Hepatology Communications最新文献

{"title":"Changes in the FXR-cistrome and alterations in bile acid physiology in Wilson disease.","authors":"Clavia Ruth Wooton-Kee, Hari K Yalamanchili, Islam Mohamed, Manal Hassan, Kenneth D R Setchell, Monica Narvaez Rivas, Ayse K Coskun, Vasanta Putluri, Nagireddy Putluri, Prasun Jalal, Michael L Schilsky, David D Moore","doi":"10.1097/HC9.0000000000000707","DOIUrl":"10.1097/HC9.0000000000000707","url":null,"abstract":"<p><strong>Background: </strong>Wilson disease (WD) is an autosomal recessive disorder that results in excessive hepatic copper, causing hepatic steatosis, inflammation, fibrosis, cirrhosis, and liver failure. Previous studies have revealed dysregulation of many farnesoid X receptor (FXR) metabolic target genes in WD, including the bile salt exporter pump, the major determinant of bile flow.</p><p><strong>Methods: </strong>We tested the hypothesis that the FXR-cistrome is decreased in Atp7b-/- mice in accord with dysregulated bile acid homeostasis.</p><p><strong>Results: </strong>FXR binding within Atp7b-/- mouse livers displayed surprising complexity: FXR binding was increased in distal intergenic regions but decreased in promoter regions in Atp7b-/- versus wild-type mice. Decreased FXR occupancy in Atp7b-/- versus wild-type mice was observed in hepatocyte metabolic and bile acid homeostasis pathways, while enrichment of FXR binding was observed in pathways associated with cellular damage outside of hepatocytes. Indeed, disparate FXR occupancy was identified in parenchymal and non-parenchymal marker genes in a manner that suggests decreased FXR activity in parenchymal cells, as expected, and increased FXR activity in non-parenchymal cells. Consistent with altered FXR function, serum and liver bile acid concentrations were higher in Atp7b-/- mice than in wild-type mice. Comparison of bile acid profiles in the serum of WD patients with \"liver,\" \"neurological,\" or \"mixed\" disease versus healthy controls also revealed increases in specific bile acids in WD-liver versus healthy controls.</p><p><strong>Conclusions: </strong>We identified novel FXR-occupancy across the genome that varied in parenchymal and non-parenchymal cells, demonstrating complex FXR regulation of metabolic and hepatocellular stress pathways in Atp7b-/- mice. Dynamic changes in FXR activity support our novel finding of altered bile acid metabolism in Atp7b-/- mice and WD patients.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 6","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12106221/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144132262","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":"Critical commentary on the study comparing TIPS, tunneled peritoneal catheter, and ascites pump in refractory ascites.","authors":"Ibrahim Nagmeldin Hassan","doi":"10.1097/HC9.0000000000000725","DOIUrl":"10.1097/HC9.0000000000000725","url":null,"abstract":"","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 6","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12106195/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144132310","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":"VLDL lipidomics reveals hepatocellular lipidome changes in metabolic dysfunction-associated steatotic liver disease.","authors":"David Guardamino Ojeda, Yusuf Yalcin, Yered Pita-Juarez, Aaron Hakim, Susmita Bhattarai, Zsu-Zsu Chen, John M Asara, Margery A Connelly, Melissa R Miller, Michelle Lai, Z Gordon Jiang","doi":"10.1097/HC9.0000000000000716","DOIUrl":"10.1097/HC9.0000000000000716","url":null,"abstract":"<p><strong>Background: </strong>The production of VLDL is one of the primary mechanisms through which liver cells regulate intracellular lipid homeostasis. We hypothesize that the disease characteristics of metabolic dysfunction-associated steatotic liver disease (MASLD) differentially impact VLDL lipid composition. This study comprehensively examines the relationship between VLDL-lipidome and MASLD histology and disease-associated genetics, aiming to define MASLD-related VLDL changes.</p><p><strong>Methods: </strong>We performed untargeted lipidomics on serum VLDL particles in a cohort of biopsy-proven MASLD patients to examine the relationship between VLDL-lipidome and MASLD disease features as well as MASLD-related genetic variants.</p><p><strong>Results: </strong>Among 1514 detected lipid species in VLDL, triglyceride (TG), phosphatidylcholine (PC), and ceramide (Cer) were the top classes. Moderate to severe hepatic steatosis was associated an increase in VLDL-TG, especially those with palmitic acid (C16:0). A unified acyl chain distribution analysis revealed that steatosis was associated with increases in TGs with saturated and monounsaturated fatty acyl chains, but decreases in polyunsaturated fatty acyl chains, a pattern that was not mirrored in acyl chains from VLDL-PC or VLDL-Cer. Lobular inflammation was associated with reductions in lipids with polyunsaturated acyl chains, particularly docosahexaenoic acid (C22:6). Meanwhile, patients with advanced liver fibrosis (stages 3-4) had reductions in VLDL-TGs with both saturated and polyunsaturated acyl chains and overall enrichment in Cer species. Furthermore, MASLD-associated genetic variants in PNPLA3, TM6SF2, GPAM, HSD17B13, and MTARC1 demonstrated distinct VLDL-lipidomic signatures in keeping with their biology in lipoprotein metabolism.