Journal of Clinical and Translational Hepatology最新文献

{"title":"Exploring the Pathogenesis of Autoimmune Liver Diseases from the Heterogeneity of Target Cells.","authors":"Zi-Xuan Qiu, Lin-Xiang Huang, Xiao-Xiao Wang, Zi-Long Wang, Xiao-He Li, Bo Feng","doi":"10.14218/JCTH.2023.00531","DOIUrl":"10.14218/JCTH.2023.00531","url":null,"abstract":"<p><p>The incidence of autoimmune liver diseases (ALDs) and research on their pathogenesis are increasing annually. However, except for autoimmune hepatitis, which responds well to immunosuppression, primary biliary cholangitis and primary sclerosing cholangitis are insensitive to immunosuppressive therapy. Besides the known effects of the environment, genetics, and immunity on ALDs, the heterogeneity of target cells provides new insights into their pathogenesis. This review started by exploring the heterogeneity in the development, structures, and functions of hepatocytes and epithelial cells of the small and large bile ducts. For example, cytokeratin (CK) 8 and CK18 are primarily expressed in hepatocytes, while CK7 and CK19 are primarily expressed in intrahepatic cholangiocytes. Additionally, emerging technologies of single-cell RNA sequencing and spatial transcriptomic are being applied to study ALDs. This review offered a new perspective on understanding the pathogenic mechanisms and potential treatment strategies for ALDs.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"12 7","pages":"659-666"},"PeriodicalIF":3.1,"publicationDate":"2024-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11233981/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141590440","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":"Real-world Effectiveness and Tolerability of Interferon-free Direct-acting Antiviral for 15,849 Patients with Chronic Hepatitis C: A Multinational Cohort Study.","authors":"Fanpu Ji, Sally Tran, Eiichi Ogawa, Chung-Feng Huang, Takanori Suzuki, Yu Jun Wong, Hidenori Toyoda, Dae Won Jun, Liu Li, Haruki Uojima, Akito Nozaki, Makoto Chuma, Cheng-Hao Tseng, Yao-Chun Hsu, Masatoshi Ishigami, Takashi Honda, Masanori Atsukawa, Hiroaki Haga, Masaru Enomoto, Huy Trinh, Carmen Monica Preda, Phillip Vutien, Charles Landis, Dong Hyun Lee, Tsunamasa Watanabe, Hirokazu Takahashi, Hiroshi Abe, Akira Asai, Yuichiro Eguchi, Jie Li, Xiaozhong Wang, Jia Li, Junping Liu, Jing Liang, Carla Pui-Mei Lam, Rui Huang, Qing Ye, Hongying Pan, Jiajie Zhang, Dachuan Cai, Qi Wang, Daniel Q Huang, Grace Wong, Vincent Wai-Sun Wong, Junyi Li, Son Do, Norihiro Furusyo, Makoto Nakamuta, Hideyuki Nomura, Eiji Kajiwara, Eileen L Yoon, Sang Bong Ahn, Koichi Azuma, Kazufumi Dohmen, Jihyun An, Do Seon Song, Hyun Chin Cho, Akira Kawano, Toshimasa Koyanagi, Aritsune Ooho, Takeaki Satoh, Kazuhiro Takahashi, Ming-Lun Yeh, Pei-Chien Tsai, Satoshi Yasuda, Yunyu Zhao, Yishan Liu, Tomomi Okubo, Norio Itokawa, Mi Jung Jun, Toru Ishikawa, Koichi Takaguchi, Tomonori Senoh, Mingyuan Zhang, Changqing Zhao, Raluca Ioana Alecu, Wei Xuan Tay, Pooja Devan, Joanne Kimiko Liu, Ritsuzo Kozuka, Elena Vargas-Accarino, Ai-Thien Do, Mayumi Maeda, Wan-Long Chuang, Jee-Fu Huang, Chia-Yen Dai, Ramsey Cheung, Maria Buti, Junqi Niu, Wen Xie, Hong Ren, Seng Gee Lim, Chao Wu, Man-Fung Yuen, Jia Shang, Qiang Zhu, Yoshiyuki Ueno, Yasuhito Tanaka, Jun Hayashi, Ming-Lung Yu, Mindie H Nguyen","doi":"10.14218/JCTH.2024.00089","DOIUrl":"10.14218/JCTH.2024.00089","url":null,"abstract":"<p><strong>Background and aims: </strong>As practice patterns and hepatitis C virus (HCV) genotypes (GT) vary geographically, a global real-world study from both East and West covering all GTs can help inform practice policy toward the 2030 HCV elimination goal. This study aimed to assess the effectiveness and tolerability of DAA treatment in routine clinical practice in a multinational cohort for patients infected with all HCV GTs, focusing on GT3 and GT6.</p><p><strong>Methods: </strong>We analyzed the sustained virological response (SVR12) of 15,849 chronic hepatitis C patients from 39 Real-World Evidence from the Asia Liver Consortium for HCV clinical sites in Asia Pacific, North America, and Europe between 07/01/2014-07/01/2021.