Hepatology Communications最新文献

{"title":"Prospective validation of a real-time natural language processing pipeline for the extraction of elastography results from electronic health record data.","authors":"Lale A Ertuglu, Christina Grimes, Dameia Brewster, Cathy A Jenkins, Qingxia Chen, Dario Giuse, Ashley Spann","doi":"10.1097/HC9.0000000000001000","DOIUrl":"10.1097/HC9.0000000000001000","url":null,"abstract":"","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"10 8","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13671591/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148561858","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":"Neoadjuvant therapy in primary liver cancer: From the missing piece to a new paradigm.","authors":"Zhe Li, Kui Ming Chan, Haojie Jin","doi":"10.1097/HC9.0000000000000977","DOIUrl":"10.1097/HC9.0000000000000977","url":null,"abstract":"","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"10 7","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13313668/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148338381","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":"Financial burden among liver transplant candidates is associated with financial distress and work impairment: A U.S. multicenter study.","authors":"Elizabeth S Aby, Melanie Hundt, Jonathan Rice, Mike Kriss, Kali Zhou, Lauren Nephew, Sarah R Lieber, Alvaro Noriega Ramirez, Brett E Fortune, Clara Tow, Paola Mejia, Deepika Devuni, Anita Krisharao, Shari Rogal, Alan Noll, Stela Celaj, Nathaly Cortez Bazan, Patricia Jones, Hersh Shroff, Krista Hunt, Areej Mazhar, Dempsey Hughes, Jackie B Henson, Lindsay Y King, Thomas M Leventhal, Enya Zhu, Grace Bizup, Lucinda Li, Malia Armstrong, Anushka Dalvi, Lina Nurhussien, Nora Horick, Chengbo Zeng, Nneka N Ufere","doi":"10.1097/HC9.0000000000000985","DOIUrl":"10.1097/HC9.0000000000000985","url":null,"abstract":"<p><strong>Background: </strong>The financial impact of chronic liver disease among adults undergoing liver transplant (LT) evaluation remains understudied. We performed a cross-sectional multicenter study to explore high financial burden, defined as medical out-of-pocket expenses ≥10% of income (per prior literature), among adult LT candidates. We aimed to identify associations between high financial burden and (1) work productivity impairment; (2) financial distress (material, behavioral, and psychological consequences of financial burden); (3) financial toxicity (health-related quality of life, HRQOL).</p><p><strong>Methods: </strong>From May 2023 to April 2024, 453 patients from 13 United States transplant centers were included. Patients completed questionnaires assessing financial burden, financial distress, financial toxicity (EuroQol EQ-5D-5L instrument), and work productivity and impairment (Work Productivity and Activity Impairment Questionnaire: Specific Health Problem Version).</p><p><strong>Results: </strong>Among LT candidates, 23.3% reported a high financial burden, and only 27.6% were employed. High financial burden was associated with a higher rate of absenteeism from work (34.1% vs. 16.9%, p=0.018) among employed participants. In adjusted models, high financial burden was significantly associated with inability to pay for basic necessities (aOR 4.76, 95% CI: 2.34-9.67), delayed or foregone medical care (aOR 4.02, 95% CI: 2.30-7.02), and psychological distress (aOR 4.63, 95% CI: 1.95-10.98) but was not associated with HRQOL (EQ-5D β: -0.04, 95% CI: -0.08 to 0.00; EQ-5D-VAS β: -4.53, 95% CI: -10.1 to 1.02).</p><p><strong>Conclusion: </strong>These results highlight the critical importance of implementing routine screening for financial burden in this high-risk population and developing strategies to mitigate associated adverse outcomes.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"10 7","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13313665/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148351772","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":"Reply: Rethinking sustained recompensation in MASLD cirrhosis: The value of pharmacological maintenance.","authors":"Alba Jiménez-Masip, Juan Manuel Pericàs Pulido","doi":"10.1097/HC9.0000000000000986","DOIUrl":"10.1097/HC9.0000000000000986","url":null,"abstract":"","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"10 7","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13286434/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148277306","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":"Methylation plus alpha-fetoprotein blood test for early detection of HCC in at-risk populations.","authors":"Neehar D Parikh, Chun-Chi Liu, Matthew DeMaio, Angela H Yeh, Mary L Stackpole, Shuo Li, Vatche G Agopian, Wenyuan Li, Xianghong Jasmine Zhou, Xiaohui Ni, Anna S Lok, Steven-Huy B Han","doi":"10.1097/HC9.0000000000000987","DOIUrl":"10.1097/HC9.0000000000000987","url":null,"abstract":"<p><strong>Background: </strong>Semi-annual abdominal ultrasound plus alpha-fetoprotein (AFP) is recommended for HCC surveillance but has limited performance, particularly in patients with metabolic dysfunction-associated steatotic liver disease. We aimed to validate a blood-based test combining cell-free DNA methylation profiling with AFP to improve HCC detection in at-risk individuals.