Journal of Hepatology最新文献

{"title":"Impact of pre-transplant immune checkpoint inhibitor use on post-transplant outcomes in HCC: A systematic review and individual patient data meta-analysis.","authors":"Mohammad Saeid Rezaee-Zavareh, Yee Hui Yeo, Tielong Wang, Zhiyong Guo, Parissa Tabrizian, Stephen C Ward, Fatma Barakat, Tarek I Hassanein, Shravan Dave, Veeral Ajmera, Sherrie Bhoori, Vincenzo Mazzaferro, David M H Chascsa, Margaret C Liu, Elizabeth S Aby, John R Lake, Miguel Sogbe, Bruno Sangro, Maen Abdelrahim, Abdullah Esmail, Andreas Schmiderer, Yasmina Chouik, Mark Rudolph, Davendra Sohal, Heloise Giudicelli, Manon Allaire, Mehmet Akce, Jessica Guadagno, Clara Y Tow, Hatef Massoumi, Paolo De Simone, Elise Kang, Robyn D Gartrell, Mercedes Martinez, Ricardo Paz-Fumagalli, Beau B Toskich, Nguyen H Tran, Gabriela Azevedo Solino, Dra Mariana Poltronieri Pacheco, Richard S Kalman, Vatche G Agopian, Neil Mehta, Neehar D Parikh, Amit G Singal, Ju Dong Yang","doi":"10.1016/j.jhep.2024.06.042","DOIUrl":"10.1016/j.jhep.2024.06.042","url":null,"abstract":"<p><strong>Background & aims: </strong>Treatment with immune checkpoint inhibitors (ICIs) for hepatocellular carcinoma (HCC) prior to liver transplantation (LT) has been reported; however, ICIs may elevate the risk of allograft rejection and impact other clinical outcomes. This study aims to summarize the impact of ICI use on post-LT outcomes.</p><p><strong>Methods: </strong>In this individual patient data meta-analysis, we searched databases to identify HCC cases treated with ICIs before LT, detailing allograft rejection, HCC recurrence, and overall survival. We performed Cox regression analysis to identify risk factors for allograft rejection.</p><p><strong>Results: </strong>Among 91 eligible patients, with a median (IQR) follow-up of 690.0 (654.5) days, there were 24 (26.4%) allograft rejections, 9 (9.9%) HCC recurrences, and 9 (9.9%) deaths. Age (adjusted hazard ratio [aHR] per 10 years 0.72, 95% CI 0.53-0.99, p = 0.044) and ICI washout time (aHR per 1 week 0.92, 95% CI 0.86-0.99, p = 0.022) were associated with allograft rejection. The median (IQR) washout period for patients with ≤20% probability of allograft rejection was 94 (196) days. Overall survival did not differ between cases with and without allograft rejection (log-rank test, p = 0.2). Individuals with HCC recurrence had fewer median (IQR) ICI cycles than those without recurrence (4.0 [1.8] vs. 8.0 [9.0]; p = 0.025). The proportion of patients within Milan post-ICI was lower for those with recurrence vs. without (16.7% vs. 65.3%, p = 0.032).</p><p><strong>Conclusion: </strong>Patients have acceptable post-LT outcomes after ICI therapy. Age and ICI washout length relate to the allograft rejection risk, and a 3-month washout may reduce it to that of patients without ICI exposure. Number of ICI cycles and tumor burden may affect recurrence risk. Large prospective studies are necessary to confirm these associations.</p><p><strong>Impact and implications: </strong>This systematic review and individual patient data meta-analysis of 91 patients with hepatocellular carcinoma and immune checkpoint inhibitor use prior to liver transplantation suggest acceptable overall post-transplant outcomes. Older age and longer immune checkpoint inhibitor washout period have a significant inverse association with the risk of allograft rejection. A 3-month washout may reduce it to that of patients without immune checkpoint inhibitor exposure. Additionally, a higher number of immune checkpoint inhibitor cycles and tumor burden within Milan criteria at the completion of immunotherapy may predict a decreased risk of hepatocellular carcinoma recurrence, but this observation requires further validation in larger prospective studies.</p>","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":" ","pages":"107-119"},"PeriodicalIF":26.