Hepatology Communications最新文献

{"title":"Recent TIPS increases postoperative mortality: A national cohort study.","authors":"Helen Tang, David E Kaplan, Samir Abu-Gazala, Nadim Mahmud","doi":"10.1097/HC9.0000000000000577","DOIUrl":"https://doi.org/10.1097/HC9.0000000000000577","url":null,"abstract":"<p><strong>Background: </strong>Patients with cirrhosis have an increased risk of postoperative mortality, which is partially attributable to portal hypertension. Preoperative TIPS placement may reduce operative risk. Studies suggesting the benefits of preoperative TIPS are limited by residual confounding and lack of longitudinal laboratory data. To address these limitations, we used granular longitudinal data from the Veterans Health Administration.</p><p><strong>Methods: </strong>This retrospective cohort study of Veterans Health Administration patients with cirrhosis who underwent major surgery from 2008 to 2022 identified patients who underwent TIPS placement within 6 months before surgery. Demographics, comorbidities, surgery type, and longitudinal laboratory data were incorporated into a propensity score using 5:1 caliper matching for receipt of TIPS. The propensity-matched cohort included 39 patients with preoperative TIPS and 171 without.</p><p><strong>Results: </strong>Baseline characteristics were similar between groups. In Cox regression, recent TIPS was associated with an increased risk of postoperative mortality (HR: 2.69, 95% CI: 1.37-5.30, p = 0.004), redemonstrated in 500 random resampling events (median HR: 1.71). TIPS and non-TIPS patients had similar albumin, bilirubin, and international normalized ratio 6 months before surgery; however, immediately before surgery, TIPS patients had lower albumin (p = 0.009), higher bilirubin (p = 0.001), and higher international normalized ratio (p = 0.001).</p><p><strong>Conclusions: </strong>In a propensity-matched analysis of patients with cirrhosis undergoing major surgery, recent TIPS was associated with increased postoperative mortality and worsened liver synthetic function in the immediate preoperative period. TIPS placement should be carefully considered in patients with cirrhosis who may undergo surgery.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"8 12","pages":""},"PeriodicalIF":5.6,"publicationDate":"2024-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11608713/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142768548","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 protein risk stratification score for diagnostic evaluation of metabolic dysfunction-associated steatohepatitis.","authors":"Michelle Lai, Simon T Dillon, Xuesong Gu, Tina L Morhardt, Yuyan Xu, Noel Y Chan, Beibei Xiong, Handan Can, Long H Ngo, Lina Jin, Xuehong Zhang, Claudia C Moreira, Nathalie C Leite, Cristiane A Villela-Nogueira, Hasan H Otu, Jörn M Schattenberg, Detlef Schuppan, Nezam H Afdhal, Towia A Libermann","doi":"10.1097/HC9.0000000000000586","DOIUrl":"https://doi.org/10.1097/HC9.0000000000000586","url":null,"abstract":"<p><strong>Background: </strong>Reliable, noninvasive tools to diagnose at-risk metabolic dysfunction-associated steatohepatitis (MASH) are urgently needed to improve management. We developed a risk stratification score incorporating proteomics-derived serum markers with clinical variables to identify high-risk patients with MASH (NAFLD activity score >4 and fibrosis score >2).</p><p><strong>Methods: </strong>In this 3-phase proteomic study of biopsy-proven metabolic dysfunction-associated steatotic fatty liver disease, we first developed a multi-protein predictor for discriminating NAFLD activity score >4 based on SOMAscan proteomics quantifying 1305 serum proteins from 57 US patients. Four key predictor proteins were verified by ELISA in the expanded US cohort (N = 168) and enhanced by adding clinical variables to create the 9-feature MASH Dx score, which predicted MASH and also high-risk MASH (F2+). The MASH Dx score was validated in 2 independent, external cohorts from Germany (N = 139) and Brazil (N = 177).</p><p><strong>Results: </strong>The discovery phase identified a 6-protein classifier that achieved an AUC of 0.93 for identifying MASH. Significant elevation of 4 proteins (THBS2, GDF15, SELE, and IGFBP7) was verified by ELISA in the expanded discovery and independently in the 2 external cohorts. MASH Dx score incorporated these proteins with established MASH risk factors (age, body mass index, ALT, diabetes, and hypertension) to achieve good discrimination between MASH and metabolic dysfunction-associated steatotic fatty liver disease without MASH (AUC: 0.87-discovery; 0.83-pooled external validation cohorts), with similar performance when evaluating high-risk MASH F2-4 (vs. MASH F0-1 and metabolic dysfunction-associated steatotic fatty liver disease without MASH).