Journal of Clinical and Translational Hepatology最新文献

{"title":"Ursolic Acid Modulates Estrogen Conversion to Relieve Inflammation in Metabolic Dysfunction-associated Steatotic Liver Disease via HSD17B14.","authors":"Simin Gu, Hui Zhang, Zhekun Xiong, Chong Chen, Junmin Wang, Dan Fang, Yiyuan Zheng, Yong Li","doi":"10.14218/JCTH.2024.00414","DOIUrl":"https://doi.org/10.14218/JCTH.2024.00414","url":null,"abstract":"<p><strong>Background and aims: </strong>The incidence of metabolic dysfunction-associated steatotic liver disease (MASLD) has been escalating annually, positioning it as the leading cause of chronic liver disease worldwide. Ursolic acid has demonstrated promising therapeutic efficacy in managing MASLD, thereby justifying the need for an in-depth exploration of its pharmacological mechanisms. This study aimed to investigate elucidate the therapeutic mechanisms by which ursolic acid modulates estrogen conversion in the treatment of MASLD.</p><p><strong>Methods: </strong>Building upon prior studies that have highlighted the potent anti-inflammatory effects of ursolic acid and its specific targeting of 17β-hydroxysteroid dehydrogenase 14 (HSD17B14), this investigation employed a western diet to induce MASLD in murine models with varying severities over different time intervals.</p><p><strong>Results: </strong>The protein expression of HSD17B14 initially increased, followed by a subsequent decrease. This trend was accompanied by corresponding changes in 17β-estradiol (E2) and estrone (E1) levels. Intervention with ursolic acid resulted in a reduction in HSD17B14 and E1 levels during the phase of high HSD17B14 expression, while simultaneously elevating E2 levels. In steatotic hepatocytes, E1 promoted cellular inflammation, whereas E2 exhibited anti-inflammatory effects. However, the alleviated effects of E2 were antagonized by HSD17B14. As expected, ursolic acid modulated HSD17B14, thereby mitigating the inflammatory response in steatotic hepatocytes.</p><p><strong>Conclusions: </strong>HSD17B14, a crucial enzyme regulating the balance between E1 and E2, catalyzes the conversion of estrogen E2 into E1, thereby exacerbating tissue inflammation induced by metabolic stress. Ursolic acid, by modulating HSD17B14-mediated estrogen conversion, appears to ameliorate immune-related inflammation in MASLD.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"13 4","pages":"269-277"},"PeriodicalIF":3.1,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11976441/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144020906","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":"Liver Injury in Immune Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis: Five New Classification Types.","authors":"Rolf Teschke","doi":"10.14218/JCTH.2024.00402","DOIUrl":"https://doi.org/10.14218/JCTH.2024.00402","url":null,"abstract":"<p><p>Liver injury in Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) is a multifaceted disorder, lacking cohort homogeneity due to a variety of potential causes, including drugs, arsenic and other heavy metals, glyphosate, infections, and ultraviolet radiation. The goals of this review were (1) to analyze the role of diagnostic algorithms in assessing causality for potential culprits involved in the development of liver injury associated with immune-mediated SJS and TEN, which represent immune-based variant disorders within a continuous spectrum. Milder forms are classified as SJS or SJS/TEN overlap, while TEN is known as the most serious form; and (2) to interpret the findings that allow for the characterization of the different types of these disorders. The manuscript is based on an extensive literature search for single case reports, case cohorts, and review articles. Search terms included: Stevens-Johnson Syndrome, Toxic Epidermal Necrolysis, and specific diagnostic algorithms such as the Roussel Uclaf Causality Assessment Method (RUCAM) and the Algorithm of Drug Causality for Epidermal Necrolysis (ALDEN). For the purpose of basic feature description, the uniform term SJS/TEN is used in the current analysis. SJS/TEN presents with five different cohort types: SJS/TEN type (1), which refers to a cohort of SJS/TEN caused by drugs, as assessed by both ALDEN and RUCAM; type (2), representing SJS/TEN due to drugs and assessed by ALDEN only, but not by RUCAM; type (3), which includes a cohort of SJS/TEN caused by drugs, assessed by non-ALDEN and non-RUCAM tools; type (4), which focuses on a cohort of SJS/TEN caused by non-drug culprits, assessed by various tools; and type (5), which considers a cohort of SJS/TEN caused by unknown culprits. Using this new SJS/TEN typology will help better characterize individual features, personalize treatment, and clarify pathogenetic specifics for each of the five disease types. This new SJS/TEN typology provides clarity by replacing issues of inhomogeneity with cohort homogeneity.