</p><p><strong>Methods: </strong>Between September 1, 2023, and April 30, 2025, 135 patients with HCC and 167 at risk for HCC were prospectively recruited at 2o medical centers; archived samples (46 HCC and 32 at-risk) were also included. A cell-free DNA methylation assay was performed to generate methylation scores, and AFP testing was conducted as part of standard of care. A pretrained model integrated methylation scores and AFP levels for HCC detection.</p><p><strong>Results: </strong>The combination of methylation and AFP tests achieved an AUC of 0.94 (95% CI, 0.92-0.96) for detecting HCC in at-risk individuals, significantly outperforming both methylation alone (AUC: 0.92, 95% CI, 0.89-0.95; p=0.001) and AFP alone (AUC: 0.83, 95% CI, 0.79-0.87; p<0.0001). In patients with early-stage HCC (within Milan Criteria), the combined test achieved an AUC of 0.90 (95% CI, 0.86-0.94), outperforming methylation alone (AUC: 0.88, 95% CI, 0.83-0.92; p=0.002) and AFP alone (AUC: 0.81, 95% CI, 0.76-0.86; p<0.0001). At 92.0% specificity, sensitivity for early-stage HCC was 73% (95% CI, 64%-80%) with the combined test, compared with 62% (95% CI, 52%-71%; p=0.025) for methylation alone and 52% (95% CI, 43%-62%; p<0.0001) for AFP alone. Sensitivity improvements were consistent across major demographic and etiologic subgroups.</p><p><strong>Conclusions: </strong>The combination of cell-free DNA methylation with AFP shows promising performance for early-stage HCC detection in this case-control validation study and warrants further validation.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"10 7","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13286316/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148277221","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":"Progression of MASH to cirrhosis, decompensation, and mortality, and the utility of NITs for detection and risk stratification.","authors":"Philip N Newsome, Claudio Sartini, Heather L Morris, Derek Gazis, Andrea R Mospan, A Sidney Barritt, Michael W Fried, Salvador Augustin, Mandy Fraessdorf, Bryan Rudolph, Rohit Loomba, Arun Sanyal","doi":"10.1097/HC9.0000000000000962","DOIUrl":"10.1097/HC9.0000000000000962","url":null,"abstract":"<p><strong>Background: </strong>Recognition and management of metabolic dysfunction-associated steatohepatitis (MASH) are hindered by variability in diagnostic practices and limited real-world data on disease progression. This study assessed the use of non-invasive testing (NIT) in MASH identification and estimated incidence rates and time-to-disease progression.</p><p><strong>Methods: </strong>Adults in the TARGET-NASH cohort (enrolled 2016-2023) were included. MASH was confirmed via medical records, NITs, pathology reports, and imaging. Patients with MASH and significant/advanced fibrosis/cirrhosis (F2/F3/F4) were included. Outcomes included progression to cirrhosis, liver-related complications, and all-cause mortality.</p><p><strong>Results: </strong>Among 1964 patients (median age 59, median BMI 34), 79% had data to calculate Fibrosis-4 score (FIB-4), 36% had FibroScan, and 29% had biopsy. Among the 776 F2-F3 patients, 17% progressed to cirrhosis over a median follow-up (mFU) time of 64.6 months. In F2-F3 patients, one unit increase in FIB-4 was associated with 14% increased hazard of cirrhosis; similarly, incidence rates for cirrhosis in patients with liver stiffness measurements (LSMs) 10-15 kPa were 60.8/1000PY (per 1000 person-years; 3.5× higher than those with LSM <10 kPa). Among the 794 patients with compensated cirrhosis (cF4), 46% experienced progression events, 13% died, and 1.3% had a liver transplant (mFU=66.0 months). Among the 394 patients with decompensated cirrhosis (dF4), 29.4% died, and 9.6% had a liver transplant (mFU=62.0 months). Higher FIB-4 was associated with increased risk of decompensation and mortality in cF4 patients. Similarly, patients with LSM ≥15 kPa had a greater incidence rate of mortality (9.1/1000PY vs. 4.3/1000PY and 3.8/1000PY for LSM 10-15 kPa and <10 kPa, respectively).</p><p><strong>Conclusions: </strong>The burden of MASH underscores the urgency of standardizing NIT use and diagnosis. Expanding FibroScan use, automating FIB-4 calculation, and increasing awareness of NITs can improve early detection and risk stratification, thereby improving patient outcomes.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"10 7","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13286308/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148277209","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":"The PERK-GADD45A axis is a key driver of hepatic stellate cell activation.","authors":"Nipuni Barupala, Jagannath Misra, Emely Bibian, Reese Baxter, Vandana Singh, Noah Xique, Ethan D Goins, Alex Jackson, Scott M Ebert, Christopher M Adams, Jessica L Maiers","doi":"10.1097/HC9.0000000000000980","DOIUrl":"10.1097/HC9.0000000000000980","url":null,"abstract":"<p><strong>Background: </strong>Hepatic stellate cells (HSCs) play a pivotal role in driving fibrosis during chronic liver injury. HSCs produce vast amounts of fibrotic proteins, causing endoplasmic reticulum (ER) stress and initiating the unfolded protein response (UPR). While the UPR is important for fibrogenesis, how signaling through UPR transducer Protein Kinase R-like ER Kinase (PERK) and its effectors impact HSC activation and fibrogenesis is unclear. Here, we sought to uncover the role of PERK and its effector GADD45A in liver fibrosis.