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11655254/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141600226","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Implications of mycophenolate mofetil in a reproductive age patient cohort: Maternal fetal medicine point of view.","authors":"Fabrizio Zullo, Vincenzo Cardinale, Domenico Alvaro","doi":"10.1016/j.jhep.2024.06.010","DOIUrl":"10.1016/j.jhep.2024.06.010","url":null,"abstract":"","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":" ","pages":"e35-e36"},"PeriodicalIF":26.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141327578","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting the liver clock improves fibrosis by restoring TGF-β signaling.","authors":"Emilie Crouchet, Mayssa Dachraoui, Frank Jühling, Natascha Roehlen, Marine A Oudot, Sarah C Durand, Clara Ponsolles, Cloé Gadenne, Laura Meiss-Heydmann, Julien Moehlin, Romain Martin, Nicolas Brignon, Fabio Del Zompo, Yuji Teraoka, Hiroshi Aikata, Hiromi Abe-Chayama, Kazuaki Chayama, Antonio Saviano, Danijela Heide, Mihaela Onea, Lucas Geyer, Thibaut Wolf, Emanuele Felli, Patrick Pessaux, Mathias Heikenwälder, Pierre Chambon, Catherine Schuster, Joachim Lupberger, Atish Mukherji, Thomas F Baumert","doi":"10.1016/j.jhep.2024.07.034","DOIUrl":"10.1016/j.jhep.2024.07.034","url":null,"abstract":"<p><strong>Background & aims: </strong>Liver fibrosis is the major driver of hepatocellular carcinoma and liver disease-related death. Approved antifibrotic therapies are absent and compounds in development have limited efficacy. Increased TGF-β signaling drives collagen deposition by hepatic stellate cells (HSCs)/myofibroblasts. Here, we aimed to dissect the role of the circadian clock (CC) in controlling TGF-β signaling and liver fibrosis.</p><p><strong>Methods: </strong>Using CC-mutant mice, enriched HSCs and myofibroblasts obtained from healthy and fibrotic mice in different CC phases and loss-of-function studies in human hepatocytes and myofibroblasts, we investigated the relationship between CC and TGF-β signaling. We explored hepatocyte-myofibroblast communication through bioinformatic analyses of single-nuclei transcriptomes and performed validation in cell-based models. Using mouse models for MASH (metabolic dysfunction-associated steatohepatitis)-related fibrosis and spheroids from patients with liver disease, we performed proof-of-concept studies to validate pharmacological targetability and clinical translatability.</p><p><strong>Results: </strong>We discovered that the CC oscillator temporally gates TGF-β signaling and this regulation is broken in fibrosis. We demonstrate that HSCs and myofibroblasts contain a functional CC with rhythmic expression of numerous genes, including fibrogenic genes. Perturbation studies in hepatocytes and myofibroblasts revealed a reciprocal relationship between TGF-β activation and CC perturbation, which was confirmed in patient-derived ex vivo and in vivo models. Pharmacological modulation of CC-TGF-β signaling inhibited fibrosis in mouse models in vivo as well as in patient-derived liver spheroids.</p><p><strong>Conclusion: </strong>The CC regulates TGF-β signaling, and the breakdown of this control is associated with liver fibrosis in patients. Pharmacological proof-of-concept studies across different models have uncovered the CC as a novel therapeutic target for liver fibrosis - a growing unmet medical need.</p><p><strong>Impact and implications: </strong>Liver fibrosis due to metabolic diseases is a global health challenge. Many liver functions are rhythmic throughout the day, being controlled by the circadian clock (CC). Here we demonstrate that regulation of the CC is perturbed upon chronic liver injury and this perturbation contributes to fibrotic disease. By showing that a compound targeting the CC improves liver fibrosis in patient-derived models, this study provides a novel therapeutic candidate strategy to treat fibrosis in patients. Additional studies will be needed for clinical translation. Since the findings uncover a previously undiscovered profibrotic mechanism and therapeutic target, the study is of interest for scientists investigating liver disease, clinical hepatologists and drug developers.</p>","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":" ","pages":"120-133"},"PeriodicalIF":26.