</p><p><strong>Conclusions: </strong>The MASH Dx score offers the first reliable noninvasive approach combining novel, biologically plausible ELISA-based fibrosis markers and clinical parameters to detect high-risk MASH in patient cohorts from the United States, Brazil, and Europe.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"8 12","pages":""},"PeriodicalIF":5.6,"publicationDate":"2024-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11608748/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142768549","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":"Blocking interleukin-1 receptor type 1 (IL-1R1) signaling in hepatocytes slows down diethylnitrosamine-induced liver tumor growth in obese mice.","authors":"Nadine Gehrke, Lea J Hofmann, Beate K Straub, Dirk A Ridder, Ari Waisman, Leonard Kaps, Peter R Galle, Jörn M Schattenberg","doi":"10.1097/HC9.0000000000000568","DOIUrl":"https://doi.org/10.1097/HC9.0000000000000568","url":null,"abstract":"<p><strong>Background: </strong>An increasing number of HCC develops in the context of metabolic dysfunction-associated steatotic liver disease and its inflammatory form, metabolic dysfunction-associated steatohepatitis, even in the absence of cirrhosis. Chronic metabolic inflammation is the driving force of metabolic dysfunction-associated steatotic liver disease progression and a key factor in hepatocarcinogenesis. Given the prominent role of IL-1 signaling in inflammation and metabolic diseases, we investigated the relevance of the hepatocyte-specific IL-1 receptor type 1 knockout in metabolic dysfunction-associated steatohepatitis-related noncirrhotic HCC.</p><p><strong>Methods: </strong>For HCC induction, Il1r1Hep-/- mice received a single i.p. injection of diethylnitrosamine at 2 weeks and were fed with high-fat plus high-carbohydrate diet, starting from 4 weeks. After 18 weeks of diet intervention, mice were sacrificed, and macroscopic and microscopic tumor loads were assessed.</p><p><strong>Results: </strong>Knockout of the hepatic IL-1 receptor type 1 pathway significantly reduced liver tumor growth. Il1r1Hep-/- mice were also less susceptible to hepatic steatosis, insulin resistance, and associated hepatic c-Jun N-terminal kinase activation than their wild-type (WT) littermates. Reduced Ki-67 and cyclin D1 levels, as well as decreased phosphorylation of signal transducer and activator of transcription 3, occur in Il1r1Hep-/- livers, lowering cancer cell proliferation and growth. Additionally, in Il1r1Hep-/- livers, the chemokine (C-X-C motif) ligand 1/2-driven accumulation of myeloid-derived suppressor cells and CD8+ T-cell infiltration were reduced compared to the wild type.</p><p><strong>Conclusions: </strong>Metabolic inflammation mediated by the hepatocytic IL-1 receptor type 1 is a cofactor in mutagenic hepatocarcinogenesis. Targeting IL-1 signaling could be an adjunct strategy to the current immunomodulatory HCC treatments.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"8 12","pages":""},"PeriodicalIF":5.6,"publicationDate":"2024-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11608749/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142768545","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":"Missense variants in the TRPMr7 α-kinase domain are associated with recurrent pediatric acute liver failure.","authors":"Lea D Schlieben, Melanie T Achleitner, Billy Bourke, Max Diesner, René G Feichtinger, Alexander Fichtner, Christa Flechtenmacher, Nedim Hadzic, Robert Hegarty, Andreas Heilos, Andreas Janecke, Vassiliki Konstantopoulou, Dominic Lenz, Johannes A Mayr, Thomas Müller, Holger Prokisch, Georg F Vogel","doi":"10.1097/HC9.0000000000000598","DOIUrl":"10.1097/HC9.0000000000000598","url":null,"abstract":"<p><strong>Background: </strong>Pediatric acute liver failure (PALF) is a rare and life-threatening condition. In up to 50% of PALF cases, the underlying etiology remains unknown during routine clinical testing. This lack of knowledge complicates clinical management and liver transplantation decisions. Recently, whole-exome sequencing has identified genetic disorders in a large number of cases without specific laboratory biomarkers or metabolic fingerprints.