Journal of Clinical and Translational Hepatology最新文献

{"title":"Non-variceal Extrahepatic Portosystemic Shunts: A Review of Pathogenesis, Diagnosis, and Treatment.","authors":"Nicole M Anastasio, George Y Wu","doi":"10.14218/JCTH.2024.00315","DOIUrl":"10.14218/JCTH.2024.00315","url":null,"abstract":"<p><p>Extrahepatic portosystemic shunts (EPS) are abnormal connections between the portal and systemic circulations. Acquired EPS occur most commonly in adults and are usually associated with portal hypertension due to cirrhosis. Acquired EPS cases can be further subdivided into two types: variceal (pre-existing) EPS and non-variceal EPS (NVEPS). Variceal EPS arise from originally small vessels with pre-existing dual portal and systemic drainage. Due to elevated portal pressure, these vessels dilate and undergo a reversal of flow, sending blood back to the systemic circulation. A much less common and, therefore, underappreciated subset of acquired EPS is NVEPS, which consists of aberrant connections that did not previously exist between the portal vein and large systemic vessels, usually in the presence of portal hypertension. Neoangiogenesis results in the development of abnormal anastomoses between the portal vein and other large veins, resulting in splenorenal, gastrorenal, portocaval, and mesocaval shunts. While not uncommon, they are frequently overlooked in the diagnosis and treatment of portal hypertension and can pose significant diagnostic and therapeutic challenges. Because the treatment of variceal EPS and NVEPS can differ markedly, it is important to correctly diagnose NVEPS and institute appropriate management. The aim of this article was to review acquired EPS, with particular attention to NVEPS, updating the pathogenesis, diagnosis, and treatment.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"13 5","pages":"425-433"},"PeriodicalIF":3.1,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12078168/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144093844","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GTF3C2 Promotes the Proliferation of Hepatocellular Carcinoma Cells through the USP21/MEK2/ERK1/2 Pathway.","authors":"Yani Wu, Yingnan Yang, Youju Zhang, Qiuran Xu, Dongsheng Huang, Kangsheng Tu","doi":"10.14218/JCTH.2024.00386","DOIUrl":"10.14218/JCTH.2024.00386","url":null,"abstract":"<p><strong>Background and aims: </strong>General transcription factor IIIC subunit 2 (GTF3C2) is one of the polymerase III transcription-related factors. Previous studies have revealed that GTF3C2 is involved in regulating cell proliferation. However, the role of GTF3C2 in hepatocellular carcinoma (HCC) remains unclear. This study aimed to determine its expression, biological function, and mechanism in HCC.</p><p><strong>Methods: </strong>The expression of GTF3C2 in HCC and non-tumor tissues, along with its clinical significance, was investigated using public databases and clinical samples. Reverse transcription-quantitative polymerase chain reaction and Western blot assays were performed to detect the expression of GTF3C2, ubiquitin specific peptidase 21 (USP21), mitogen-activated protein kinase 2 (MEK2), extracellular signal-regulated kinase 1/2 (ERK1/2), and p-ERK1/2 in cells. A luciferase reporter assay was conducted to explore the regulatory effect of GTF3C2 on USP21 transcription. Cell Counting Kit-8, 5-ethynyl-2'-deoxyuridine, and colony formation assays were performed to assess HCC cell proliferation. Subcutaneous injection of HCC cells into nude mice was used to evaluate tumor growth <i>in vivo</i>.</p><p><strong>Results: </strong>GTF3C2 expression was upregulated in HCC tissues and was positively correlated with advanced tumor stages and high tumor grades. HCC patients with high GTF3C2 expression had significantly worse survival outcomes. Knockdown of GTF3C2 suppressed the proliferation of Hep3B and HCCLM3 cells, while overexpression of GTF3C2 facilitated the proliferation of SNU449 and Huh7 cells. GTF3C2 promoted USP21 expression by activating its transcription, which subsequently increased the levels of MEK2 and p-ERK1/2 in HCC cells. Overexpression of both USP21 and MEK2 counteracted the GTF3C2 knockdown-induced inactivation of the ERK1/2 pathway. Moreover, GTF3C2 promoted HCC cell proliferation <i>in vitro</i> and tumor growth <i>in vivo</i> by regulating the USP21/MEK2/ERK1/2 pathway.