{"title":"PSMA immunohistochemistry as a diagnostic biomarker of hepatocellular carcinoma","authors":"Killian Véron , Etienne Becht , Astrid Laurent-Bellue , Rémy Nicolle , Miguel Albuquerque , Samira Laouirem , Hélène Cazier , Clément Bailly , Mohamed Bouattour , Mickaël Lesurtel , Catherine Guettier , Rachida Lebtahi , Valérie Vilgrain , Valérie Paradis , Jérôme Cros , Aurélie Beaufrère","doi":"10.1016/j.jhepr.2025.101542","DOIUrl":"10.1016/j.jhepr.2025.101542","url":null,"abstract":"<div><h3>Background & Aims</h3><div>A combination of three immunohistological markers (Glypican 3, heat shock protein 70 [HSP70], and glutamine synthetase [GS]) is routinely used to differentiate hepatocellular carcinoma (HCC), but this panel’s sensitivity is suboptimal. Our aim was to assess the diagnostic value of prostate-specific membrane antigen (PSMA) expression for diagnosing HCC in a series of hepatocellular nodules and compare its performance with that of routinely used markers.</div></div><div><h3>Methods</h3><div>We included 320 hepatocellular nodules from 188 patients in a test cohort and 87 hepatocellular nodules from 48 patients in an external validation cohort distributed as follows: regenerative nodules (RN, n = 39+22), low-grade dysplastic nodules (LGDN, n = 38+16), high-grade dysplastic nodules (HGDN, n = 30+8), early HCC (≤2-cm nodules) (n = 107+24), HCC (n = 106+17), and corresponding non-tumour livers (NTL, n = 152+37). PSMA, HSP70, Glypican 3, and GS expression was assessed by immunohistochemistry on tissue microarrays. For each marker or combination of markers, sensitivity, specificity, and accuracy were calculated.</div></div><div><h3>Results</h3><div>In the test cohort, PSMA was expressed in 83% of HCC (n = 88/106), 77% of early HCC (n = 82/107), 27% of HGDN (n = 8/30), 21% of LGDN (n = 8/38), 18% of RN (n = 7/39), and 3% of NTL (n = 5/152). In the validation cohort, the sensitivity and specificity of PSMA for HCC diagnosis were 0.95 and 0.77, respectively, and its accuracy was 0.83. The sensitivity and the specificity of the Glypican 3–HSP70–GS (≥2 positive markers) combination for HCC diagnosis were 0.41 and 0.99, respectively, and its accuracy was 0.80. Adding PSMA to this combination increased the sensitivity and accuracy to 0.85 and 0.86, respectively.</div></div><div><h3>Conclusions</h3><div>PSMA alone has shown good performance in diagnosing HCC, outperforming the combination of the three routinely used markers. When sufficient material is available, adding Glypican 3, HSP70, and GS to PSMA could be recommended.</div></div><div><h3>Impact and implications</h3><div>Differentiating hepatocellular nodules, particularly high-grade dysplastic nodules and hepatocellular carcinoma (HCC), based on histologic criteria remains challenging. In this study, we assess the diagnostic value of a new immunohistochemical marker, prostate-specific membrane antigen (PSMA), for diagnosing HCC in two independent series of hepatocellular nodules and compare its performance with that of routinely used markers (Glypican 3, heat shock protein 70 [HSP70], and glutamine synthetase [GS]). PSMA alone has demonstrated good performance in diagnosing HCC, superior to the combination of the three routinely used markers, and could be useful in practice for differentiating difficult-to-classify hepatocellular nodules. When the material is sparse, using PSMA alone could be recommended, whereas when sufficient material is available, adding PSMA to ","PeriodicalId":14764,"journal":{"name":"JHEP Reports","volume":"7 11","pages":"Article 101542"},"PeriodicalIF":7.5,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145218822","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":"Relative exchangeable copper: A highly specific and sensitive biomarker for Wilson disease diagnosis","authors":"Nouzha Djebrani-Oussedik , Clément Desjardins , Mickaël Alexandre Obadia , Djamila Rahli , Corinne Collet , France Woimant , Joël Poupon , Dominique Debray , Aurélia Poujois","doi":"10.1016/j.jhepr.2025.101537","DOIUrl":"10.1016/j.jhepr.2025.101537","url":null,"abstract":"<div><h3>Background & Aims</h3><div>Wilson disease (WD) is an autosomal recessive disorder characterized by copper accumulation in various organs, primarily the liver and brain. Standard assessment of copper metabolism includes total serum copper, serum ceruloplasmin, and urinary copper excretion. Quantitative measurement of non-ceruloplasmin-bound copper, known as exchangeable copper (CuEXC), was developed in 2009. Subsequently in 2011, relative exchangeable copper (REC), defined as the ratio of CuEXC to total serum copper, was proposed as a diagnostic biomarker. This study aimed to validate the REC cut-off for the diagnosis of WD in a large cohort and to refine the reference ranges for CuEXC.