Journal of Hepatology最新文献

{"title":"From the Editor’s Desk...","authors":"","doi":"10.1016/j.jhep.2024.07.008","DOIUrl":"10.1016/j.jhep.2024.07.008","url":null,"abstract":"","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":null,"pages":null},"PeriodicalIF":26.8,"publicationDate":"2024-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142048171","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":"Porto-sinusoidal vascular liver disorder with portal hypertension: Natural History and Long-Term Outcome.","authors":"Marta Magaz, Heloïse Giudicelli-Lett, Juan G Abraldes, Oana Nicoară-Farcău, Fanny Turon, Neil Rajoriya, Ashish Goel, Karlien Raymenants, Sophie Hillaire, Luis Téllez, Laure Elkrief, Bogdan Procopet, Lara Orts, Filipe Nery, Akash Shukla, Hélène Larrue, Helena Degroote, Victoria Aguilera, Elba LLop, Laura Turco, Federica Indulti, Stefania Gioia, Giulia Tosetti, Niccolò Bitto, Chiara Becchetti, Edilmar Alvarado, Cristina Roig, Raquel Diaz, Michael Praktiknjo, Anna-Lena Konicek, Pol Olivas, José Ignacio Fortea, Helena Masnou, Ángela Puente, Alba Ardèvol, Carmen A Navascués, Marta Romero-Gutiérrez, Bernhard Scheiner, Georg Semmler, Mattias Mandorfer, Filipe Damião, Anna Baiges, Asunción Ojeda, Macarena Simón-Talero, Carlos González-Alayón, Alba Díaz, Ángeles García-Criado, Andrea De Gottardi, Manuel Hernández-Guerra, Joan Genescà, Nicolas Drilhon, Carlos Noronha Ferreira, Thomas Reiberger, Manuel Rodríguez, Rosa María Morillas, Javier Crespo, Jonel Trebicka, Rafael Bañares, Càndid Villanueva, Annalisa Berzigotti, Massimo Primignani, Vincenzo La Mura, Oliviero Riggio, Filippo Schepis, Xavier Verhelst, José Luis Calleja, Christophe Bureau, Agustín Albillos, Frederik Nevens, Virginia Hernández-Gea, Dhiraj Tripathi, Pierre-Emmanuel Rautou, Juan Carlos García-Pagán","doi":"10.1016/j.jhep.2024.07.035","DOIUrl":"https://doi.org/10.1016/j.jhep.2024.07.035","url":null,"abstract":"<p><strong>Background & aims: </strong>Current knowledge of the natural history of patients with porto-sinusoidal vascular disorder (PSVD) is derived from small studies. The aim of the present study was to determine natural history and prognostic factors using a large multicenter cohort of PSVD patients.</p><p><strong>Methods: </strong>Retrospective multicentric study of PSVD patients and signs of portal hypertension (PH) prospectively registered in 27 centers.</p><p><strong>Results: </strong>587 patients were included, median age of 47 years and 38% were women. Four-hundred and one patient had an associated condition, that was graded as severe in 157. Median follow-up was 68 months. At diagnosis, 64% of patients were asymptomatic while 36% had a PH-related complication: PH-related bleeding in 112 patients; ascites in 117 and hepatic encephalopathy in 11. In those not presenting with bleeding, the incidence of first bleeding was of 15% at 5 years, with a 5-year rebleeding rate of 18%. Five-year cumulative incidence of new or worsening ascites was of 18% and of developing PVT of 16%. Fifty (8.5%) patients received a liver transplantation and 109 (19%) died, including 55 non-liver related death. Transplant-free survival was 97%, and 83% at 1 and 5 years. Variables independently associated with transplant-free survival were age, ascites, serum bilirubin, albumin and creatinine levels at diagnosis and severe associated conditions. This allowed the creation of a Nomogram that accurately predicted prognosis.</p><p><strong>Conclusions: </strong>Prognosis of PSVD is strongly determined by the severity of the associated underlying conditions and parameters of liver and renal function.