Hepatology International国际肝病学

Hepatology International(英文缩写 HEPATOL INT),ISSN 1936-0533,eISSN 1936-0541,中文译名:国际肝病学 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。

2026 年数据 · 影响因子
7.800
JCR 分区
Q1
CAS 分区
B1
近一年发文量
277
本站 PubMed 收录统计

发文量统计区间:2025-11-01 至 2026-10-31,按本站收录文献的发表日期统计。

ISSN: 1936-0533 · eISSN: 1936-0541 · 缩写: HEPATOL INT ·中文: 国际肝病学

期刊介绍

选择期刊介绍栏目

期刊简介

《Hepatology International》是亚太肝病学会的官方期刊,聚焦肝病学临床与转化研究。主要领域涵盖病毒性肝炎、肝硬化、肝癌、脂肪性肝病及肝移植等。读者群包括肝病科医师、胃肠病学家、移植外科医生及基础研究人员,旨在促进亚太地区与全球肝病学界的学术交流。

研究方向

期刊发表肝病学相关的原创研究、综述、专家共识和临床指南,重点方向包括病毒性肝炎、代谢相关脂肪性肝病、肝纤维化与肝硬化、肝细胞癌、肝衰竭及肝移植。论文类型以临床研究、转化医学和流行病学调查为主,兼收高质量病例报告。

期刊特色

研究取向强调临床实用性与区域流行病学特点,尤其关注亚太地区高发的乙型肝炎和肝癌。论文通常要求有明确临床意义或转化价值,适合肝病专科医生、研究人员及研究生阅读参考,对希望了解亚太肝病防治进展的读者尤为有益。

投稿难度

投稿难度中等偏上,作为Q1区期刊对创新性和数据质量要求较高。建议研究设计严谨、样本量充分,并突出临床或转化意义。亚太地区流行病学相关研究可能更具优势,但需注意英文写作规范和伦理审查要求,避免仅凭分区判断录用可能性。

历年影响因子趋势

JCR 数据年份影响因子JCR 分区
20219.046Q1
20226.600Q1
20235.900Q1
20246.100Q1
20257.800Q1

Hepatology International 最新收录文献

  1. JCR分区: Q1 CAS分区: B1 影响因子: 7.8

    1. Clinical and pathological significance of serum anti-PD-1 autoantibodies in acute-onset and chronic autoimmune hepatitis.

    1. 血清抗PD-1自身抗体在急性起病型和慢性自身免疫性肝炎中的临床及病理学意义
    作者:
    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
    日期:
    2026-09-29

    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). 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. 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. 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.

  2. JCR分区: Q1 CAS分区: B1 影响因子: 7.8

    2. Circulating fibronectin levels are linked to liver function, matrix remodeling, and hemostatic complications in advanced chronic liver disease.

    2. 循环纤连蛋白水平与晚期慢性肝病中的肝功能、基质重塑和止血并发症相关
    作者:
    Georg Kramer, Irina Andreea Lie-Ungurean, Benedikt Silvester Hofer, Lukas Hartl, Mathias Jachs, Lorenz Balcar, Georg Semmler, Christian Sebesta, Paul Thöne, Marlene Hintersteininger, Paula Höfinger, Rodrig Marculescu, Thomas Perkmann, Philipp Schwabl, Michael Trauner, Mattias Mandorfer, Thomas Reiberger, Benedikt Simbrunner
    日期:
    2026-09-25

    Fibronectin is a multifunctional matrix glycoprotein involved in tissue remodeling and hemostasis; however, its clinical relevance in cirrhosis remains unclear. This study characterized circulating fibronectin across stages of advanced chronic liver disease (ACLD) and assessed its correlation to pathophysiological biomarkers and predictive value for liver-related complications. Patients with ACLD undergoing hepatic venous pressure gradient (HVPG) measurement were prospectively enrolled with circulating fibronectin measured simultaneously. Associations were assessed using correlation analyses and systems modeling. Competing-risk regression was used to evaluate clinical outcomes. Among 298 patients (median HVPG 17 [12-21] mmHg; MELD 3.0 12 [9-17]), fibronectin levels were lower in decompensated than compensated ACLD (30.3 vs. 38.8 mg/dL; p < 0.001). Fibronectin correlated with hepatic synthesis (cholinesterase: Spearman's r = 0.64) and MELD 3.0 (r = - 0.47; both p < 0.001) while showing an independent positive association with ELF (β = 0.19; p < 0.001). In systems modeling, hepatic synthesis explained most of fibronectin variance (cholinesterase: 37%), followed by fibrinolysis (antiplasmin: 14%) and matrix remodeling (ELF: 12%). In exploratory analyses, higher fibronectin levels were independently associated with variceal bleeding (aSHR 1.04, p = 0.017), and lower fibronectin levels with portal vein thrombosis (aSHR 0.95, p = 0.031), when adjusted for HVPG, MELD 3.0, or IL-6. Fibronectin was not associated with other hepatic decompensation events, hepatocellular carcinoma, or liver-related mortality. Circulating fibronectin reflects hepatic synthetic capacity and matrix remodeling. Its divergent exploratory associations with variceal bleeding and portal vein thrombosis suggest that fibronectin may capture aspects of hemostatic vulnerability. NCT03267615.