</div></div><div><h3>Methods</h3><div>Data were collected from 778 individual<del>s</del> at the French National Reference Centre for WD from January 2009 to 2025. The cohort included 204 patients with WD, 359 healthy heterozygous carriers, and 215 controls. All participants underwent clinical evaluation, assessment of copper metabolism, including CuEXC and REC, and genetic testing for <em>ATP7B</em>. Receiver operating characteristic curve analysis was used to assess the diagnostic performance of REC and to determine the optimal cut-off for diagnosing WD.</div></div><div><h3>Results</h3><div>Patients with WD had significantly higher CuEXC and REC values compared with heterozygous carriers and controls. The optimal REC cut-off for diagnosing WD was identified as 14% with 95.6% sensitivity and 99.8% specificity. This cut-off was validated in both pediatric and adult subgroups with similar sensitivity and specificity. Reference ranges for CuEXC (0.50–1.38 μmol/L) and for REC (2.6–9.5%) were refined using control group data. Age-specific ranges were also determined.</div></div><div><h3>Conclusion</h3><div>This study supports the use of REC in clinical practice and confirms its central role in the diagnostic algorithm for WD, as recognized in the recently published EASL 2025 guidelines.</div></div><div><h3>Impact and implications</h3><div>The study established relative exchangeable copper (REC) as a robust diagnostic biomarker for Wilson disease (WD), demonstrating high sensitivity and specificity across age groups in a large cohort including 204 patients with WD. By refining the optimal REC cut-off, this research provides crucial insights for improving WD diagnostic accuracy and patient outcomes. These findings confirm the need to incorporate REC into routine clinical practice and WD management guidelines, potentially reducing the reliance on invasive liver biopsies to assess hepatic copper levels. Consequently, this advancement in diagnostic methodology could facilitate earlier detection and treatment, thereby preventing irreversible tissue damage and enhancing the quality of life for patients with WD.</div></div>","PeriodicalId":14764,"journal":{"name":"JHEP Reports","volume":"7 10","pages":"Article 101537"},"PeriodicalIF":7.5,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144988841","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}
JHEP ReportsPub Date : 2025-07-31DOI: 10.1016/j.jhepr.2025.101533
Kyungchul Song , Yu-Jin Kwon
{"title":"Reply to: “Rethinking risk indices in pediatric MASLD”","authors":"Kyungchul Song , Yu-Jin Kwon","doi":"10.1016/j.jhepr.2025.101533","DOIUrl":"10.1016/j.jhepr.2025.101533","url":null,"abstract":"","PeriodicalId":14764,"journal":{"name":"JHEP Reports","volume":"7 10","pages":"Article 101533"},"PeriodicalIF":7.5,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144913784","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}
JHEP ReportsPub Date : 2025-07-24DOI: 10.1016/j.jhepr.2025.101524
Jiwon Yang , Sun Young Yim , Kunhee Kim , Hye Won Lee , Jonggi Choi
{"title":"Incidence and risk factors of hepatocellular carcinoma in patients with autoimmune hepatitis in Asia","authors":"Jiwon Yang , Sun Young Yim , Kunhee Kim , Hye Won Lee , Jonggi Choi","doi":"10.1016/j.jhepr.2025.101524","DOIUrl":"10.1016/j.jhepr.2025.101524","url":null,"abstract":"<div><h3>Background & Aims</h3><div>A recent European multicenter study reported a low incidence of hepatocellular carcinoma (HCC) in autoimmune hepatitis (AIH), even after cirrhosis development. In this study, we evaluated the incidence and predictors of HCC in Asian patients with AIH.</div></div><div><h3>Methods</h3><div>We conducted a multicenter, retrospective study on adult patients diagnosed with AIH between January 2000 and October 2023 registered in the rare intractable disease registry of the Korean National Health Insurance Database. The primary outcome was HCC incidence by competing risk analysis, with death and liver transplantation (LT) considered as competing risk factors. The secondary outcome was LT-free survival. Therapeutic efficacy was also evaluated based on the International Autoimmune Hepatitis Group response criteria.