</p><p><strong>Conclusions: </strong>Hepatic steatosis and liver fibrosis in MASLD are associated with distinct VLDL-lipidomic signatures, respectively. This relationship is further modified by MASLD-genetics, suggesting a differential impact of pathogenic features on hepatocellular lipid homeostasis.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 6","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12106201/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144132326","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":"Skeletal muscle and MASLD: Mechanistic and clinical insights.","authors":"Thomas Marjot, Matthew J Armstrong, Jonathan G Stine","doi":"10.1097/HC9.0000000000000711","DOIUrl":"10.1097/HC9.0000000000000711","url":null,"abstract":"<p><p>Metabolic dysfunction-associated steatotic liver disease (MASLD) is intrinsically linked with widespread metabolic perturbations, including within skeletal muscle. Indeed, MASLD is associated with a range of skeletal muscle abnormalities, including insulin resistance, myosteatosis, and sarcopenia, which all converge on the liver to drive disease progression and adverse patient outcomes. This review explores the mechanistic links between skeletal muscle and MASLD, including the role of abnormal glycemic control, systemic inflammation, and disordered myokine signaling. In turn, we discuss how intrinsic liver pathology can feed back to further exacerbate poor skeletal muscle health. Given the central importance of skeletal muscle in MASLD pathogenesis, it offers clinicians an opportunity to intervene for therapeutic benefit. We, therefore, summarize the role of nutrition and physical activity on skeletal muscle mass, quality, and metabolic function and discuss the knock-on effect this has on the liver. An awareness of these treatment strategies is particularly important in the era of effective pharmacological and surgical weight loss interventions, which can be associated with the development of sarcopenia. Finally, we highlight a number of promising drug agents in the clinical trial pipeline that specifically target skeletal muscle in an attempt to improve metabolic and physical functioning.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 6","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12106243/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144132323","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":"Parental liver disease mortality is associated with unfavorable outcomes in patients with alcohol-associated hepatitis.","authors":"Wanzhu Tu, Samer Gawrieh, Lauren Nephew, Craig McClain, Qing Tang, Srinivasan Dasarathy, Vatsalya Vatsalya, Douglas A Simonetto, Carla Kettler, Gyongyi Szabo, Bruce Barton, Yunpeng Yu, Patrick S Kamath, Arun J Sanyal, Laura Nagy, Mack C Mitchell, Suthat Liangpunsakul, Vijay H Shah, Naga Chalasani, Ramon Bataller","doi":"10.1097/HC9.0000000000000666","DOIUrl":"10.1097/HC9.0000000000000666","url":null,"abstract":"<p><strong>Background: </strong>How parental alcohol use disorder and liver disease-related mortality influence the risk and the outcomes of alcohol-associated hepatitis (AH) in the offspring is unknown.</p><p><strong>Methods: </strong>We analyzed data from 2 prospective observational studies of AH cases and heavy drinking controls (HDCs). Family history of parental alcohol use disorder and liver disease mortality was assessed at the study entry. Logistic regression and Cox proportional hazard models were used to assess the influences of family history on AH development and outcome.</p><p><strong>Results: </strong>Data from 1356 participants in two prospective cohorts (926 AH cases and 430 HDC) were combined and analyzed. Parental alcohol use disorder was found in 56.9% of AH cases and 61.1% of HDC; parental death due to liver disease was reported in 7.5% of AH cases and 5.7% of HDC. Multivariable logistic regression showed that parental liver disease-related mortality was associated with more than a doubled risk of AH development in the offspring after controlling for their demographic characteristics and drinking behavior (OR=2.26, 95% CI: [1.22, 4.20]). Moreover, among the AH cases, having a parent die of liver disease significantly increased the 90-day mortality of study participants after adjusting for the effects of other risk factors (HR=2.26, 95% CI: [1.05, 4.86]).</p><p><strong>Conclusions: </strong>The study highlights the influences of parental death due to liver disease on AH development and mortality. Identifying patients at risk of AH through family history might help facilitate discussions on reducing alcohol consumption.