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142036031","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transposon-based oncogene integration in Abcb4(Mdr2)^-/- mice recapitulates high susceptibility to cholangiocarcinoma in primary sclerosing cholangitis.","authors":"Pinzhu Huang, Guangyan Wei, Jesse D Kirkpatrick, Yi Lin, Li Tan, Heansika Matta, Imad Nasser, Mingzhe Huang, Li Chen, Mathieu Petitjean, Disha Skelton-Badlani, Wen Gao, Kahini Vaid, Shuangshuang Zhao, Alicia Lugovskoy, Maram Alenzi, Xin Chen, Gregory J Gores, Yury V Popov","doi":"10.1016/j.jhep.2024.07.016","DOIUrl":"10.1016/j.jhep.2024.07.016","url":null,"abstract":"<p><strong>Background & aims: </strong>Cholangiocarcinoma (CCA) is a dreaded complication of primary sclerosing cholangitis (PSC) that is difficult to diagnose and associated with high mortality. A lack of animal models of CCA recapitulating the hepatic microenvironment of sclerosing cholangitis has hindered the development of novel treatments. Herein, we sought to develop a mouse model of PSC-associated CCA.</p><p><strong>Methods: </strong>Ten-week-old Mdr2^-/- mice with congenital PSC-like disease, and healthy wild-type littermates were subjected to either modified retrograde biliary instillation or hydrodynamic tail vein injection of a sleeping beauty transposon-transposase plasmid system with activated AKT (myr-AKT) and Yap (YapS127A) proto-oncogenes (SB AKT/YAP1). The role of TGFβ was interrogated via ALK5 inhibitor (SB-525334) administration. Tumor phenotype, burden and desmoplastic reaction were analyzed histologically and via RNA sequencing.</p><p><strong>Results: </strong>While SB AKT/YAP1 plasmids administered via retrograde biliary injection caused tumors in Mdr2^-/-, only 26.67% (4/15) of these tumors were CCA. Alternatively, hydrodynamic tail vein injection of SB AKT/YAP1 resulted in robust tumorigenesis in all fibrotic Mdr2^-/- mice with high CCA burden compared to healthy mice. Tumors phenotypically resembled human CCA, expressed multiple CCA (but not hepatocellular carcinoma) markers, and exhibited a profound desmoplastic reaction. RNA sequencing analysis revealed profound transcriptional changes in CCA evolving in a PSC-like context, with specific alterations in multiple immune pathways. Pharmacological TGFβ inhibition led to enhanced immune cell tumor infiltration, reduced tumor burden and suppressed desmoplastic collagen accumulation compared to placebo.</p><p><strong>Conclusion: </strong>We established a new high-fidelity cholangiocarcinoma model in mice, termed SB CCA.Mdr2^-/-, which recapitulates the increased susceptibility to CCA in the setting of biliary injury and fibrosis observed in PSC. Through transcriptomics and pharmacological studies, we show dysregulation of multiple immune pathways and TGFβ signaling as potential drivers of CCA in a PSC-like microenvironment.</p><p><strong>Impact and implications: </strong>Animal models for primary sclerosing cholangitis (PSC)-related cholangiocarcinoma (PSC-CCA) are lacking. Thus, we have developed and characterized a new mouse model of PSC-CCA, termed SB CCA.Mdr2^-/-, which features reliable tumor induction on a PSC-like background of biliary injury and fibrosis. Global gene expression alterations were identified and standardized tools, including automated whole slide image analysis methodology for tumor burden and feature analysis, were established to enable systematic research into PSC-CCA biology and formal preclinical drug testing.</p>","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":" ","pages":"84-96"},"PeriodicalIF":26.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11655257/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141875028","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inclusive healthcare in light of the new MASLD guidelines: Should people living with HIV be screened for liver fibrosis?","authors":"Giada Sebastiani, Felice Cinque, Antonio Cascio, Jürgen K Rockstroh, Giovanni Guaraldi","doi":"10.1016/j.jhep.2024.06.026","DOIUrl":"10.1016/j.jhep.2024.06.026","url":null,"abstract":"","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":" ","pages":"e18-e20"},"PeriodicalIF":26.