</p><p><strong>Methods: </strong>We describe how further analysis of whole-exome sequencing data combined with proteomic analyses in 5 previously unsolved PALF patients, where no pathogenic variants in genes previously associated with acute liver failure were identified, revealed rare biallelic variants in transient receptor potential cation channel subfamily M member 7 (TRPM7).</p><p><strong>Results: </strong>We establishe TRPM7 as a novel disease gene for PALF. Yet, the cation channel kinase TRPM7 has not been associated with any Mendelian disorder. No homozygous loss-of-function variants were found in in-house exomes or publicly available databases. Rare biallelic TRPM7-variants were significantly enriched in the PALF cohort compared with a pediatric control cohort. Viral infections preceded the majority of PALF episodes. Recurrent PALF episodes characterized the disease course with rapid progression, leading to early death in 3 cases. Proteomic analyses of patient fibroblasts unveiled significantly reduced TRPM7 protein levels, indicative of functional impairment. Severely reduced Mg2+ levels in one individual with a mutation in the channel domain suggests a potential interaction between disturbed Mg2+ homeostasis and PALF. The consistent presence of mutations in the TRPM7 protein-kinase-domain across all patients suggests its specific relevance in PALF.</p><p><strong>Conclusions: </strong>Our data extend the genetic spectrum of recurrent PALF and prompt consideration of TRPM7 in children with unexplained liver failure.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"8 12","pages":""},"PeriodicalIF":5.6,"publicationDate":"2024-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11608757/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142768546","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":"Modeling metabolic-associated steatohepatitis with human pluripotent stem cell-derived liver organoids.","authors":"Xiaoshan Wu, Dacheng Jiang, Yuchen Wang, Xin Li, Chenyu Liu, Yanhao Chen, Wei Sun, Ruikun He, Yi Yang, Xiaosong Gu, Chunping Jiang, Qiurong Ding","doi":"10.1097/HC9.0000000000000585","DOIUrl":"https://doi.org/10.1097/HC9.0000000000000585","url":null,"abstract":"<p><strong>Background: </strong>Metabolic-associated steatohepatitis (MASH) is one of the most prevalent liver diseases worldwide, with a global prevalence estimated between 3% and 5%, posing a significant health burden. Human liver organoids (HLOs) have previously been generated to model steatohepatitis, offering a potential cellular disease model for studying MASH. However, the current HLO model lacks detailed molecular characterizations and requires further improvement.</p><p><strong>Methods: </strong>HLOs derived from human pluripotent stem cells were treated with oleic acid and TGFβ to mimic the MASH progression. Treated HLOs were then analyzed using both bulk and single-cell RNA sequencing. Functional characterization was performed through staining with BODIPY, TMRM, CellROX, and Collagen I, as well as terminal deoxynucleotidyl transferase dUTP nick end labeling and ELISA assays. In addition, a test using the MASH HLO model to validate the hepatoprotective effects of several herb extracts was also conducted.</p><p><strong>Results: </strong>Both RNA-seq and single-cell RNA sequencing demonstrated a close resemblance of multiple molecular signatures and key intercellular communications in and between hepatocyte-like cells and stellate-like cells in the MASH HLO model, compared to human MASH. Furthermore, functional characterizations revealed progressive features of human MASH in the MASH HLO model, including severe steatosis, oxidative stress, mitochondrial dysfunction, inflammation, and fibrosis. In addition, the Schisandra extracts have been demonstrated to have significant antioxidative, anti-inflammatory, and antifibrotic properties in the context of MASH.</p><p><strong>Conclusions: </strong>This study offers an improved HLO disease model of human MASH, which can be potentially applied to facilitate the understanding of the MASH pathogenesis and the discovery of effective treatments.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"8 12","pages":""},"PeriodicalIF":5.6,"publicationDate":"2024-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11608672/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142768547","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 pyruvate dehydrogenase kinase inhibitor dichloroacetate mitigates alcohol-induced hepatic inflammation and metabolic disturbances in mice.","authors":"Jianguo Wu, Emily Huang, Megan R McMullen, Vaibhav Singh, Marko Mrdjen, Annette Bellar, Li Wang, Nicole Welch, Jaividhya Dasarathy, Srinivasan Dasarathy, David Streem, J Mark Brown, Laura E Nagy","doi":"10.1097/HC9.0000000000000547","DOIUrl":"https://doi.org/10.1097/HC9.0000000000000547","url":null,"abstract":"<p><strong>Background: </strong>Dichloroacetate (DCA), a pan-pyruvate dehydrogenase kinase inhibitor, ameliorates multiple pathological conditions and tissue injury and shows strong potential for clinical applications. Here, we investigated the preventive effects of DCA in a murine model of alcohol-associated liver disease.