</p>","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":null,"pages":null},"PeriodicalIF":26.8,"publicationDate":"2024-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142055736","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":"Identifying the optimal measurement timing and hemodynamic targets of portal pressure gradient after TIPS in patients with cirrhosis and variceal bleeding: a prospective cohort study.","authors":"Yong Lv, Qiuhe Wang, Bohan Luo, Wei Bai, Menghao Li, Kai Li, Zhengyu Wang, Dongdong Xia, Wengang Guo, Xiaomei Li, Jie Yuan, Na Zhang, Xing Wang, Huahong Xie, Yanglin Pan, Yongzhan Nie, Zhanxin Yin, Daiming Fan, Guohong Han","doi":"10.1016/j.jhep.2024.08.007","DOIUrl":"https://doi.org/10.1016/j.jhep.2024.08.007","url":null,"abstract":"<p><strong>Background & aims: </strong>The optimal timing of measurement and hemodynamic targets of portacaval pressure gradient (PPG) after TIPS remains inconclusive. This study aimed to identify the ideal moment of hemodynamic measurements and the optimal target of PPG in patients undergoing covered TIPS for variceal bleeding.</p><p><strong>Methods: </strong>Between May 2018 and December 2021, 466 consecutive patients with recurrent variceal bleeding treated with covered TIPS were prospectively included. Post-TIPS PPG were measured immediately (immediate PPG), 24-72 hours (early PPG), and again 1 month (late PPG) after TIPS placement. The agreement among PPGs measured at different time points was assessed by intra-class correlation coefficient (ICC) and Bland-Altman method. The unadjusted and confounder-adjusted effects of PPGs on the clinical outcomes (portal hypertension complications [PHC], overt hepatic encephalopathy [OHE], further decompensation, and death) were assessed using Fine and Gray competing risk regression models.</p><p><strong>Results: </strong>The agreement between early PPG and late PPG (ICC: 0.34) was better than that between immediate PPG and late PPG (ICC: 0.23, p<0.001). Early PPG revealed an excellent predictive value for PHC risk (early PPG ≥ vs <12 mmHg: adjusted HR [95%CI]: 2.17 [1.33-3.55], p=0.002) as well as OHE (0.40 [0.17-0.91], p=0.030) while immediate PPG did not. Late PPG showed a predictive value for PHC risk but not OHE. By targeting the lowest risk of further decompensation, we identified an optimal hemodynamic target with early PPG ranging 11 to 14 mmHg that was associated with a decreased risk of OHE while effectively preventing PHC.</p><p><strong>Conclusions: </strong>PPG measured 24 to 72 hours after TIPS correlates with long term PPG and clinical outcomes, and hemodynamic target with a PPG 11-14 mmHg reduced encephalopathy but not compromised clinical efficacy.</p><p><strong>Impact and implications: </strong>The optimal timing of measurement and hemodynamic targets of portacaval pressure gradient (PPG) after transjugular intrahepatic portosystemic shunt (TIPS) remains inconclusive. Here we show that post-TIPS PPG measured at least 24 hours but not immediately after the procedure correlated with long-term PPG and clinical events, therefore should be used for decision making in order to improve clinical outcomes. Targeting post-TIPS PPG at 11-14 mmHg or 20%-50% relative reduction from pre-TIPS baseline that measured 24-72 hours after procedure reduced encephalopathy but not compromised clinical efficacy, therefore could be used to guide TIPS creation and revision in patients with cirrhosis and variceal bleeding undergoing covered TIPS.</p><p><strong>Clinical trial registration number: </strong>ClinicalTrials.gov, ID: NCT03590288.</p>","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":null,"pages":null},"PeriodicalIF":26.8,"publicationDate":"2024-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142055735","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":"Variation in intention-to-treat survival by MELD subtypes: all models created for end-stage liver disease are not equal.","authors":"Craig Rosenstengle, Marina Serper, Sumeet K Asrani, Therese Bittermann, Jinyu Du, Tsung-Wei Ma, David Goldberg, Pere Gines, Patrick S Kamath","doi":"10.1016/j.jhep.2024.08.006","DOIUrl":"https://doi.org/10.1016/j.jhep.2024.08.006","url":null,"abstract":"<p><strong>Background & aims: </strong>Kidney dysfunction is a major determinant of prognosis in patients with decompensated cirrhosis awaiting transplantation. We hypothesized that for identical MELD scores at listing, outcomes before and after liver transplantation may vary if the predominant driver of the MELD score is serum creatinine versus serum bilirubin or INR.