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"13 4","pages":"339-357"},"PeriodicalIF":3.1,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11976437/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144006143","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":"Hepatocellular Carcinoma and the Role of Liver Transplantation: An Update and Review.","authors":"Lynette M Sequeira, N Begum Ozturk, Leandro Sierra, Merve Gurakar, Merih Deniz Toruner, Melanie Zheng, Cem Simsek, Ahmet Gurakar, Amy K Kim","doi":"10.14218/JCTH.2024.00432","DOIUrl":"https://doi.org/10.14218/JCTH.2024.00432","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is the fourth leading cause of cancer-related death worldwide. Multiple treatment modalities are available for the management of HCC, depending on its stage as determined by the Barcelona Clinic Liver Cancer staging system. Because liver transplantation (LT) theoretically removes the cancer and replaces the organ at risk for future malignancy, LT is often considered the most definitive and one of the most efficacious treatment options for HCC. Nevertheless, the success and efficacy of liver transplantation depend on various tumor characteristics. As a result, multiple criteria have been developed to assess the appropriateness of a case of HCC for LT, with the pioneering Milan Criteria established in 1996. Over the past 20 to 30 years, these criteria have been critically evaluated, expanded, and often liberalized to make LT for patients with HCC a more universally applicable option. Furthermore, the development of other treatment modalities has enabled downstaging and bridging strategies for HCC prior to LT. In this narrative and comprehensive review, we provided an update on recent trends in the epidemiology of HCC, selection criteria for LT, implementation of LT across different regions, treatment modalities available as bridges, downstaging strategies, alternatives to LT, and, finally, post-LT surveillance.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"13 4","pages":"327-338"},"PeriodicalIF":3.1,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11976436/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144007743","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":"Patients with AMA/anti-sp100/anti-gp210 Positivity and Cholestasis Can Manifest Conditions Beyond Primary Biliary Cholangitis.","authors":"Xin Zeng, Tingting Lv, Shuxiang Li, Sha Chen, Buer Li, Zhijiao Lu, Yu Wang, Xiaojuan Ou, Xinyan Zhao, Hong You, Weijia Duan, Jidong Jia","doi":"10.14218/JCTH.2024.00374","DOIUrl":"10.14218/JCTH.2024.00374","url":null,"abstract":"<p><strong>Background and aims: </strong>The diagnostic value of primary biliary cholangitis (PBC)-specific antibodies in patients with elevated alkaline phosphatase (ALP) and gamma-glutamyl transferase (GGT) levels, and other identifiable causes, was unclear. Our study aimed to determine whether etiological treatments in PBC-specific antibody-positive patients could improve liver biochemical tests, thereby distinguishing them from individuals with PBC.</p><p><strong>Methods: </strong>We enrolled patients who were positive for PBC-specific antibodies and elevated ALP and/or GGT levels but with other identifiable etiologies. Changes in liver biochemistry following non-ursodeoxycholic acid etiological treatments were monitored.</p><p><strong>Results: </strong>A total of 155 patients with positive PBC-specific antibodies and elevated ALP and/or GGT levels due to non-PBC diseases were enrolled. Among them, 100 patients were diagnosed with non-PBC liver diseases, mainly metabolic-associated fatty liver disease, drug-induced liver injury, and autoimmune hepatitis. Additionally, 55 patients had non-liver diseases, predominantly connective tissue diseases. The median follow-up duration was 15.9 (4.7-25.6) months. Among 141 patients who completed follow-up after receiving etiological treatments, 85.1% (120/141) showed improvement in ALP and/or GGT levels, with 51.8% (73/141) achieving normalization of both ALP and GGT. However, 68 patients continued to exhibit elevated ALP and/or GGT, with 55 patients displaying isolated GGT elevation and 11 patients showing liver histological changes not consistent with PBC.