Hepatology Communications最新文献

{"title":"Sex and racial disparities in clinical outcomes and health resource use among patients with primary biliary cholangitis in the United States.","authors":"Julius M Wilder, Hongbo Yang, Su Zhang, Dongni Ye, Sherry Shi, Anyu Zhu, Ashley Jowell, Larissa Lushniak, Nisreen Shamseddine","doi":"10.1097/HC9.0000000000001030","DOIUrl":"10.1097/HC9.0000000000001030","url":null,"abstract":"<p><strong>Background: </strong>Racial and sex disparities have been described in liver conditions, including primary biliary cholangitis (PBC). This study sought to understand how race/ethnicity and sex-based differences impact access to diagnosis, clinical outcomes, health resource use (HRU), and treatment among patients with PBC in the United States (US).</p><p><strong>Methods: </strong>Komodo Research Database claims data (2016-2023) for adults diagnosed with PBC were analyzed retrospectively. Patients were grouped by race/ethnicity (White, Black, Hispanic, Asian, and Other) and separately by sex (male or female). Clinical characteristics, treatment patterns, and HRU outcomes were assessed pre-index and post-index. The index date was defined as the first claim with a PBC diagnosis code. Statistical significance for comparisons was defined as p<0.05.</p><p><strong>Results: </strong>In total, 9554 and 11,591 patients were included in the race/ethnicity and sex analyses. Black and Hispanic patients (versus [vs.] White) and male patients (vs. female) had higher comorbidity burden and PBC-related symptoms pre-index. Post-index, Black patients (vs. White) had significantly higher risks of liver transplant and hospitalization due to hepatic decompensation (adjusted hazard ratio [HR] of 2.09 and 1.37, respectively). Hispanic patients (vs. White) had a significantly higher risk of developing cirrhosis (adjusted HR of 1.19). Males had a higher risk than females for all adverse outcomes. Most HRU outcomes were significantly higher for Black patients vs. White, while treatment rates and response rates to ursodeoxycholic acid were significantly lower for Black patients vs. White and male patients vs. female.</p><p><strong>Conclusions: </strong>These results highlight significant differences in disease management and treatment initiation across race/ethnicity and sex groups in the US. Improved provider awareness of such differences in PBC is required to support individualized management and ensure equitable access to PBC treatment.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"10 10","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13623276/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149080788","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 multicenter multistate modeling on the natural history of liver decompensation: Longitudinal analysis of 1777 patients.","authors":"Eunice X X Tan, Nicole Shu Ying Tang, Nicholas Syn, Daniel Q Huang, Anand V Kulkarni, Ming-Hua Zheng, Vincent L Chen, Chitchai Rattananukrom, Jimmy Che-To Lai, Karn Wijarnpreecha, Rahul Kumar, Apichat Kaewdech, Masayuki Ueno, Akash Roy, Ken Liu, Toru Nakamura, Yanhang Gao, Masato Yoneda, Yuya Seko, Takefumi Kimura, Mazen Nourredin, Mohammad Shadab Siddiqui, Hirokazu Takahashi, Cheng Han Ng, Mark Muthiah","doi":"10.1097/HC9.0000000000001042","DOIUrl":"10.1097/HC9.0000000000001042","url":null,"abstract":"<p><strong>Background: </strong>Cirrhosis often remains silent until decompensation, after which survival deteriorates sharply. Contemporary, transition-aware estimates are limited, especially in Asian-predominant cohorts. We analyzed trajectories from compensated advanced chronic liver disease (cACLD) through sequential decompensations to death.</p><p><strong>Method: </strong>In this multicenter study, we analyzed retrospective data from an adult cohort with liver stiffness ≥15 kPa from vibration-controlled transient elastography across 19 institutions internationally. Decompensation included ascites, hepatic encephalopathy, spontaneous bacterial peritonitis, or variceal bleeding. Multistate models were constructed to characterize patient trajectories across 4 main clinically meaningful states: baseline cACLD, first decompensation, a subsequent second decompensation, and death. Etiology-specific subgroup analyses were conducted, and the effects of univariable predictors on transitions were also examined.</p><p><strong>Results: </strong>Among 1777 patients, 265 (14.9%) developed a first decompensation over a median follow-up of 4.25 years. In the main multistate analysis cohort, from baseline cACLD, first decompensation occurred in 215 patients at 3.10 per 100 person-years, while death occurred at a rate of 1.01 per 100 person-years. The rate of a second decompensation was higher following the first decompensation, at 42.73 per 100 person-years. Patients with alcohol-associated liver disease had the highest rate of progression from baseline to first decompensation, whereas patients with hepatitis B etiology had the lowest progression rate into a second decompensation following a first decompensating event.