the problem and the available solutions. Alcohol causes dysbiosis and also disrupts gut barrier function, consequently promoting the translocation of microbial lipopolysaccharide into the portal circulation and liver. Therefore, probiotics, prebiotics, antibiotics, or transplantation of gut microbiota are likely to attenuate the dysbiosis-related liver insult. Fecal microbiota transplantation (FMT) is expected to have a role in managing alcoholic liver disease in general and SAH in particular by correcting dysbiosis, the primary insult. Results from mouse studies have suggested beyond doubt that alcohol-related liver injury is transferrable and also treatable by adopting FMT from suitable donors. Initial human trials from our center have affirmed benefits in human subjects with SAH as well, with both improvements in disease severity and as well as the rate of survival. Further studies addressing the head-to-head comparison of steroids and FMT are ongoing. Available preliminary data are promising and FMT and/or gut microbial modulation might become the standard of care in the near future for managing alcohol-related liver diseases, especially alcoholic hepatitis, with greater applicability, improved acceptability, and minimal side effects.

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Liver fibrosis, cirrhosis, and portal hypertension

Hepatic venous pressure gradient: clinical use in chronic liver disease
Ki Tae Suk
Clin Mol Hepatol 2014;20(1):6-14.
Published online March 26, 2014
DOI: https://doi.org/10.3350/cmh.2014.20.1.6

Portal hypertension is a severe consequence of chronic liver diseases and is responsible for the main clinical complications of liver cirrhosis. Hepatic venous pressure gradient (HVPG) measurement is the best available method to evaluate the presence and severity of portal hypertension. Clinically significant portal hypertension is defined as an increase in HVPG to >10 mmHg. In this condition, the complications of portal hypertension might begin to appear. HVPG measurement is increasingly used in the clinical fields, and the HVPG is a robust surrogate marker in many clinical applications such as diagnosis, risk stratification, identification of patients with hepatocellular carcinoma who are candidates for liver resection, monitoring of the efficacy of medical treatment, and assessment of progression of portal hypertension. Patients who had a reduction in HVPG of ≥20% or to ≤12 mmHg in response to drug therapy are defined as responders. Responders have a markedly decreased risk of bleeding/rebleeding, ascites, and spontaneous bacterial peritonitis, which results in improved survival. This review provides clinical use of HVPG measurement in the field of liver disease.

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Original Articles
The usefulness of transient elastography to diagnose cirrhosis in patients with alcoholic Liver disease
Sang Gyune Kim, M.D., Young Seok Kim, M.D., Seung Won Jung, M.D., Hee Kyung Kim, M.D.1, Jae Young Jang, M.D., Jong Ho Moon, M.D., Hong Soo Kim, M.D., Joon Seong Lee, M.D., Moon Sung Lee, M.D., Chan Sup Shim, M.D., Boo Sung Kim, M.D.
Korean J Hepatol 2009;15(1):42-51.
Published online March 31, 2009
DOI: https://doi.org/10.3350/kjhep.2009.15.1.42
Backgrounds/Aims
It is not easy to differentiate between patients with cirrhosis and those with alcoholic liver disease. Liver biopsy is generally considered the gold standard for assessing hepatic fibrosis; however, this protocol frequently carries a risk of severe complications and false-negative results. Transient elastography (Fibroscan, Echosens, Paris, France), which is a noninvasive method of measuring liver stiffness, has become available for assessing liver fibrosis. Liver stiffness reportedly differs markedly with the cirrhosis etiology. The aim of this study was thus to determine the diagnostic accuracy of the Fibroscan in the detection of cirrhosis in patients with alcoholic liver disease. Methods: We enrolled 45 patients with alcoholic liver disease. Fibroscan, abdominal ultrasonography, aspartate aminotransferase/platelet ratio index (APRI), and liver biopsy were performed on all patients. Fibrosis stage was assessed using the Batts-Ludwig scoring system. Results: The stage of fibrosis (F1-F4) was distributed among the cohort as follows: 5 patients at F1, 4 patients at F2, 7 patients at F3, and 29 patients at F4. Liver stiffness differed significantly between each fibrosis stage (P<0.001). For the diagnosis of cirrhosis, the area under the receiver operating characteristic curve was 0.97 for transient elastography (95% confidence interval, CI, 0.93-1.01), 0.81 for ultrasonography (95% CI, 0.68-0.94), and 0.83 for APRI score (95% CI, 0.70-0.95). The optimal cut-off value of liver stiffness for detecting cirrhosis was 25.8 kPa, with a sensitivity of 90% and a specificity of 87%. Conclusions: Transient elastography is a useful method for diagnosing cirrhosis in patients with alcoholic liver disease. (Korean J Hepatol 2008;15:42-51)