</p><p><strong>Methods: </strong>We evaluated all adult patients registered for liver transplantation (LT) between 2016 - 2020 and excluded patients receiving MELD exceptions or undergoing dual organ transplantation. Using K-Means clustering analysis, we classified each patient as MELD-Br, MELD-INR or MELD-Cr depending on the dominant variable for their MELD score. The primary outcome was intent-to-treat survival, defined as survival within 1 year from listing with or without LT.</p><p><strong>Results: </strong>MELD scores of LT waitlist registrants clustered into 3 subtypes: MELD-Br (n=13,658), MELD-INR (n=13,809), and MELD-Cr (n=12,412). One-year ITT survival was 78% (MELD-Br), 75% (MELD-INR), and 65% (MELD-Cr), p<0.01. ITT survival was lower for each MELD subtype for females compared to males (e.g. MELD Cr 63% females vs 67% males, p<0.0001). MELD-Cr subtype had the highest MELD at listing (MELD Cr 23.4 vs MELD-Br 19.2 vs MELD INR 21.0) and the largest decline in MELD over 3 months (23% vs. 12% vs 21%). In adjusted analyses including MELD Na, MELD-Cr compared to the other subtypes was associated with higher WL mortality (HR 1.339, 95% CI 1.279-1.402) and lower LT rates (HR 0.688, 95% CI 0.664-0.713).</p><p><strong>Conclusions: </strong>For equivalent listing practices, registrants with MELD-Cr subtype have lower ITT survival. MELD subtype may serve as a more sophisticated variable for dynamic assessment of risk of mortality, to inform models for organ allocation.</p><p><strong>Impact and implications: </strong>The MELD score is an excellent predictor of waitlist mortality; however, our work highlights that the driver of a patient's score MELD score matters and particularly those driven by elevated creatinine have a lower 1-year ITT mortality. The 1-year ITT mortality is also lower for women compared to men within the Cr-dominant subtype. These results are important for physicians and patients undergoing LT evaluation as creatinine may serve as a marker of prognosis and even if the creatinine improves the prognosis remains poor, necessitating discussion about alternative pathways for transplant. Our work also highlights that the type of kidney injury matters, in that those AKI were more likely to die or remain on the waitlist compared to those with CKD within the creatinine dominant subtype.</p>","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":null,"pages":null},"PeriodicalIF":26.8,"publicationDate":"2024-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142055788","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":"ACMSD inhibition corrects fibrosis, inflammation, and DNA damage in MASLD/MASH.","authors":"Yasmine J Liu, Masaki Kimura, Xiaoxu Li, Jonathan Sulc, Qi Wang, Sandra Rodríguez-López, Angelique M L Scantlebery, Keno Strotjohann, Hector Gallart-Ayala, Archana Vijayakumar, Robert P Myers, Julijana Ivanisevic, Riekelt H Houtkooper, G Mani Subramanian, Takanori Takebe, Johan Auwerx","doi":"10.1016/j.jhep.2024.08.009","DOIUrl":"https://doi.org/10.1016/j.jhep.2024.08.009","url":null,"abstract":"<p><strong>Background & aims: </strong>Recent findings reveal the importance of tryptophan-initiated de novo nicotinamide adenine dinucleotide (NAD⁺) synthesis in the liver, a process previously considered secondary to biosynthesis from nicotinamide. The enzyme α-amino-β-carboxymuconate-ε-semialdehyde decarboxylase (ACMSD), primarily expressed in liver and kidney, acts as a modulator of de novo NAD⁺ synthesis. Boosting NAD⁺ levels has previously demonstrated remarkable metabolic benefits in mouse models. In this study, we aimed to investigate the therapeutic implications of ACMSD inhibition in the treatment of metabolic dysfunction-associated steatotic liver disease/steatohepatitis (MASLD/MASH).