Ruoqi Zhou, Jiyang Chen, Rui Huang, Yida Yang, Yu Shi
{"title":"The Failure Rate of Liver Stiffness Measured by Vibration-controlled Transient Elastography in the United States and Relevant Factors.","authors":"Ruoqi Zhou, Jiyang Chen, Rui Huang, Yida Yang, Yu Shi","doi":"10.14218/JCTH.2024.00261","DOIUrl":"10.14218/JCTH.2024.00261","url":null,"abstract":"","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"12 12","pages":"1067-1069"},"PeriodicalIF":3.1,"publicationDate":"2024-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11622204/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142794491","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":"Emerging Roles of High-mobility Group Box-1 in Liver Disease.","authors":"Lu Wang, Zhiwei Dong, Yeqiong Zhang, Liang Peng","doi":"10.14218/JCTH.2024.00317","DOIUrl":"10.14218/JCTH.2024.00317","url":null,"abstract":"<p><p>High-mobility group box-1 (HMGB1) is an architectural chromosomal protein with various roles depending on its cellular localization. Extracellular HMGB1 functions as a prototypical damage-associated molecular pattern that triggers inflammation and adaptive immune responses, mediated by specific cell surface receptors, including receptors for advanced glycation end products and toll-like receptors. Post-translational modifications of HMGB1 significantly impact various cellular processes that contribute to the pathogenesis of liver diseases. Recent studies have highlighted the close relationship between HMGB1 and the pathogenesis of acute liver injuries, including acetaminophen-induced liver injury, hepatic ischemia-reperfusion injury, and acute liver failure. In chronic liver diseases, HMGB1 plays a role in nonalcoholic fatty liver disease, alcohol-associated liver disease, liver fibrosis, and hepatocellular carcinoma. Targeting HMGB1 as a therapeutic approach, either by inhibiting its release or blocking its extracellular function, is a promising strategy for treating liver diseases. This review aimed to summarize the available evidence on HMGB1's role in liver disease, focusing on its multifaceted signaling pathways, impact on disease progression, and the translation of these findings into clinical interventions.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"12 12","pages":"1043-1056"},"PeriodicalIF":3.1,"publicationDate":"2024-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11622203/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142794894","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}
Editorial Office Of Journal Of Clinical And Translational Hepatology
{"title":"2024 Reviewer Acknowledgement.","authors":"Editorial Office Of Journal Of Clinical And Translational Hepatology","doi":"10.14218/JCTH.2024.000RA","DOIUrl":"https://doi.org/10.14218/JCTH.2024.000RA","url":null,"abstract":"","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"12 12","pages":"1070-1073"},"PeriodicalIF":3.1,"publicationDate":"2024-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11622205/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142903255","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":"Exploring Circulating Tumor Cells: Detection Methods and Biomarkers for Clinical Evaluation in Hepatocellular Carcinoma.","authors":"Chin-Mu Hsu, Yi-Chang Liu, Jee-Fu Huang","doi":"10.14218/JCTH.2024.00230","DOIUrl":"10.14218/JCTH.2024.00230","url":null,"abstract":"<p><p>Circulating tumor cells (CTCs), originating from primary neoplastic tissues, infiltrate blood vessels, migrate through the bloodstream, and establish secondary tumor foci. The detection of CTCs holds significant promise for early-stage identification, diagnostic precision, therapeutic monitoring, and prognostic evaluation. It offers a non-invasive approach and has broad clinical relevance in cancer management. This comprehensive review primarily focused on CTCs as biomarkers in the diagnostic, therapeutic, and prognostic surveillance of hepatocellular carcinoma, compared their correlation with key clinical parameters and the identification of gene characteristics. It also highlighted current methodologies in CTC detection. Despite approval by the U.S. Food and Drug Administration for select malignancies, the comprehensive integration of CTCs into routine clinical practice requires procedural standardization and a deeper understanding of the underlying molecular intricacies. The challenges in CTC detection, including limited quantity, technical impediments, and cellular heterogeneity, call for concerted and further investigational efforts to advance precision in cancer diagnostics and prognostication, thus realizing the objectives of precise and personalized medicine.