</p><p><strong>Methods: </strong>C57BL/6J mice were subjected to the acute-on-chronic model of alcohol-associated liver disease and treated with DCA. Livers were assessed in liver histology, biochemistry, and gene expression. Mass spectrometry was used to compare protein expression and metabolite levels.</p><p><strong>Results: </strong>DCA inhibited hepatic expression of inflammatory genes but did not prevent steatosis and hepatocellular injury in ethanol-fed mice. Consistently, DCA repressed the expression of mRNAs for inflammatory genes in LPS-stimulated murine bone-marrow-derived macrophages and human monocytic THP-1 cells and inhibited both gene expression and protein release of interleukin-1 beta. DCA prevented hepatic accumulation of isovaleric acid in ethanol-fed mice, a short-chain fatty acid primarily produced by gut microbiota. In vitro, isovaleric acid potentiated LPS's effects, while DCA prevented this proinflammatory action. Ethanol feeding increased the expression of proteins involved in diverse metabolic pathways, including branched-chain amino acid (BCAA) degradation. In ethanol-fed mice, hepatic Fischer's ratio (the molar ratio of BCAAs to aromatic amino acids Phe and Tyr) and BTR (the molar ratio of BCAAs to Tyr) showed a decrease compared to pair-fed mice; however, this decrease was not observed in DCA-treated ethanol-fed mice. DCA blunted the ethanol-induced increase of BCKDHA, the rate-limiting enzyme in BCAA catabolism, and cytochrome P450 2E1.</p><p><strong>Conclusions: </strong>Ethanol-induced hepatic inflammatory responses and metabolic disturbances were prevented by DCA in mice, indicating the potential to develop pyruvate dehydrogenase kinase inhibitors as an effective therapy to treat alcohol-associated liver disease.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"8 12","pages":""},"PeriodicalIF":5.6,"publicationDate":"2024-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11608733/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142768550","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":"Validation of the Hospital Anxiety and Depression Scale in patients with decompensated cirrhosis.","authors":"Chengbo Zeng, John Donlan, Teresa Indriolo, Lucinda Li, Enya Zhu, Joyce C Zhou, Malia E Armstrong, Kedie Pintro, Nora Horick, Raymond T Chung, Areej Ei-Jawahri, Maria O Edelen, Nneka N Ufere","doi":"10.1097/HC9.0000000000000588","DOIUrl":"https://doi.org/10.1097/HC9.0000000000000588","url":null,"abstract":"","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"8 12","pages":""},"PeriodicalIF":5.6,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142846533","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Predicting long-term survival among patients with HCC.","authors":"David Goldberg, Peter P Reese, David A Kaplan, Yalda Zarnegarnia, Neelima Gaddipati, Sirisha Gaddipati, Binu John, Catherine Blandon","doi":"10.1097/HC9.0000000000000581","DOIUrl":"10.1097/HC9.0000000000000581","url":null,"abstract":"<p><strong>Background: </strong>Prognosticating survival among patients with HCC and cirrhosis must account for both the tumor burden/stage, as well as the severity of the underlying liver disease. Although there are many staging systems used to guide therapy, they have not been widely adopted to predict patient-level survival after the diagnosis of HCC. We sought to develop a score to predict long-term survival among patients with early- to intermediate-stage HCC using purely objective criteria.</p><p><strong>Methods: </strong>Retrospective cohort study among patients with HCC confined to the liver, without major medical comorbidities within the Veterans Health Administration from 2014 to 2023. Tumor data were manually abstracted and combined with clinical and laboratory data to predict 5-year survival from HCC diagnosis using accelerated failure time models. The data were randomly split using a 75:25 ratio for training and validation. Model discrimination and calibration were assessed and compared to other HCC staging systems.