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Background/Aims
Most liver diseases lead to a pathobiochemical reaction termed liver fibrosis. Hepatic fibrosis is not a uniform phenomenon and it comprises increased deposition of the liver connective tissue components(collagen, noncollagenous glycoprotein, proteoglycan) in the intercellular space, leading to disturbances of intrahepatic blood flow and hindrance of exchange processes between blood and cells, Fibrosis can be determined by morphological examination o f the liver, but this approach cannot be used to assess accurately the activity of collagen synthesis at any given point in time, Thus, the development of biochemical markers of hepatic fihrosis might allow a promising diagnostic approach for the identification and quantitation of this process, Aminoterminal procollagen III pn)peptide(PIIINP) and carboxytermina1 procollagen I propeptide(PICP) are known as the most widely used parameter for evaluating liver fibrosis, but it is diAicult to find previous report discribing the correlation ot each other. To elucidate the clinical significance of the corretation of PICP(x) and PIIINP(y) concentrations in patients with chronic liver diseases, radioimmunoassay was employed in this investigation. Methods:Sera tested were obtained from pathologically proven 43 patients;4 cases of fatly liver, 11 cases of chronic persistent hepatitis, 13 cases of chronic active hepatitis, l5 cases of liver cirrhosis. All the patients except 4 cases ot fatty liver were shown positivity of HBsAg. PICP and PIIlNP radioimmunoassay kits(Farrnos Diagnostica, Oulunsalo, Finland) wcre purchased for this study. Results:In the patients among the three groups of chronic active hepatitis, liver cirrhosis, chmnic persistent hepatitis, the correlations were significant in orders(y= - 10.27 +0.l3938x, r=0.92286, p=0.000007;y=-1.185+0.06611x, r=0.73656, p=0.001737;y=1.1174+0.03273x, r=0.56879, p=0.067849). Four cases of fatty liver reveal no signiticant correlation(y=4,8671- 0,0079x, r= 0.1959, p=0.804054). Conclusion:0n the basis of these data, we s st that the correlation of each showed a significant increase with heightening degree of inflammation, activity of diseases and fibrosis.
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Evaluation of Angiogenin Concentrations using ELISA in Sera from the Patients with Chronic Liver Diseases.
Kee Woon Kweon, Soong Hwan Lee, Seong Hee Lee, Hong Ju Kim, Chang Hwa Lee, Byoung Hun Kim, In Kyu Paik, Dong Il Park, Sung Soo Park, Dong Hoo Lee
Korean J Hepatol 1996;2(1):29-36.
Backgroud:Liver fibrosis by the progression of the chronic processes of the liver diseases induces deforrned microcirculations of the hepatic lobules. And this eventually resolted in portal hypertension. On the other hands, angiogenic stimu4nt factors are physiologically activated in order to repair the tissue damage. Overexpression of angiogenic factors, however, can stimulate neovascularization as in a fonnation of the tumor that liberates uncontrolled overgrowing of the tumor cells. Methods: To elucidate the dynamic changes of the serum concentration of angiogenin in chronic liver diseases, this study is intended to employ an ELISA in 44 pathologically proven patients. Quantikiae human angiogenin kit (R & D,systems Inc. Mmneapolis, MN) was used for this investigation. Results:Mean value and standard error of angiogenin concentration (ng/ml) of the sera was 238.92+ 50.95 in 5 cases of chronic persistent hepatitis, 184.47+ 12.75 in 6 cases of chronic active hepatitis, 131.36+ 10.99 in 19 cases of liver cirrhosis, and 211.03+ 19.08 in 14 cases of hepatocellular carcinoma, respectively. Serum angiogenin level in the liver cirrhosis was significantly lower than in chronic persistent hepatitis(p=0.00336), and than in chronic active hepatitis(p=0.018673). Angiogenin concentration in hepatocellular carcinomas was significantly higher than the level of the liver cirrhosis investigated(p=0.00569). Conclusions:These data support that persistent inflammatory insults in the chronic hepatitis were compensated by the elevation of angiogenin but complete fibrosis as in liver cirrhosis showed the depressed level. And emerging of the hepatocellular carcinoma is accompanied by the elevated stimuli of angiogenin for the neovascularization.
