Journal of Hepatology最新文献

{"title":"Register now for the EASL Liver Cancer Summit 2025, 20-22 February in Paris","authors":"","doi":"10.1016/s0168-8278(24)02673-4","DOIUrl":"https://doi.org/10.1016/s0168-8278(24)02673-4","url":null,"abstract":"No Abstract","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":"75 1","pages":""},"PeriodicalIF":25.7,"publicationDate":"2024-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142825546","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":"JHEP at a Glance January 2025","authors":"","doi":"10.1016/s0168-8278(24)02695-3","DOIUrl":"https://doi.org/10.1016/s0168-8278(24)02695-3","url":null,"abstract":"No Abstract","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":"36 1","pages":""},"PeriodicalIF":25.7,"publicationDate":"2024-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142825484","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":"LIVERSCREEN aims to establish a population-based screening programme for liver fibrosis utilising non-invasive markers","authors":"","doi":"10.1016/s0168-8278(24)02674-6","DOIUrl":"https://doi.org/10.1016/s0168-8278(24)02674-6","url":null,"abstract":"No Abstract","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":"14 1","pages":""},"PeriodicalIF":25.7,"publicationDate":"2024-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142825547","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":"From the Editor’s Desk...","authors":"Philip N. Newsome, Frank Tacke, Heiner Wedemeyer, Lorenza Rimassa, Annalisa Berzigotti, Tom H. Karlsen, Vlad Ratziu","doi":"10.1016/j.jhep.2024.10.033","DOIUrl":"https://doi.org/10.1016/j.jhep.2024.10.033","url":null,"abstract":"<h2>Section snippets</h2><section><section><section><h2>Targeting the liver clock improves fibrosis by restoration of TGF-β signalling</h2>The circadian clock (CC) regulates several functions in the liver and perturbations have been shown to be associated with liver disease. <span><span>Crouchet, Dachraoui and coworkers</span><svg aria-label=\"Opens in new window\" focusable=\"false\" height=\"20\" viewbox=\"0 0 8 8\"><path d=\"M1.12949 2.1072V1H7V6.85795H5.89111V2.90281L0.784057 8L0 7.21635L5.11902 2.1072H1.12949Z\"></path></svg></span> studied the functional role of CC as a driver and therapeutic target in liver fibrosis. The authors show that CC oscillators are present in both hepatocytes and stellate cells, with the hepatocyte CC influencing stellate cell gene expression. They also demonstrated that the <strong>CC oscillator modulates the expression of TGF-β</strong></section></section></section><section><section><section><h2>A new mouse model resembling cholangiocellular carcinoma development in chronic cholangiopathies</h2>Primary sclerosing cholangitis (PSC) is associated with a high risk of cholangiocarcinoma (CCA), which is difficult to diagnose and is associated with a high mortality rate. <span><span>Huang, Wei and coworkers</span><svg aria-label=\"Opens in new window\" focusable=\"false\" height=\"20\" viewbox=\"0 0 8 8\"><path d=\"M1.12949 2.1072V1H7V6.85795H5.89111V2.90281L0.784057 8L0 7.21635L5.11902 2.1072H1.12949Z\"></path></svg></span> aimed to develop a mouse model of PSC-associated CCA using <em>Mdr2</em><sup>-/-</sup> mice, which exhibit a PSC-like cholestatic injury pattern, and injected them with proto-oncogenes AKT and Yap to induce tumour formation. They found that <strong>hydrodynamic tail vein injection of these genes led to robust tumour growth,</strong></section></section></section><section><section><section><h2>Induction of steatosis in primary human hepatocytes recapitulates key pathophysiological aspects of MASLD</h2>Efficacy in animal models of metabolic dysfunction-associated steatotic liver disease (MASLD) often fails to translate into efficacy in humans, thereby requiring adjunctive systems to bridge this divide. In this issue, <span><span><strong>Kwon and coworkers</strong></span><svg aria-label=\"Opens in new window\" focusable=\"false\" height=\"20\" viewbox=\"0 0 8 8\"><path d=\"M1.12949 2.1072V1H7V6.85795H5.89111V2.90281L0.784057 8L0 7.21635L5.11902 2.1072H1.12949Z\"></path></svg></span> <strong>demonstrate the utility of a cryopreserved primary human hepatocyte model in testing putative therapies</strong>. Their model recapitulated aspects of human MASLD in response to incubation with free fatty acids, which were corrected