Hepatology Communications最新文献

{"title":"Sexual health and function in liver disease.","authors":"Alberto Ferrarese, Ivonne Hurtado Díaz de León, Elliot B Tapper, Patrizia Burra","doi":"10.1097/HC9.0000000000000691","DOIUrl":"10.1097/HC9.0000000000000691","url":null,"abstract":"<p><p>Sex is a central aspect of human life and is significantly impacted by chronic illness. Cirrhosis, due to its unique pathophysiology and the side effects of common therapies, serves as a paradigmatic example, being associated with very high rates of sexual dysfunction in both men and women. Liver transplantation can modify certain hormonal and pathophysiological aspects related to sexual dysfunction, but complete recovery occurs in only a relatively small percentage of patients. This review examines the pathophysiology, epidemiology, and management of sexual and reproductive dysfunction in patients with cirrhosis and those undergoing liver transplantation. It provides a framework for understanding the sources of dysfunction, tools for identifying it in clinical settings, and interventions to improve sexual health and functioning in these patients.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 4","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11970893/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143772076","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Depletion of tumor-reactive HSCs reveals their significance during different stages of liver metastasis.","authors":"Aitor Benedicto, Alba Herrero, Aritz Lopategi, Scott L Friedman, Maria Dolores Boyano, Beatriz Arteta","doi":"10.1097/HC9.0000000000000669","DOIUrl":"10.1097/HC9.0000000000000669","url":null,"abstract":"<p><strong>Background: </strong>Activated HSCs play a major role in tissue repair, extracellular matrix regulation, immune response, and inflammation. However, their contributions to the hepatic tumor microenvironment are underexplored and need to be clarified.</p><p><strong>Methods: </strong>In vitro, we analyzed the responses of freshly isolated LSECs and HSCs to tumor cell supernatants and secretome-driven activation of both primary cell types. For in vivo HSC depletion, transgenic mice expressing the herpes simplex virus-thymidine kinase (HSV-Tk) gene driven by the mouse glial fibrillary acidic protein promoter were used. MC38 colon carcinoma or B16 melanoma was intrasplenically injected to generate liver metastasis to further analyze metastatic growth, collagen accumulation, angiogenesis, and immunosuppression.</p><p><strong>Results: </strong>Metastatic tumor cells arrest and adhere in the liver 48 hours after intrasplenic injection. The 65% of arrested tumor cells were surrounded by α-smooth muscle actin-expressing cells. In vitro, tumor-activated LSEC-derived secretomes stimulated α-smooth muscle actin expression, migration, VEGF, and LSEC promigratory factor release by HSCs. Tumor cell secretomes stimulated HSC proliferation and the secretion of proangiogenic and protumoral mediators. HSC depletion reduced the foci number and metastatic area in colorectal cancer and melanoma models. Moreover, livers from transgenic mice showed reduced key tumor microenvironment parameters, including intratumoral collagen accumulation, neoangiogenesis, and recruitment of myeloid-derived suppressor cells.</p><p><strong>Conclusions: </strong>Depletion of tumor-reactive proliferating HSCs implicates these cells as the required spark for the initiation and progression of liver metastasis, making them a good candidate for new therapies targeting the tumor microenvironment to treat liver metastasis of different primary origins.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 4","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11936575/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143700323","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A systematic review of noninvasive laboratory indices and elastography to predict hepatic decompensation.","authors":"John Grady, Michael Song, Whitney Townsend, Nadim Mahmud, Elliot B Tapper, Neehar D Parikh","doi":"10.1097/HC9.0000000000000675","DOIUrl":"10.1097/HC9.0000000000000675","url":null,"abstract":"<p><strong>Background: </strong>Hepatic decompensation carries profound implications for patient quality of life and risk of mortality. We lack comparative data on how noninvasive tools perform in risk stratification for those with compensated cirrhosis. We performed a systematic review to assess the performance of laboratory and transient elastography-based models for predicting hepatic decompensation in patients with compensated cirrhosis.</p><p><strong>Methods: </strong>The following databases were searched by an informationist to identify relevant studies, including adult patients with compensated cirrhosis from inception to August 2023: Medline, Embase, Scopus, Web of Science, and ClinicalTrials.gov. Title and abstract screening followed by full-text review were performed by 2 independent reviewers, and data abstraction was completed using standardized forms. Studies of patients with decompensation at baseline (defined by ascites, variceal bleeding, and HE) or any primary hepatic malignancy were excluded. The primary outcome was hepatic decompensation, as defined above. Pooled HRs were calculated using the common-effect inverse-variance model.