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"12 12","pages":"1020-1042"},"PeriodicalIF":3.1,"publicationDate":"2024-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11622199/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142794895","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":"Ferroptosis and Intrinsic Drug-induced Liver Injury by Acetaminophen and Other Drugs: A Critical Evaluation and Historical Perspective.","authors":"Hartmut Jaeschke, Anup Ramachandran","doi":"10.14218/JCTH.2024.00324","DOIUrl":"10.14218/JCTH.2024.00324","url":null,"abstract":"<p><p>Drug-induced hepatotoxicity is a significant clinical issue worldwide. Given the limited treatment options for these liver injuries, understanding the mechanisms and modes of cell death is crucial for identifying novel therapeutic targets. For the past 60 years, reactive oxygen species and iron-dependent lipid peroxidation (LPO) have been hypothesized to be involved in many models of acute drug-induced liver injury. However, this mechanism of toxicity was largely abandoned when apoptosis became the primary focus of cell death research. More recently, ferroptosis-a novel, non-apoptotic form of cell death-was identified in NRAS-mutant HT-1080 fibrosarcoma cells exposed to erastin and other NRLs. Ferroptosis is characterized by glutathione depletion and the impairment of glutathione peroxidase 4 activity, which hinders the detoxification of lipid hydroperoxides. These hydroperoxides then serve as substrates for iron-dependent LPO propagation. This cell death mechanism is now receiving widespread attention, extending well beyond its original identification in cancer research, including in the field of drug-induced liver injury. However, concerns arise when such mechanisms are applied across different cell types and disease states without sufficient validation. This review critically evaluated the historical evidence for iron-dependent LPO as a mechanism of drug-induced hepatotoxicity and explored how these earlier findings have led to the current concept of ferroptosis. Overall, the published data support the idea that multi-layered endogenous antioxidant defense mechanisms in the liver limit the occurrence of pathophysiologically relevant LPO under normal conditions. Only when these defense mechanisms are severely compromised does ferroptosis become a significant mode of drug-induced cell death.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"12 12","pages":"1057-1066"},"PeriodicalIF":3.1,"publicationDate":"2024-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11622198/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142794896","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}
Robert Lam, Dhanpat Jain, Yanhong Deng, Eesha Acharya, Joseph K Lim
{"title":"Advanced Liver Fibrosis Predicts Liver Outcomes in Biopsy-proven Metabolic Dysfunction-associated Steatotic Liver Disease: A U.S.-based Single-center Retrospective Cohort Study.","authors":"Robert Lam, Dhanpat Jain, Yanhong Deng, Eesha Acharya, Joseph K Lim","doi":"10.14218/JCTH.2024.00189","DOIUrl":"10.14218/JCTH.2024.00189","url":null,"abstract":"<p><strong>Background and aims: </strong>Data regarding risk factors and long-term outcomes of U.S. patients with biopsy-proven metabolic dysfunction-associated steatotic liver disease (MASLD) are limited. This study aimed to investigate the role of clinical and histologic risk factors on long-term outcomes in patients with MASLD.</p><p><strong>Methods: </strong>A retrospective cohort study of 451 adults with biopsy-proven MASLD was conducted at a U.S. academic hospital from 2012 to 2020. An experienced pathologist evaluated the index liver biopsy. Patients with a prior liver transplant or alternative etiologies of chronic liver disease were excluded. The duration of the risk exposure was determined from the date of the index liver biopsy to an outcome event or the last follow-up examination. Outcome events of interest included incident liver-related events, liver decompensation, and all-cause mortality.