by firsocostat. These data provide</section></section></section><section><section><section><h2>Long-term outcomes after HOPE in a real-world setting (HOPE-REAL study)</h2>Preservation by liver machine perfusion is increasingly being implemented in clinical practice and helps overcome organ shortages by increasing ut","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":"22 1","pages":""},"PeriodicalIF":25.7,"publicationDate":"2024-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142825482","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":"All-cause and cause-specific mortality in patients with chronic hepatitis B and concurrent steatotic liver disease","authors":"Shang-Chin Huang, Tung-Hung Su, Tai-Chung Tseng, Shih-Jer Hsu, Chun-Ming Hong, Ting-Yuan Lan, Chen-Hua Liu, Hung-Chih Yang, Chun-Jen Liu, Jia-Horng Kao","doi":"10.1016/j.jhep.2024.12.009","DOIUrl":"https://doi.org/10.1016/j.jhep.2024.12.009","url":null,"abstract":"<h3>Background &amp; Aims</h3>Steatotic liver disease (SLD) is prevalent among patients with chronic hepatitis B (CHB). However, the effects of metabolic dysfunction–associated SLD (MASLD) on the long-term survival of such patients remain unknown. Accordingly, this study investigated the mortality risks in patients with CHB and concurrent SLD.<h3>Methods</h3>Consecutive patients with CHB and concurrent SLD were retrospectively recruited at National Taiwan University Hospital. MASLD was defined by the presence of cardiometabolic risk factors (CMRF). The cumulative incidences of all-cause and cause-specific mortality were compared.<h3>Results</h3>A total of 8,718 patients with CHB and concurrent SLD were included from 2006 to 2021. At baseline, the MASLD group (n=6,562) was older and had a lower proportion of hepatitis B e antigen positivity and lower hepatitis B virus DNA levels compared with the non-MASLD group (n=2,156). After a median follow-up period of 9.1 years, the MASLD group exhibited a higher risk of all-cause mortality compared with the non-MASLD group (adjusted hazard ratio [aHR]: 1.79, 95% confidence interval [CI]: 1.24–2.58, <em>p</em>=0.002). Furthermore, cumulative CMRF dose-dependently elevated the risks of all-cause, liver-related, and cardiovascular mortality (all <em>p</em>&lt;0.05). During the follow-up period, new-onset diabetes mellitus, hypertension, and significant weight gain further increased the risks of all-cause and liver-related mortality (all <em>p</em>&lt;0.05). However, patients with SLD had a lower mortality risk than non-SLD patients after propensity score matching (HR: 0.62, 95% CI: 0.53 – 0.74, <em>p</em>&lt;0.001).<h3>Conclusions</h3>Among patients with CHB and SLD, metabolic burden dose-dependently increases the all-cause, liver-related, and cardiovascular mortality risks. Patients with SLD have a lower mortality risk than those without SLD. Identifying these metabolic dysfunctions is crucial for stratifying the level of risk in daily care.<h3>Impact and Implications</h3>Concurrent steatotic liver disease (SLD) is prevalent among patients with chronic hepatitis B (CHB); however, the effects of the associated cardiometabolic risk factors on all-cause and cause-specific mortality remain unknown. This study demonstrated that cumulative metabolic burden dose-dependently increased the risks of all-cause, liver-related, and cardiovascular mortality in patients with CHB and SLD. Moreover, new-onset diabetes mellitus, hypertension, and weight gain during the follow-up period further exacerbated these risks. However, patients with SLD had a lower risk of mortality than those without SLD. Thus, routine screening and monitoring of metabolic dysfunctions constitute a key element of daily care for patients with CHB.","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":"119 1","pages":""},"PeriodicalIF":25.7,"publicationDate":"2024-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142820732","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":"A new generation of non-invasive tests of liver fibrosis with improved accuracy in MASLD","authors":"Paul Calès, Clémence M. Canivet, Charlotte Costentin, Adrien Lannes, Frédéric Oberti, Isabelle Fouchard, Gilles Hunault, Victor de Lédinghen, Jérôme Boursier","doi":"10.1016/j.jhep.2024.11.049","DOIUrl":"https://doi.org/10.1016/j.jhep.2024.11.049","url":null,"abstract":"<h3>Background &amp; aims</h3>The accuracy of non-invasive tests (NITs) should be ≥80% (EASL recommendation). We aimed to compare the accuracies of the recommended NITs for advanced fibrosis in MASLD and improve NIT accuracy.