</p><p><strong>Conclusions: </strong>PBC-specific antibodies, along with elevated ALP and GGT levels, may occur in various non-PBC diseases. Etiological treatments may improve or even resolve cholestatic biochemistry. For these patients, initiating etiological treatment rather than immediately starting ursodeoxycholic acid therapy would be justified.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"13 3","pages":"200-206"},"PeriodicalIF":3.1,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11894394/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143615734","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":"Chinese Guidelines on the Management of Hepatic Encephalopathy in Cirrhosis (2024).","authors":"Xiaoyuan Xu, Huiguo Ding, Wengang Li, Ying Han, Yujuan Guan, Jinghang Xu, Yifan Han, Jidong Jia, Lai Wei, Zhongping Duan, Yuemin Nan, Hui Zhuang","doi":"10.14218/JCTH.2024.00484","DOIUrl":"10.14218/JCTH.2024.00484","url":null,"abstract":"<p><p>With progress in basic and clinical research on hepatic encephalopathy in cirrhosis worldwide, the Chinese Society of Hepatology of the Chinese Medical Association has invited experts in relevant fields to revise the 2018 \"Chinese Guidelines on the Management of Hepatic Encephalopathy in Cirrhosis.\" The updated guidelines provide recommendations for the clinical diagnosis, treatment, and both primary and secondary prevention of hepatic encephalopathy in cirrhosis.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"13 3","pages":"253-267"},"PeriodicalIF":3.1,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11894390/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143615661","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":"SOX9 Overexpression Ameliorates Metabolic Dysfunction-associated Steatohepatitis Through Activation of the AMPK Pathway.","authors":"Juan Deng, Kai Ding, Shuqing Liu, Fei Chen, Ru Huang, Bonan Xu, Xin Zhang, Weifen Xie","doi":"10.14218/JCTH.2024.00197","DOIUrl":"10.14218/JCTH.2024.00197","url":null,"abstract":"<p><strong>Background and aims: </strong>The transcription factor sex-determining region Y-related high-mobility group-box gene 9 (SOX9) plays a critical role in organ development. Although SOX9 has been implicated in regulating lipid metabolism <i>in vitro</i>, its specific role in metabolic dysfunction-associated steatohepatitis (MASH) remains poorly understood. This study aimed to investigate the role of SOX9 in MASH pathogenesis and explored the underlying mechanisms.</p><p><strong>Methods: </strong>MASH models were established using mice fed either a methionine- and choline-deficient (MCD) diet or a high-fat, high-fructose diet. To evaluate the effects of SOX9, hepatocyte-specific SOX9 deletion or overexpression was performed. Lipidomic analyses were conducted to assess how SOX9 influences hepatic lipid metabolism. RNA sequencing was employed to identify pathways modulated by SOX9 during MASH progression. To elucidate the mechanism further, HepG2 cells were treated with an adenosine monophosphate-activated protein kinase (AMPK) inhibitor to test whether SOX9 acts via AMPK activation.</p><p><strong>Results: </strong>SOX9 expression was significantly elevated in hepatocytes of MASH mice. Hepatocyte-specific SOX9 deletion exacerbated MCD-induced MASH, whereas overexpression of SOX9 mitigated high-fat, high-fructose-induced MASH. Lipidomic and RNA sequencing analyses revealed that SOX9 suppresses the expression of genes associated with lipid metabolism, inflammation, and fibrosis in MCD-fed mice. Furthermore, SOX9 deletion inhibited AMPK pathway activation, while SOX9 overexpression enhanced it. Notably, administration of an AMPK inhibitor negated the protective effects of SOX9 overexpression, leading to increased lipid accumulation in HepG2 cells.</p><p><strong>Conclusions: </strong>Our findings demonstrate that SOX9 overexpression alleviates hepatic lipid accumulation in MASH by activating the AMPK pathway. These results highlight SOX9 as a promising therapeutic target for treating MASH.