</p><p><strong>Conclusions: </strong>Upregulation of GTF3C2 is frequently observed in HCC tissues and predicts poor prognosis. GTF3C2 promotes HCC cell proliferation via the USP21/MEK2/ERK1/2 pathway.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"13 5","pages":"374-384"},"PeriodicalIF":3.1,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12078175/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144093632","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibition of Cyclooxygenase-2 Upregulates the Nuclear Factor Erythroid 2-related Factor 2 Signaling Pathway to Mitigate Hepatocyte Ferroptosis in Chronic Liver Injury.","authors":"Zhu Yang, Yang Tai, Tian Lan, Chong Zhao, Jin-Hang Gao, Cheng-Wei Tang, Huan Tong","doi":"10.14218/JCTH.2024.00440","DOIUrl":"10.14218/JCTH.2024.00440","url":null,"abstract":"<p><strong>Background and aims: </strong>Ferroptosis plays an essential role in chronic liver diseases, and cyclooxygenase-2 (COX-2) affects liver fibrosis through multiple mechanisms. However, research on COX-2 regulation of ferroptosis in chronic liver injury remains limited. This study aimed to investigate whether and how COX-2 regulates ferroptosis in chronic liver injury.</p><p><strong>Methods: </strong><i>In vivo</i>, a thioacetamide (TAA)-induced chronic liver injury model, characterized by significant liver lipid peroxidation and oxidative stress, was used. <i>COX-2</i> ^+/+ and <i>COX-2</i> ^-/- mice were treated with TAA or normal saline. <i>In vitro</i>, primary mouse hepatocytes were isolated and treated with dimethyl sulfoxide (DMSO), erastin+DMSO, etoricoxib+erastin+DMSO, and tBHQ+erastin+DMSO. Mitochondrial morphology, iron metabolism, lipid peroxidation, and oxidative stress were assessed to verify ferroptosis. The nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway was measured to investigate the relationship between COX-2 and ferroptosis.</p><p><strong>Results: </strong>TAA-treated <i>COX-2</i> ^-/- mice presented milder liver fibrosis, whereas TAA-treated <i>COX-2</i> ^-/- mice livers and etoricoxib+erastin+DMSO-treated primary hepatocytes exhibited alleviated mitochondrial damage compared with TAA-treated <i>COX-2</i> ^+/+ littermates and erastin+DMSO-treated primary hepatocytes, respectively. The knockout of COX-2 decreased ferrous ion concentration (<i>p</i> < 0.01) and mitigated lipid peroxidation in TAA-treated livers (<i>p</i> < 0.05). Furthermore, both COX-2 knockout and etoricoxib restored reduced glutathione (<i>p</i> < 0.05) and glutathione peroxidase 4 (<i>p</i> < 0.05), while decreasing malondialdehyde levels (<i>p</i> < 0.05). Additionally, COX-2 inhibition upregulated Nrf2, which helped alleviate erastin+DMSO-induced ferroptosis (<i>p</i> < 0.01).</p><p><strong>Conclusions: </strong>Ferroptosis contributes to the progression of chronic liver injury. Inhibition of COX-2 upregulates Nrf2, mitigating hepatocyte ferroptosis in chronic liver injury.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"13 5","pages":"409-417"},"PeriodicalIF":3.1,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12078174/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144093645","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"FTO Promotes Hepatocellular Carcinoma Progression by Mediating m6A Modification of BUB1 and Targeting TGF-βR1 to Activate the TGF-β Signaling Pathway.","authors":"Lin Zhang, Li Gan, Yuru Lin, Zhechuan Mei, Shengtao Liao","doi":"10.14218/JCTH.2025.00007","DOIUrl":"10.14218/JCTH.2025.00007","url":null,"abstract":"<p><strong>Background and aims: </strong>Fat mass and obesity-associated protein (FTO) has been linked to various cancers, though its role in hepatocellular carcinoma (HCC) remains unclear. This study aimed to investigate FTO expression, its clinical relevance, functional role in HCC progression, and the underlying molecular mechanisms.</p><p><strong>Methods: </strong>Quantitative reverse-transcription polymerase chain reaction and immunohistochemical analysis were used to assess FTO expression in HCC. Functional assays, including proliferation, invasion, and epithelial-mesenchymal transition studies, were conducted using HCC cell lines with FTO knockdown. N6-methyladenosine (m6A) RNA immunoprecipitation and RNA stability assays further elucidated the role of FTO in BUB1 mRNA methylation and stability. Co-immunoprecipitation studies were employed to confirm the interaction between BUB1 and TGF-βR1. <i>In vivo</i> studies in nude mice were conducted to evaluate tumor growth following FTO knockdown.