Hepatology最新文献

{"title":"Erratum: Lipocalin-2 activates hepatic stellate cells and promotes nonalcoholic steatohepatitis in high-fat diet-fed Ob/Ob mice.","authors":"Kyung Eun Kim, Jaewoong Lee, Hyun Joo Shin, Eun Ae Jeong, Hye Min Jang, Yu Jeong Ahn, Hyeong Seok An, Jong Youl Lee, Meong Cheol Shin, Soo Kyoung Kim, Won Gi Yoo, Won Ho Kim, Gu Seob Roh","doi":"10.1097/HEP.0000000000001287","DOIUrl":"https://doi.org/10.1097/HEP.0000000000001287","url":null,"abstract":"","PeriodicalId":177,"journal":{"name":"Hepatology","volume":" ","pages":""},"PeriodicalIF":12.9,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143717811","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: Targeted enteral feeding for malnutrition in Liver Transplant candidates.","authors":"Brooke Chapman, Darren Wong, Marie Sinclair, Penelope Hey, Ryma Terbah, Paul Gow, Avik Majumdar, Adam Testro","doi":"10.1097/HEP.0000000000001319","DOIUrl":"https://doi.org/10.1097/HEP.0000000000001319","url":null,"abstract":"","PeriodicalId":177,"journal":{"name":"Hepatology","volume":" ","pages":""},"PeriodicalIF":12.9,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143707882","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: Primary sclerosing cholangitis and autoimmune hepatitis - distinct or common autoimmune penetrance?","authors":"Lisbet Grønbæk, Hendrik Vilstrup, Peter Jepsen","doi":"10.1097/HEP.0000000000001325","DOIUrl":"https://doi.org/10.1097/HEP.0000000000001325","url":null,"abstract":"","PeriodicalId":177,"journal":{"name":"Hepatology","volume":" ","pages":""},"PeriodicalIF":12.9,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143707865","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":"Deciphering the spatial tumor microenvironment in intrahepatic cholangiocarcinoma","authors":"Rocio I.R. Macias, Stephanie Roessler, Monique M.A. Verstegen","doi":"10.1097/hep.0000000000001322","DOIUrl":"https://doi.org/10.1097/hep.0000000000001322","url":null,"abstract":"","PeriodicalId":177,"journal":{"name":"Hepatology","volume":"34 1","pages":""},"PeriodicalIF":13.5,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143695491","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":"Erratum: Primary biliary cholangitis: Personalizing second-line therapies","authors":"Cynthia Levy, Christopher L. Bowlus","doi":"10.1097/hep.0000000000001275","DOIUrl":"https://doi.org/10.1097/hep.0000000000001275","url":null,"abstract":"","PeriodicalId":177,"journal":{"name":"Hepatology","volume":"96 1","pages":""},"PeriodicalIF":13.5,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143695492","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":"Proton density fat fraction for diagnosis of metabolic dysfunction associated steatotic liver disease.","authors":"Nikolaos Panagiotopoulos, Tanya Wolfson, David T Harris, Danielle Batakis, Rashmi Agni, Lael Ceriani, Yesenia Covarrubias, Gavin Hamilton, Michael S Middleton, Vitor F Martins, Anthony C Gamst, Thekla H Oechtering, Ryan Sappenfield, Santiago Horgan, Eduardo Grunvald, Luke M Funk, Garth R Jacobsen, Anne O Lidor, James A Goodman, Sami B Khoury, Claude B Sirlin, Scott B Reeder","doi":"10.1097/HEP.0000000000001318","DOIUrl":"10.1097/HEP.0000000000001318","url":null,"abstract":"<p><strong>Background aims: </strong>Prior work has shown that magnetic resonance imaging (MRI)-derived proton density fat fraction (PDFF) can diagnose metabolic dysfunction-associated steatotic liver disease (MASLD) noninvasively, but there is a paucity of data on the performance of PDFF to classify more advanced forms of the MASLD spectrum. The purpose of this study was to assess the diagnostic performance of PDFF for the diagnoses of MASLD, metabolic dysfunction-associated steatohepatitis (MASH), and fibrotic MASH in adults with obesity undergoing bariatric surgery, using contemporaneous intraoperative liver biopsy as reference.