</p><p><strong>Methods: </strong>In vitro experiments were conducted in primary rodent hepatocytes, Huh7 human liver carcinoma cells and iPSC-derived human liver organoids (HLOs). C57BL/6J male mice were fed a western-style diet and housed at thermoneutrality to recapitulate key aspects of MASLD/MASH. Pharmacological ACMSD inhibition was given therapeutically, following disease onset. Steatohepatitis HLO models were used to assess the DNA damage responses by ACMSD inhibition in human contexts.</p><p><strong>Results: </strong>Inhibiting ACMSD with a novel specific pharmacological inhibitor promotes de novo NAD⁺ synthesis and reduces DNA damage ex vivo, in vivo, and in HLO models. In mouse models of MASLD/MASH, de novo NAD⁺ biosynthesis is suppressed, and transcriptomic DNA damage signatures correlate with disease severity; in humans, Mendelian randomization-based genetic analysis suggests a notable impact of genomic stress on liver disease susceptibility. Therapeutic inhibition of ACMSD in mice increases liver NAD⁺ and reverses MASLD/MASH, mitigating fibrosis, inflammation, and DNA damage, as were observed in HLO models of steatohepatitis.</p><p><strong>Conclusions: </strong>Our findings highlight the benefits of ACMSD inhibition to enhance hepatic NAD⁺ levels and enable genomic protection, underscoring its therapeutic potential in MASLD/MASH.</p><p><strong>Impact and implications: </strong>Enhancing NAD⁺ levels has shown remarkable health benefits in mouse models of MASLD/MASH, yet liver-specific NAD⁺ boosting strategies remain underexplored. Here, we present a novel pharmacological approach to enhance liver NAD⁺de novo synthesis by inhibiting ACMSD, an enzyme highly expressed in the liver. Inhibiting ACMSD increases NAD⁺ levels, enhances mitochondrial respiration, and maintains genomic stability in hepatocytes ex vivo and in vivo. These molecular benefits prevent disease progression in both mouse and human liver organoid models of steatohepatitis. Our preclinical study identifies ACMSD as a promising target for MASLD/MASH management and lays the groundwork for developing ACMSD inhibitors as a clinical treatment.</p>","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":null,"pages":null},"PeriodicalIF":26.8,"publicationDate":"2024-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142055734","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":"Thyroid hormone receptor-beta agonist HSK31679 alleviates MASLD by modulating gut microbial sphingolipids.","authors":"Yu-Hang Zhang, Ran Xie, Chen-Shu Dai, Hong-Wei Gao, Gan Zhou, Tian-Tian Qi, Wen-Yu Wang, Hua Wang, Yi-Min Cui","doi":"10.1016/j.jhep.2024.08.008","DOIUrl":"https://doi.org/10.1016/j.jhep.2024.08.008","url":null,"abstract":"<p><strong>Background & aims: </strong>As the first approved medication for metabolic dysfunction-associated steatohepatitis (MASH), thyroid hormone receptor-beta (THR-β) agonist MGL-3196 (Resmetirom) is highly spotlighted as the liver-directed, bioactive oral drug. However, it was also identified with remarkable heterogeneity of individual clinical efficacy and its interference with gut microbiota in host hepatoenteral circulation was still undocumented.</p><p><strong>Methods: </strong>We compared MASH attenuation by MGL-3196 and its derivative drug HSK31679 between germ-free (GF) and specific-pathogen free (SPF) mice to evaluate the role of gut microbiota. Then cross-omics analyses of microbial metagenome, metabolome and single-cell RNA-sequencing were applied into the randomized, double-blind, placebo-controlled multiple-ascending-dose (MAD) cohort of HSK31679 treatment (n = 40), to comprehensively investigate the altered gut microbiota metabolism and circulating immune signatures.