Journal of Hepatology最新文献

{"title":"Upadacitinib for refractory Primary Biliary Cholangitis","authors":"Mirjam Kolev, Burkhard Möller, Annalisa Berzigotti, Nasser Semmo","doi":"10.1016/j.jhep.2025.03.004","DOIUrl":"https://doi.org/10.1016/j.jhep.2025.03.004","url":null,"abstract":"<h2>Section snippets</h2><section><section><h2>Financial support</h2>The authors received no specific funding for this work.</section></section><section><section><h2>Authors' contributions</h2>MK: acquisition of data, drafting the article; MK, BM, AB, NS: interpretation of data, revising article critically for important intellectual content, final approval of the submitted version.</section></section><section><section><h2>Declaration of Competing Interest</h2>The authors declare that they have no conflicts of interest.Please refer to the accompanying ICMJE disclosure forms for further details.</section></section>","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":"7 1","pages":""},"PeriodicalIF":25.7,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143599112","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":"Underrepresentation of Asians in diagnostic test development and drug trials in MASLD","authors":"Lung-Yi Mak, Terry Cheuk-Fung Yip, Chi-Ho Lee, Jimmy Che-To Lai, Vincent Wai-Sun Wong","doi":"10.1016/j.jhep.2025.03.005","DOIUrl":"https://doi.org/10.1016/j.jhep.2025.03.005","url":null,"abstract":"<h2>Section snippets</h2><section><section><h2>Authors' contributions</h2>Conceptualization: LYM and VWSW; Data curation: LYM, TCFY, CHL, JCTL and VWSW; Writing – original draft preparation: LYM. Writing – reviewing and editing: LYM, TCFY, CHL, JCTL and VWSW</section></section><section><section><h2>Data availability statement</h2>The authors confirm that the data supporting the findings of this study are available within the article.</section></section><section><section><h2>Financial support</h2>None</section></section><section><section><h2>Declaration of Competing Interest</h2>Please refer to the accompanying ICMJE disclosure forms for further details.</section></section>","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":"14 1","pages":""},"PeriodicalIF":25.7,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143599113","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":"Reply: Revisiting the use of albumin in patients with cirrhosis – trial design matters","authors":"Marten A. Lantinga, Elliot B. Tapper, Joost P.H. Drenth","doi":"10.1016/j.jhep.2025.03.006","DOIUrl":"https://doi.org/10.1016/j.jhep.2025.03.006","url":null,"abstract":"<h2>Section snippets</h2><section><section><h2>Uncited reference</h2>8.</section></section><section><section><h2>Authors' contributions</h2>All authors contributed equally to the conception, design, and writing of the article.</section></section><section><section><h2>Financial support</h2>None.</section></section><section><section><h2>Declaration of Competing Interest</h2>The authors declare that they have no competing interests.Please refer to the accompanying ICMJE disclosure forms for further details.</section></section>","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":"32 1","pages":""},"PeriodicalIF":25.7,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143599614","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":"Sour neuronal signalling attenuates macrophage mediated liver injury","authors":"Xi Zhou, Zhibo Ma, Qi Cheng, Na Jiang, Junbo Li, Tianao Zhan, Naonao Yuan, Yanyu Chen, Lu Wang, Jingzeng Wang, Qingwen Li, Wenlong Jia, Bowen Xie, Yuanyuan Zhao, Bo Zhang, Bo Yang, Chen Dai, Lai Wei, Jing Liu, Zhishui Chen, Peixiang Lan","doi":"10.1016/j.jhep.2025.02.026","DOIUrl":"https://doi.org/10.1016/j.jhep.2025.02.026","url":null,"abstract":"<h3>Background</h3>Liver injury, a common pathophysiological basis of various liver diseases, is associated with inflammation. Hepatic nerves regulate inflammation. However, the specific signals that trigger inflammation and methods to treat inflammation by targeting nerves remain unknown.<h3>Methods</h3>First, we constructed an animal model to detect the effect of sour stimuli on liver ischemia and reperfusion injury (IRI) in mice. Next, we analyzed the altered gene expression of neurons during liver IRI by single-cell sequencing. In additional, we explored the mechanism of sour stimuli on liver IRI in mice. Finally, we designed clinical trials to explore the effect of sour stimuli on liver IRI during hepatectomy.