</p><p><strong>Approach results: </strong>PDFF was evaluated alone and with other potential classifiers (imaging, serum and anthropometric), using Bayesian Information Criterion-based stepwise logistic regression models. Areas under the receiver operating characteristic (ROC) curves (AUC) were computed for all models and single classifiers. Cross-validated sensitivity and specificity were calculated at Youden-based PDFF classification thresholds. Data analysis from 140 patients demonstrated that PDFF was the most accurate single classifier, with high AUC for MASLD (0.95), MASH (0.85), and fibrotic MASH (0.82) (all p<0.001). Multivariable models including PDFF outperformed those without PDFF. The Youden-based threshold for PDFF was 4.4% for MASLD (sensitivity: 87%, specificity: 86%), 6.9% for MASH (sensitivity: 77%, specificity: 66%), and 13.5% for fibrotic MASH (sensitivity: 67%, specificity: 85%).</p><p><strong>Conclusions: </strong>PDFF was the most accurate single classifier for diagnosing MASLD, MASH, and fibrotic MASH. The most accurate multivariable classification models for MASLD, MASH, and fibrotic MASH included PDFF, demonstrating the central importance of PDFF for noninvasive assessment of the MASLD spectrum.</p>","PeriodicalId":177,"journal":{"name":"Hepatology","volume":" ","pages":""},"PeriodicalIF":12.9,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143707867","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: targeted enteral feeding for malnutrition in liver transplant candidates","authors":"Qingyu Chen","doi":"10.1097/hep.0000000000001317","DOIUrl":"https://doi.org/10.1097/hep.0000000000001317","url":null,"abstract":"","PeriodicalId":177,"journal":{"name":"Hepatology","volume":"93 1","pages":""},"PeriodicalIF":13.5,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143695502","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Liver Transplant Comorbidity Index (LTCI) : A composite index of ambulatory Pre-LT factors to identify patients at increased risk of Post-LT Mortality.","authors":"Jennifer C Lai, Amy M Shui, Michele Molinari, Robert Rahimi, Daniela Ladner, Daniel Ganger, Matthew Kappus, Elizabeth King, Amit Tevar, Michael Volk, Andres Duarte-Rojo, Elizabeth C Verna","doi":"10.1097/HEP.0000000000001320","DOIUrl":"https://doi.org/10.1097/HEP.0000000000001320","url":null,"abstract":"<p><strong>Background: </strong>Frailty is strongly associated with mortality after liver transplantation. However, national guidelines discourage its use as a sole reason to decline a patient for liver transplantation, as some frail patients have acceptable outcomes. We aimed to develop a composite index, the Liver Transplant Comorbidity Index (LTCI), integrating frailty and other comorbidities, as a risk factor for longer-term (3-year) post-transplant mortality.</p><p><strong>Methods: </strong>This 8-center prospective Functional Assessment in Liver Transplantation (FrAILT) Study included adult recipients of a primary deceased donor liver transplant from 2012-2022. Frailty was measured using the Liver Frailty Index (LFI ≥4.5=frail). Other candidate variables included demographics, laboratories, and comorbidities. Cox proportional hazards regression with best subset selection was used to identify risk factors of 3-year post-transplant death. The final model was selected based on Aikaike Information Criterion and clinical pragmatism.</p><p><strong>Results: </strong>Of 1,472 liver transplant recipients. 290 (20%) were frail. Three-year post-transplant mortality was higher in frail versus non-frail patients (13 vs. 8%; p=0.03). The final LTCI included 5 variables: frailty, coronary artery disease, hepatocellular carcinoma, renal dysfunction, and diabetes. Three-year post-transplant mortality in low-, moderate-, and high-risk LTCI groups was 93%, 87%, and 80% respectively. In multivariable analysis, after adjusting for donor factors (age, DCD), both moderate- (HR 2.23; 95% CI 1.46-3.40; p<0.001) and high-risk (HR 2.78; 95% CI 1.67-4.64; p<0.001) status were associated with 3-year post-transplant mortality.