Hepatology InternationalPub Date : 2026-10-01Epub Date: 2026-07-11DOI: 10.1007/s12072-026-11127-y
Glenn Jun Kit Ho, Asvin Selvakumar, Lucas Yang Yuxu Yeo, Mako Eguchi, Ryan Yanzhe Lim, Benedix Kuan Loon Sim, Daniel Tung, Apoorva N Sasikumar, Shirley Huey Shin Bong, Ethan Kai Jun Tham, Jia Hao Law, Eunice Xiang-Xuan Tan, Brian J Wentworth, Won-Mook Choi, Aparna Goel, David N Assis, Benjamin Nah, Vincent L Chen
{"title":"Epidemiology of primary sclerosing cholangitis in general and IBD populations: a systematic review and meta-analysis.","authors":"Glenn Jun Kit Ho, Asvin Selvakumar, Lucas Yang Yuxu Yeo, Mako Eguchi, Ryan Yanzhe Lim, Benedix Kuan Loon Sim, Daniel Tung, Apoorva N Sasikumar, Shirley Huey Shin Bong, Ethan Kai Jun Tham, Jia Hao Law, Eunice Xiang-Xuan Tan, Brian J Wentworth, Won-Mook Choi, Aparna Goel, David N Assis, Benjamin Nah, Vincent L Chen","doi":"10.1007/s12072-026-11127-y","DOIUrl":"10.1007/s12072-026-11127-y","url":null,"abstract":"<p><strong>Background & aims: </strong>Primary Sclerosing Cholangitis (PSC) is a chronic cholestatic liver condition that is closely associated with inflammatory bowel disease (IBD). PSC is associated with substantial long-term hepatobiliary morbidity, including an increased risk of cholangiocarcinoma. Reported prevalence and incidence estimates of PSC vary widely across different populations and study designs. This meta-analysis aims to provide an updated estimate of the prevalence of PSC in the general and IBD populations, and PSC incidence in the general population.</p><p><strong>Methods: </strong>A systematic search of MEDLINE (Ovid) and Embase from inception to October 20, 2025, for population- or cohort-based studies reporting PSC prevalence or incidence was performed. Seventy-four studies met the inclusion criteria. Random-effects meta-analyses were performed to pool prevalence and incidence estimates. Subgroup analyses, meta-regression, and sensitivity analyses were conducted to assess robustness and sources of heterogeneity.</p><p><strong>Results: </strong>Seventeen studies including 196,635,709 individuals showed a pooled overall PSC prevalence of 8.06 per 100,000 (95% CI 4.75-13.36) in the general population. Among 516,548 patients with IBD in thirty-four studies, pooled PSC prevalence was 15.2 per 1,000 (95% CI 10.7-21.7). PSC prevalence was higher in ulcerative colitis (20.6 per 1,000) than in Crohn's disease (10.2 per 1,000). Using Crohn's disease as the reference group, ulcerative colitis was associated with higher odds of PSC (OR 1.787, 95% CI 1.066-2.996, p = 0.028). Thirteen studies reported a pooled incidence of PSC in the general population of 0.892 per 100,000 person-years (95% CI 0.705-1.130).</p><p><strong>Conclusion: </strong>This meta-analysis provides an updated synthesis of PSC epidemiology, extending prior work by incorporating detailed subgroup analyses across IBD phenotype, PSC subtype, geographic region, socioeconomic context, diagnostic modality, case-ascertainment method, and time period, which are dimensions not comprehensively addressed in previous meta-analyses. PSC remains a rare disease in the general population but is substantially more prevalent among individuals with IBD. Marked geographic and methodological heterogeneity, with notable underrepresentation of data from lower-SDI regions and the African Region, underscores the need for standardized case definitions and improved epidemiological surveillance across diverse settings. Given the markedly increased risk of cholangiocarcinoma in PSC, these findings highlight the clinical importance of recognizing PSC in higher-risk IBD populations and provide an epidemiological foundation for future studies evaluating risk stratification, early detection, and surveillance.</p>","PeriodicalId":12901,"journal":{"name":"Hepatology International","volume":" ","pages":"1463-1478"},"PeriodicalIF":7.8,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13676655/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148420648","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}
Hepatology InternationalPub Date : 2026-10-01Epub Date: 2026-07-27DOI: 10.1007/s12072-026-11133-0
Thomas Sorz-Nechay, Benedikt S Hofer, Philipp Königshofer, Alexis Treitler, Georg Semmler, Benedikt Simbrunner, Vlad Taru, Katharina Bonitz, Henriette Horstmeier, Georg Kramer, Kerstin Zinober, Katharina Regnat, Barbara Neudert, Christopher C Kaltenecker, Behrang Mozayani, Renate Kain, Michael Trauner, Mattias Mandorfer, Philipp Schwabl, Thomas Reiberger