</p><p><strong>Results: </strong>The mean age was 62±13 years, with 49.6% male. The demographic breakdown was 91.1% Asian (52.9% Japanese, 25.7% Chinese/Taiwanese, 5.4% Korean, 3.3% Malaysian, and 2.9% Vietnamese), 6.4% White, 1.3% Hispanic/Latino, and 1% Black/African-American. Additionally, 34.8% had cirrhosis, 8.6% had hepatocellular carcinoma (HCC), and 24.9% were treatment-experienced (20.7% with interferon, 4.3% with direct-acting antivirals). The largest group was GT1 (10,246 [64.6%]), followed by GT2 (3,686 [23.2%]), GT3 (1,151 [7.2%]), GT6 (457 [2.8%]), GT4 (47 [0.3%]), GT5 (1 [0.006%]), and untyped GTs (261 [1.6%]). The overall SVR12 was 96.9%, with rates over 95% for GT1/2/3/6 but 91.5% for GT4. SVR12 for GT3 was 95.1% overall, 98.2% for GT3a, and 94.0% for GT3b. SVR12 was 98.3% overall for GT6, lower for patients with cirrhosis and treatment-experienced (TE) (93.8%) but ≥97.5% for treatment-naive patients regardless of cirrhosis status. On multivariable analysis, advanced age, prior treatment failure, cirrhosis, active HCC, and GT3/4 were independent predictors of lower SVR12, while being Asian was a significant predictor of achieving SVR12.</p><p><strong>Conclusions: </strong>In this diverse multinational real-world cohort of patients with various GTs, the overall cure rate was 96.9%, despite large numbers of patients with cirrhosis, HCC, TE, and GT3/6. SVR12 for GT3/6 with cirrhosis and TE was lower but still excellent (>91%).</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"12 7","pages":"646-658"},"PeriodicalIF":3.1,"publicationDate":"2024-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11233980/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141590442","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":"Mesenchymal Stem Cells Alleviate Acute Liver Failure through Regulating Hepatocyte Apoptosis and Macrophage Polarization.","authors":"Yachao Tao, Yonghong Wang, Menglan Wang, Hong Tang, Enqiang Chen","doi":"10.14218/JCTH.2023.00557","DOIUrl":"10.14218/JCTH.2023.00557","url":null,"abstract":"<p><strong>Background and aims: </strong>Acute liver failure (ALF) is a life-threatening clinical problem with limited treatment options. Administration of human umbilical cord mesenchymal stem cells (hUC-MSCs) may be a promising approach for ALF. This study aimed to explore the role of hUC-MSCs in the treatment of ALF and the underlying mechanisms.</p><p><strong>Methods: </strong>A mouse model of ALF was induced by lipopolysaccharide and d-galactosamine administration. The therapeutic effects of hUC-MSCs were evaluated by assessing serum enzyme activity, histological appearance, and cell apoptosis in liver tissues. The apoptosis rate was analyzed in AML12 cells. The levels of inflammatory cytokines and the phenotype of RAW264.7 cells co-cultured with hUC-MSCs were detected. The C-Jun N-terminal kinase/nuclear factor-kappa B signaling pathway was studied.</p><p><strong>Results: </strong>The hUC-MSCs treatment decreased the levels of serum alanine aminotransferase and aspartate aminotransferase, reduced pathological damage, alleviated hepatocyte apoptosis, and reduced mortality <i>in vivo</i>. The hUC-MSCs co-culture reduced the apoptosis rate of AML12 cells <i>in vitro</i>. Moreover, lipopolysaccharide-stimulated RAW264.7 cells had higher levels of tumor necrosis factor-α, interleukin-6, and interleukin-1β and showed more CD86-positive cells, whereas the hUC-MSCs co-culture reduced the levels of the three inflammatory cytokines and increased the ratio of CD206-positive cells. The hUC-MSCs treatment inhibited the activation of phosphorylated (p)-C-Jun N-terminal kinase and p-nuclear factor-kappa B not only in liver tissues but also in AML12 and RAW264.7 cells co-cultured with hUC-MSCs.</p><p><strong>Conclusions: </strong>hUC-MSCs could alleviate ALF by regulating hepatocyte apoptosis and macrophage polarization, thus hUC-MSC-based cell therapy may be an alternative option for patients with ALF.