  3. JCR分区: Q1 CAS分区: B1 影响因子: 7.8

    3. The Global ACLF Consensus : the 'Istanbul Document'.

    作者:
    Anand V Kulkarni, Ashok Choudhury, Vinod Arora, Abdul Kadir Dokmeci, Abraham Koshy, Ahmet Gurakar, Ajay Duseja, Akash Roy, Akash Shukla, Aleksander Krag, Alfred Wei Chieh Kow, Ananta Shrestha, Apichat Kaewdech, Ashish Goel, Ashish Kumar, Ashwani K Singal, Aung Hlaing Bwa, Chanunta Hongthanakorn, Cosmas Rinaldi Adithya Lesmana, Daniel Huang, Darrell Crawford, Debbie Shawcross, Deniz Balchi, Dhiraj Agrawal, Diana A Payawal, Do Seon Song, Dong Joon Kim, Fernando Bessone, George K Lau, Giacomo Germani, Girish Kumar Pati, Grace L Su, Guan-Huei Lee, Gupse Adali, Gyongyi Szabo, Hasmik Ghazinian, Jacob George, James Fung, Jasmohan Bajaj, P Javed, Jidong Jia, Jimmy Che-To Lai, Jin Jun Chen, Jonel Trebicka, Jun Li, Kavish Patidar, Kemal Fariz Kalista, Ken Liu, Kessarin Thanapirom, Lai Wei, M Golam Azam, Madhumita Premkumar, Madunil Niriella, Manasa Alla, Mangesh Pagadala, Manoj Kumar, Manuel Mendizabal, Mario Guimaraes Pessoa, Mark Dhinesh Muthiah, Masao Omata, Mazen Noureddin, Md Fazal Karim, Mithun Sharma, Mohamed Alboraie, Mohamed Elbasiony, Murat Harputluoglu, Narendra Singh Choudhary, Nazia Selzner, Necati Ormeci, Nelia Hernandez, Nipun Verma, Paolo Angeli, Phunchai Charatcharoenwitthaya, Prabir Maji, Pravin Rathi, R K Dhiman, Rahul Kumar, Rakhi Maiwall, Ramazan Idilman, Richard Moreau, Rino A Gani, Rosmawati Mohamed, S S Hamid, Sanjeev Sachdeva, Senamjit Kaur, Shahinul Alam, Soe Thiha Maung, Soek-Siam Tan, T R Sowmya, K C Sudhamshu, Sumana Ramachandra, Sunil Kumar Dadhich, Sunil Taneja, Suprabhat Giri, Surender Singh, Tao Chen, Tarana Gupta, Tushar Madke, V M Dayal, Venishetty Shantan, Viniyendra Pamecha, Wong Yu Jun, Xiaolong Qi, Yoon Jun Kim, Zaigham Abbas, Zobair M Younossi, Shiv Kumar Sarin
    日期:
    2026-09-24