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A Study on the Efficacy and Safety of Dipheny - dimethyl - dicarboxylate in Patients with Chronic Liver disease
Hyoung Sik kim , Soo Taek Lee , Dae Gon kim , Deuk Soo Ahn
Korean J Hepatol 1996;2(1):54-60.
Background/Aims
The spectrum of clinical features of chronic liver disease bas wide range from asymptomatic cases to hepatic failure, The natural course and long-term prognosis of chronic liver disease also varies greately, and this diversity makes it diflicult to predict the clinical course of individual patient. The two majar approaches to the treatment of chronic liver disease are 1) directed toward the eradication of the virus and 2)designed to modulate cellular and humeral immunity. Progress has been made in the development of antiviral chernotherapeutic agents for hepatitis. But as yet no safe and reliably effective treatment or combination of treatrnents is available. In tkis study, we performed trial of diphenyl-dimethyl-dicarboxylate to evaluate the therapeutic effect and safety of it. Methods: The ciinical trials of DDB(complex capsule of diphenyl dimethyl dicarboxylate 7.5mg and polysorbate 80 1,5mg and polyethylene glycol 6000 66mg) were carried out in 30 patients with chronic liver disease for 6 months. All patients had abnormal liver function test ouer a period of 6 months. Results:In selected groups mean serum aspartate aminotransferase and alanine aminotrans- ferase dropped from pretreatment level of' 115.9+ 74.1 IU/L and 201.6+ 173.0 1U/L to posttreatment level of46.6+ 21.6 UU/L and 28.7- 15.4IU/L, respectively(p<0.01). There was no significant hernatological and biochemical change after administration of DDB. Untoward side effects were easily controlled by discontinuing the drugs, Conclusions:Administration of DDB(for 6 months) appears to be effective for decrement of transaminase level and safe for the treatment of patients with chronic liver disease.
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The Detection of Hepatitis G Virus RNA by RT - PCR in Various Liver Diseases
Kwang Hyub Han , Won Choi , Young Nyun Park , Young Woong Hwang , Wang Sik Ryu , Eun Sin Park , Kwan Sik Lee , Chae Yoon Chon , Young Myoung Moon , Chan Il Park
Korean J Hepatol 1997;3(2):123-132.
Background/Aims
Recently, nucleotide sequences from a novel virus, termed hepatitis G virus (HGV), were identified in serum from a patient with cryptogenic hepatitis and suggested as agent of non A-E hepatitis. HGV has been isolated from patients with various liver diseases but clinical implications of this new agent remain largely unresolved. In Korea, the etiology of substantial fraction of hepatitis has remained undefined and there has been no report concerning HGV. Methods: To determine the infection rate of HGV, RT-PCR of 5 UTR of HGV was performed, and to understand the clinical implication of HGV, medical records of 115 patients with various liver diseases were reviewed. Of 115 patients, 63 were male and 52 were female. Their mean age was 44 years (19-74) and their mean AST and ALT were 121.3+278.7 IU/L and 172.2+253.3 IU/L, respectively. Of 115 patients, 58 (50.4%) had no specific cause of liver diseases, 37 (32.2%) were infected with hepatitis B and/or C virus and 20 (17.4%) had non-viral identifiable liver diseases. Results: 1. HGV RNA was detected in 15 (13.0%) patients of 115 patients. 2, Among the 15 HGV RNA positive cases, 7 were male and 8 were female. Their mean age was 48 years (19-72) and their mean AST and ALT were 71.9+45.2 IU/L, 97.4+66.8 IU/I respectively. 3. HGV RNA was detected in 8(13.8%) of 58 patients without obvious causes of their liver diseases and in 7 (18.9%) of 37 patients infected with HBV and/or HCV. However, HGV RNA was not detected fram 20 patients with non-viral liver diseases such as alcoholic liver diseases, autoimmune hepatitis, PBC, or fatty liver. 4. HGV RNA was detected in 5 (19.2%) of 26 patients with acute hep- atitis, in 6 (9.4%) of 64 patients with chronic hepatitis, in 1 (14.3%) of 7 patients with liver cirrhasis, and iB 3 (27.3%) Of 11 pafients with hepatocellular caIcinoma. 5. These was no slatistically significant difference in sex, age, history of transfusion, serum ALT level, etiologies and status of liver diseases between HGV RNA positve and negative group. Conclusions: the prevalence of HGV infection is quite high among the patients who have no specific cause of acute or chronic liver diseases and HGV can be coinfected with HBV and/ar HCV infection in Korea.