</p><p><strong>Conclusion: </strong>Most patients with cACLD remain compensated over 10 years of follow-up, but once decompensation occurs, trajectories accelerate, and survival worsens. Transition-aware, etiology-stratified estimates enable individualized prognostication and earlier risk-guided intervention, including timely transplant referral.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"10 10","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13623273/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149080731","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":"Ferroptosis in liver biology and diseases.","authors":"Peng Cao, Peijian He, Kuo Du, Hartmut Jaeschke, John J Lemasters, Yiling Chen, Carmen Chak-Lui Wong, Wen-Xing Ding","doi":"10.1097/HC9.0000000000001058","DOIUrl":"10.1097/HC9.0000000000001058","url":null,"abstract":"<p><p>Ferroptosis is a form of non-apoptotic cell death driven by iron-dependent lipid peroxidation (LPO). Ferroptosis is closely associated with hepatic metabolic pathways, particularly those involving iron, fatty acids, amino acids, and redox changes. This review aims to provide a comprehensive overview of the current molecular pathways and regulatory mechanisms underlying iron homeostasis and intracellular compartmentation in liver biology, emphasizing the roles of ferroptosis in several liver diseases, such as ischemia-reperfusion injury, drug-induced liver injury, viral hepatitis, metabolic dysfunction-associated steatotic liver disease, alcohol-associated liver disease, fibrosis, and hepatocellular carcinoma. We have also discussed the challenges of interpreting ferroptosis-related data, proposed a framework for defining ferroptosis, and highlighted future research directions as well as the therapeutic potential of targeting ferroptosis in the treatment of various liver diseases.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"10 10","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13623292/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149080691","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":"Alcohol use trajectories and liver enzyme changes in adolescents with MASLD: A longitudinal multicenter cohort.","authors":"Nhat Quang N Thai, Laura A Wilson, Cynthia A Behling, Jeanne M Clark, Jean P Molleston, Kimberly P Newton, Rany M Salem, Gretchen Bandoli, John Alcaraz, Noe Crespo, Jeffrey B Schwimmer","doi":"10.1097/HC9.0000000000001056","DOIUrl":"10.1097/HC9.0000000000001056","url":null,"abstract":"<p><strong>Objectives: </strong>To characterize longitudinal patterns of alcohol use and evaluate associations with liver enzyme changes in youth with metabolic dysfunction-associated steatotic liver disease (MASLD).</p><p><strong>Methods: </strong>We analyzed 1172 children with biopsy-confirmed MASLD and longitudinal Alcohol Use Disorders Identification Test-Consumption (AUDIT-C) data. Group-based trajectory modeling identified alcohol use patterns over time. Linear mixed models assessed associations between alcohol trajectory groups and alanine aminotransferase (ALT), aspartate aminotransferase (AST), and gamma-glutamyl transferase (GGT). Generalized linear mixed models evaluated predictors of alcohol use, including age, sex, body mass index (BMI), fibrosis stage, and household income.</p><p><strong>Results: </strong>Among participants diagnosed with MASLD in childhood, 206 (17.6%) reported alcohol use during adolescence or early adulthood. Three alcohol-use groups were identified: non-users, adolescent initiators, and adult initiators. Heavy episodic drinking was reported by 48 of 71 adolescent initiators (67.6%) and 53 of 135 adult initiators (39.3%). Compared with non-users, alcohol initiators had lower liver chemistry values at enrollment but greater annual increases during follow-up. Adolescent initiators had a 4% greater annual increase in ALT, while adult initiators had 6%, 4%, and 3% greater annual increases in ALT, AST, and GGT, respectively.</p><p><strong>Conclusions: </strong>Nearly 1 in 5 youth with MASLD reported alcohol use during adolescence or early adulthood despite ongoing subspecialty care. Alcohol-use trajectories were associated with greater annual increases in liver chemistries, particularly among participants with heavy episodic drinking. These findings support routine alcohol screening and developmentally tailored anticipatory guidance in pediatric MASLD care.