<h3>Results</h3>In this study, single-cell sequencing data from the liver and celiac ganglion showed that TAFA2 was induced in neurones during liver IRI, whereas sour stimuli decreased TAFA2 production and liver injury. In vivo studies showed that TAFA2 ablation and specific knockdown in neurones reduce liver injury. Using FLAG-tagged TAFA2, we found that TAFA2 interacted with Chemokine C-C-Motif Receptor 2 (CCR2) and promoted macrophage activation, consistent with RNA sequencing data showing that TAFA2 induced the expression of inflammatory genes in wild-type macrophages, but not in CCR2 knockout macrophages. Moreover, patients exposed to sour stimuli exhibited less severe liver IRI during hepatectomy.<h3>Conclusions</h3>Our results reveal a neuroimmune interaction in which neurones derived TAFA2 recruit CCR2+ macrophages to the liver and trigger liver injury, which is at least partly reduced by sour stimuli nerve signalling, which is related to acid with low pH. Our findings provide new insights into the brain-liver axis and therapeutic perspectives for liver injury.<h3>Clinical trial number</h3>This clinical trial was registered with the Chinese Clinical Trial Registry (ChiCTR2400088096)<h3>Impact and implications</h3>● This study clarified that sour stimuli, which is related to acid (low pH value), is at least partly responsible for reducing human and mouse liver ischemia and reperfusion injury through nerves, and confirmed the important role of brain-liver axis in liver ischemia and reperfusion injury.● This study found that brain-liver axis to increase liver ischemia-reperfusion injury through the secretion of TAFA2 protein, and proved that TAFA2 protein mediated liver ischemia-reperfusion injury through the recruitment and activation of macrophages.● This study found that CCR2 is the receptor for TAFA2 protein, and TAFA2 and CCL2 produce a different transcriptional profile by RNA sequencing.","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":"11 1","pages":""},"PeriodicalIF":25.7,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143569473","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":"Hot and Cold Fibrosis: The Role of Serum Biomarkers to assess the Immune Mechanisms and ECM-Cell Interactions in Human Fibrosis","authors":"A. Zawadzki, D.J. Leeming, A.J. Sanyal, Q.M. Anstee, J.M. Schattenberg, S.L. Friedman, S.D. Schuppan, M.A. Karsdal","doi":"10.1016/j.jhep.2025.02.039","DOIUrl":"https://doi.org/10.1016/j.jhep.2025.02.039","url":null,"abstract":"Fibrosis is a pathological condition characterized by excessive accumulation of extracellular matrix (ECM) components, particularly collagens, leading to tissue scarring and organ dysfunction. In fibrosis, an imbalance between collagen synthesis (fibrogenesis) and degradation (fibrolysis) results in the deposition of fibrillar collagens disrupting the structural integrity of the ECM and, consequently, the tissue architecture. Fibrosis is associated with a wide range of chronic diseases, including liver cirrhosis, kidney fibrosis, pulmonary fibrosis, and autoimmune diseases. Recently, the concept of \"hot\" and \"cold\" fibrosis has emerged, referring to the immune status within fibrotic tissues and the nature of fibrogenic signaling. Hot fibrosis is characterized by active immune cell infiltration and inflammation, while cold fibrosis is associated with auto- and paracrine myofibroblast activation, immune cell exclusion and quiescence.This article aims to explore the relationship between hot and cold fibrosis, the role of various types of collagens and their biologically active fragments in modulating the immune system, and how serological ECM biomarkers can help the understanding of the disease-relevant interactions between immune and mesenchymal cells in fibrotic tissues. Additionally, we draw lessons from immuno-oncology research in solid tumors to shed light on potential strategies for fibrosis treatment and highlight the advantage of having a “hot fibrotic environment” to treat fibrosis by enhancing collagen degradation through modulation of the immune system.","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":"85 4 1","pages":""},"PeriodicalIF":25.7,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143569469","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":"Clinical and Pathophysiological Characteristics of Non-acute Decompensation of Cirrhosis","authors":"Nipun Verma, Parminder Kaur, Pratibha Garg, Vivek Ranjan, Samonee Ralmilay, Sahaj Rathi, Arka De, Madhumita Premkumar, Sunil Taneja, Akash Roy, Mahesh Goenka, Ajay Duseja, Rajiv Jalan","doi":"10.1016/j.jhep.2025.02.028","DOIUrl":"https://doi.org/10.1016/j.jhep.2025.02.028","url":null,"abstract":"<h3>Background &amp; Aims</h3>The heterogenous presentation patterns in decompensated cirrhosis confers variable outcomes. While acute decompensation (AD) is well-characterised with poorest prognosis, presentation as non-acute decompensation (NAD) remain unclear. This study aimed to characterize clinical and pathophysiological features of NAD in comparison with healthy (HC), compensated cirrhosis (CC) and AD and identify predictors of progression in NAD.