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"12 6","pages":"571-580"},"PeriodicalIF":3.1,"publicationDate":"2024-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11224903/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141554925","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 GRIM19 Loss Induces Liver Fibrosis through NLRP3/IL33 Activation via Reactive Oxygen Species/NF-кB Signaling.","authors":"Xiaohui Xu, Jinmei Feng, Xin Wang, Xin Zeng, Ying Luo, Xinyu He, Meihua Yang, Tiewei Lv, Zijuan Feng, Liming Bao, Li Zhao, Daochao Huang, Yi Huang","doi":"10.14218/JCTH.2023.00562","DOIUrl":"10.14218/JCTH.2023.00562","url":null,"abstract":"<p><strong>Background and aims: </strong>Hepatic fibrosis (HF) is a critical step in the progression of hepatocellular carcinoma (HCC). Gene associated with retinoid-IFN-induced mortality 19 (GRIM19), an essential component of mitochondrial respiratory chain complex I, is frequently attenuated in various human cancers, including HCC. Here, we aimed to investigate the potential relationship and underlying mechanism between GRIM19 loss and HF pathogenesis.</p><p><strong>Methods: </strong>GRIM19 expression was evaluated in normal liver tissues, hepatitis, hepatic cirrhosis, and HCC using human liver disease spectrum tissue microarrays. We studied hepatocyte-specific <i>GRIM19</i> knockout mice and clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein-9 (Cas9) lentivirus-mediated <i>GRIM19</i> gene-editing in murine hepatocyte AML12 cells <i>in vitro</i> and <i>in vivo</i>. We performed flow cytometry, immunofluorescence, immunohistochemistry, western blotting, and pharmacological intervention to uncover the potential mechanisms underlying GRIM19 loss-induced HF.</p><p><strong>Results: </strong>Mitochondrial GRIM19 was progressively downregulated in chronic liver disease tissues, including hepatitis, cirrhosis, and HCC tissues. Hepatocyte-specific <i>GRIM19</i> heterozygous deletion induced spontaneous hepatitis and subsequent liver fibrogenesis in mice. In addition, GRIM19 loss caused chronic liver injury through reactive oxygen species (ROS)-mediated oxidative stress, resulting in aberrant NF-кB activation via an IKK/IкB partner in hepatocytes. Furthermore, GRIM19 loss activated NLRP3-mediated IL33 signaling via the ROS/NF-кB pathway in hepatocytes. Intraperitoneal administration of the NLRP3 inhibitor MCC950 dramatically alleviated GRIM19 loss-driven HF <i>in vivo</i>.</p><p><strong>Conclusions: </strong>The mitochondrial GRIM19 loss facilitates liver fibrosis through NLRP3/IL33 activation via ROS/NF-кB signaling, providing potential therapeutic approaches for earlier HF prevention.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"12 6","pages":"539-550"},"PeriodicalIF":3.1,"publicationDate":"2024-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11224902/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141554926","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":"\"Treat-all\" Strategy for Patients with Chronic Hepatitis B Virus Infection in China: Are We There Yet?","authors":"Mengyang Zhang, Yuanyuan Kong, Xiaoqian Xu, Yameng Sun, Jidong Jia, Hong You","doi":"10.14218/JCTH.2024.00091","DOIUrl":"10.14218/JCTH.2024.00091","url":null,"abstract":"<p><p>Chronic hepatitis B remains the primary cause of liver-related events in China. The World Health Organization set a goal to eliminate viral hepatitis as a public health threat by 2030. However, achieving this goal appears challenging due to the current low rates of diagnosis and treatment. The \"Treat-all\" strategy, which proposes treating all patients with detectable hepatitis B virus (HBV) DNA or even all patients with positive HBsAg, has been suggested to simplify anti-HBV treatment. In 2022, the Chinese Society of Hepatology and the Chinese Society of Infectious Diseases updated the guidelines for the prevention and treatment of chronic hepatitis B in China, expanding antiviral indications and simplifying the treatment algorithm. According to this latest guideline, nearly 95% of patients with detectable HBV DNA are eligible for antiviral treatment. This review aimed to provide a detailed interpretation of the treatment indications outlined in the Chinese <i>Guidelines for the Prevention and Treatment of Chronic Hepatitis B</i> (version 2022) and to identify gaps in achieving the \"Treat-all\" strategy in China.