Hepatology Communications最新文献

{"title":"Neighborhood-level deprivation mediates racial and ethnic disparities in HCC diagnosis in Texas.","authors":"Itunu O Sokale, Aaron P Thrift, Hashem B El-Serag, Abiodun O Oluyomi","doi":"10.1097/HC9.0000000000000536","DOIUrl":"10.1097/HC9.0000000000000536","url":null,"abstract":"<p><strong>Background: </strong>Texas has the highest HCC rates in the United States, and the greatest burden is among Hispanics. Racial and ethnic disparities in HCC incidence have multiple underpinning factors. We conducted a mediation analysis to examine the role of neighborhood disadvantage (Area Deprivation Index) as a potential mediator of the association between neighborhood race and ethnicity distribution and neighborhood HCC case counts in Texas.</p><p><strong>Methods: </strong>The primary outcome measure was counts of new HCC diagnoses per census tract based on Texas Department of State Health Services Texas Cancer Registry data. The primary exposure of interest was the race and ethnicity-based Index of Concentration at the Extremes (non-Hispanic Black ICE or Hispanic ICE). We assessed Area Deprivation Index as a potential mediator of the association between Black/Hispanic ICE and HCC case counts. We adjusted the analyses for selected census tract characteristics.</p><p><strong>Results: </strong>We analyzed 4934 census tracts containing 13,632 new HCC diagnoses reported to Texas Cancer Registry between 2016 and 2020. Racial minority (Black/Hispanic ICE)-concentrated neighborhoods had a higher socioeconomic disadvantage. The results of the mediation analyses showed that compared to non-Hispanic White-concentrated census tracts, non-Hispanic Black-concentrated census tracts and Hispanic-concentrated census tracts had higher case counts of HCC (total effects: adjusted case count ratio: 1.03 [95% CI, 1.02-1.04] and adjusted case count ratio: 1.09 [95% CI, 1.08-1.10], respectively). Approximately 48% and 15% of the neighborhood-level disparity in HCC case counts were attributable to neighborhood socioeconomic disadvantage in Black and Hispanic minoritized neighborhoods, respectively.</p><p><strong>Conclusions: </strong>Neighborhood HCC case counts varied by neighborhood race and ethnicity distribution. The variations were partly explained by neighborhood deprivation, with a stronger effect among Black-concentrated census tracts.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"8 11","pages":""},"PeriodicalIF":5.6,"publicationDate":"2024-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11495745/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142931609","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":"FAK inhibition delays liver repair after acetaminophen-induced acute liver injury by suppressing hepatocyte proliferation and macrophage recruitment.","authors":"Qing Li, Qi Xu, Jialin Shi, Wei Dong, Junfei Jin, Chong Zhang","doi":"10.1097/HC9.0000000000000531","DOIUrl":"10.1097/HC9.0000000000000531","url":null,"abstract":"<p><strong>Background: </strong>Overdose of acetaminophen (APAP), a commonly used antipyretic analgesic, can lead to severe liver injury and failure. Current treatments are only effective in the early stages of APAP-induced acute liver injury (ALI). Therefore, a detailed examination of the mechanisms involved in liver repair following APAP-induced ALI could provide valuable insights for clinical interventions.</p><p><strong>Methods: </strong>4D-label-free proteomics analysis was used to identify dysregulated proteins in the liver of APAP-treated mice. RNA-Seq, hematoxylin-eosin staining, immunohistochemical staining, immunofluorescence staining, quantitative PCR, western blotting, transwell were used to explore the underlying mechanisms.