<h3>Methods</h3>A prospective, two-center study enrolled patients across the cirrhosis spectrum from India between 2020-2023: CC (n=29), NAD (n=311), AD (n=201), and HC (n=10). Clinical and laboratory parameters, cytokine levels (IL-6, TNF, IL-10, MCP-1), and cell death markers (M30, M65, Gasdermin-D, Receptor-interacting-protein-kinase; RIPK3, Mixed lineage kinase domain-like; MLKL) were assessed at baseline. Patients were followed for 12 month-survival. The predictors of progression to AD and mortality were evaluated in NAD.<h3>Results</h3>Patients with NAD had a poorer survival (81.7%) compared to CC (100%), but superior to AD (31.2%) (p&lt;0.001). Despite no significant systemic inflammation, patients with NAD exhibited elevated levels of cell death markers, particularly Gasdermin-D and RIPK3, compared to healthy and patients with CC. Both inflammatory and cell death markers were most pronounced in AD. Over 12 months, the cumulative incidence of progression to AD among NAD was 55.1%, significantly reducing their survival (68.2% vs. 95.3%, p&lt;0.001). Predictors of such progression to AD included severe ascites, lower IGF-1, albumin, BMI, and higher bilirubin, CTP, MELD, Gasdermin-D, and RIPK3 levels.<h3>Conclusions</h3>NAD represents a clinically, prognostically and pathophysiologically distinct entity in cirrhosis. Patients with NAD express elevated cell death markers and remain at risk of progression to AD and mortality. Identifying such high-risk patients should prompt interventions to prevent progression. Modulation of cell death is a potentially disease-modifying target in cirrhosis.<h3>Impact and Implications</h3>This study highlights non-acute decompensation as a clinically, prognostically and pathophysiologically distinct subset of cirrhosis, underscoring the importance of understanding its progression dynamics. Identifying key predictors of acute decompensation, including ascites severity, low IGF-1 levels, and elevated cell death markers such as Gasdermin-D and RIPK3, potentially suggests new therapeutic avenues. These findings are crucial for hepatologists and researchers in risk stratifying patients and optimizing transplant candidacy. Interventions targeting necroptosis and pyroptosis pathways may improve outcomes, providing a significant shift towards precision medicine in cirrhosis care.","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":"17 1","pages":""},"PeriodicalIF":25.7,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143569477","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":"Recompensation of decompensated cirrhosis in hepatitis C patients after SVR: Prognostic implications","authors":"Yolanda Sánchez-Torrijos, Paula Fernández-Álvarez, Jose Miguel Rosales, Celia Pérez-Estrada, Paloma Alañón-Martínez, Manuel Rodríguez-Perálvarez, Carlota Jimeno, Pilar del Pino, Alberto García-García, Ángeles López-Garrido, Miren García-Cortés, Gema Romero, Manuel Romero-Gómez, Marta Casado, Isabel Carmona, Javier Ampuero","doi":"10.1016/j.jhep.2025.02.041","DOIUrl":"https://doi.org/10.1016/j.jhep.2025.02.041","url":null,"abstract":"<h3>Backgound&amp;Aims</h3>The Baveno VII consensus introduced the term “recompensated cirrhosis,” though few studies have examined its clinical relevance. We analyzed the rate and predictors of recompensation in hepatitis C (HCV) patients after sustained virological response (SVR) and evaluated its impact on mortality and hepatocellular carcinoma (HCC) compared to compensated and decompensated cirrhosis.<h3>Methods</h3>Multicenter observational study enrolling 916 HCV-related cirrhotic patients, with a minimum follow-up period of 12 months after SVR. Subjects were categorized into three mutually exclusive groups: compensated, decompensated, and recompensated group. Patients were followed until the occurrence of liver transplantation, death, or the last follow-up date, whichever came first.<h3>Results</h3>During the study (4.5±2.5 years), 12% (110/916) experienced a decompensating event, 7.7% (71/916) were diagnosed with HCC, and 14.9% (137/916) died. Among 23% (216/916) patients who were decompensated at baseline, 63.4% (137/216) achieved recompensation at 12 months. Child-Pugh score [OR 0.69 (95% CI 0.53-0.89); p=0.005] and the number of past decompensating events were associated with recompensation. The compensated cohort exhibited a lower mortality rate (4.2% (28/663)) than recompensated (36.5% (50/137)), and decompensated subjects (50% (30/60)) (p=0.0001). Along with age [CSHR 1.03 (95% CI 1.01-1.05); p=0.0009], albumin [CSHR 0.67 (95% CI 0.45-0.98); p=0.038], INR, [CSHR 1.88 (95% CI 1.14-3.10); p=0.014], bilirubin levels [CSHR 1.28 (95% CI 1.08-1.50);p=0.003], recompensated [CSHR 0.30 (95% CI 0.19-0.49); p=0.0001] and compensated states [CSHR 0.09 (95% CI 0.05-0.16); p=0.0001] were associated with mortality. By contrast, HCC occurrence was significantly lower in compensated (4.4% (29/662)) than recompensated (14.4% (19/132)), and decompensated patients (12.1% (7/58)) (p=0.0001).