    The Kyoto Consensus introduced a key conceptual shift in characterizing acute-on-chronic liver failure (ACLF) patients into Type-A and Type-B phenotypes. A day-long meeting was convened at Istanbul during APASL 2026 to assess the real-world applicability of Type-A and Type-B ACLF across continents. The objective was that physicians could recognize ACLF as a unified disease entity, and quality research and new therapeutic options with defined end-points could be undertaken. Data from APASL ACLF Research Consortium (AARC), EASL-CLIF and NACSELD were assessed and discussed in detail. While the applicability of Type-A and Type-B varied across cohorts, the definition required to be appended. The experts unanimously agreed that 'liver failure' as identified by serum bilirubin of ≥ 5 mg/dl and INR ≥ 1.5 should be the 'core' for both Type-A and Type-B ACLF. Type-A ACLF is considered when "a patient with compensated advanced chronic liver disease or compensated cirrhosis presents with index decompensation as liver failure followed by development of ascites and/or hepatic encephalopathy within 4 weeks." Type-B ACLF is considered when "a patient with prior or concurrent decompensated cirrhosis presents with acute decompensation as liver failure accompanied by one or more extrahepatic organ failures." New definitions of organ dysfunction and failure, as well as endpoints for clinical trials, were also deliberated and finalized. The "Istanbul Report", presents a milestone evidence based consensus document carrying harmonization of various aspects of ACLF, incorporating current evidence, critically analyzed unanimous recommendations, and key areas for future studies.

  4. JCR分区: Q1 CAS分区: B1 影响因子: 7.8

    4. Dynamic changes in controlled attenuation parameter (CAP) improve prognostic prediction for CHB patients with significant fibrosis and cirrhosis.

    作者:
    Xiaowei Ai, Mengyang Zhang, Shuyan Chen, Xinyu Zhao, Jialing Zhou, Tongtong Meng, Bingqiong Wang, Chenglin Sun, Xiao Han, Yankun Gao, Xiaoning Wu, Hong You, Yameng Sun
    日期:
    2026-09-19

    The coexistence of hepatic steatosis and chronic hepatitis B (CHB) is becoming increasingly common. Although the controlled attenuation parameter (CAP) has been widely used to quantify hepatic steatosis in CHB patients, the prognostic value of longitudinal changes in CAP remains unknown. This study aimed to evaluate whether dynamic changes in CAP are associated with liver-related events (LREs) in CHB patients undergoing antiviral therapy. CHB patients with significant fibrosis or cirrhosis before antiviral therapy were included. CAP was used to assess hepatic steatosis. LREs were defined as hepatic decompensations, hepatocellular carcinoma (HCC), liver transplantation, or liver-related death. Joint models were employed to analyze associations between longitudinal measurements and risk of LREs. A total of 573 CHB patients were followed for a median of 6.9 years, during which 51 LREs occurred. CAP-dynamics independently predicted LREs (per 10 dB/m increase aHR 0.86, 95% CI 0.78-0.96, p = 0.006). After adjusting for LSM-dynamics, CAP-dynamics remained an independent factor for LREs (per 10 dB/m increase aHR 0.85, 95% CI 0.77-0.95, p = 0.005). The multivariate joint model integrating CAP and LSM dynamics improved predictive performance compared with LSM alone, with the 7-year AUROC increasing from 0.70 to 0.75. CAP exceeding 236 dB/m over time was associated with a reduced risk of LREs (aHR 0.67, 95% CI 0.53-0.84, p < 0.001). In on-treatment CHB patients with significant fibrosis, the dynamics of CAP were associated with the risk of LREs. Longitudinal monitoring of CAP can offer extra prognostic value.

  5. JCR分区: Q1 CAS分区: B1 影响因子: 7.8

    5. Coronary atherosclerosis across stages of metabolic dysfunction-associated steatotic liver disease: a VCTE-CCTA study.

    5. 冠状动脉粥样硬化在代谢功能障碍相关脂肪性肝病各阶段中的表现:一项VCTE-CCTA研究
    作者:
    Gediz Dogay Us, Francesco Innocenti, Ozgur Muhammet Koc, Sevval İlke Ebeoglu, Baris Okcun, İhsan Nuri Akpinar, Melih Hulusi Us, Ger H Koek
    日期:
    2026-09-16