</p><p><strong>Methods: </strong>PERK-GADD45A signaling was assessed in primary and immortalized HSCs treated with TGFβ, and mouse models of fibrosis. Genetic and pharmacological disruption of PERK or GADD45A was used to assess the role of PERK or GADD45A in HSC activation, proliferation, and fibrogenesis. HSC-specific Gadd45a-null mice were utilized to investigate the role of GADD45A on CCl4-induced fibrosis.</p><p><strong>Results: </strong>We found that TGFβ-induction of collagen I drives activation of PERK signaling in HSCs. Furthermore, loss or inhibition of PERK limits long-term HSC activation as illustrated by reduced levels of collagen I and fibronectin, impaired collagen I deposition, and reduced cell proliferation in vitro. Next, we show that PERK signaling induces expression of GADD45A during HSC activation, and loss of GADD45A disrupts HSC activation and expression of proliferation and cell-cycle-associated genes in immortalized and primary HSCs. Finally, HSC-specific GADD4Aa loss limits CCl4-driven fibrogenesis in vivo.</p><p><strong>Conclusion: </strong>PERK signaling is critical for HSC activation, and loss of the PERK downstream effector GADD45A limits fibrosis progression. Disruption of HSC activation and proliferation, coupled with dysregulation of cell-cycle-associated genes upon PERK or GADD45A loss, suggests that PERK-GADD45A signaling impacts multiple facets of HSC pathophysiology.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"10 7","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13286415/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148277304","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":"Rethinking sustained recompensation in MASLD cirrhosis: The value of pharmacological maintenance.","authors":"Nobuyuki Toshikuni, Masaaki Shimatani","doi":"10.1097/HC9.0000000000000984","DOIUrl":"10.1097/HC9.0000000000000984","url":null,"abstract":"","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"10 7","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13286431/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148277289","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":"Long-term protection following a primary series of hepatitis B vaccine in Alaska Native children and adults.","authors":"Jonathan Steinberg, Ian Blake, Timothy Stevenson, Heather Wheelock, Dana Bruden, Lisa Townshend-Bulson, Joseph Klejka, Mark Peterson, Emily J Cartwright, Jan Drobeniuc, Heather M Scobie, Michael G Bruce, Marc Fischer, Brian McMahon","doi":"10.1097/HC9.0000000000000978","DOIUrl":"10.1097/HC9.0000000000000978","url":null,"abstract":"<p><strong>Background: </strong>Vaccination is effective at preventing chronic HBV infection and its complications, but the duration of protection and need for booster doses have not been determined.</p><p><strong>Methods: </strong>We administered a 3-dose primary series of plasma-derived hepatitis B vaccine to Alaska Native persons aged 6 months or above who resided in an HBV-endemic area of western Alaska. Persons with antibody to hepatitis B surface antigen (anti-HBs) ≥10 milli-international units per milliliter (mIU/mL) at 6 months after series completion were followed through 41 years after vaccination. Beginning at 22 years, participants with anti-HBs <10 mIU/mL were offered a booster dose (ie, challenge dose) of recombinant hepatitis B vaccine and retested 4 weeks later as a surrogate for immune memory. Combining these immune-memory data with a survival model estimating anti-HBs persistence, we estimated the overall proportion with serologic evidence of protection at 22, 30, 35, and 41 years. We also described breakthrough hepatitis B infections.</p><p><strong>Results: </strong>During 1981-1982, 1351 persons completed the hepatitis B vaccine primary series and had anti-HBs ≥10 mIU/mL at 6 months after vaccination; median age at enrollment was 13 years (range: 0.5-77). The overall proportion with serologic evidence of protection was 95% at 22 years, 95% at 30 years, 88% at 35 years, and 91% at 41 years after vaccination. At 41 years, 32% had circulating anti-HBs ≥10 mIU/mL, and 59% had immune memory. During 41 years of follow-up, 16 (1%) persons had evidence of a breakthrough infection; none developed chronic hepatitis B.</p><p><strong>Conclusions: </strong>We found serologic evidence of protection among Alaska Native persons 41 years after primary hepatitis B vaccination. Our findings support the recommendation that booster doses are not needed in endemic areas.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"10 7","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13286331/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148277183","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":"Reply: High mortality at safety-net hospitals for patients with cirrhosis.","authors":"Rebecca G Kim, Andrea Wallace, Jennifer C Price","doi":"10.1097/HC9.0000000000000965","DOIUrl":"10.1097/HC9.0000000000000965","url":null,"abstract":"","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"10 7","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13286337/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148277268","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}