<h3>Methods</h3>1051 MASLD patients were allocated to derivation (n=637) and validation (n=414) sets. The main outcome (Kleiner F3+F4) was primarily evaluated by accuracy. Conventional NITs were FIB-4, Fibrotest, FibroMeter, liver stiffness measurement (LSM by Fibroscan), Elasto-FibroMeter (FibroMeter-LSM combination), and ELF in 396 patients. We used machine-learning-optimized multitargeting to develop new NITs: FIB-9 (including 9 usual biomarkers), FIB-11 (adding 2 specialized blood markers) and FIB-12 (adding LSM).<h3>Results</h3>In the whole population, the accuracies of recommended NITs were insufficient, Fibrotest: 68.0%, FIB-4: 71.2%, FibroMeter: 75.1%, LSM: 75.9%, Elasto-FibroMeter: 78.6%. Therefore, new NITs (FIB-9, FIB-11, FIB-12) were developed in the derivation set. In the validation set, AUROCs were, FIB-4: 0.757, Fibrotest: 0.766, FibroMeter: 0.850, LSM: 0.852, FIB-9: 0.863, FIB-11: 0.880, Elasto-FibroMeter: 0.894, FIB-12: 0.912 (p&lt;0.001). The FIB-12 AUROC was superior to the ELF AUROC (0.906 vs 0.865, p=0.039). Accuracies were, FIB-4: 68.8%, Fibrotest: 68.6%, LSM: 75.4%, FibroMeter: 76.3%, FIB-9: 78.7%, Elasto-FibroMeter: 79.7%, FIB-11: 80.2%, FIB-12: 83.3% (p&lt;0.001 between all NITs). Scores were segmented by ≥90% sensitivity and specificity cut-offs or NIT match, which individualized subgroups with NIT accuracies ≥80%, e.g. for FIB-9: 85.8% in 68.1% of patients using two cut-offs and 83.2% in 71.7% of patients where FIB-9 agreed with FIB-4.<h3>Conclusions</h3>Recommended NITs had accuracies &lt;80% for advanced fibrosis in MASLD. Several NIT segmentations individualized subgroups with accuracies ≥80%. New NITs further improved accuracy. The simple FIB-9 (available via a free calculator) provided accuracy equaling or surpassing recommended NITs. FIB-12 outperformed other NITs.<h3>Impact and implications</h3>Currently recommended non-invasive tests (NITs) have insufficient accuracy (&lt;80%) for the diagnosis of advanced fibrosis in MASLD. Therefore, we developed three new NITs with new statistical techniques. Thus, FIB-9 (available via a free calculator), including nine usual blood markers, equaled the performance of patented NITs. FIB-11, adding two specialized blood markers, and FIB-12, adding liver stiffness, had accuracy &gt;80%. FIB-12, outperformed all other NITs. FIB-9 is suitable for screening and FIB-11 or FIB-12 for diagnosis.","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":"1 1","pages":""},"PeriodicalIF":25.7,"publicationDate":"2024-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142815924","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":"Gut bacterial membrane components as pathogenic signalling molecules in PSC-IBD","authors":"David C. Trampert","doi":"10.1016/j.jhep.2024.11.024","DOIUrl":"https://doi.org/10.1016/j.jhep.2024.11.024","url":null,"abstract":"<h2>Section snippets</h2><section><section><h2>Background and context</h2>Primary sclerosing cholangitis (PSC) is an immune-mediated sclerosing cholangiopathy characterized by stricturing of the biliary tree and a strong association with inflammatory bowel disease (IBD).¹ This is emphasized by the observations of a higher recurrence rate of PSC after liver transplantation in individuals with active IBD and a protective effect of colectomy on PSC progression. “Gut-liver axis” signalling includes microbiota-related molecules passing an impaired intestinal barrier with</section></section><section><section><h2>Objectives, methods, and findings</h2>The authors isolated OMVs from intestinal bacteria and studied the migratory capacity of OMVs to the liver and their hepatic inflammatory and fibrogenic effects. They used the <em>Mdr2</em>^<em>-/-</em> mouse model to resemble PSC and an additional model of PSC-IBD by crossing <em>Mdr2</em>^<em>-/-</em> and <em>Casp8</em>^{<em>ΔIEC</em>} mice.¹¹ Bacterial OMV transport was visualized <em>in vivo</em> in the <em>Rosa26.tdTomato</em> mouse model inoculated by oral gavage with <em>E. Coli</em>^<em>Cre</em> or <em>E. Coli</em>^<em>GFP</em>.¹² For the proof-of-concept experiment, OMVs isolated from <em>K. pneumoniae</em></section></section><section><section><h2>Significance of findings</h2>Dorner <em>et al.