</p><p><strong>Results: </strong>The cohort included 1325 patients with confirmed HCC. A risk score using baseline clinical, laboratory, and HCC-related survival had excellent discrimination (integrated AUC: 0.71 in the validation set) and calibration (based on calibration plots and Brier scores). Models had superior performance to the BCLC and ALBI scores and similar performance to the combined BCLC-ALBI score.</p><p><strong>Conclusions: </strong>We developed a risk score using purely objective data to accurately predict long-term survival for patients with HCC. This score, if validated, can be used to prognosticate survival for patients with HCC, and, in the setting of liver transplantation, can be incorporated to consider the net survival benefit of liver transplantation versus other curative options.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"8 11","pages":""},"PeriodicalIF":5.6,"publicationDate":"2024-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11537595/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142567059","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 healthy lifestyle is prospectively associated with lower onset of metabolic dysfunction-associated steatotic liver disease.","authors":"Laura S Grinshpan, Yaara Even Haim, Dana Ivancovsky-Wajcman, Naomi Fliss-Isakov, Yuval Nov, Muriel Webb, Oren Shibolet, Revital Kariv, Shira Zelber-Sagi","doi":"10.1097/HC9.0000000000000583","DOIUrl":"10.1097/HC9.0000000000000583","url":null,"abstract":"<p><strong>Background: </strong>Metabolic dysfunction-associated steatotic liver disease (MASLD) is associated with an unhealthy lifestyle. However, there is limited prospective evidence regarding the association between combined lifestyle factors and MASLD. This study aims to test the association of a combination of lifestyle components, expressed as a healthy lifestyle index (HLI), and unhealthful eating behavior habits with MASLD, insulin resistance (IR), liver fibrosis, and metabolic dysfunction-associated steatohepatitis.</p><p><strong>Methods: </strong>A prospective cohort study was conducted among participants of metabolic and hepatic screening surveys. MASLD was evaluated by ultrasonography or controlled attenuation parameter at 2 time points to assess new-onset, persistence, or remission, and IR was estimated by homeostasis model assessment. Presumed liver fibrosis and metabolic dysfunction-associated steatohepatitis were evaluated using FibroMax biomarkers. The HLI was calculated as the sum of 4 lifestyle components: nonsmoking, healthy weight, healthy diet, and physical activity.</p><p><strong>Results: </strong>The final cohort included 315 subjects with 6.7 years of follow-up, 40-70 years old. In multivariable analyses, a favorable lifestyle (≥3 components) was independently associated with lower odds of new-onset MASLD (OR = 0.42; 95% CI: 0.19-0.90). Similarly, a favorable lifestyle was associated with lower odds of new-onset/persistent (vs. never/remission) MASLD and IR, respectively (OR = 0.49; 95% CI: 0.30-0.80; OR = 0.40; 95% CI: 0.24-0.66). There was a dose-response association between HLI and new-onset/persistent MASLD and IR. A favorable lifestyle was associated with lower odds of new-onset metabolic dysfunction-associated steatohepatitis (OR = 0.50; 95% CI: 0.27-0.95). Adjusting for HLI, unhealthful eating behavior habits were associated with higher odds of MASLD prevalence (OR = 1.81; 95% CI: 1.07-3.06).</p><p><strong>Conclusions: </strong>Adherence to a healthy lifestyle is prospectively associated with lower odds of MASLD, markers of liver damage, and IR. A holistic approach that considers overall lifestyle and eating behavior may be useful for preventing MASLD.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"8 11","pages":""},"PeriodicalIF":5.6,"publicationDate":"2024-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11537571/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142566915","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":"Hepatopulmonary syndrome associated with common variable immunodeficiency: Is it reasonable to investigate?","authors":"Ubiratan Cassano-Santos, Eduardo Sica, Renata M Perez, Guilherme F M Rezende","doi":"10.1097/HC9.0000000000000537","DOIUrl":"10.1097/HC9.0000000000000537","url":null,"abstract":"","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"8 11","pages":""},"PeriodicalIF":5.6,"publicationDate":"2024-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11537557/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142567029","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}