    [中文摘要] 代谢功能障碍相关脂肪性肝病(MASLD)与冠状动脉疾病(CAD)具有共同的病理生理通路。然而,不同阶段的MASLD与不同冠状动脉粥样硬化表型之间的关系仍不明确。我们使用配对的振动控制瞬态弹性成像(VCTE)和冠状动脉计算机断层扫描血管造影(CCTA)评估了肝脏脂肪变性和纤维化与冠状动脉疾病结局的关联。共纳入425名在三个月内同时接受VCTE和CCTA检查的成年人。MASLD定义为受控衰减参数(CAP)≥248 dB/m,显著纤维化定义为肝脏硬度测量值(LSM)≥8 kPa。冠状动脉结局根据冠状动脉疾病报告和数据系统指南进行评估。主要结局为斑块存在;次要结局包括阻塞性狭窄、钙化斑块、高节段受累和CAD严重程度。多变量 logistic 回归模型逐步调整了人口学、生活方式和心脏代谢因素。47.3%的参与者存在MASLD。与无MASLD者相比,MASLD患者的总体斑块患病率更高(81.6% vs 60.7%,p<0.001),而两组之间的阻塞性狭窄无差异。完全调整后,MASLD与总体斑块存在的较高比值比独立相关(OR 2.22,95% CI 1.04-4.73;p=0.038)。在探索性分析中,MASLD并未增加阻塞性狭窄、钙化斑块或CAD严重程度的比值比。相比之下,LSM每增加1 kPa与阻塞性狭窄(OR 1.14,95% CI 1.00-1.30)和钙化斑块(OR 1.18,95% CI 1.04-1.34)的较高比值比相关,但与CAD的存在和严重程度无关。MASLD与冠状动脉粥样硬化斑块的存在独立相关。探索性分析进一步提示,较大的肝脏硬度可能与阻塞性狭窄和钙化斑块相关,这提高了更晚期肝病与晚期冠状动脉疾病特定特征相关的可能性。尚需在更大规模的前瞻性研究中加以证实。

    [英文摘要] Metabolic dysfunction-associated steatotic liver disease (MASLD) and coronary artery disease (CAD) share common pathophysiologic pathways. However, the relationship between different stages of MASLD and distinct coronary atherosclerosis phenotypes remains unclear. We evaluated the association of hepatic steatosis and fibrosis with coronary artery disease outcomes using paired vibration-controlled transient elastography (VCTE) and coronary computed tomography angiography (CCTA). 425 adults who underwent both VCTE and CCTA within a three-month interval were included. MASLD was defined as controlled attenuation parameter (CAP) ≥248 dB/m, and significant fibrosis was defined as Liver Stiffness Measurement (LSM) ≥8 kPa. Coronary outcomes were assessed according to Coronary Artery Disease Reporting and Data System guidance. The primary outcome was plaque presence; secondary outcomes included obstructive stenosis, calcified plaque, high segment involvement, and CAD severity. Multivariable logistic regression models were progressively adjusted for demographic, lifestyle, and cardiometabolic factors. MASLD was present in 47.3% of participants. Individuals with MASLD had a higher prevalence of overall plaque than those without (81.6% vs 60.7%, p<0.001), whereas obstructive stenosis did not differ between groups. MASLD was independently associated with higher odds of overall plaque presence after full adjustment (OR 2.22, 95% CI 1.04-4.73; p=0.038). In exploratory analyses, MASLD did not increase the odds of obstructive stenosis, calcified plaque, or CAD severity. In contrast, 1 kPa increase in LSM was associated with higher odds of obstructive stenosis (OR 1.14, 95% CI 1.00-1.30) and calcified plaque (OR 1.18, 95% CI 1.04-1.34), but not CAD presence and severity. MASLD was independently associated with the presence of coronary atherosclerotic plaque. Exploratory analyses further suggested that greater liver stiffness may be associated with obstructive stenosis and calcified plaque, raising the possibility that more advanced liver disease relates to specific features of advanced coronary artery disease. Confirmation in larger prospective studies is warranted.

  6. JCR分区: Q1 CAS分区: B1 影响因子: 7.8

    6. How to apply artificial intelligence (AI) to facilitate and enhance MASH trials.

    6. 如何应用人工智能(AI)来促进和增强MASH试验
    作者:
    Daniel Yan Zheng Lim, Wei Qiang Leow, Daniela S Allende, Wai Kay Seto, Terry Cheuk-Fung Yip, George Boon Bee Goh
    日期:
    2026-09-16

    Metabolic dysfunction-associated steatohepatitis (MASH) is one of the most common liver diseases, but thus far only two drugs (resmetirom and semaglutide) have received conditional approval for use. Successful MASH trials are thus highly desired to fill the therapeutic and evidence gap. Concurrently, AI has powered advances in multiple areas of medicine. We consider in this review the potential applications of AI to enhance MASH trials. We conduct a narrative review of AI uses in MASH, with a focus on current and potential applications in MASH trials. We describe current digital pathology and AI technologies for MASH grading, a mature application where specific models have been qualified by the FDA and EMA for endpoint determination in MASH trials. We also cover the use of contemporary AI risk models to facilitate patient enrollment, and large language models to facilitate patient interactions including recruitment and retention. Finally, we consider lessons from innovative uses of AI in other medical domains, and how current guidelines shape our thinking about the use of AI in MASH trials. AI has made inroads into the world of MASH trials and shows high potential to further enhance their safety, efficacy, and scientific validity.