</p><p><strong>Results: </strong>HSK31679 outperformed MGL-3196 in ameliorating MASH diet-induced steatohepatitis of SPF mice but not GF mice. In the MAD cohort of HSK31679, relative abundance of B. thetaiotaomicron was significantly enriched to impair glucosylceramide synthase (GCS)-catalyzed monoglucosylation of microbial Cer(d18:1/16:0) and Cer(d18:1/24:1). In stark contrast to the non-inferiority MASH resolution between MGL-3196 and HSK31679 for GF^BTΔGCS mice, HSK31679 manifested superior steatohepatitis alleviation than MGL-3196 for GF^BTWT mice, due to its steric hindrance with R123 and Y401 of gut microbial GCS. For participants with high fecal GCS activity, the administration of 160 mg HSK31679 induced a shift in peripheral compartments towards an immunosuppressive niche, characterized by decreased CD8α⁺ dendritic cells and MINCLE⁺ macrophages.</p><p><strong>Conclusions: </strong>This study provided novel insights into the indispensable gut microbiota for HSK31679 treatment, which revealed microbial GCS may serve as its prognostic biomarker of MASH treatment, as well as the new target for further strategies of microbiota-based MASH therapeutics.</p><p><strong>Impact and implications: </strong>Remarkable heterogeneity of individual clinical efficacy of THR-β agonists and their interferences with microbiome in host hepatoenteral circulation are poorly understood. In our current germ-free mice models and randomized, double-blind multiple-dose cohort study, we identified microbial GCS as the prognostic biomarker of HSK31679 treatment, as well as the new target for further strategies of microbiota-based MASLD therapeutics.</p>","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":null,"pages":null},"PeriodicalIF":26.8,"publicationDate":"2024-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142055737","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":"https://doi.org/10.1016/j.jhep.2024.07.034","url":null,"abstract":"<p><strong>Background & aims: </strong>Liver fibrosis is the major driver for hepatocellular carcinoma and liver disease related death. Approved anti-fibrotic therapies are absent and compounds in development have limited efficacy. Increased TGF-β signaling drives collagen deposition by hepatic stellate cells (HSC)/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 validation in cell-based models. Using mouse models for MASH 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 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 uncover the CC as a therapeutic candidate target for liver fibrosis - a rising global 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 the 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 uncovers 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":null,"pages":null},"PeriodicalIF":26.8,"publicationDate":"2024-08-20","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":"Addressing the impact of stigma in liver diseases: A call for proper language and responsibility allocation.","authors":"Juan Vaz, José Willemse, Peter Jepsen","doi":"10.1016/j.jhep.2024.08.004","DOIUrl":"10.1016/j.jhep.2024.08.004","url":null,"abstract":"","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":null,"pages":null},"PeriodicalIF":26.8,"publicationDate":"2024-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142036030","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":"In Memoriam: Professor Paul McMaster (1943 to 2024)","authors":"","doi":"10.1016/j.jhep.2024.06.025","DOIUrl":"10.1016/j.jhep.2024.06.025","url":null,"abstract":"","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":null,"pages":null},"PeriodicalIF":26.8,"publicationDate":"2024-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0168827824023316/pdfft?md5=a58880949d6d0ee330590b34f3923c5b&pid=1-s2.0-S0168827824023316-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142242267","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":"Changes of hepatic myeloid cells in chronic viral hepatitis and after cure and their clinical significance - Reply.","authors":"Ang Cui, Raymond T Chung, Nadia Alatrakchi","doi":"10.1016/j.jhep.2024.08.001","DOIUrl":"https://doi.org/10.1016/j.jhep.2024.08.001","url":null,"abstract":"","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":null,"pages":null},"PeriodicalIF":26.8,"publicationDate":"2024-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142017726","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}