</div></div><div><h3>Results</h3><div>We analyzed 838 patients with biopsy-proven AIH. The median age of patients was 57.7 years, and 709 (84.6%) patients were women. Cirrhosis was present upon diagnosis in 365 (43.6%) patients. During the median follow-up period of 4.6 years, 21 (2.5%) patients developed HCC, with an annual incidence of 4.29/1,000 person-years (PY). The annual incidence of LT-free mortality was 16.44/1,000 PYs. The risk factors for HCC included cirrhosis (subdistribution hazard ratio [HR] 6.55) and hepatic decompensation (subdistribution HR 2.89). Treatment status, diabetes, cirrhosis, hepatic decompensation, and variant syndrome (adjusted HR: 5.12, 2.00, 5.50, 3.05, and 2.01, respectively; all <em>p</em> <0.05) were significantly associated with poor LT-free survival. Insufficient responders had a higher incidence of HCC (4.45/1,000 PYs) and poorer LT-free survival (20.3/1,000 PYs) than complete biochemical responders.</div></div><div><h3>Conclusions</h3><div>The incidence of HCC in Asian patients with AIH was higher than that reported in a recent European study. The risk factors included cirrhosis and hepatic decompensation at diagnosis.</div></div><div><h3>Impact and implications</h3><div>Autoimmune hepatitis (AIH) is rare, and the annual incidence of hepatocellular carcinoma (HCC) in patients with AIH is lower than that of other liver diseases, varying according to age, sex, and ethnicity, leading to an ongoing debate regarding the necessity for regular HCC surveillance in patients with AIH. However, most studies have focused on Western patients, and few have investigated HCC incidence in Asian populations, where the incidence of HCC is higher. Our multicenter study revealed that HCC incidence was higher in Asian populations than in Western populations. Regardless, this incidence did not meet the threshold for cost-effective surveillance. Our findings underscore the need for a nuanced approach to screening, balancing the low incidence of HCC with the presence of significant risk factors in Asian patients with AIH.</div></div>","PeriodicalId":14764,"journal":{"name":"JHEP Reports","volume":"7 10","pages":"Article 101524"},"PeriodicalIF":7.5,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145096421","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}
JHEP ReportsPub Date : 2025-07-24DOI: 10.1016/j.jhepr.2025.101525
Tomohiro Tanaka , Jennifer C. Lai , David Axelrod , Daniel Sewell
{"title":"MELD 3.i: A Bayesian framework for updating the model for end-stage liver disease score","authors":"Tomohiro Tanaka , Jennifer C. Lai , David Axelrod , Daniel Sewell","doi":"10.1016/j.jhepr.2025.101525","DOIUrl":"10.1016/j.jhepr.2025.101525","url":null,"abstract":"<div><h3>Background & Aims</h3><div>The model for end-stage liver disease (MELD) score has been central to liver transplant (LT) allocation since 2002, with iterative updates culminating in MELD 3.0. However, given temporal changes and variations in liver disease epidemiology across allocation systems that utilize MELD, continuous refinements are essential to ensure its optimal performance across diverse patient populations and transplant frameworks.</div></div><div><h3>Methods</h3><div>This retrospective cohort study included all US adult LT candidates listed between July 13, 2023 to June 30, 2024. Candidates from the first two-thirds of listing dates formed the training set, while the last third comprised the validation set. We applied a Bayesian proportional hazards model, using MELD 3.0 as informative priors to generate posterior coefficient distributions. The resulting model, MELD 3.1, represents the first iteration within the MELD 3.i framework. Model performance was assessed using concordance (C-) statistics, and reclassification analyses evaluated patient redistribution and mortality risk across MELD tiers.</div></div><div><h3>Results</h3><div>The cohort included 13,764 candidates (41.1% female). MELD 3.1 assigned a higher coefficient for female sex and a lower coefficient for creatinine, and showed improved C-statistics for 90-day waitlist mortality in the validation set (0.7195 <em>vs.</em> 0.7152 for MELD 3.0, <em>p</em> = 0.036). MELD 3.1 led to a net 3.1% up-categorization of patients who died or dropped out while on the waitlist, with the net gain entirely accounted for by female candidates. MELD 3.1 also showed net gains across age groups and liver disease etiologies.