</p><p><strong>Results: </strong>FTO was significantly upregulated in HCC tissues compared to normal liver tissues, with higher expression observed in advanced tumor-node-metastasis stages and metastatic HCC. Elevated FTO correlated with poor overall survival in patients. Silencing FTO decreased HCC cell proliferation, colony formation, invasion, epithelial-mesenchymal transition, and tumor growth in nude mice. Mechanistically, FTO downregulation led to increased m6A modification of BUB1 mRNA, thereby promoting its degradation via the YTH domain family 2-dependent pathway and reducing BUB1 protein levels. Additionally, BUB1 physically interacted with TGF-βR1, activating downstream TGF-β signaling.</p><p><strong>Conclusions: </strong>FTO is overexpressed in HCC and is associated with poor clinical outcomes. Mechanistically, FTO promotes HCC progression by stabilizing BUB1 mRNA through an m6A-YTH domain family 2-dependent pathway, which activates TGF-β signaling. Targeting the FTO-BUB1-TGF-βR1 regulatory network may offer a promising therapeutic strategy for HCC.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"13 5","pages":"385-394"},"PeriodicalIF":3.1,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12078176/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144093919","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Key Points and Future Directions from the 2024 Chinese Guidelines for Fatty Liver Disease.","authors":"Maria Tampaki, Evangelos Cholongitas","doi":"10.14218/JCTH.2025.00051","DOIUrl":"10.14218/JCTH.2025.00051","url":null,"abstract":"","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"13 5","pages":"434-439"},"PeriodicalIF":3.1,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12078172/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144093726","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Analysis of the Disease Spectrum Characteristics of Inherited Metabolic Liver Diseases in Two Hepatology Specialist Hospitals in Beijing over the Past 20 Years.","authors":"Wei Hou, Yuanzhi Huang, Tang Shang, Zheng Wang, Wei Zhang, Kefi Wang, Yinjie Gao, Min Zhang, Sujun Zheng","doi":"10.14218/JCTH.2025.00030","DOIUrl":"10.14218/JCTH.2025.00030","url":null,"abstract":"<p><strong>Background and aims: </strong>Inherited metabolic liver diseases (IMLDs) have complex etiologies and vary widely in clinical presentation, with a significant overall incidence. With the advancements in diagnostic and treatment technologies, an increasing number of children with inherited metabolic diseases are surviving into adolescence and adulthood. These advancements have improved our understanding of the IMLD disease spectrum and clinical outcomes. This study aimed to analyze changes in the disease spectrum and epidemiological characteristics of inherited metabolic liver diseases (IMLD) over the past 20 years in two specialized liver disease hospitals in northern China.</p><p><strong>Methods: </strong>A retrospective analysis was conducted on IMLD cases diagnosed between January 1, 2002, and December 31, 2023, at two liver disease specialty hospitals in Beijing. Data were obtained from inpatient and outpatient hospital information systems, with diagnoses based on national and international IMLD diagnosis and treatment guidelines.</p><p><strong>Results: </strong>A total of 2,103 IMLD patients were analyzed, including 1,213 adults and 890 children. IMLD accounted for 4.58‰ of hospitalized liver disease patients during this period. The most common IMLD was Wilson's disease, comprising 68% of all IMLD cases. The number of diagnosed IMLD types increased from 15 to 32 across two 11-year periods (2002-2012 and 2013-2023). Among pediatric patients, glycogen storage disease and Alagille syndrome were more prevalent in those under one year of age, while Wilson's disease was prevalent across all age groups. In adult IMLD patients, Wilson's disease, polycystic liver disease, and hereditary hyperbilirubinemia were more frequently observed.