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"13 3","pages":"189-199"},"PeriodicalIF":3.1,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11894392/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143615737","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":"The Role of Solute Carrier Family Transporters in Hepatic Steatosis and Hepatic Fibrosis.","authors":"Chi Zhang, Xuanran Yang, Yi Xue, Huan Li, Chuanfei Zeng, Mingkai Chen","doi":"10.14218/JCTH.2024.00348","DOIUrl":"10.14218/JCTH.2024.00348","url":null,"abstract":"<p><p>Solute carrier (SLC) family transporters are crucial transmembrane proteins responsible for transporting various molecules, including amino acids, electrolytes, fatty acids, and nucleotides. To date, more than fifty SLC transporter subfamilies have been identified, many of which are linked to the progression of hepatic steatosis and fibrosis. These conditions are often caused by factors such as non-alcoholic fatty liver disease and non-alcoholic steatohepatitis, which are major contributors to the global liver disease burden. The activity of SLC members regulates the transport of substrates across biological membranes, playing key roles in lipid synthesis and metabolism, mitochondrial function, and ferroptosis. These processes, in turn, influence the function of hepatocytes, hepatic stellate cells, and macrophages, thereby contributing to the development of hepatic steatosis and fibrosis. Additionally, some SLC transporters are involved in drug transport, acting as critical regulators of drug-induced hepatic steatosis. Beyond substrate transport, certain SLC members also exhibit additional functions. Given the pivotal role of the SLC family in hepatic steatosis and fibrosis, this review aimed to summarize the molecular mechanisms through which SLC transporters influence these conditions.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"13 3","pages":"233-252"},"PeriodicalIF":3.1,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11894391/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143615740","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":"Dose-dependent Relationship between Alcohol Consumption and the Risks of Hepatitis B Virus-associated Cirrhosis and Hepatocellular Carcinoma: A Meta-analysis and Systematic Review.","authors":"Yin-Ping Wu, Xue-Yan Yang, Yu-Xin Tian, Jin Feng, Yee Hui Yeo, Fan-Pu Ji, Ming-Hua Zheng, Yu-Chen Fan","doi":"10.14218/JCTH.2024.00379","DOIUrl":"10.14218/JCTH.2024.00379","url":null,"abstract":"<p><strong>Background and aims: </strong>The quantitative effects of alcohol consumption on cirrhosis and hepatocellular carcinoma (HCC) in hepatitis B virus (HBV) infection are unknown. This study aimed to establish a dose-dependent model of alcohol consumption on the risks of cirrhosis and HCC.</p><p><strong>Methods: </strong>PubMed, Embase, the Cochrane Library, Web of Science, and four Chinese databases were searched for studies published from their inception to 15 May 2024. A random-effects model was used to pool the data on the incidence of cirrhosis and HCC, and a dose-dependent model of alcohol's effect on cirrhosis and HCC was established.</p><p><strong>Results: </strong>A total of 33,272 HBV patients from 45 studies were included. Compared with non-drinkers, the overall pooled odds ratio (OR) for cirrhosis was 2.61 (95% confidence interval [CI]: 1.46-4.66; I² = 94%, <i>p</i> < 0.001), and the OR for HCC was 2.27 (95% CI: 1.50-3.43; I² = 90%, <i>p</i> < 0.001) among drinkers. Compared with low-level drinkers, the estimated pooled OR for cirrhosis was 2.34 (95% CI: 1.59-3.44; I² = 87%, <i>p</i> < 0.001), and the OR for HCC was 2.42 (95% CI: 1.90-3.09; I² = 80%, <i>p</i> < 0.001) among high-level drinkers. Furthermore, a linear dose-dependent analysis showed that each daily consumption of 12 g of alcohol increased the risk of cirrhosis by 6.2% and the risk of HCC by 11.5%.</p><p><strong>Conclusions: </strong>Alcohol dose-dependently increases the risks of cirrhosis and HCC in patients with HBV infection, and patients with daily alcohol consumption of more than 12 g should be strictly monitored.