</p><p><strong>Results: </strong>In the final cohort of 406 patients followed for a median of 3.7 years (interquartile range: 4.8 years), 35 patients died, 41 developed hepatic decompensation, and 70 experienced a liver-related event. Among histologic risk factors, stage 3 (adjusted Hazard ratio (aHR) 2.68, 95% confidence interval (CI) 1.18-6.11) and stage 4 (aHR 6.96, 95% CI 3.55-13.64) fibrosis were associated with incident liver-related events compared to stage 0-1 fibrosis. Stage 4 (aHR 8.46, 95% CI 3.26-21.99) fibrosis alone was associated with incident liver decompensation events compared to stage 0-1 fibrosis. Among clinical risk factors, hypertension (aHR 2.58, 95% CI 1.05-6.34) was associated with incident liver decompensation.</p><p><strong>Conclusions: </strong>In a U.S. single-center cohort of patients with biopsy-proven MASLD, advanced fibrosis was the primary risk factor for incident liver decompensation and liver-related events.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"12 12","pages":"988-996"},"PeriodicalIF":3.1,"publicationDate":"2024-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11622200/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142794892","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}
Yue Chen, Wenkang Gao, Huikuan Chu, Afnan Ahmed Mohamed Al-Asbahi, Shengqi Yan, Hang Yuan, Jiake Che, Zilu Cheng, Zexuan Li, Jin Ye, Rong Lin, Xiaohua Hou, Fan Du, Ling Yang
{"title":"Anti-hepatitis B Virus Treatment with Tenofovir Amibufenamide Has No Impact on Blood Lipids: A Real-world, Prospective, 48-week Follow-up Study.","authors":"Yue Chen, Wenkang Gao, Huikuan Chu, Afnan Ahmed Mohamed Al-Asbahi, Shengqi Yan, Hang Yuan, Jiake Che, Zilu Cheng, Zexuan Li, Jin Ye, Rong Lin, Xiaohua Hou, Fan Du, Ling Yang","doi":"10.14218/JCTH.2024.00237","DOIUrl":"10.14218/JCTH.2024.00237","url":null,"abstract":"<p><strong>Background and aims: </strong>The effect of tenofovir amibufenamide (TMF) on blood lipid profiles in patients with chronic hepatitis B (CHB) remains unclear. This study aimed to explore whether TMF affects blood lipids during 48 weeks in patients with CHB.</p><p><strong>Methods: </strong>A total of 91 patients with CHB undergoing TMF treatment for 48 weeks were divided into two groups: Lipid Normal (n = 42) and Lipid Abnormal (n = 49), based on baseline blood lipid levels. Lipid indices, virological responses, and biochemical indicators were compared between the two groups. Clinical observations were further verified through <i>in vitro</i> experiments.</p><p><strong>Results: </strong>After an average follow-up of 373 ± 121 days, lipid indices in all 91 patients had not significantly changed compared with baseline (total cholesterol: 4.67 vs. 4.69 mmol/L, <i>P</i> = 0.2499; triglycerides: 1.08 vs. 1.04 mmol/L, <i>P</i> = 0.4457; high-density lipoprotein cholesterol: 1.25 vs. 1.25 mmol/L, <i>P</i> = 0.3063; low-density lipoprotein cholesterol: 3.03 vs. 3.02 mmol/L, <i>P</i> = 0.5765). Subgroup comparisons showed lipid indices remained stable. Among treatment-naïve patients (n = 82), complete viral suppression rates were 23.2%, 59.8%, 70.7%, and 86.6% at four, 12, 24, and 48 weeks, respectively. Cellular experiments revealed that TMF did not promote lipid metabolism in primary hepatocytes and AML12 cells.</p><p><strong>Conclusions: </strong>Regardless of baseline blood lipid characteristics, 48 weeks of antiviral treatment with TMF in patients with CHB had no significant lipid-raising effect.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"12 12","pages":"997-1008"},"PeriodicalIF":3.1,"publicationDate":"2024-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11622202/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142794893","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":"Prolonged Direct Hyperbilirubinemia Following Acute Hepatitis: When Not to Worry?","authors":"Danzhu Zhao, George Y Wu","doi":"10.14218/JCTH.2024.00265","DOIUrl":"10.14218/JCTH.2024.00265","url":null,"abstract":"","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"12 12","pages":"985-987"},"PeriodicalIF":3.1,"publicationDate":"2024-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11622201/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142794488","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}