</div></div><div><h3>Conclusion</h3><div>Our findings provide proof-of-concept for the MELD updating framework (MELD 3.i) as a sustainable and adaptive approach for periodically refining MELD using contemporary data and Bayesian methods. This iterative process enhances predictive accuracy, ensuring MELD remains responsive to evolving demographics and clinical practices in the US and other allocation systems.</div></div><div><h3>Impact and implications</h3><div>We present MELD 3.i, a Bayesian framework for ongoing refinement of the MELD score, with MELD 3.1 as its first iteration. The findings demonstrate improved predictive accuracy for 90-day waitlist mortality compared to the original MELD 3.0, particularly for women. These results are important for clinicians, transplant centers, and policymakers aiming to optimize organ allocation while addressing persistent sex disparities. By enabling adaptive refinements within an existing model structure, this approach has the potential to offer a practical method to align liver transplant prioritization with evolving patient demographics and varying practices across nations and regions.</div></div>","PeriodicalId":14764,"journal":{"name":"JHEP Reports","volume":"7 10","pages":"Article 101525"},"PeriodicalIF":7.5,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145155330","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}
JHEP ReportsPub Date : 2025-07-22DOI: 10.1016/j.jhepr.2025.101521
Jörn M. Schattenberg , Henning Grønbæk , Iris Kliers , Steen Ladelund , Michelle T. Long , Sune Boris Nygård , Arun J. Sanyal , Melanie J. Davies
{"title":"Proteomic signatures reflect effects of semaglutide treatment for MASH","authors":"Jörn M. Schattenberg , Henning Grønbæk , Iris Kliers , Steen Ladelund , Michelle T. Long , Sune Boris Nygård , Arun J. Sanyal , Melanie J. Davies","doi":"10.1016/j.jhepr.2025.101521","DOIUrl":"10.1016/j.jhepr.2025.101521","url":null,"abstract":"<div><h3>Background & Aims</h3><div>Proteomic technology has emerged as a non-invasive method for grading and staging metabolic dysfunction-associated steatohepatitis (MASH). The aims of this <em>post hoc</em> analysis of the STEP 1 and STEP 2 trials were to assess the distribution of SomaSignal-derived MASH components, evaluate the effect of semaglutide (2.4 mg and 1.0 mg) on these components, and test concordance with biopsy-based MASH histology from the phase IIb Sema-MASH trial.</div></div><div><h3>Methods</h3><div>Participants with overweight or obesity (STEP 1) and type 2 diabetes (STEP 2), who received once-weekly semaglutide or placebo for 68 weeks and had available biological samples, were included. In addition, participants with biopsy-confirmed MASH from the phase IIb Sema-MASH trial who received once-daily semaglutide or placebo for 72 weeks were included.</div></div><div><h3>Results</h3><div>SomaSignal-derived steatosis was prevalent in both STEP 1 (43.2%) and STEP 2 (71.7%). At week 68, participants who received semaglutide had significantly lower odds of exhibiting SomaSignal-defined MASH components compared with those on placebo. They were also more likely to have a less severe SomaSignal-derived stage of metabolic dysfunction-associated steatotic liver disease, with odds ratios for semaglutide 2.4 mg of 5.26 (95% CI 3.59–7.72) in STEP 1 and 4.90 (95% CI 2.86–8.40) in STEP 2; both <em>p</em> <0.0001. SomaSignal-derived MASH components correlated with histologic changes, standard liver-related biomarkers, and measures of glycemic control.</div></div><div><h3>Conclusions</h3><div>These findings suggest that SomaSignal MASH component testing may be useful for evaluating the potential therapeutic effects of semaglutide in patients with MASH and related comorbidities. However, prospective randomized clinical trials are necessary to confirm these results.</div></div><div><h3>Clinical trial registration numbers</h3><div>STEP 1: NCT03548935; STEP 2: NCT03552757; MASH phase IIb trial: NCT02970942.</div></div><div><h3>Impact and implications</h3><div>Liver biopsy is the current gold standard for the diagnosis of metabolic dysfunction-associated steatohepatitis (MASH); however, this procedure is invasive and time consuming for patients living with MASH. The use of non-invasive tests to diagnose MASH is becoming increasingly popular and many clinicians see this approach as the diagnostic future. SomaSignal is a proteomics-based model designed to non-invasively test for and validate MASH components as well as detect the prevalence of metabolic dysfunction-associated steatotic liver disease stages, against biopsy results. In the future, SomaSignal MASH components may have an impact on future clinical practice by providing clinicians with an alternative option for non-invasive assessment of treatment effects in the early clinical stages of therapeutic development.