</p><p><strong>Results: </strong>Forty-four full-text studies met the inclusion criteria. Across 52,589 patients, the cumulative incidence of any decompensation was 17.9% over a follow-up time of 111,401 patient years. Pooled risk estimates for all-cause decompensation demonstrated that MELD (HR: 1.08; 95% CI: 1.06-1.10), albumin-bilirubin (HR: 2.13, 95% CI: 1.92-2.36), fibrosis-4 (HR: 1.04, 95% CI: 1.03-1.06), albumin-bilirubin-fibrosis-4 (HR: 1.25, 95% CI: 1.18-1.33), and liver stiffness by transient elastography (HR: 1.04; 95% CI: 1.04-1.05) predict decompensation.</p><p><strong>Conclusions: </strong>Available blood and imaging-based biomarkers can risk-stratify patients for hepatic decompensation. Changes in albumin-bilirubin appear to have the highest discrimination in predicting decompensation events.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 4","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11936601/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143700319","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aerobic exercise interventions lead to MASH resolution in clinical trials: Pooled analysis using the MASH resolution index.","authors":"Shelley E Keating, Patrick J Owen, Christopher J A Pugh, Daniel J Cuthbertson, Jonathan G Stine","doi":"10.1097/HC9.0000000000000681","DOIUrl":"10.1097/HC9.0000000000000681","url":null,"abstract":"","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 4","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11936640/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143700321","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multiple cell-type interactions drive invariant NKT cell hepatitis.","authors":"Jiaxin Tan, Longshan Ji, Qian Li, Ruowen Guo, Yawen Hao, Peng Xiao, Qiuhong Zai, Xuewei Zhang, Yating Gao, Xin Zhang, Miao Fang, Yanhang Gao, Weidong Zhao, Yong He, Yueqiu Gao, Man Li","doi":"10.1097/HC9.0000000000000592","DOIUrl":"10.1097/HC9.0000000000000592","url":null,"abstract":"<p><strong>Background: </strong>α-Galactosylceramide (α-Galcer), a specific ligand for invariant natural killer T (NKT) cell activation, has been actively investigated in clinical trials such as antitumor therapy; however, treatment with α-Galcer is well known to induce acute hepatitis due to enriched NKT cells in the liver. The molecular mechanisms underlying NKT-mediated hepatitis still remain obscure. The object of this study was to investigate whether and how myeloid cells affect NKT-mediated hepatitis.</p><p><strong>Methods: </strong>α-Galcer-induced NKT hepatitis was used in this study. microRNA-223 (miR-223) and neutrophil cytosolic factor 1 (Ncf1)-deficent mice were generated and subjected to α-Galcer-induced NKT hepatitis.</p><p><strong>Results: </strong>In this study, we demonstrated that α-Galcer-induced NKT cell activation resulted in neutrophil and monocyte-derived macrophage accumulation in the liver. Importantly, serum levels of several hepatic myeloid cell infiltration-related cytokines and chemokines were significantly elevated after α-Galcer administration. Among these myeloid cells, blockade of neutrophil or macrophage migration through using different inhibitors of (C-X-C Motif) receptor 2, (C-C motif) receptor 2, and (C-C motif) receptor 5 signaling ameliorated α-Galcer-induced liver injury, mainly due to the decrease of reactive oxygen species production and inflammation. Depletion of neutrophils reduced α-Galcer-induced liver injury and hepatitis. Interestingly, genetic deletion of neutrophil-specific miR-223 markedly enhanced while Ncf1 deficiency significantly ameliorated liver inflammation and oxidative damage caused by α-Galcer.</p><p><strong>Conclusions: </strong>Neutrophil and macrophage infiltration through multiple inflammatory mediators is required for NKT cell activation-induced hepatitis, which sheds light on the myeloid cell infiltration-related molecular mechanisms of NKT cell-mediated liver injury. Our study may provide a novel therapeutical strategy for the treatment of NKT cell hepatitis.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 4","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11936566/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143700328","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Moderate alcohol-associated hepatitis: A real-world multicenter study.","authors":"Francisco Idalsoaga, Luis Antonio Díaz, Winston Dunn, Heer Mehta, Karen Muñoz, Vicente Caldentey, Jorge Arnold, Gustavo Ayares, Rokhsana Mortuza, Shiv K Sarin, Rakhi Maiwall, Wei Zhang, Steve Qian, Douglas Simonetto, Ashwani K Singal, Mohamed A Elfeki, Carolina Ramirez-Cadiz, Gurpreet Malhi, Adan Ahmed, Hoomam Homsi, Zinia Abid, Joaquín Cabezas, Victor Echavarría, Maria Poca, German Soriano, Berta Cuyas, Meritxell Ventura Cots, María Fátima Higuera-De La Tijera, Maria Ayala-Valverde, Diego Perez, Jaime Gomez, Juan G Abraldes, Mustafa Al-Karaghouli, Prasun K Jalal, Mohamad Ali Ibrahim, Guadalupe García-Tsao, Daniela Goyes, Lubomir Skladaný, Daniel J Havaj, Karolina Sulejova, Svetlana Adamcova Selcanova, Diego Rincón, Kristina R Chacko, Juan C Restrepo, Pamela Yaquich, Luis G Toro, Vijay Shah, Marco Arrese, Patrick S Kamath, Ramon Bataller, Juan Pablo Arab","doi":"10.1097/HC9.0000000000000673","DOIUrl":"10.1097/HC9.0000000000000673","url":null,"abstract":"<p><strong>Background: </strong>Severe alcohol-associated hepatitis (sAH) is a well-characterized disease with high short-term mortality. However, there is limited research on those with a \"less severe condition\" (moderate AH). This study aims to characterize in-depth patients with moderate AH (mAH), including the performance of mortality scoring systems, key prognostic factors, and survival over time.