</p><p><strong>Results: </strong>Utilizing high throughput 4D-label-free proteomics analysis, we observed a notable increase in proteins related to the \"focal adhesion\" pathway in the livers of APAP-treated mice. Inhibiting focal adhesion kinase (FAK) activation with a specific inhibitor, 1,2,4,5-Benzenetetraamine tetrahydrochloride (also called Y15), resulted in reduced macrophage numbers, delayed necrotic cell clearance, and inhibited liver cell proliferation in the necrotic regions of APAP-treated mice. RNA-Seq analysis demonstrated that Y15 downregulated genes associated with \"cell cycle\" and \"phagosome\" pathways in the livers of APAP-treated mice. Furthermore, blocking extracellular matrix (ECM)-integrin activation with a competitive peptide inhibitor, Gly-Arg-Gly-Asp-Ser (GRGDS), suppressed FAK activation and liver cell proliferation without affecting macrophage recruitment to necrotic areas. Mechanistically, ECM-induced FAK activation upregulated growth-promoting cell cycle genes, leading to hepatocyte proliferation, while CCL2 enhanced FAK activation and subsequent macrophage recruitment via F-actin rearrangement.</p><p><strong>Conclusions: </strong>Overall, these findings underscore the pivotal role of FAK activation in liver repair post-APAP overdose by promoting liver cell proliferation and macrophage recruitment.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"8 11","pages":""},"PeriodicalIF":5.6,"publicationDate":"2024-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11495758/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142931604","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 tyrosine kinase Yes1 is a druggable host factor of HEV.","authors":"Jil Alexandra Haase, Abarna Baheerathan, Xin Zhang, Rebecca Menhua Fu, Maximilian Klaus Nocke, Charlotte Decker, Viet Loan Dao Thi, Daniel Todt, Johan Neyts, Suzanne J F Kaptein, Eike Steinmann, Volker Kinast","doi":"10.1097/HC9.0000000000000553","DOIUrl":"10.1097/HC9.0000000000000553","url":null,"abstract":"<p><strong>Background: </strong>HEV is a positive-sense, single-stranded RNA virus of the Hepeviridae family. Although HEV accounts for more than 3 million symptomatic cases of viral hepatitis per year, specific anti-HEV therapy and knowledge about HEV pathogenesis are scarce.</p><p><strong>Methods: </strong>To gain a deeper understanding of the HEV infectious cycle and guide the development of novel antiviral strategies, we here used an RNAi mini screen targeting a selection of kinases, including mitogen-activated protein kinases, receptor tyrosine kinases, and Src-family kinases. Further, we used state-of-the-art HEV infection models, including primary human hepatocytes and athymic nude rats.</p><p><strong>Results: </strong>Upon knockdown of the Src-family kinase Yes1, a significant reduction of HEV susceptibility could be observed, suggesting an important role of Yes1 in the HEV infectious cycle. Selective inhibition of Yes1 kinase activity resulted in significant inhibition of HEV infection in hepatoma cells and primary human hepatocytes, as well as in a rat HEV in vivo model system. Subsequent analysis of Y1KI during the HEV infectious life cycle indicated a role of Yes1 kinase activity in the early onset of HEV infection.</p><p><strong>Conclusions: </strong>We identified the dependence of HEV on Yes1 signaling, which may contribute to the so far scarce knowledge of HEV's pathogenesis in the future. Moreover, we provide Y1KI as a novel antiviral drug candidate specifically targeting an HEV host factor.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"8 11","pages":""},"PeriodicalIF":5.6,"publicationDate":"2024-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11495762/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142667334","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":"Serum levels of total bile acids are associated with an increased risk of HCC in patients with cirrhosis.","authors":"Hashem B El-Serag, Aaron P Thrift, Hao Duong, Jing Ning, Saira Khaderi, Amit G Singal, Sumeet K Asrani, Jorge A Marrero, Hannah Powell, Kinza Rizwan, Omar Najjar, Christopher I Amos, Michelle Luster, Abeer Al-Sarraj, Emad Salem, Michael E Scheurer, Jagpreet Chhatwal, Salma Kaochar, Fasiha Kanwal","doi":"10.1097/HC9.0000000000000545","DOIUrl":"10.1097/HC9.0000000000000545","url":null,"abstract":"<p><strong>Background: </strong>Previous studies have reported higher circulating bile acid levels in patients with HCC compared to healthy controls. However, the association between prediagnostic bile acid levels and HCC risk among patients with cirrhosis is unclear.