{"title":"Histomorphometry indicates distinct contributions of myofibroblast activation and sinusoidal capillarization to portal hypertension.","authors":"Thomas Sorz-Nechay, Benedikt S Hofer, Philipp Königshofer, Alexis Treitler, Georg Semmler, Benedikt Simbrunner, Vlad Taru, Katharina Bonitz, Henriette Horstmeier, Georg Kramer, Kerstin Zinober, Katharina Regnat, Barbara Neudert, Christopher C Kaltenecker, Behrang Mozayani, Renate Kain, Michael Trauner, Mattias Mandorfer, Philipp Schwabl, Thomas Reiberger","doi":"10.1007/s12072-026-11133-0","DOIUrl":"10.1007/s12072-026-11133-0","url":null,"abstract":"<p><strong>Background and aims: </strong>Portal hypertension (PH) is a severe consequence of cirrhosis and the primary driver of hepatic decompensation. We aimed to investigate the link between histological myofibroblast activation (alpha-smooth-muscle-actin: αSMA) and sinusoidal capillarization (CD34) markers to PH severity in patients with chronic liver disease (CLD).</p><p><strong>Methods: </strong>Patients with CLD underwent hepatic venous pressure gradient (HVPG) measurement and liver biopsy. Liver samples were stained by picrosirius-red for collagen proportionate area (CPA) and for αSMA/CD34. Quantitative histomorphometry was performed on full-slide scans.</p><p><strong>Results: </strong>102 patients (63.7% male, median age 56.4 years, mainly steatotic liver disease: 58.8%) were included. The median HVPG was 13 [10-18] mmHg and severe PH (HVPG ≥ 16 mmHg, PH16) was found in 35.3%. Median liver-stiffness was 30.6 [19.1-57.6] kPa. In PH16 patients, fibrosis (CPA: 28.39 vs 17.72%), myofibroblast activation (αSMA: 10.84 vs 3.75%), and capillarization (CD34: 5.45 vs 2.67%) were significantly more pronounced (all p < 0.001 vs. no PH16). CD34 showed a higher correlation to HVPG (rho = 0.505) than CPA (rho = 0.472) and αSMA (rho = 0.347, all p < 0.001). CD34 expression was independently correlated with enhanced liver fibrosis (ELF) test and von Willebrand factor (VWF). When partially adjusting for fibrosis severity, patients with less severe fibrosis and high αSMA or CD34 had a trend for higher HVPG, whereas in intermediate fibrosis, only CD34-high patients trended higher HVPG.</p><p><strong>Conclusion: </strong>CPA, CD34 and αSMA expression all correlate with PH severity. CD34 represents a histologic sinusoidal capillarization marker that correlates with circulating VWF and ELF. αSMA and CD34 represent potential histologic markers of PH beyond the static component.</p>","PeriodicalId":12901,"journal":{"name":"Hepatology International","volume":" ","pages":"1432-1445"},"PeriodicalIF":7.8,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13676638/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148602350","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}
Hepatology InternationalPub Date : 2026-10-01Epub Date: 2026-02-26DOI: 10.1007/s12072-026-11073-9
Jiehua Han, Xiaoyan Zhang
{"title":"Comment on \"BRIX1 activated by mTORC1-SP1 signaling regulates ribosome biogenesis and alternative splicing to promote hepatocellular carcinoma progression\".","authors":"Jiehua Han, Xiaoyan Zhang","doi":"10.1007/s12072-026-11073-9","DOIUrl":"10.1007/s12072-026-11073-9","url":null,"abstract":"","PeriodicalId":12901,"journal":{"name":"Hepatology International","volume":" ","pages":"1553-1554"},"PeriodicalIF":7.8,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147289788","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}
Hepatology InternationalPub Date : 2026-10-01Epub Date: 2026-03-30DOI: 10.1007/s12072-026-11080-w
Yuanqin Zhang, Yang He, Yifei Chen, Fang Nie
{"title":"Re-examining the incremental benefit of TACE-TKI-PD-1 triplet therapy: time-related bias and treatment pathways in a real-world HCC cohort.","authors":"Yuanqin Zhang, Yang He, Yifei Chen, Fang Nie","doi":"10.1007/s12072-026-11080-w","DOIUrl":"10.1007/s12072-026-11080-w","url":null,"abstract":"","PeriodicalId":12901,"journal":{"name":"Hepatology International","volume":" ","pages":"1555-1556"},"PeriodicalIF":7.8,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147581288","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}
Hepatology InternationalPub Date : 2026-10-01Epub Date: 2026-06-23DOI: 10.1007/s12072-026-11112-5
Ji Won Han, Seunghee Na, Kyungdo Han, Kyu Na Lee, Do Young Kim, Sang Hoon Ahn, Mi Na Kim