</em> elegantly show that in models for PSC-IBD, OMVs from PSC-associated bacterial strains, as opposed to the bacteria themselves, translocate to the liver. The OMVs elicit pathogenic effects in PSC-IBD, mainly through pro-inflammatory and pro-fibrotic hepatic and bile duct changes. Similarities in the phenotype between <em>Mdr2</em>^<em>-/-</em> mice injected with OMVs and <em>Casp8</em>^{<em>ΔIEC</em>}x<em>Mdr2</em>^<em>-/-</em> mice suggests that intestinal microbial and inflammatory signaling molecules both contribute to hepatobiliary</section></section><section><section><h2>Financial support</h2>The author did not receive any financial support to produce this manuscript.</section></section><section><section><h2>Conflict of interest</h2>The author declares no conflict of interest with regard to this work.Please refer to the accompanying ICMJE disclosure forms for further details.</section></section>","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":"40 1","pages":""},"PeriodicalIF":25.7,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142809537","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":"Impact of metabolism-disrupting chemicals and folic acid supplementation on liver injury and steatosis in mother-child pairs","authors":"Sandra India-Aldana, Vishal Midya, Larissa Betanzos-Robledo, Meizhen Yao, Cecilia Alcalá, Syam S. Andra, Manish Arora, Antonia M. Calafat, Jaime Chu, Andrea Deierlein, Guadalupe Estrada-Gutierrez, Ravikumar Jagani, Allan C. Just, Itai Kloog, Julio Landero, Youssef Oulhote, Ryan W. Walker, Shirisha Yelamanchili, Andrea A. Baccarelli, Robert O. Wright, Damaskini Valvi","doi":"10.1016/j.jhep.2024.11.050","DOIUrl":"https://doi.org/10.1016/j.jhep.2024.11.050","url":null,"abstract":"<h3>Background and Aims</h3>Scarce knowledge about the impact of metabolism-disrupting chemicals (MDCs) on steatotic liver disease limits opportunities for intervention. We evaluated pregnancy MDC-mixture associations with liver outcomes, and effect modification by folic acid (FA) supplementation in mother-child pairs.<h3>Methods</h3>We studied ∼200 mother-child pairs from the Mexican PROGRESS cohort, with measured 43 MDCs during pregnancy (estimated air pollutants, blood/urine metals or metalloids, urine high- and low-molecular-weight phthalate [HMWPs, LMWPs] and organophosphate-pesticide [OP] metabolites), and serum liver enzymes (ALT, AST) at ∼9 years post-parturition. Outcomes included elevated liver enzymes in children and established clinical scores for steatosis and fibrosis in mothers (i.e., AST:ALT, FLI, HSI, FIB-4). Bayesian Weighted Quantile Sum regression assessed MDC-mixture associations with liver outcomes. We further examined chemical-chemical interactions and effect modification by self-reported FA supplementation.<h3>Results</h3>In children, many MDC-mixtures were associated with liver injury. Per quartile HMWP-mixture increase, ALT increased by 10.1% (95%CI: 1.67%, 19.4%) and AST by 5.27% (95% CI: 0.80%, 10.1%). LMWP-mixtures and air pollutant-mixtures were associated with higher AST and ALT, respectively. Air pollutant and non-essential metal/element associations with liver enzymes were attenuated by maternal cobalt blood concentrations (<em>p</em>-interactions&lt;0.05). In mothers, only the LMWP-mixture was associated with odds for steatosis [OR=1.53 (95%CI: 1.01, 2.28) for HSI&gt;36, and OR=1.62 (95%CI: 1.05, 2.49) for AST:ALT&lt;1]. In mothers and children, most associations were attenuated (null) at FA supplementation≥600mcg/day (<em>p</em>-interactions&lt;0.05).<h3>Conclusions</h3>Pregnancy MDC exposures may increase risk for liver injury and steatosis, particularly in children. Adequate FA supplementation and maternal cobalt levels may attenuate these associations.