</p><p><strong>Methods: </strong>We measured total BA (TBA) concentration in serum samples collected from a prospective cohort of patients with cirrhosis who were followed until the development of HCC, death, or last study date. Competing risk proportional hazard-adjusted models were used to estimate the association between tertiles of serum TBA levels and the risk of developing HCC. We quantified the incremental predictive value of serum bile acid when added to a previously validated clinical model.</p><p><strong>Results: </strong>We analyzed data from 940 patients with cirrhosis, of whom 68 patients progressed to HCC during 3406 person-years of follow-up. Higher baseline serum TBA level was significantly associated with an increased risk of developing HCC with an adjusted HR of 3.69 (95% CI = 1.85-7.37) for the highest versus lowest tertile. TBA levels significantly increased predictive ability for progression to HCC at 2 years of follow-up; the c statistic increased from 0.74 to 0.80 (p < 0.001). There was evidence for a significant interaction between TBA level and hepatitis C (p = 0.04).</p><p><strong>Conclusions: </strong>In a large prospective cohort study, the prediagnostic serum level of TBAs was associated with a significant increase in the risk of developing HCC among patients with multi-etiology cirrhosis. The TBA-associated risk was additive to that of established demographic and clinical predictors.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"8 11","pages":""},"PeriodicalIF":5.6,"publicationDate":"2024-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11469875/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142800578","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":"Impact of social determinants of health on hepatocellular carcinoma surveillance, treatment, and health care costs.","authors":"Amit G Singal, Karl M Kilgore, Elizabet Shvets, Neehar D Parikh, Neil Mehta, A Burak Ozbay, Christie Teigland, Omar Hafez, Amy Schroeder, Audrey Yang, Jill Schinkel","doi":"10.1097/HC9.0000000000000517","DOIUrl":"10.1097/HC9.0000000000000517","url":null,"abstract":"<p><strong>Background: </strong>The impact of clinical factors and social determinants of health on treatment patterns and health care costs among patients with HCC is unknown.</p><p><strong>Methods: </strong>Using 100% Medicare Fee-For-Service claims and a commercial multipayor claims database, we identified patients diagnosed with HCC from January 1, 2017, to December 31, 2020. Surveillance receipt was defined 12 months prior to HCC diagnosis, whereas treatment and health care costs were assessed post-HCC diagnosis. Multinomial logistic regression was used to assess the association between demographics, social determinants of health, and surveillance or HCC treatment. Multivariable generalized linear regression was used to identify factors associated with total health care costs.</p><p><strong>Results: </strong>Of the 32,239 patients with HCC (mean age 68 y, 67% male, 73% White), 70% received surveillance and only half (51%) received any treatment. Curative treatment receipt was higher among those with prior surveillance (24% with CT/MRI and 18% with ultrasound vs. 9% with no surveillance). Curative treatment was independently associated with HCC surveillance and inversely associated with Black race, lower education level, and diagnosis in the year 2020 (COVID-19 year). Higher health care costs were independently associated with Black race, low English proficiency, living alone, and diagnosis in 2018-2020, and inversely associated with CT/MRI-based surveillance.</p><p><strong>Conclusions: </strong>Race and social determinants of health were independently associated with curative treatment receipt and health care costs. Increasing access to high-quality HCC surveillance may improve treatment receipt and reduce health disparities among patients with HCC.