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 6","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12106198/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144132315","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":"Cholangiocarcinoma cells direct fatty acids to support membrane synthesis and modulate macrophage phenotype.","authors":"Michele Dei Cas, Stefania Mantovani, Barbara Oliviero, Aida Zulueta, Linda Montavoci, Monica Falleni, Delfina Tosi, Camillo Morano, Sara Penati, Annalisa Chiocchetti, Riccardo Sinella, Camilla Barbero Mazzucca, Matteo Donadon, Cristiana Soldani, Gaetano Piccolo, Matteo Barabino, Paolo Pietro Bianchi, Marcello Maestri, Ana Lleo, Jesus M Banales, Mario U Mondelli, Anna Caretti","doi":"10.1097/HC9.0000000000000717","DOIUrl":"10.1097/HC9.0000000000000717","url":null,"abstract":"<p><strong>Background and aims: </strong>Cholangiocarcinoma (CCA) is a globally rare, increasingly incident cancer. Metabolic reprogramming is common in cancer cells, and altered lipid homeostasis favors tumor development and progression. Previous studies have described lipid deregulation in HCC cells, while in CCA, the lipidome profile is still poorly characterized.</p><p><strong>Methods: </strong>We used liquid chromatography-tandem mass spectrometry to examine the lipid level profile of intrahepatic CCA (iCCA) and non-tumor surrounding tissue from patients, as well as in patients' and healthy controls' sera.</p><p><strong>Results: </strong>All lipid classes were upregulated in tumor specimens and iCCA-derived sera. Newly synthesized fatty acids (FAs) accumulated in iCCA and were only marginally directed to mitochondrial β-oxidation and scarcely folded in lipid droplets as neutral species. Metabolic flux assay showed that FAs were instead redirected toward plasma membrane formation and remodeling, being incorporated into phospholipids and sphingomyelin. A distinct lipid droplet and macrophage distribution was revealed by immunohistochemistry and Imaging Mass Cytometry. Lipid droplets were fewer in iCCA than in normal tissue and present mainly in the intratumoral fibrous septa and in M2 macrophages. Monocytes modified their lipid content and phenotype in the presence of iCCA cells, and the same effect could be recapitulated by FA supplementation.</p><p><strong>Conclusions: </strong>Our results reveal a profound alteration in the lipid content of iCCA tissues and demonstrate that FA accumulation prompts iCCA aggressiveness by supporting membrane biogenesis, generating bioactive lipids that boost proliferation, and by modifying macrophage phenotype.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 6","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12106197/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144132307","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":"HCC surveillance in hepatitis C: A longitudinal algorithm improves alpha-fetoprotein screening.","authors":"Tracey L Marsh, Janet M Johnston, Chriss Homan, Lisa J Townshend-Bulson, Nicole J Kim, Trang VoPham, Xiaohong Li, Qianchuan He, Brian J McMahon, George N Ioannou, Ziding Feng","doi":"10.1097/HC9.0000000000000719","DOIUrl":"10.1097/HC9.0000000000000719","url":null,"abstract":"<p><strong>Background: </strong>Surveillance for HCC remains important after hepatitis C cure. Improved sensitivity of screening with alpha-fetoprotein (AFP) by using a parametric empirical Bayes (PEB) algorithm, which incorporates an individual patient's longitudinal AFP measurements, was previously demonstrated in a retrospective analysis of clinical trial data prior to widespread hepatitis C cure.</p><p><strong>Methods: </strong>We analyzed de-identified data extracted from the medical records of participants in the Alaska Hepatitis C Study, which aims to enroll all Alaska Native persons living in Alaska with a history of hepatitis C.We compared the performance characteristics of AFP as a screening test using the PEB method versus a fixed cutoff (FC) method in an observational setting, separately for HCC surveillance in active and cured hepatitis C.</p><p><strong>Results: </strong>The PEB and FC methods were applied to AFP levels from participants with F3/F4 fibrosis who had active hepatitis C (173 no HCC, 14 HCC) or after they achieved hepatitis C cure (162 no HCC, 12 HCC). Compared to a fixed 20 ng/mL cutoff, demonstrating 91.2% specificity in active hepatitis C, PEB increased sensitivity from 64.3% to 71.4%. After cure, a fixed 7.2 ng/mL cutoff demonstrated 91.2% specificity, and PEB increased sensitivity from 58.3% to 91.7%.</p><p><strong>Conclusions: </strong>The PEB algorithm can increase sensitivity and lead to earlier detection of HCC among patients with F3/F4 fibrosis, both in active and even more so in cured hepatitis C. Lower AFP levels after cure indicate that for either PEB or FC methods, screening parameters, such as cutoffs for a target specificity, should be specified separately by hepatitis C treatment status for HCC surveillance.