  7. JCR分区: Q1 CAS分区: B1 影响因子: 7.8

    7. Noninvasive surrogate endpoints in MASH trials: current perspectives and challenges.

    7. MASH试验中的无创替代终点:当前观点与挑战
    作者:
    Hye Won Lee, Luis Antonio Díaz, Vincent Wai-Sun Wong, Wah Kheong Chan
    日期:
    2026-09-13

    Metabolic dysfunction-associated steatohepatitis (MASH) is a leading cause of cirrhosis and liver-related morbidity. Current regulatory pathways rely on histology and long-term clinical outcomes, but repeated liver biopsy is noninvasive and poorly reproducible; regulators have signaled interest in noninvasive tests (NITs) as surrogate endpoints. This review synthesizes contemporary regulatory perspectives, the evidentiary framework for biomarker qualification, and the published performance of leading noninvasive tests (vibration-controlled transient elastography [VCTE], magnetic resonance elastography [MRE], and the enhanced liver fibrosis [ELF] test). We summarize diagnostic, prognostic, monitoring and response assessment data from cohort studies, meta-analyses and trial datasets, and outline the analytical and clinical validation steps required for reasonably likely surrogate endpoint (RLSE) qualification. Evidence shows that baseline values and longitudinal changes in liver stiffness measurement (LSM by VCTE and MRE) and ELF correlate with histological stage and predict liver-related events. VCTE offers broad accessibility and a mature outcome linkage; MRE provides superior accuracy and repeatability; ELF supplies a scalable prognostic blood signal. However, variability in measurement, limited trial-level surrogacy data, and low-event rates in pre-cirrhotic cohorts constrain definitive qualification. Composite or tiered strategies and prospective trial datasets linking on-treatment NIT changes to major adverse liver outcomes are needed. NITs show promise as surrogate endpoints for MASH trials, but full qualification as RLSE requires standardized assays, robust prospective evidence that treatment‑induced biomarker changes predict hard clinical outcomes, and close collaboration among academia, industry, and regulators.

  8. JCR分区: Q1 CAS分区: B1 影响因子: 7.8

    8. Antiviral therapies are associated with reduced mortality but under-utilized in patients with viral hepatocellular carcinoma: a multinational REAL-HCC study.

    8. 抗病毒治疗与病毒性肝细胞癌患者死亡率降低相关但未得到充分利用:一项跨国REAL-HCC研究
    作者:
    Taotao Yan, Pei-Chien Tsai, Ming-Lun Yeh, Dae Won Jun, Hidenori Toyoda, Yao-Chun Hsu, Jennifer Leong, Xiaozhong Wang, Xu Qiang, Hiroshi Abe, Takanori Suzuki, Chia-Yen Dai, Jee-Fu Huang, Wan-Long Chuang, Chung-Feng Huang, Yao-Li Chen, Ping-Yi Lin, Satoshi Yasuda, Joanne Kimiko Liu, Mayumi Maeda, Eiichi Ogawa, Cheng-Hao Tseng, Maria Buti, Philip Vutien, Yu Jun Wong, Huy Trinh, Takashi Honda, Haruki Uojima, Masaru Enomoto, Yasuhito Tanaka, Myron Schwartz, Ramsey Cheung, Ming-Lung Yu, Mindie H Nguyen
    日期:
    2026-09-11