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"10 10","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13623281/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149080713","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":"Timing and trajectory of acute kidney injury predict mortality in alcohol-associated hepatitis: A multinational cohort study.","authors":"Butros Fakhoury, Ali Khan, Pojsakorn Danpanichkul, Omar Albhaisi, Kriti Soni, Ximena Parraga, Francisco Idalsoaga, Arun Valsan, Gowripriya Nair, Jorge Arnold, María Ayala-Valverde, Carolina Ramirez-Cadiz, Juan Pablo Roblero, Daniela Simian, José Antonio Velarde-Ruiz Velasco, Jacqueline Córdova, Manuel Mendizabal, Sebastián Marciano, Kristina R Chacko, Lubomir Skladaný, Michał Kukla, Arun J Sanyal, Vijay H Shah, Patrick S Kamath, Marco Arrese, Winston Dunn, Ashwani K Singal, Ramon Bataller, Luis Antonio Díaz, Juan Pablo Arab","doi":"10.1097/HC9.0000000000001047","DOIUrl":"10.1097/HC9.0000000000001047","url":null,"abstract":"<p><strong>Background: </strong>Acute kidney injury (AKI) is common in alcohol-associated hepatitis (AH) and associated with poor outcomes, yet the prognostic implications of AKI timing and early renal trajectory remain unclear.</p><p><strong>Methods: </strong>In this prospective multicenter cohort from the Global AlcHep Prospective Database, patients with AH were classified as no AKI, prevalent AKI at admission, or incident AKI during hospitalization. The primary outcome was 90-day mortality, using competing-risks regression with liver transplantation as the competing event. A 7-day landmark analysis assessed the prognostic impact of AKI trajectory among prevalent AKI patients.</p><p><strong>Results: </strong>Among 581 patients, 37% had prevalent AKI, and 11% developed incident AKI. The 90-day mortality was 18.2% (11 transplantations, 1.9%). Prevalent AKI was predominantly functional (84%), while incident AKI had a higher proportion of structural injury (44%). Despite lower baseline severity [median mDF 59.8 vs. 69.3 and lower rates of ACLF grade 3 (23.4% vs. 45.3%)], incident AKI conferred mortality of similar magnitude to prevalent AKI (sHR 2.18, 95% CI 1.19-3.99 vs. sHR 1.80, 95% CI 1.02-3.16). Among 7-day survivors (N=457), prevalent AKI without progression had mortality similar to no AKI (sHR 1.27, p=0.52), while prevalent AKI with progression carried the worst prognosis (sHR 3.34, 95% CI 1.44-7.77).</p><p><strong>Conclusion: </strong>Both prevalent and incident AKI independently predict mortality in AH. Incident AKI confers equivalent risk despite lower disease severity and a distinct etiologic profile with higher rates of intrinsic renal injury. Early renal trajectory refines risk beyond baseline AKI status, where absence of progression approximates outcomes of those without AKI, while progressive AKI identifies the highest-risk subgroup.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"10 10","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13585329/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148982557","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":"Mild alkaline phosphatase elevation associates with increased mortality and major adverse liver outcomes in MASLD.","authors":"Jingyi Hu, Christopher Okarski, Pooja Rangan, Blake Czapla, Kira Zhao, Ethan Grey, Suranjan Bantupalli, Leanne Nasser, Majd Aboona, Karn Wijarnpreecha, Vincent L Chen","doi":"10.1097/HC9.0000000000001044","DOIUrl":"10.1097/HC9.0000000000001044","url":null,"abstract":"<p><strong>Background: </strong>Alkaline phosphatase (ALP) elevation is commonly observed in patients with metabolic dysfunction-associated steatotic liver disease (MASLD), but its clinical implications in MASLD are unclear. We evaluated whether longitudinal patterns of mild ALP elevation are associated with mortality and major adverse liver outcomes (MALO).</p><p><strong>Methods: </strong>We performed a multicenter retrospective cohort study of adults with MASLD from Michigan Medicine and the Banner Health system. We included patients with MASLD defined as hepatic steatosis on imaging and at least one cardiometabolic comorbidity, with at least 1 ALP measurement within 1 year of the imaging date. Mild ALP elevation was defined as >1 to ≤1.5× the upper limit of normal and categorized as persistently normal, transiently elevated, or persistently elevated. Primary outcomes were all-cause mortality and MALO. Mortality was modeled as a Cox proportional hazards model, and MALO as Fine-Gray competing risk models.</p><p><strong>Results: </strong>Among 32,753 patients, persistently elevated ALP was present in ~10% of both cohorts. After multivariable adjustment, persistently elevated ALP was associated with increased mortality and MALO in both Michigan (mortality HR 1.51, 95% CI 1.20-1.89; MALO SHR 2.45, 95% CI 1.55-3.88) and Banner (mortality HR 1.81, 95% CI 1.19-2.75; MALO SHR 2.13, 95% CI 1.55-2.94). Associations were most consistent in low-risk and intermediate-risk FIB-4 groups. Associations remained significant in sensitivity analyses excluding baseline cirrhosis and restricting to patients with at least 2 ALP measurements.