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"13 3","pages":"179-188"},"PeriodicalIF":3.1,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11894389/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143615663","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":"Fluorescence-guided Surgery for Hepatocellular Carcinoma: From Clinical Practice to Laboratories.","authors":"Tian Xiao, Didi Chen, Li Peng, Zhuoxia Li, Wenming Pan, Yuping Dong, Jinxiang Zhang, Min Li","doi":"10.14218/JCTH.2024.00375","DOIUrl":"10.14218/JCTH.2024.00375","url":null,"abstract":"<p><p>Fluorescence navigation is a novel technique for accurately identifying hepatocellular carcinoma (HCC) lesions during hepatectomy, enabling real-time visualization. Indocyanine green-based fluorescence guidance has been commonly used to demarcate HCC lesion boundaries, but it cannot distinguish between benign and malignant liver tumors. This review focused on the clinical applications and limitations of indocyanine green, as well as recent advances in novel fluorescent probes for fluorescence-guided surgery of HCC. It covers traditional fluorescent imaging probes such as enzymes, reactive oxygen species, reactive sulfur species, and pH-sensitive probes, followed by an introduction to aggregation-induced emission probes. Aggregation-induced emission probes exhibit strong fluorescence, low background signals, excellent biocompatibility, and high photostability in the aggregate state, but show no fluorescence in dilute solutions. Design strategies for these probes may offer insights for developing novel fluorescent probes for the real-time identification and navigation of HCC during surgery.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"13 3","pages":"216-232"},"PeriodicalIF":3.1,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11894393/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143615667","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":"Effectiveness and Safety of Tenofovir Amibufenamide in the Treatment of Chronic Hepatitis B: A Real-world, Multicenter Study.","authors":"Yaping Li, Yongmei Lin, Guoe Gou, Dandan Cui, Xiaohong Gao, Guanghua Xu, Hongmei Zu, Shuangsuo Dang","doi":"10.14218/JCTH.2024.00364","DOIUrl":"10.14218/JCTH.2024.00364","url":null,"abstract":"<p><strong>Background and aims: </strong>Chronic hepatitis B (CHB) remains a significant global health challenge, and effective antiviral therapies are essential for long-term management. This study aimed to evaluate the real-world effectiveness and safety of tenofovir amibufenamide (TMF) in a cohort of patients with chronic hepatitis B (CHB).</p><p><strong>Methods: </strong>In this multicenter, prospective, real-world cohort study, 194 CHB patients were recruited from four hospitals between August 2021 and August 2022. Patients were divided into treatment-naïve (TN, n = 123) and treatment-experienced (TE, n = 71) groups. The TN group was further subdivided into TMF (n = 63) and tenofovir disoproxil fumarate (TDF, n = 60) subgroups. In the TE group, patients transitioned from prior antiviral therapies (entecavir or TDF) to TMF after meeting criteria for poor virological response or safety concerns. Treatment response was evaluated in terms of virological effectiveness and alanine transaminase normalization rates. Virological response (VR), ALT normalization rates, renal function markers, and lipid profiles were monitored.</p><p><strong>Results: </strong>In the TN cohort, VR rates at 24 and 48 weeks were 42.86% and 90.48% for TMF, and 60.00% and 83.33% for TDF. ALT normalization rates at 24 and 48 weeks for TMF were 56.82% and 70.45% (according to AASLD 2018 standards). In the TE group, VR rates at 24 and 48 weeks were 83.1% and 91.55%, respectively. ALT normalization rates were 86.67% and 93.33% (local standards), and 66.67% and 76.67% (AASLD 2018 standards) (z = -2.822, <i>P</i> = 0.005). Additionally, TMF showed improved renal safety over TDF, with no significant differences in lipid concentrations.</p><p><strong>Conclusions: </strong>TMF is comparable to TDF in terms of CHB treatment effectiveness, with better renal safety and no impact on lipid levels. In TE patients, transitioning to TMF therapy does not affect antiviral treatment outcomes.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"13 3","pages":"207-215"},"PeriodicalIF":3.1,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11894395/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143615665","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}