</div></div>","PeriodicalId":14764,"journal":{"name":"JHEP Reports","volume":"7 10","pages":"Article 101521"},"PeriodicalIF":7.5,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145019812","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":"GTX-11 improves portal hypertension, liver fibrosis, and sinusoidal cells phenotype in experimental MASH","authors":"María Andrés-Rozas , Zoe Boyer-Diaz , Eugènia Ruiz-Cánovas , Peio Aristu-Zabalza , Sergi Guixé-Muntet , Cristina Fernández-Asensio , Juan José Lozano , Noemí García-Delgado , Carla Fuster , Jaume Mercade , Jaime Bosch , Jordi Gracia-Sancho","doi":"10.1016/j.jhepr.2025.101497","DOIUrl":"10.1016/j.jhepr.2025.101497","url":null,"abstract":"<div><h3>Background & Aims</h3><div>Steatotic liver disease can lead to the development of metabolic dysfunction-associated steatohepatitis (MASH), the prevalence of which is rapidly increasing, intensifying the need to find an effective treatment. GTX-11 is a first-in-class drug with anti-inflammatory and antifibrotic properties mediated by the modulation of the transforming growth factor beta pathway. The present study evaluated the effects of GTX-11 on hepatic hemodynamics and liver fibrosis, as well as its underlying mechanisms, in a preclinical model of MASH, and in human precision-cut liver slices (hPCLS).</div></div><div><h3>Methods</h3><div>Male Wistar MASH rats received GTX-11 (1 and 10 mg/kg/day) or vehicle, for 14 days (n = 15/group). <em>In vivo</em> systemic and hepatic hemodynamics, fibrosis, biochemical parameters, and hepatic cells phenotype were analyzed. hPCLS were obtained from human hepatic resections and incubated with the active metabolite of GTX-11 (GTX-11m) (1 μM or 10 μM) or vehicle for 24 h. Gene expression changes were evaluated by RNA sequencing and gene deconvolution analysis was performed (n = 6/group).</div></div><div><h3>Results</h3><div>MASH rats receiving GTX-11 showed a significant dose-dependent reduction in portal pressure compared with the vehicle (-8.4% <em>p</em> = 0.05 and -11.7% <em>p</em> <0.01 for 1 and 10 mg/kg, respectively), associated with lower hepatic fibrosis at 10 mg/kg (-28%, <em>p</em> <0.01). At the cellular level, GTX-11-treated rats showed hepatic stellate cells (HSCs) deactivation and endothelial cells redifferentiation. Transcriptomic analysis from hPCLS revealed that GTX-11m promoted HSCs deactivation and inhibition of pro-fibrogenic pathways, as well as extracellular matrix remodeling. Gene deconvolution analysis confirmed the beneficial effects of GTX-11m on HSCs, promoting their deactivation and rebalance.</div></div><div><h3>Conclusions</h3><div>This study demonstrates for the first time the beneficial effects of GTX-11 on portal hypertension and liver fibrosis in MASH by means of HSCs deactivation and endothelial phenotype restoration. Validation in human liver tissues encourages its clinical evaluation as a possible new treatment for this disease.</div></div><div><h3>Impact and implications</h3><div>Metabolic dysfunction-associated steatohepatitis (MASH) affects >3–6% of the world’s population, and this number continues to increase. Despite its high prevalence, there is currently no specific, generally effective, and safe treatment for the disease. This study demonstrates, for the first time, the therapeutic potential of GTX-11 in treating fibrosis and portal hypertension associated with MASH by deactivating hepatic stellate cells and enhancing endothelial phenotype. These findings highlight GTX-11 as a promising candidate for future therapeutic strategies aimed at reversing liver fibrosis and improving patient outcomes in MASH.</div></div>","PeriodicalId":14764,"journal":{"name":"JHEP Reports","volume":"7 10","pages":"Article 101497"},"PeriodicalIF":7.5,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144988842","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}
JHEP ReportsPub Date : 2025-07-12DOI: 10.1016/j.jhepr.2025.101522
Sheng Li , Qianqian Mao
{"title":"Rethinking risk indices in pediatric MASLD","authors":"Sheng Li , Qianqian Mao","doi":"10.1016/j.jhepr.2025.101522","DOIUrl":"10.1016/j.jhepr.2025.101522","url":null,"abstract":"","PeriodicalId":14764,"journal":{"name":"JHEP Reports","volume":"7 10","pages":"Article 101522"},"PeriodicalIF":7.5,"publicationDate":"2025-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144913783","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}