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Distinct Expressions of TGF - α among Chronic Hepatitis , Liver Cirrhosis , and Hepatocellular Carcinoma
Byeong Moo Yoo , Sung Soo Park , Dong Hoo Lee , Jung Dal Lee
Korean J Hepatol 1997;3(4):316-328.
Background
/Aim: Transforming growth factor-a(TGF-a) is a polypeptide cytokine related to cell proliferation and transformation. TGF- a binds to EGF receptor and stimulating DNA synthesis in liver cell. The hepatitis B virus (HBV) by itself is also believed to play a role in the hepatic carcinogenesis. Recently, it was reported that TGF- a and HBV were synergistic in action with rapid appearance of hepatocelluar carcinoma in bitransgenic mice. Although TGF- a is thought to play an important role in hepatocarcinogenesis, its expression during the natural history of HBV hepatitis was poorly understood. This investigation was performed to elucidate the dynamic changes and distinct immunohistochemical staining patterns in the course of chronic HBV hepatitis with specific reference to hepatocelluar carcinoma and to explain the role of TGF- a in the pathogenesis of hepatocelluar carcinoma. Materials/Methods: Employing TGF- a monoclonal antibody, signal detection was carried out by peroxidase-conjugated streptavidin in deparaffinized liver tissue sections taken from HBsAg positive patients. All of the liver tissue sections were proven HBV DNA positive by in situ hybridization. Immunohistochemical staining was performed in the tissue sections obtained from four normal controls, six from patients with chronic persistent hepatitis, five with chronic active hepatitis, eight with liver cirrhosis and eleven with hepatocellular carcinoma. Results: The patterns of TGF- a immunoreactivity were cytoplasmic-grain types in normal controls and chronic persistent hepatitis, honeycomb types in chronic active hepatitis, occasional cytoplasmic-flooding types in liver cirrhosis, and cytoplasmic-grape types in hepatocellular carcinoma. A Shapiro-Wilk W test for frequency table analysis for the expression of TGF- a in these different disease groups was statistically significant. Conclusion: These data suggest that step-wise distinct expression of TGF-a enhancement in HBV associated chranic liver diseases which eventually resulted in the development of hepatocellular carcinoma were conceivably due to dysregulation of liver cell cycles by both HBV and TGF- a during the persistent repetition of cell cycles. (Korean J Hepatol 1997;7:316 328)
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Validation of the Korean Version of Liver Disease Quality of Life (LDQOL 1.0) Instrument
Sehyun Kim, Ph.D.1, Ki Hyun Choi, M.D.2, Seong Gyu Hwang, M.D.2, Ji Hyun Lee, M.D.2, Sun Young Kwak, M.D.2, Pil Won Park, M.D.2, Yukyung Kim, M.D.2, Hye Ja Park, Ph.D.3, Soon Joo Kim, M.A.4, Kyu Sung Rim2, M.D.
Korean J Hepatol 2007;13(1):44-50.
Background/Aims
Assessment of Health-related quality of life (HRQOL) outcomes in treatment of chronic disease is increasingly important. The objective of this study was to validate a Korean translation of the Liver Disease Quality of Life instrument (LDQOL version 1.0) for use in patients with chronic liver disease. Methods: Two native Korean speakers with fluent English translated LDQOL including instructions, items, and response choices. This Korean translation of the LDQOL was administered to 121 patients with chronic liver disease. Cronbach's alpha coefficients were applied to test an internal consistency reliability of disease-specific scales of the LDQOL. MELD and modified CTP scores were calculated for all patients. Associations of MELD and modified CTP scores with severity of liver disease were analyzed with LDQOL. Results: Internal consistency reliability was good (Cronbach's Alpha=0.69-0.94) in liver disease specific scales, except for the quality of social interaction scale (Cronbach's Alpha= 0.56). Mean modified CTP score and MELD score were 6.2±1.9 and 9.3±5.3, respectively. Both MELD score and modified CTP score showed correlations with most of the scores of liver disease specific scales of LDQOL 1.0, except for the quality of social interaction and sleep scale.
Conclusions
The Korean version of the liver disease specific scales of the LDQOL 1.0 is validated and useful for measuring HRQOL in Korean patients with chronic liver disease. (Korean J Hepatol 2007;13: 44-50)
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