Jian-Gao Fan, Xiao-Yuan Xu, Rui-Xu Yang, Yue-Min Nan, Lai Wei, Ji-Dong Jia, Hui Zhuang, Jun-Ping Shi, Xiao-Ying Li, Chao Sun, Jie Li, Vincent Wai-Sun Wong, Zhong-Ping Duan
{"title":"Guideline for the Prevention and Treatment of Metabolic Dysfunction-associated Fatty Liver Disease (Version 2024).","authors":"Jian-Gao Fan, Xiao-Yuan Xu, Rui-Xu Yang, Yue-Min Nan, Lai Wei, Ji-Dong Jia, Hui Zhuang, Jun-Ping Shi, Xiao-Ying Li, Chao Sun, Jie Li, Vincent Wai-Sun Wong, Zhong-Ping Duan","doi":"10.14218/JCTH.2024.00311","DOIUrl":"10.14218/JCTH.2024.00311","url":null,"abstract":"<p><p>With the rising epidemic of obesity, metabolic syndrome, and type 2 diabetes mellitus in China, metabolic dysfunction-associated non-alcoholic fatty liver disease has become the most prevalent chronic liver disease. This condition frequently occurs in Chinese patients with alcoholic liver disease and chronic hepatitis B. To address the impending public health crisis of non-alcoholic fatty liver disease and its underlying metabolic issues, the Chinese Society of Hepatology and the Chinese Medical Association convened a panel of clinical experts to revise and update the \"Guideline of prevention and treatment of non-alcoholic fatty liver disease (2018, China)\". The new edition, titled \"Guideline for the prevention and treatment of metabolic dysfunction-associated fatty liver disease (Version 2024)\", offers comprehensive recommendations on key clinical issues, including screening and monitoring, diagnosis and evaluation, treatment, and follow-up for metabolic dysfunction-associated fatty liver disease and metabolic dysfunction-associated steatotic liver disease. Metabolic dysfunction-associated fatty liver disease is now the preferred English term and is used interchangeably with metabolic dysfunction-associated steatotic liver disease. Additionally, the guideline emphasizes the importance of multidisciplinary collaboration among hepatologists and other specialists to manage cardiometabolic disorders and liver disease effectively.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"12 11","pages":"955-974"},"PeriodicalIF":3.1,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11557364/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142621258","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}
Mariana M Ramírez-Mejía, Stephany M Castillo-Castañeda, Shreya C Pal, Xingshun Qi, Nahum Méndez-Sánchez
{"title":"The Multifaceted Role of Bilirubin in Liver Disease: A Literature Review.","authors":"Mariana M Ramírez-Mejía, Stephany M Castillo-Castañeda, Shreya C Pal, Xingshun Qi, Nahum Méndez-Sánchez","doi":"10.14218/JCTH.2024.00156","DOIUrl":"10.14218/JCTH.2024.00156","url":null,"abstract":"<p><p>Bilirubin, the primary breakdown product of hemoproteins, particularly hemoglobin, plays a key role in the diagnosis, prognosis, and monitoring of liver diseases. In acute liver diseases, such as acute liver failure, drug-induced liver injury, and viral hepatitis, bilirubin serves as a biomarker reflecting the extent of hepatocyte loss and liver damage. Chronic liver diseases, including alcohol-related liver disease, chronic hepatitis C virus infection, metabolic dysfunction-associated fatty liver disease, and autoimmune liver diseases, are marked by persistent liver injury and inflammation. Bilirubin levels in chronic liver diseases provide insight into liver function, disease severity, and prognosis. As a versatile biomarker, bilirubin offers valuable information on the pathophysiology of liver diseases and aids in guiding clinical decision-making regarding the treatment of liver diseases and their complications. This review aimed to explore the multifunctional role of bilirubin in liver diseases by analyzing its biological functions beyond its role as a biomarker of liver damage.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"12 11","pages":"939-948"},"PeriodicalIF":3.1,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11557368/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142621276","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}