<h3>Impact and Implications</h3>The effects of environmental chemical exposures on steatotic liver diseases are not well understood. In a parallel investigation of mothers and children, we found that pregnancy exposures to metabolism-disrupting chemicals may increase the risk for liver injury and steatosis, especially in the child, and that these associations could be attenuated by higher folic acid and/or cobalt levels. These findings can inform policies to decrease environmental chemical pollution and contribute to the design of clinical interventions addressing the MASLD epidemic.","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":"5 1","pages":""},"PeriodicalIF":25.7,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142809538","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":"Impaired whole blood thrombin generation is associated with procedure-related bleeding in acutely decompensated cirrhosis.","authors":"Alberto Zanetto, Elena Campello, Cristiana Bulato, Ruth Willems, Joke Konings, Mark Roest, Sabrina Gavasso, Giorgia Nuozzi, Serena Toffanin, Patrizia Burra, Francesco Paolo Russo, Marco Senzolo, Bas de Laat, Paolo Simioni","doi":"10.1016/j.jhep.2024.12.008","DOIUrl":"https://doi.org/10.1016/j.jhep.2024.12.008","url":null,"abstract":"<h3>Background &amp; Aims</h3>The clinical utility of thrombomodulin-modified thrombin generation (TM-TG) in cirrhosis is uncertain. We conducted a prospective study to evaluate the prognostic value of TM-TG in cirrhosis.<h3>Methods</h3>Patients were recruited during outpatient clinics (compensated and stable decompensated) or if admitted to our inpatient service (acutely decompensated, AD). We performed whole blood (WB) and platelet-poor plasma (PPP) TM-TG at recruitment. All patients were prospectively followed-up for bleeding/thrombosis, hepatic decompensation, and liver-related death.<h3>Results</h3>We included 231 patients: 80 compensated, 70 stable decompensated, and 81 AD. Median follow-up was 414 days (range: 77-668). Eleven patients, all AD, experienced procedure-related bleeding. Both WB-TG and PPP-TG were more altered in bleeding vs. non-bleeding individuals (lower endogenous thrombin potential [ETP] and peak-height). However, only WB-TG could identify - at individual-patient level - those experiencing major bleeding (all having pre-procedural ETP &lt;350 nmol/L*min). In AD, the area under the ROC curve of WB-TG ETP for bleeding was 0.854 (95%CI: 0.732-0.976), which was higher than that of PPP-TG ETP (0.676; 95%CI: 0.524-0.809). Neither WB-TG nor PPP-TG could predict development of thrombosis, mostly PVT (n=15). In compensated cirrhosis, WB-TG and PPP-TG were comparable between patients who experienced decompensation and those who did not. In decompensated cirrhosis, WB-TG and PPP-TG were more significantly altered in patients experiencing further decompensation/ACLF/liver-related death. A higher WB-TG ETP was linked to a lower risk of progression independently of MELD, Child-Pugh, and C-reactive protein (HR: 0.4, 95%CI: 95%: 0.21-0.79; p&lt;0.01).<h3>Conclusions</h3>In compensated cirrhosis, WB-TG and PPP-TG do not improve risk stratification. In decompensated cirrhosis, WB-TG may be a promising tool for estimating procedure-related bleeding risk.<h3>Trial registration number</h3>NA","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":"649 1","pages":""},"PeriodicalIF":25.7,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142804826","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":"CKM: A New Approach to Managing Metabolic Comorbidities in MASLD?","authors":"Tianyuan Yang, Tong Bu, Bingqing Yang, Yuanying Zhao, Qi Wang","doi":"10.1016/j.jhep.2024.12.014","DOIUrl":"https://doi.org/10.1016/j.jhep.2024.12.014","url":null,"abstract":"<h2>Section snippets</h2><section><section><h2>Uncited reference</h2>3.; 4.; 5.; 3.; 4.; 5..</section></section><section><section><h2>Authors' contributions</h2>TY and QW contributed to the concept of the letter. TY and TB wrote the first draft of the manuscript and performed the statistical analyses. All authors contributed to the methodology, critically revised the manuscript, and approved its final draft.</section></section><section><section><h2>Financial support</h2>This study was funded by the National Natural Science Foundation of China (82170591), and Natural Science Foundation of Beijing (7222097). All authors were involved in the decision to submit the article for publication.</section></section><section><section><h2>Declaration of Competing Interest</h2>The authors declare that they do not have any conflict of interest to disclose in terms of funding for this manuscript.Please refer to the accompanying ICMJE disclosure forms for further details.</section></section>","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":"1 1","pages":""},"PeriodicalIF":25.7,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142804828","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}