</p><p><strong>Conclusion: </strong>The LTCI, comprising 5 pre-transplant clinical parameters, effectively identifies patients at increased risk of post-transplant mortality. By integrating frailty in the context of other co-morbidities, the LTCI can help providers better weigh the relative transplant risks and benefits and standardize selection of transplant candidates.</p>","PeriodicalId":177,"journal":{"name":"Hepatology","volume":" ","pages":""},"PeriodicalIF":12.9,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143707908","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":"Erratum: HDV RNA assays: Performance characteristics, clinical utility, and challenges.","authors":"Heiner Wedemeyer, Mitchell Leus, Thomas R Battersby, Jeffrey Glenn, Emmanuel Gordien, Saleem Kamili, Hema Kapoor, Harald H Kessler, Oliver Lenz, Marc Lütgehetmann, Tonya Mixson-Hayden, Christian O Simon, Michael Thomson, Gabriel Westman, Veronica Miller, Norah Terrault, Pietro Lampertico","doi":"10.1097/HEP.0000000000001262","DOIUrl":"https://doi.org/10.1097/HEP.0000000000001262","url":null,"abstract":"","PeriodicalId":177,"journal":{"name":"Hepatology","volume":" ","pages":""},"PeriodicalIF":12.9,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143699263","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":"Neutrophil serine proteases NE and PR3 controlled by the miR-223/STAT3 axis potentiate MASH and liver fibrosis.","authors":"Pengfei Zhang, Dongyang Liu, Lihong Wu, Xiaoqin Wu, Kaixuan Yan, Mengqi Fan, Danqi Zou, Erfei Song, Yumeng Jiang, Ying Xu, Xiaoping Wu, Shufei Zang, Fei Zhu, Yuqi Chen, Zhikang Cen, Mengqiao Bi, Yuying Zhang, Xicheng Wang, Wei Liu, Rongxin Zhang, Cunchuan Wang, Ruby Lai Chong Hoo, Aimin Xu, Dewei Ye","doi":"10.1097/HEP.0000000000001309","DOIUrl":"https://doi.org/10.1097/HEP.0000000000001309","url":null,"abstract":"<p><strong>Background aims: </strong>Metabolic dysfunction-associated steatohepatitis (MASH) and its related liver fibrosis represent a substantial public health burden with limited treatment options. Although MASH is associated with enhanced neutrophil infiltration in the liver, the mediators and mechanisms underlying neutrophil-driven progression of MASH and fibrosis remain largely unknown. This study aimed to investigate the role of neutrophil serine proteases neutrophil elastase (NE) and proteinase 3 (PR3) in the development of MASH and fibrosis.</p><p><strong>Approach: </strong>Liver biopsies from 121 morbidly obese patients were recruited for analysis. NE-/-, PR3-/-, microRNA-223 (miR-223)-/- mice and their wild type controls were fed a choline-deficient, L-amino acid-defined, high-fat diet to induce MASH fibrosis. Bone marrow transplantation was performed to generate mice with miR-223 chimerism in bone marrow-derived cells.</p><p><strong>Results: </strong>NE and PR3 content in human liver with MASH and fibrosis was markedly increased in close association with histological features. Genetic ablation or AAV-mediated inhibition of NE and PR3 substantially alleviated MASH and liver fibrosis in mice. Mechanistic study revealed that miR-223 suppressed neutrophilic NE and PR3 by targeting STAT3. MiR-223 deficiency augmented inflammation and fibrosis in mouse liver. Bone marrow transplantation-induced miR-223 chimerism significantly affected hepatic NE/PR3 content and the progression of MASH fibrosis in mice.</p><p><strong>Conclusions: </strong>Our findings reveal that NE and PR3 are key factors triggering liver inflammation to potentiate the development of MASH and liver fibrosis, offering insight into the development of new therapeutic approaches that target NE and PR3.</p>","PeriodicalId":177,"journal":{"name":"Hepatology","volume":" ","pages":""},"PeriodicalIF":12.9,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143672888","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}