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141457361","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The association between primary hypobetalipoproteinemia and hepatic diseases: Evidence from genetic studies.","authors":"Yifan Zhang, Jie Chen, Shengyuan Su","doi":"10.1016/j.jhep.2024.06.022","DOIUrl":"10.1016/j.jhep.2024.06.022","url":null,"abstract":"","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":" ","pages":"e48-e49"},"PeriodicalIF":26.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141457363","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Induction of steatosis in primary human hepatocytes recapitulates key pathophysiological aspects of metabolic dysfunction-associated steatotic liver disease.","authors":"Yun Kwon, Pascal Gottmann, Surui Wang, Joel Tissink, Karsten Motzler, Revathi Sekar, Wiebke Albrecht, Cristina Cadenas, Jan G Hengstler, Annette Schürmann, Anja Zeigerer","doi":"10.1016/j.jhep.2024.06.040","DOIUrl":"10.1016/j.jhep.2024.06.040","url":null,"abstract":"<p><strong>Background & aims: </strong>Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most common cause of chronic liver disease. Owing to limited available treatment options, novel pre-clinical models for target selection and drug validation are warranted. We have established and extensively characterized a primary human steatotic hepatocyte in vitro model system that could guide the development of treatment strategies for MASLD.</p><p><strong>Methods: </strong>Cryopreserved primary human hepatocytes from five donors varying in sex and ethnicity were cultured with free fatty acids in a 3D collagen sandwich for 7 days and the development of MASLD was followed by assessing classical hepatocellular functions. As proof of concept, the effects of the drug firsocostat (GS-0976) on in vitro MASLD phenotypes were evaluated.</p><p><strong>Results: </strong>Incubation with free fatty acids induced steatosis, insulin resistance, mitochondrial dysfunction, inflammation, and alterations in prominent human gene signatures similar to patients with MASLD, indicating the recapitulation of human MASLD in this system. The application of firsocostat rescued clinically observed fatty liver disease pathologies, highlighting the ability of the in vitro system to test the efficacy and potentially characterize the mode of action of drug candidates.</p><p><strong>Conclusions: </strong>Altogether, our human MASLD in vitro model system could guide the development and validation of novel targets and drugs for the treatment of MASLD.</p><p><strong>Impact and implications: </strong>Due to low drug efficacy and high toxicity, clinical treatment options for metabolic dysfunction-associated steatotic liver disease (MASLD) are currently limited. To facilitate earlier stop-go decisions in drug development, we have established a primary human steatotic hepatocyte in vitro model. As the model recapitulates clinically relevant MASLD characteristics at high phenotypic resolution, it can serve as a pre-screening platform and guide target identification and validation in MASLD therapy.</p>","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":" ","pages":"18-27"},"PeriodicalIF":26.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141558926","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of PNPLA3 risk variant with steatotic liver disease among lean people with HIV mono-infection.","authors":"Win Min Han, Tanakorn Apornpong, Natthaya Chuaypen, Pisit Tangkijvanich, Anchalee Avihingsanon","doi":"10.1016/j.jhep.2024.08.017","DOIUrl":"10.1016/j.jhep.2024.08.017","url":null,"abstract":"","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":" ","pages":"e32-e34"},"PeriodicalIF":26.