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 6","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12106215/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144132313","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":"Treatment of pruritus in primary sclerosing cholangitis: Analysis of the consortium for autoimmune liver disease registry.","authors":"Richard Dean, Maryam Yazdanfar, Joseph Zepeda, Cynthia Levy, Craig Lammert, Daniel Pratt, Stuart C Gordon, Lisa Forman, David N Assis, Ashleigh McGirr, Megan McLaughlin, Sumanta Mukherjee, Usha Gungabissoon, Christopher L Bowlus","doi":"10.1097/HC9.0000000000000703","DOIUrl":"10.1097/HC9.0000000000000703","url":null,"abstract":"<p><strong>Background: </strong>Cholestasis from primary sclerosing cholangitis (PSC) frequently causes pruritus. However, the prevalence of pruritus and its management have not been well studied. Investigating the Cholestatic Pruritus of Primary Sclerosing Cholangitis (ItCh-PSC) includes a retrospective medical record review to determine the prevalence, severity, and treatment patterns of pruritus.</p><p><strong>Methods: </strong>Data was collected at 5 academic medical centers in the United States. Medical records were searched for the terms \"itch\" and \"pruritus\" and data abstracted related to itch severity, number of encounters, and treatment.</p><p><strong>Results: </strong>Among 724 patients with PSC, 359 (50%) of patients had a documented history of pruritus, including 40%, 39%, and 21% with mild, moderate, or severe itch. Itch was less common in those with small ducts compared to large duct PSC (p=0.02) and more frequent in those of Hispanic versus non-Hispanic ethnicity (p=0.001). Compared to patients with mild itch, patients with moderate or severe itch were younger, and had more elevated liver biochemistries, more encounters with itch, and more frequently prescribed 2 or more anti-pruritic medications. Bile acid-binding resins were prescribed in 36%, hydroxyzine in 23%, rifampin in 11%, and fenofibrate in 4% of patients with any itch. The prevalence and severity of pruritus were not affected by cirrhosis, hepatic decompensation, or inflammatory bowel disease.</p><p><strong>Conclusion: </strong>Itch is common in patients with PSC and is often associated with multiple prescriptions of antipruritic agents. Effective treatments for pruritus in patients with PSC remain an unmet need.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 5","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12055165/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143995252","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":"Single-cell transcription reveals hepatocyte-to-cholangiocyte reprogramming and biliary gene profile in biliary atresia.","authors":"Lingdu Meng, Min Du, Haodong Li, Fanyang Kong, Jiajian Yang, Rui Dong, Shan Zheng, Gong Chen, Zhen Shen, Junfeng Wang","doi":"10.1097/HC9.0000000000000710","DOIUrl":"10.1097/HC9.0000000000000710","url":null,"abstract":"<p><strong>Background: </strong>Ductular reaction (DR), characterized by the expansion of biliary epithelial cells in the portal area, is a typical hepatic pathology for biliary atresia (BA). The cellular source and function of DR remain poorly understood. Herein, we performed single-cell RNA sequencing (scRNA-seq) in BA to resolve the complexity of DR in BA.</p><p><strong>Methods: </strong>A total of 4 BA and 3 normal control livers underwent scRNA-seq. The epithelial cells were extracted from all cells for further analysis. The cell types, functions, and differentiational trajectory of epithelial cells were determined. The biliary markers and transcription factors (TFs) were identified by combing public bulk and scRNA-seq data and validated by immunohistochemistry.</p><p><strong>Results: </strong>ScRNA-seq identified the existence of biliary reprogramming in BA, and the reprogrammed cells expressed both hepatocyte and cholangiocyte markers. When compared with hepatocytes, genes of epithelial-mesenchymal transition, fibrosis, inflammation, and RNA metabolism were enriched in cholangiocytes and upregulated in BA. Pseudotime analysis depicted a differentiation trajectory from hepatocytes across reprogrammed cells to cholangiocytes in BA. Matrix metalloproteinase 7 (MMP7), VTCN1, and LAMC2 were identified as the biliary markers, and KLF5 and HNF1B were determined as the biliary TFs in BA. All the biliary markers and TFs were upregulated in BA when compared with controls.</p><p><strong>Conclusions: </strong>Dissecting the cellular source and function of cholangiocytes is essential to understand the pathological role of DR in BA. The identified specific biliary markers and TFs provide important insights into its potential diagnosis and mechanism exploration for BA in the future.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 5","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12055120/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143970112","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":"Letter to the editor: Refining risk stratification in hepatic encephalopathy-External validation of the BABS score in European cohorts.","authors":"Nadja G Østberg, Gabriele Berg-Beckhoff, Lea L Grønkjær, Elise Jonasson, Eva Maria Schleicher, Simon J Gairing, Christian Labenz, Mette M Lauridsen","doi":"10.1097/HC9.0000000000000688","DOIUrl":"10.1097/HC9.0000000000000688","url":null,"abstract":"","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 5","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12055061/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144001738","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}