</p><p><strong>Conclusions: </strong>Persistent ALP elevation was associated with increased risk of mortality and MALO in MASLD, particularly among patients with low-risk and intermediate-risk FIB-4 scores. These findings suggest that ALP may serve as a clinically meaningful biomarker in early MASLD.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"10 10","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13585302/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148982537","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: Physical frailty is the most important predictor of early mortality in hospitalized patients with decompensated cirrhosis.","authors":"Chun-Mei Li, Xian Feng","doi":"10.1097/HC9.0000000000001037","DOIUrl":"10.1097/HC9.0000000000001037","url":null,"abstract":"","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"10 9","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13533487/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148864815","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":"MSCs overexpressing FGF21 alleviate acetaminophen-induced acute liver injury by eliciting macrophage-mediated phagocytosis.","authors":"Qian Huai, Cheng Zhu, Haoran Huang, Long Cheng, Xiaoqin Deng, Yue Wang, Tianyin Sun, Lijuan Mao, Yongkang Zhang, Mengwei Wu, Shi Yin, Hanren Dai, Xiaolei Li, Hua Wang","doi":"10.1097/HC9.0000000000001018","DOIUrl":"10.1097/HC9.0000000000001018","url":null,"abstract":"<p><strong>Background: </strong>Acetaminophen (APAP) is a widely used analgesic and antipyretic agent that is safe at therapeutic doses. However, due to its extensive misuse, APAP-induced liver injury has become a major public health concern. Although mesenchymal stem/stromal cells (MSCs) represent a promising emerging therapy for APAP-induced liver injury, considerable research has focused on enhancing their efficacy, notably through genetic modification. Fibroblast growth factor 21 (FGF21), an endocrine hormone activated by metabolic stress, is known to regulate energy homeostasis, glucose and lipid metabolism, and to promote the homing of MSCs to sites of injury. Consequently, this study was designed to determine whether genetically engineering MSCs to overexpress FGF21 (FGF21-MSCs) augments their therapeutic potential against APAP-induced acute liver injury (ALI).</p><p><strong>Methods: </strong>In this investigation, MSCs were employed as a platform for FGF21 gene delivery. The MSCs were transduced with lentiviral vectors encoding the FGF21 gene to facilitate sustained FGF21 overexpression. We subsequently assessed the therapeutic potential of these FGF21-MSCs in a murine model of APAP-induced ALI. The extent of liver injury was comprehensively evaluated. Furthermore, the underlying mechanisms were elucidated using techniques including immunohistochemistry, immunofluorescence, and flow cytometry.</p><p><strong>Results: </strong>Our results demonstrated that FGF21-MSCs significantly enhanced the therapeutic efficacy of conventional MSCs against APAP-induced ALI via a biphasic mechanism: attenuating oxidative stress and inflammation during the acute injury phase, while actively fostering tissue repair during the subsequent regenerative phase. This protective effect is primarily mediated through the enhancement of macrophage phagocytic capacity, thereby accelerating tissue repair and regeneration.</p><p><strong>Conclusions: </strong>Our findings demonstrate that FGF21-MSCs significantly augment therapeutic efficacy against APAP-induced ALI in mice, thereby yielding critical insights and revealing novel therapeutic targets for ALI prevention and treatment.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"10 9","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13533497/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148864818","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":"Hepatoprotective effects of resolvin D1 in mice exposed to ethanol and galactosamine.","authors":"Josiah Hardesty, Jeffrey Warner, Dennis Warner, Rui Treves, Nicolli Butzke-Souza, Jingzhi Wang, Yasmeen Abdelfadil, Dibson Gondim, Craig McClain, Irina Kirpich","doi":"10.1097/HC9.0000000000001039","DOIUrl":"10.1097/HC9.0000000000001039","url":null,"abstract":"<p><strong>Background: </strong>Alcohol-associated liver disease (ALD) is a major global health condition characterized by inflammation, hepatocellular injury, fibrosis, and impaired liver regeneration. To capture key features of severe ALD, we employed a murine model combining ethanol (EtOH) exposure with galactosamine (GalN), a hepatotoxic agent that sensitizes the liver to endotoxin-induced injury. Using this model, we evaluated the therapeutic efficacy of resolvin D1 (RvD1), a lipid mediator with potent anti-inflammatory and tissue-protective actions.