{"title":"Alcohol consumption and dementia risk in steatotic liver disease: a nationwide cohort study.","authors":"Ji Won Han, Seunghee Na, Kyungdo Han, Kyu Na Lee, Do Young Kim, Sang Hoon Ahn, Mi Na Kim","doi":"10.1007/s12072-026-11112-5","DOIUrl":"10.1007/s12072-026-11112-5","url":null,"abstract":"<p><strong>Background: </strong>The relationship between steatotic liver disease (SLD) and dementia remains unclear, particularly regarding alcohol consumption patterns. We investigated the risk of dementia across SLD subtypes classified by alcohol consumption.</p><p><strong>Methods: </strong>We analyzed 3,071,829 adults without baseline dementia who underwent health examinations in 2012. Participants were classified into No SLD, metabolic dysfunction-associated steatotic liver disease (MASLD), metabolic dysfunction-associated alcohol-related liver disease (MetALD), and ALD groups. Primary outcomes were newly diagnosed all-cause dementia, Alzheimer's disease (AD), and vascular dementia (VD).</p><p><strong>Results: </strong>Over a median follow-up of 5.4 years, 72,545 all-cause dementia, 56,999 AD, and 8923 VD cases occurred. The risk of dementia significantly increased across all dementia outcomes in SLD (all p < 0.05). Across the SLD subtypes, ALD showed the highest risk of dementia, followed by MASLD, whereas MetALD showed largely neutral associations except for a modestly increased risk of VD. When MASLD was further stratified by alcohol consumption, the MASLD-no alcohol group showed consistently increased risk of all dementia outcomes (all p < 0.05). In contrast, MASLD with within-threshold alcohol intake showed heterogeneous associations across dementia outcomes.</p><p><strong>Conclusions: </strong>The association between SLD and dementia differed according to SLD phenotype and alcohol consumption pattern. These findings should be interpreted as observational associations and warrant further validation in studies with longitudinal assessment of SLD status and alcohol exposure.</p>","PeriodicalId":12901,"journal":{"name":"Hepatology International","volume":" ","pages":"1420-1431"},"PeriodicalIF":7.8,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148307033","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":"Clinical and pathological significance of serum anti-PD-1 autoantibodies in acute-onset and chronic autoimmune hepatitis.","authors":"Takashi Oda, Akinobu Takaki, Kenichi Harada, Teruko Arinaga-Hino, Masanori Abe, Takeshi Matsui, Atsushi Takahashi, Hiromasa Ohira, Yoshiyuki Suzuki, Nobuhiro Nakamoto, Atsushi Tanaka, Kazuyuki Matsumoto, Jinpeng Li, Nozomi Miyake, Masahiko Sue, Takuya Adachi, Yasuto Takeuchi, Hideki Onishi, Miwa Kawanaka, Motoyuki Otsuka","doi":"10.1007/s12072-026-11152-x","DOIUrl":"https://doi.org/10.1007/s12072-026-11152-x","url":null,"abstract":"<p><strong>Background: </strong>Acute-onset autoimmune hepatitis (A-AIH) poses diagnostic challenges because autoantibodies are frequently absent or serum IgG levels may only be mildly elevated. Autoantibodies against the immune checkpoint molecule PD-1 have been detected in patients with chronic AIH (C-AIH). To clarify the clinical and pathological significance of anti-PD-1 autoantibodies, we examined their association with the clinical features of patients with liver diseases, including A-AIH, C-AIH, primary biliary cholangitis (PBC), and drug-induced liver injury (DILI).</p><p><strong>Methods: </strong>We compared the clinical characteristics and serum anti-PD-1 autoantibody titers of patients with A-AIH, C-AIH, PBC, and DILI (n = 72, 45, 41, and 19, respectively). Correlations between autoantibody titers and biochemical parameters were assessed to identify the factors that discriminate between the diseases. To reduce non-specific IgG response, anti-PD-1 autoantibody titers were normalized to the serum IgG levels. The liver histology was evaluated in a subset of patients with AIH.</p><p><strong>Results: </strong>A-AIH caused severe liver parenchymal and portal inflammation. The anti-PD-1/IgG ratio showed positive correlations with AST and ALT, but only weak correlations with ALP and γ-GTP. Anti-PD-1/IgG ratio was the highest in A-AIH, followed by DILI, C-AIH and PBC. Histological findings showed that anti-PD-1/IgG ratio was associated with severe inflammation, but not with centrilobular necrosis.</p><p><strong>Conclusions: </strong>The serum anti-PD-1 autoantibody/IgG ratio was significantly elevated in A-AIH compared with that in C-AIH and PBC, and A-AIH was independently distinguished from C-AIH. These markers may assist with the assessment of acute-onset liver inflammation and clinical phenotyping of AIH.</p>","PeriodicalId":12901,"journal":{"name":"Hepatology International","volume":" ","pages":""},"PeriodicalIF":7.8,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149080606","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}