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"8 11","pages":""},"PeriodicalIF":5.6,"publicationDate":"2024-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11469853/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142406333","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":"Zinc supplementation to improve prognosis in patients with compensated advanced chronic liver disease: a multicenter, randomized, double-blind, placebo-controlled clinical trial.","authors":"Juan Bañares, Laia Aceituno, Lourdes Ruiz-Ortega, Mònica Pons, Juan G Abraldes, Joan Genescà","doi":"10.1097/HC9.0000000000000524","DOIUrl":"10.1097/HC9.0000000000000524","url":null,"abstract":"<p><p>Zinc homeostasis could play a role in compensated advanced chronic liver disease, and its supplementation has been linked to improvement in liver function, a decrease of hepatic complications, and reduction in HCC incidence. Compensated advanced chronic liver disease encompasses a heterogeneous group of patients with variable risks of clinically significant portal hypertension and clinical events. The ANTICIPATE model is a validated model for stratifying these risks. Our aim is to demonstrate that zinc administration can reduce the rate and risk of presenting clinical events (first decompensation, HCC, death, and liver transplantation). This study protocol describes an ongoing phase III, national, multicenter, randomized, double-blind clinical trial that will enroll 300 patients to receive either the trial treatment (zinc acexamate) or placebo. An inclusion period of 42 months is planned, with a minimum follow-up of 2 years. Our principal hypothesis is that zinc could modify the natural history of patients with compensated advanced chronic liver disease, with an overall improvement in prognosis.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"8 11","pages":""},"PeriodicalIF":5.6,"publicationDate":"2024-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11469812/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142406335","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":"Impact of racial, ethnic, and socioeconomic disparities on presentation and survival of HCC: A multicenter study.","authors":"Nicole E Rich, Patricia D Jones, Hong Zhu, Tanushree Prasad, Amy Hughes, Sandi Pruitt, Caitlin C Murphy, Karim Seif-El-Dahan, Darine Daher, Gloria Figueroa, Stephanie Castaneda, Lisa Quirk, Michael Gonzales, Osiris Carranza, Samantha Bourque, Nargis Baset, Adam C Yopp, Amit G Singal","doi":"10.1097/HC9.0000000000000477","DOIUrl":"10.1097/HC9.0000000000000477","url":null,"abstract":"<p><strong>Background: </strong>Racial and ethnic disparities have been reported for HCC prognosis, although few studies fully account for clinically important factors and social determinants of health, including neighborhood socioeconomic status.</p><p><strong>Methods: </strong>We conducted a retrospective multicenter cohort study of patients newly diagnosed with HCC from January 2010 through August 2018 at 4 large health systems in the United States. We used multivariable logistic regression and cause-specific Cox proportional hazard models to identify factors associated with early-stage HCC presentation and overall survival.</p><p><strong>Results: </strong>Of 2263 patients with HCC (37.6% non-Hispanic White, 23.5% non-Hispanic Black, 32.6% Hispanic, and 6.4% Asian/other), 42.0% of patients presented at an early stage (Barcelona Clinic Liver Cancer stage 0/A). In fully adjusted models, there were persistent Black-White disparities in early-stage presentation (OR: 0.63, 95% CI: 0.45-0.89) but not Hispanic-White disparities (OR: 0.93, 95% CI: 0.70-1.24). Median survival was 16.2 (IQR: 5.8-36.8) months for White patients compared to 15.7 (IQR: 4.6-34.4) months for Hispanic, 10.0 (IQR: 2.9-29.0) months for Black, and 9.5 (IQR: 3.4-31.9) months for Asian/other patients. Black-White disparities in survival persisted after adjusting for individual demographics and clinical factors (HR: 1.30, 95% CI: 1.09-1.53) but were no longer observed after adding HCC stage and treatment (HR: 1.05, 95% CI: 0.88-1.24), or in fully adjusted models (HR: 0.97, 95% CI: 0.79-1.18). In fully adjusted models, Hispanic-White (HR: 0.87, 95% CI: 0.73-1.03) and Asian/other-White (HR: 0.85, 95% CI: 0.63-1.15) differences in survival were not statistically significant, although patients in high-SES neighborhoods had lower mortality (HR: 0.69, 95% CI: 0.48-0.99).</p><p><strong>Conclusions: </strong>In a multicenter cohort of patients with HCC, racial and ethnic differences in HCC prognosis were explained in part by differences in tumor stage at diagnosis and neighborhood SES. These data inform targets to intervene and reduce disparities.