</p><p><strong>Methods: </strong>A multicenter retrospective cohort study (2009-2019) included patients with mAH (MELD score ≤20 at admission). Cox regression and receiver operating characteristic curves with AUC were used for analysis.</p><p><strong>Results: </strong>We included 1845 patients with AH (20 centers, 8 countries) between 2009 and 2019. mAH was defined as a MELD score ≤20 at admission. Twenty-four percent met the criteria for an mAH episode. Patients with mAH tend to be older and have a higher proportion of females, with a median MELD of 17 (15-19), Maddrey discriminant function (mDF) of 33 (22-40), the trajectory of serum bilirubin of 0.83 (0.60-1.21), and neutrophil-to-lymphocyte ratio (NLR) of 5 (2.96-8.60). The primary causes of death in mAH included multiple organ failure (34.1%) and infections (16.6%). The cumulative survival rates at 30, 90, and 180 days were 94.3%, 90.4%, and 88.2%, respectively. In multivariable analysis, age was the only significant predictor of 30-day mortality (HR 1.49, 95% CI: 1.27-1.76, p<0.001). Mortality prediction models showed poor performance, with AUC for MELD (0.671), mDF (0.726), trajectory of serum bilirubin (0.733), and NLR (0.697).</p><p><strong>Conclusions: </strong>Patients with moderate AH exhibited a mortality of 11.8% at 6 months, primarily driven by multiple organ failure and infections. These patients also exhibit a different clinical profile compared to those with sAH. Tailored models and therapeutic strategies are needed to improve long-term outcomes in mAH.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 4","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11936654/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143700326","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PRMT1-mediated modification of H4R3me2a promotes liver cancer progression by enhancing the transcriptional activity of SOX18.","authors":"Jing Ling, Siying Wang, Chenhe Yi, Xingling Zheng, Yangyang Zhou, Shunjia Lou, Haoyu Li, Ruobing Yu, Wei Wu, Qiangxin Wu, Xiaoxiao Sun, Yuanyuan Lv, Huijue Zhu, Qi Li, Haojie Jin, Jinhong Chen, Jiaojiao Zheng, Wenxin Qin","doi":"10.1097/HC9.0000000000000647","DOIUrl":"10.1097/HC9.0000000000000647","url":null,"abstract":"<p><strong>Background: </strong>HCC is one of the most prevalent and deadliest malignancies worldwide, with a poor prognosis. Altered histone modifications have been shown to play a significant role in HCC. However, the biological roles and clinical relevance of specific histone modifications, such as the asymmetric dimethylation on arginine 3 of histone H4 (H4R3me2a), remain poorly understood in HCC.</p><p><strong>Methods: </strong>In this study, immunohistochemical staining was performed to assess histone H4R3me2a modification in 32 pairs of HCC tissues and corresponding adjacent nontumor liver tissues. Cellular-level experiments and subcutaneous xenograft models in nude mice were used to investigate the effects of silencing protein arginine methyltransferase 1 (PRMT1) with shRNA or pharmacologically blocking PRMT1 activity on HCC cell proliferation, migration, and invasion. RNA-seq analysis combined with Chip-qPCR validation was employed to explore the regulatory mechanism of PRMT1 on SOX18 expression. The downstream target of SOX18 was identified using the JASPAR database and a dual-luciferase reporter system.</p><p><strong>Results: </strong>The level of histone H4R3me2a modification was significantly elevated in HCC tissues and closely associated with poor prognosis in patients with HCC. Silencing PRMT1 or pharmacologically inhibiting its activity effectively suppressed the proliferation, migration, and invasion of HCC cells. Mechanistically, PRMT1 was found to regulate SOX18 expression by modulating histone H4R3me2a modification in the SOX18 promoter region. LOXL1 was identified as a downstream target of the transcription factor SOX18.</p><p><strong>Conclusions: </strong>This study revealed the clinical relevance of histone H4R3me2a modification in HCC and demonstrated that PRMT1 promotes malignant behavior in HCC cells by modulating H4R3me2a modification in the SOX18 promoter region. The findings elucidate the role and molecular mechanism of PRMT1-mediated histone H4R3me2a modification in HCC progression and highlight the potential clinical applications of PRMT1 inhibitors. These results may provide new insights into the treatment of HCC.