<h3>Conclusions</h3>Two-thirds of patients with decompensated cirrhosis achieved recompensation twelve months post-SVR, leading to improved survival compared to those without recompensation, though still lower than in compensated patients. However, HCC risk remained unchanged in the recompensated cohort.","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":"91 1","pages":""},"PeriodicalIF":25.7,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143560798","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":"Letter to the editor: Several questions about the study of hypothermic oxygenated machine perfusion","authors":"Hanwen Yang, Simeng Lei, Zhili JI","doi":"10.1016/j.jhep.2025.02.043","DOIUrl":"https://doi.org/10.1016/j.jhep.2025.02.043","url":null,"abstract":"<h2>Section snippets</h2><section><section><h2>Authors' contributions</h2>Hanwen Yang (Conceptualization, Methodology, Writing— original draft, Writing—review &amp; editing), Simeng Lei (Writing—review &amp; editing), Zhili JI (Conceptualization, Methodology, Writing—review &amp; editing, Funding support)</section></section><section><section><h2>Financial support</h2>National Natural Science Foundation of China (52373294)</section></section><section><section><h2>Declaration of Competing Interest</h2>All authors state that there are no conflict of interest.Please refer to the accompanying ICMJE disclosure forms for further details.</section></section>","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":"21 4 1","pages":""},"PeriodicalIF":25.7,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143560707","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":"EUS-guided portal pressure measurement: beware of thrombosis risk","authors":"Géraldine Dahlqvist, Pierre Deprez, Nicolas Lanthier","doi":"10.1016/j.jhep.2025.02.042","DOIUrl":"https://doi.org/10.1016/j.jhep.2025.02.042","url":null,"abstract":"<h2>Section snippets</h2><section><section><h2>Authors' contributions</h2>GD wrote the manuscript, NL et PD reviewed the manuscript</section></section><section><section><h2>Financial support</h2>There is no financial support regarding this work</section></section><section><section><h2>Declaration of Competing Interest</h2>The authors have no conflict of interest regarding this workPlease refer to the accompanying ICMJE disclosure forms for further details.</section></section>","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":"191 1","pages":""},"PeriodicalIF":25.7,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143560799","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":"Reply to \"Pharmacological inhibition of ATGL as therapeutic approach for MASH: Far beyond the lipase suppression role of ATGL inhibitors\"","authors":"Emmanuel Dauda Dixon, Thierry Claudel, Michael Trauner","doi":"10.1016/j.jhep.2025.02.022","DOIUrl":"https://doi.org/10.1016/j.jhep.2025.02.022","url":null,"abstract":"<h2>Section snippets</h2><section><section><h2>Acknowledgements</h2>EDD: initial drafting of the manuscript. TC: revision of the manuscript. MT: conception and revision and final approval of the manuscript. All the authors approved the final version of the letter.</section></section><section><section><h2>Authors' contributions</h2>Arial, normal, 12</section></section><section><section><h2>Financial support</h2>This work was supported by the Austrian Science Fund FWF (SFB F73 [F7301]), the County of Styria, and the City of Graz.</section></section><section><section><h2>Declaration of Competing Interest</h2>MT has received research grants from Albireo, Alnylam, Cymabay, Falk, Genentech, Gilead, Intercept, MSD, Takeda and Ultragenyx and travel grants from Abbvie, Falk, Gilead Intercept and Jannsen. He further has advised for Abbvie, Agomab, Albireo, Agomab, BiomX, Boehringer Ingelheim, Chemomab Falk Pharma GmbH, Genfit, Gilead, Hightide, Intercept, Ipsen, Janssen, MSD, Mirum, Novartis, Phenex, Pliant, Regulus, Siemens and Shire and has served as speaker for Albireo, BMS, Boehringer Ingelheim, Falk,</section></section>","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":"35 1","pages":""},"PeriodicalIF":25.7,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143545920","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}