</p><p><strong>Conclusions: </strong>Over the past 20 years, both the number of diagnosed IMLD cases and disease diversity have significantly increased, with Wilson's disease remaining the most prevalent IMLD. These findings provide valuable insights for the long-term management of IMLD patients and the allocation of healthcare resources.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"13 5","pages":"367-373"},"PeriodicalIF":3.1,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12078171/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144093876","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochondrial Membrane Potential of CD8⁺ T Cells Predicts Bacterial Infection and Rapid Development of Acute-on-chronic Liver Failure in Cirrhotic Patients.","authors":"Xixuan Wang, Shuling Chen, Jing Fan, Yuxiang Gong, Hongli Liu, Lili Wang, Xiaoning Feng, Hui Zhou, Wenquan Zeng, Changhua Yi, Caiyun Zhang, Qingfang Xiong, Hao Ren, Yongfeng Yang","doi":"10.14218/JCTH.2024.00452","DOIUrl":"10.14218/JCTH.2024.00452","url":null,"abstract":"<p><strong>Background and aims: </strong>Patients with cirrhosis are at an increased risk of bacterial infection (BI), which is the most common precondition for acute-on-chronic liver failure (ACLF). In this study, we aimed to evaluate the ability of mitochondria-related indicators (mitochondrial mass and mitochondrial membrane potential (MMP)) of T cells in peripheral blood to predict BI and ACLF within 90 days in cirrhotic patients.</p><p><strong>Methods: </strong>We prospectively studied mitochondria-related indicators in various T cells from 235 cirrhotic patients at the Second Hospital of Nanjing. The outcomes of interest were BI and ACLF.</p><p><strong>Results: </strong>The restricted cubic spline analysis showed that the MMP of CD8⁺ T cells had a linear relationship with the risk of BI and ACLF (both <i>P</i> < 0.001). Multivariable Cox regression analysis demonstrated that the MMP of CD8⁺ T cells was an independent risk factor for both BI and ACLF (BI: hazard ratio 0.96, 95% confidence interval 0.94-0.98; <i>P</i> < 0.001; ACLF: hazard ratio 0.94, 95% confidence interval 0.90-0.97; <i>P</i> < 0.001). The MMP of CD8⁺ T cells exhibited better diagnostic efficacy than traditional indices in predicting BI (C index: 0.75). The MMP of CD8⁺ T cells, when combined with traditional models (Child-Turcotte-Pugh and model for end-stage liver disease score), improved their diagnostic efficiency in predicting both BI and ACLF. Additionally, the MMP of CD8⁺ T cells showed a significant negative correlation with inflammation-related markers (<i>P</i> < 0.05). Mitochondrial damage and abnormally activated mitochondrial autophagy were observed in CD8⁺ T cells from cirrhotic patients with low MMP.</p><p><strong>Conclusions: </strong>The MMP of CD8⁺ T cells could serve as a valuable predictor of BI and ACLF within 90 days in cirrhotic patients.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"13 5","pages":"395-408"},"PeriodicalIF":3.1,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12078170/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144093833","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>PCSK9</i> and <i>APOA4</i>: The Dynamic Duo in TMAO-induced Cholesterol Metabolism and Cholelithiasis.","authors":"Chao Shi, Jingjing Yu, Ziang Meng, Dongxu Lu, Haoran Ding, Haijun Sun, Guangxin Shi, Dongbo Xue, Xianzhi Meng","doi":"10.14218/JCTH.2024.00403","DOIUrl":"https://doi.org/10.14218/JCTH.2024.00403","url":null,"abstract":"<p><strong>Background and aims: </strong>Cholesterol synthesis and gallstone formation are promoted by trimethylamine-N-oxide (TMAO), a derivative of trimethylamine, which is a metabolite of gut microbiota. However, the underlying mechanisms of TMAO-induced lithogenesis remain incompletely understood. This study aimed to explore the specific molecular mechanisms through which TMAO promotes gallstone formation.</p><p><strong>Methods: </strong>Enzyme-linked immunosorbent assays were used to compare serum concentrations of TMAO, apolipoprotein A4 (APOA4), and proprotein convertase subtilisin/kexin type 9 (PCSK9) between patients with cholelithiasis and normal controls. A murine model of TMAO-induced cholelithiasis was employed, incorporating assays of gallstone weight and bile cholesterol content, along with RNA sequencing of murine hepatic tissue. A TMAO-induced AML12 hepatocyte line was constructed and transfected with targeted small interfering RNAs and overexpression plasmids. <i>In vivo</i> and <i>in vitro</i> experiments were performed to determine the expression and regulation of genes related to cholesterol metabolism.