</p><p><strong>Methods: </strong>C57BL/6J male mice were fed 5% EtOH-containing liquid diet for 10 days and administered GalN (500 mg/kg, i.p.) on days 9, 10, and 11, followed by a single EtOH binge (5 g/kg) on day 11. A separate cohort also received RvD1 (500 ng/mouse, days 7-12) as a therapy. Markers of endotoxemia, liver injury, inflammation, fibrosis, and regeneration were evaluated at 9 and 48 hours after the binge.</p><p><strong>Results: </strong>The EtOH+GalN model reproduced hallmark features of advanced ALD, including acute liver injury, sustained inflammation, induction of pro-fibrotic gene markers, reduced hepatic synthetic function, and markedly impaired regenerative capacity. RvD1 treatment significantly mitigated EtOH+GalN-induced pathology, lowering plasma endotoxin and ALT levels, reducing hepatic necrosis, and limiting neutrophil infiltration. RvD1 also decreased hepatic IL-6 levels at 9 hours and reduced IFN-γ at 48 hours. In addition, RvD1 attenuated the expression of pro-fibrotic genes and improved the diminished regenerative response in EtOH+GalN-treated mice, increasing hepatocyte proliferation at 48 hours and partially restoring plasma albumin concentrations.</p><p><strong>Conclusion: </strong>This study established an EtOH+GalN exposure mouse model of severe ALD and demonstrated that RvD1 exerts significant hepatoprotective effects. The findings support RvD1 as a promising therapeutic candidate for advanced ALD and provide the rationale for further mechanistic studies and translational evaluation.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"10 9","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13533502/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148864784","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":"Measuring quality of life in advanced chronic liver disease with FACT-Hep: Findings from the PAL LIVER trial.","authors":"Manisha Verma, Binu V John, Don Rockey, Sid Barritt, Victor Navarro, Linda K Shaw, Andrzej Kosinski, Elliot B Tapper, Archita P Desai","doi":"10.1097/HC9.0000000000001043","DOIUrl":"10.1097/HC9.0000000000001043","url":null,"abstract":"<p><strong>Background: </strong>Patient-reported outcome measures (PROMs) are increasingly incorporated into hepatology research, yet few have been rigorously evaluated, particularly among patients with decompensated cirrhosis. The Functional Assessment of Cancer Therapy-Hepatobiliary (FACT-Hep) captures multidimensional liver disease-specific burden, while the disease-agnostic PROMIS-29 assesses physical and mental health broadly. We evaluated the performance of FACT-Hep and its relationship to PROMIS-29 among participants with cirrhosis or hepatocellular carcinoma (HCC) enrolled in a prospective multicenter clinical trial.</p><p><strong>Methods: </strong>Baseline data were analyzed from 935 participants enrolled in the PAL LIVER trial. This study enrolled patients with Child-Turcotte-Pugh (CTP) B/C cirrhosis and/or with HCC. Health-related quality of life (HRQoL) was assessed using FACT-Hep and PROMIS-29. Correlations and multivariable linear regression models examined associations between PROM scores and clinical characteristics.</p><p><strong>Results: </strong>Among 935 patients, the mean FACT-Hep total score was 116 (SD 28.16), with worse scores among women, young participants (age <50 y), and Whites (all p<0.05). Patients with CTP B/C cirrhosis (83%) had worse HRQoL than those with HCC alone (28%) (p<0.0001). Younger age, higher MELD 3.0, smoking, and worse ECOG status were independently associated with total FACT-Hep score. FACT-Hep correlated with PROMIS preference scores (correlation coefficient=0.78). MELD 3.0 demonstrated a stronger association with total FACT-Hep score than with PROMIS measures.</p><p><strong>Conclusions: </strong>HRQoL measures provide important information distinct from disease severity indices. HRQoL impairment in patients with advanced chronic liver disease is driven primarily by decompensation, particularly ascites and hepatic encephalopathy. FACT-Hep and PROMIS-29 correlate well. FACT-Hep is a valid measure and effectively captures the multidimensional liver disease-specific burden. PROMIS-29 measures broader aspects that may be influenced by many factors beyond liver disease.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"10 9","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13533500/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148864834","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}