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142108015","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of pemvidutide, a GLP-1/glucagon dual receptor agonist, on MASLD: A randomized, double-blind, placebo-controlled study.","authors":"Stephen A Harrison, Sarah K Browne, John J Suschak, Shaheen Tomah, Julio A Gutierrez, Jay Yang, M Scot Roberts, M Scott Harris","doi":"10.1016/j.jhep.2024.07.006","DOIUrl":"10.1016/j.jhep.2024.07.006","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background & aims: &lt;/strong&gt;This was a randomized, double-blind, placebo-controlled study to assess the effects of pemvidutide, a glucagon-like peptide-1 (GLP-1)/glucagon dual receptor agonist, on liver fat content (LFC) in individuals with metabolic dysfunction-associated steatotic liver disease (MASLD).&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;Patients with a BMI ≥28.0 kg/m&lt;sup&gt;2&lt;/sup&gt; and LFC ≥10% by magnetic resonance imaging-proton density fat fraction were randomized 1:1:1:1 to pemvidutide at 1.2 mg, 1.8 mg, or 2.4 mg, or placebo administered subcutaneously once weekly for 12 weeks. Participants were stratified according to a diagnosis of type 2 diabetes mellitus. The primary efficacy endpoint was relative reduction (%) from baseline in LFC after 12 weeks of treatment.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Ninety-four patients were randomized and dosed. Median baseline BMI and LFC across the study population were 36.2 kg/m&lt;sup&gt;2&lt;/sup&gt; and 20.6%; 29% of patients had type 2 diabetes mellitus. At week 12, relative reductions in LFC from baseline were 46.6% (95% CI -63.7 to -29.6), 68.5% (95% CI -84.4 to -52.5), and 57.1% (95% CI -76.1 to -38.1) for the pemvidutide 1.2 mg, 1.8 mg, and 2.4 mg groups, respectively, vs. 4.4% (95% CI -20.2 to 11.3) for the placebo group (p &lt;0.001 vs. placebo, all treatment groups), with 94.4% and 72.2% of patients achieving 30% and 50% reductions in LFC and 55.6% achieving normalization (≤5% LFC) at the 1.8 mg dose. Maximal responses for weight loss (-4.3%; p &lt;0.001), alanine aminotransferase (-13.8 IU/L; p = 0.029), and corrected cT1 (-75.9 ms; p = 0.002) were all observed at the 1.8 mg dose. Pemvidutide was well-tolerated at all doses with no severe or serious adverse events.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusions: &lt;/strong&gt;In patients with MASLD, weekly pemvidutide treatment yielded significant reductions in LFC, markers of hepatic inflammation, and body weight compared to placebo.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Impact and implications: &lt;/strong&gt;Metabolic dysfunction-associated steatotic liver disease, and its progressive form steatohepatitis, are strongly associated with overweight/obesity and it is believed that the excess liver fat associated with obesity is an important driver of these diseases. Glucagon-like peptide-1 receptor (GLP-1R) agonists elicit weight loss through centrally and peripherally mediated effects on appetite. Unlike GLP-1R agonists, glucagon receptor agonists act directly on the liver to stimulate fatty acid oxidation and inhibit lipogenesis, potentially providing a more potent mechanism for liver fat content reduction than weight loss alone. This study demonstrated the ability of once-weekly treatment with pemvidutide, a dual GLP-1R/glucagon receptor agonist, to significantly reduce liver fat content, hepatic inflammatory activity, and body weight, suggesting that pemvidutide may be an effective treatment for both metabolic dysfunction-associated steatohepatitis and obesity.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Clinical trial number: &lt;/strong&gt;N","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":" ","pages":"7-17"},"PeriodicalIF":26.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141603715","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Is liver fibrosis more advanced in MetALD than in MASLD?","authors":"Hideki Fujii, Yoshihiro Kamada, Akihiro Tokushige, Toshio Watanabe, Norifumi Kawada","doi":"10.1016/j.jhep.2024.07.028","DOIUrl":"10.1016/j.jhep.2024.07.028","url":null,"abstract":"","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":" ","pages":"e56-e57"},"PeriodicalIF":26.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141860033","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}