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"8 11","pages":""},"PeriodicalIF":5.6,"publicationDate":"2024-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11469814/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142817856","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":"Concordance of MASLD and NAFLD nomenclature in youth participating in the TARGET-NASH real-world cohort.","authors":"Cristian Sanchez-Torres, Ana Ramirez Tovar, Kelsey Chatman, Heather L Morris, Feng Yu, Andrea R Mospan, Anna Mae Diehl, Daniel H Leung, Preeti Viswanathan, James E Squires, Sirish Palle, Miriam B Vos","doi":"10.1097/HC9.0000000000000546","DOIUrl":"10.1097/HC9.0000000000000546","url":null,"abstract":"","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"8 11","pages":""},"PeriodicalIF":5.6,"publicationDate":"2024-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11469899/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142464076","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":"Transforming steatotic liver disease management: The emerging role of GLP-1 receptor agonists.","authors":"Ellen L Jensen, Mads Israelsen, Aleksander Krag","doi":"10.1097/HC9.0000000000000561","DOIUrl":"10.1097/HC9.0000000000000561","url":null,"abstract":"<p><p>Chronic liver disease is a major cause of mortality, with approximately 2 million deaths worldwide each year, and it poses a significant economic burden. The most common cause of chronic liver disease in the United States and Europe is steatotic liver disease (SLD), which includes metabolic dysfunction-associated SLD, metabolic dysfunction and alcohol-associated SLD, and alcohol-associated liver disease (ALD). Effective treatment of these conditions is essential to reduce the liver disease burden, with promising approaches including treating cardiometabolic risk factors and excessive alcohol intake. Glucagon-like peptide 1 receptor agonists, both as monotherapy and in combination with other drugs, are gaining attention for their beneficial impact on cardiometabolic risk factors and excessive alcohol intake. In this review, we examine the molecular and clinical effects of glucagon-like peptide 1 receptor agonists, focusing on their direct hepatic steatohepatitis and liver fibrosis but also the indirect influence on cardiometabolic risk factors and excessive alcohol intake as key features of SLD. We also explore the future implications of glucagon-like peptide 1 receptor agonists for treating metabolic dysfunction-associated SLD, metabolic dysfunction and alcohol-associated SLD, alcohol-associated liver disease, and the potential challenges.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"8 11","pages":""},"PeriodicalIF":5.6,"publicationDate":"2024-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11469819/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142406334","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":"Infections in decompensated cirrhosis: Pathophysiology, management, and research agenda.","authors":"Jessica Ferguson Toll, Elsa Solà, Maria Alejandra Perez, Salvatore Piano, Alice Cheng, Aruna K Subramanian, W Ray Kim","doi":"10.1097/HC9.0000000000000539","DOIUrl":"10.1097/HC9.0000000000000539","url":null,"abstract":"<p><p>Bacterial infections in patients with cirrhosis lead to a 4-fold increase in mortality. Immune dysfunction in cirrhosis further increases the risk of bacterial infections, in addition to alterations in the gut microbiome, which increase the risk of pathogenic bacteria. High rates of empiric antibiotic use contribute to increased incidence of multidrug-resistant organisms and further increases in mortality. Despite continous advances in the field, major unknowns regarding interactions between the immune system and the gut microbiome and strategies to reduce infection risk and improve mortality deserve further investigation. Here, we highlight the unknowns in these major research areas and make a proposal for a research agenda to move toward improving disease progression and outcomes in patients with cirrhosis and infections.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"8 10","pages":""},"PeriodicalIF":5.6,"publicationDate":"2024-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11458171/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142371729","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}