    Antiviral treatment can reduce mortality of viral hepatocellular carcinoma (HCC), but may be underutilized. In a multinational real-world consortium of HCC patients with hepatitis B (HBV-HCC) or C (HCV-HCC), we assessed nucleos(t)ide analog treatment rate in HBV-HCC (2007-2023) and direct acting antiviral treatment rate in HCV-HCC (2015-2023). Among 3973 HCC patients (3186 HBV, 647 HCV, 140 HBV/HCV), 49.7% of HBV-HCC and 63.2% of HCV-HCC received antiviral treatment. For HBV, lower treatment rates were observed in female (41.7% vs. 51.8%), older (> 60) (45.3% vs. 54.5%), non-cirrhosis and decompensated cirrhosis (vs. compensates cirrhosis: 41.3% vs. 43.2% vs. 76.7%), and Asia region (37.9% vs. 85.0%) patients; for HCV, lower rates in male (59.0% vs. 72.4%), compensated and decompensated cirrhosis (vs. noncirrhosis: 62.9% vs. 54.0% vs. 73.2%), and non-Asia region (58.2% vs. 69.9%) patients. Child A cirrhosis and Barcelona Clinic Liver Cancer (BCLC) 0/A patients had highest treatment rates followed by Child B and C or BCLC B, C, or D for both HBV (78.6%, 48.3%, 43.8%; 59.9%, 50.9%, 36.7%, 41.0%) and HCV (68.2%, 53.3%, 38.6%; 72.5%, 53.3%, 51.9%, 30.2%), all P<0.001. Factors independently associated with lower treatment rates were: female, age>60, Asia region, noncirrhosis, and BCLC B or C (vs. 0/A) for HBV; male, age>65, Child B or C cirrhosis (vs. noncirrhosis), and BCLC B or C for HCV. Antiviral treatment was independently associated with reduced mortality in both HBV-HCC and HCV-HCC patients. Despite survival benefits, antiviral therapies were substantially underutilized in both HBV-HCC and HCV-HCC, particularly advanced patients.

  9. JCR分区: Q1 CAS分区: B1 影响因子: 7.8

    9. Real-world outcomes of lenvatinib versus sorafenib as the second-line therapy after atezolizumab plus bevacizumab in patients with hepatocellular carcinoma: a large-scale multicenter study in Korea.

    9. 仑伐替尼与索拉非尼作为阿替利珠单抗联合贝伐珠单抗治疗后肝细胞癌患者二线治疗的真实世界结局:一项韩国大规模多中心研究
    作者:
    Min Ji Lee, Subin Lim, Jae Yong Shim, Mi Na Kim, DongKyu Kim, Kyu-Pyo Kim, Kang Mo Kim, Baek-Yeol Ryoo, Won-Mook Choi, Hyun-Jeong Kim, Seung-Hoon Lee, Gaeun Kang, Mira Kang, Won Chul Cha, Jung Yong Hong, Woo Kyoung Jeong, Sung Kyung Ju, Jung-Hyun Won, Doik Lee, Jiyoon Ahn, Do Young Kim
    日期:
    2026-09-11

    After first‑line atezolizumab plus bevacizumab (ATE + BEV) in hepatocellular carcinoma (HCC), optimal second‑line (2L) therapy remains unclear. This study compared the real‑world effectiveness and hepatotoxicity of lenvatinib versus sorafenib as 2L treatment after ATE + BEV. This retrospective, multicenter study used electronic medical record data from the Liver Cancer IN Korea (LINK) database. Patients who received 2L lenvatinib or sorafenib after ATE + BEV were included. The primary endpoint was overall survival (OS). Secondary endpoints included time to treatment discontinuation (TTD), time to next treatment (TTNT), hepatotoxicity, and tumor marker dynamics. Analyses were conducted in the overall cohort, with additional propensity score (PS)-matched analyses performed. A total of 295 patients were included in the analysis (2L lenvatinib, n = 132; 2L sorafenib, n = 163). Median OS was significantly longer with lenvatinib (not reached) than with sorafenib (6.67 months [95% CI 5.32-17.31]; p = 0.001). Lenvatinib also showed significantly longer TTD (5.49 months [3.75-6.04] vs. 1.84 months [1.68-2.20]; p < 0.001) and TTNT (5.72 months [4.07-7.85] vs. 3.06 months [2.56-3.48]; p = 0.001). These findings were generally consistent after PS-matching. Incidence rates of laboratory-based hepatotoxicity were lower with lenvatinib. From 2L initiation to 3 months after 2L therapy, both AFP and PIVKA-II generally declined in both groups. These findings suggest that lenvatinib may be a promising 2L option following ATE + BEV in HCC, as evidenced by improved OS, longer treatment durability, and lower rates of laboratory-based hepatotoxicity compared with sorafenib. However, given the retrospective observational design, further prospective studies are warranted to confirm these findings.

  10. JCR分区: Q1 CAS分区: B1 影响因子: 7.8

    10. Alcohol and dementia: is hepatic steatosis an innocent bystander or an active contributor to cognitive decline?

    10. 酒精与痴呆:肝脂肪变性是认知衰退的无辜旁观者,还是积极的促进因素?
    作者:
    Cameron Gofton, Elie Matar, Jacob George
    日期:
    2026-09-09

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指标接近的期刊