</p><p><strong>Results: </strong>Serum TMAO and PCSK9 levels were elevated, whereas APOA4 levels were reduced in patients with cholelithiasis. Furthermore, our murine model demonstrated that TMAO upregulated hepatic expression of PCSK9, 3-hydroxy-3-methylglutaryl-CoA reductase, and ATP-binding cassette sub-family G member 5/8, while reducing APOA4 expression, thereby modulating cholesterol metabolism and promoting lithogenesis. <i>PCSK9</i> and <i>APOA4</i> were identified as key regulatory genes in the cholesterol metabolic pathway. <i>PCSK9</i> knockdown increased <i>APOA4</i> expression, while <i>APOA4</i> overexpression led to reduced <i>PCSK9</i> expression.</p><p><strong>Conclusions: </strong>TMAO upregulated hepatic <i>PCSK9</i> expression and reduced <i>APOA4</i> expression, initiating a feedback loop that dysregulated cholesterol metabolism and promoted lithogenesis.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"13 4","pages":"295-305"},"PeriodicalIF":3.1,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11976434/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144012381","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prevalence of Hepatitis B Core Antibody in Intravenous Immunoglobulin Products by Chemiluminescent Microparticle Immunoassay.","authors":"Laura Victoria, Anu S Maharjan, Julia Kostka, Raphael Assenso-Bediako, Wesley Merkert, Lisa Chirch, Kevin Dieckhaus","doi":"10.14218/JCTH.2024.00464","DOIUrl":"https://doi.org/10.14218/JCTH.2024.00464","url":null,"abstract":"","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"13 4","pages":"358-360"},"PeriodicalIF":3.1,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11976438/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143968379","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prevalence of Hepatitis D Virus Antibody Positivity in Chinese Patients with Chronic Hepatitis B Virus Infection.","authors":"Xieer Liang, Qiaoqiao Chen, Hong Tang, Yujuan Guan, Minfeng Liang, Peng Hu, Wen Xie, Huiying Rao, Junqi Niu, Liang Chen, Li Yan, Xiaowei Chen, Xiaohe Li, Yulin Zhao, Oliver Lenz, Michael Biermer, Jinlin Hou","doi":"10.14218/JCTH.2024.00313","DOIUrl":"https://doi.org/10.14218/JCTH.2024.00313","url":null,"abstract":"<p><strong>Background and aims: </strong>Large-scale data on the hepatitis D virus (HDV)/hepatitis B virus (HBV) co-infection rate is needed to estimate the current epidemiology of HDV in China. This study aimed to estimate the current epidemiology of HDV.</p><p><strong>Methods: </strong>Patients with chronic HBV infection, with documented serum hepatitis B surface antigen (HBsAg) positivity for more than six months, were enrolled across China. Blood samples were collected at baseline for central evaluations of HDV antibody and HBsAg quantification. Assessments for antibodies of hepatitis A virus, hepatitis C virus, hepatitis E virus, and human immunodeficiency virus, as well as HDV RNA quantification, were performed in patients who tested positive for HDV antibodies.</p><p><strong>Results: </strong>Of the 5,044 enrolled patients between September 24, 2021, and December 28, 2022, 4,936 patients were included in the analysis. The mean age (±standard deviation) was 42.9 ± 9.9 years, and 69.8% of patients were male. The mean alanine aminotransferase level was 34 ± 58 U/L, and 1,509 (30.6%) patients were hepatitis B e antigen-positive. The mean (standard deviation) HBsAg level at baseline was 3,535 ± 11,292 IU/mL among 4,842 patients who were HBsAg positive. The rate of HBV infection and HDV antibody positivity was 0.24% (95% confidence interval: 0.1-0.4%), and only one patient was HDV RNA positive.</p><p><strong>Conclusions: </strong>The prevalence of HDV antibody positivity was 0.24% in Chinese patients with chronic HBV infection, and only one patient with both anti-HDV antibody and HDV RNA positivity was observed in this study.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"13 4","pages":"278-283"},"PeriodicalIF":3.1,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11976442/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143982600","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}