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 4","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11936655/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143700330","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum: Pervasive role of pruritus in impaired quality of life in patients with primary biliary cholangitis: Data from the GLIMMER study.","authors":"Helen T Smith, Sugato Das, James Fettiplace, Robyn von Maltzahn, Philip J F Troke, Megan M McLaughlin, David E Jones, Andreas E Kremer","doi":"10.1097/HC9.0000000000000698","DOIUrl":"10.1097/HC9.0000000000000698","url":null,"abstract":"","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 4","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11927640/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143752425","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advances in radiation therapy for HCC: Integration with liver-directed treatments.","authors":"Orly Yariv, Neil B Newman, Mark Yarchoan, Atoosa Rabiee, Bradford J Wood, Riad Salem, Jonathan M Hernandez, Christine K Bang, Ted K Yanagihara, Freddy E Escorcia","doi":"10.1097/HC9.0000000000000653","DOIUrl":"10.1097/HC9.0000000000000653","url":null,"abstract":"<p><p>HCC is the fourth leading cause of cancer-related mortality with increasing incidence worldwide. Historically, treatment for early disease includes liver transplantation, surgical resection, and/or other local therapies, such as thermal ablation. As a result of technical advances and high-quality prospective data, the use of definitive external beam radiotherapy with ablative doses has emerged. Intermediate-stage disease has been generally addressed with arterially directed therapies (eg, chemoembolization or radioembolization) and external beam radiotherapy, while advanced stages have been addressed by systemic therapy or best supportive care. The role of each local/locoregional therapy has rapidly evolved in the context of novel pharmacotherapies, including immunotherapies and antiangiogenic agents. The combinations, indications, and timing of treatments vary widely among specialties and geographies. Here, we aim to synthesize the best quality evidence available regarding the efficacy and safety of different liver-directed modalities, with a focus on recent prospective clinical data of external beam radiotherapy within the context of other available liver-directed therapies across Barcelona Liver Classification (BCLC) stages.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 4","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11927661/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143752424","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evidence-based criteria for identifying at-risk individuals requiring liver disease screening.","authors":"Fredrik Åberg, Ville Männistö, Juho Asteljoki, Veikko Salomaa, Antti Jula, Annamari Lundqvist, Satu Männistö, Markus Perola, Panu K Luukkonen","doi":"10.1097/HC9.0000000000000679","DOIUrl":"10.1097/HC9.0000000000000679","url":null,"abstract":"<p><strong>Background: </strong>Liver fibrosis screening is recommended in at-risk groups, but a clear definition of \"at risk\" for entry criteria is lacking. We analyzed different combinations of established risk factors to define specific screening entry criteria with a prespecified sensitivity requirement.</p><p><strong>Methods: </strong>Data regarding individuals aged 40-70 years from Finnish health-examination surveys (FINRISK 2002-2012 and Health 2000, n=15,057) and the UK Biobank (n=454,990) were linked with healthcare registries for liver cirrhosis-related events (LREs; liver-related hospitalizations, cancer, or death). The predictive performance of 1919 combinations of risk factors, including alcohol consumption, metabolic disturbances, abnormal liver function tests, and Chronic Liver Disease risk score, was assessed for 10-year LRE risk requiring a minimum 90% sensitivity. Validations were performed using liver stiffness measurement (LSM) >12 kPa in the NHANES 2017-2020 sample (n=3367).</p><p><strong>Results: </strong>Optimal entry criteria for predicting 10-year LRE risk with >90% sensitivity included any one of: hazardous alcohol use, severe obesity, metabolic syndrome, an AST-to-ALT ratio >0.8 with elevated ALT, and an intermediate-to-high Chronic Liver Disease risk score. The sensitivity and specificity for this strategy were 91% and 51% for LREs, respectively, in the Finnish cohort, and 91% and 41% for LSM >12 kPa in the US sample. In the US sample, applying these entry criteria followed by fibrosis-4 ≥1.3 for predicting LSM >12 kPa reduced the sensitivity to 45% (specificity: 85%), which was attributed to the suboptimal sensitivity of fibrosis-4.</p><p><strong>Conclusions: </strong>This study identifies an inexpensive risk factor-based strategy with >90% sensitivity for predicting LRE and LSM >12 kPa, which is practical and scalable for targeted liver fibrosis screening to improve population outcomes. However, a more sensitive first-line noninvasive fibrosis test is needed.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 4","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11927647/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143673410","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}