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"12 6","pages":"589-593"},"PeriodicalIF":3.1,"publicationDate":"2024-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11224901/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141554924","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":"Association of Mosaic Chromosomal Alterations and Genetic Factors with the Risk of Cirrhosis.","authors":"Xinyuan Ge, Lu Zhang, Maojie Liu, Xiao Wang, Xin Xu, Yuqian Yan, Chan Tian, Juan Yang, Yang Ding, Chengxiao Yu, Jing Lu, Longfeng Jiang, Qiang Wang, Qun Zhang, Ci Song","doi":"10.14218/JCTH.2023.00575","DOIUrl":"10.14218/JCTH.2023.00575","url":null,"abstract":"<p><strong>Background and aims: </strong>Age-related mosaic chromosomal alterations (mCAs) detected from genotyping of blood-derived DNA are structural somatic variants that indicate clonal hematopoiesis. This study aimed to investigate whether mCAs contribute to the risk of cirrhosis and modify the effect of a polygenic risk score (PRS) on cirrhosis risk prediction.</p><p><strong>Methods: </strong>mCA call sets of individuals with European ancestry were obtained from the UK Biobank. The PRS was constructed based on 12 susceptible single-nucleotide polymorphisms for cirrhosis. Cox proportional hazard models were applied to evaluate the associations between mCAs and cirrhosis risk.</p><p><strong>Results: </strong>Among 448,645 individuals with a median follow-up of 12.5 years, we identified 2,681 cases of cirrhosis, 1,775 cases of compensated cirrhosis, and 1,706 cases of decompensated cirrhosis. Compared to non-carriers, individuals with copy-neutral loss of heterozygosity mCAs had a significantly increased risk of cirrhosis (hazard ratio (HR) 1.42, 95% confidence interval (CI) 1.12-1.81). This risk was higher in patients with expanded cell fractions of mCAs (cell fractions ≥10% vs. cell fractions <10%), especially for the risk of decompensated cirrhosis (HR 2.03 [95% CI 1.09-3.78] vs. 1.14 [0.80-1.64]). In comparison to non-carriers of mCAs with low genetic risk, individuals with expanded copy-neutral loss of heterozygosity and high genetic risk showed the highest cirrhosis risk (HR 5.39 [95% CI 2.41-12.07]).</p><p><strong>Conclusions: </strong>The presence of mCAs is associated with increased susceptibility to cirrhosis risk and could be combined with PRS for personalized cirrhosis risk stratification.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"12 6","pages":"562-570"},"PeriodicalIF":3.1,"publicationDate":"2024-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11224905/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141556467","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":"Transjugular Intrahepatic Portosystemic Shunt Linked to Increased Risk of Hepatocellular Carcinoma: A VA Matched Cohort Study.","authors":"Shalini Bansal, Tamar Taddei, Rebecca Wells, Marina Serper, Theresa Bittermann, Nadim Mahmud, David E Kaplan","doi":"10.14218/JCTH.2023.00554","DOIUrl":"10.14218/JCTH.2023.00554","url":null,"abstract":"<p><p></p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"12 5","pages":"534-538"},"PeriodicalIF":3.1,"publicationDate":"2024-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11106346/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141081607","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":"Dopamine Inhibits the Expression of Hepatitis B Virus Surface and e Antigens by Activating the JAK/STAT Pathway and Upregulating Interferon-stimulated Gene 15 Expression.","authors":"Xiaoquan Liu, Xiuqing Pang, Zhiping Wan, Jinhua Zhao, Zhiliang Gao, Hong Deng","doi":"10.14218/JCTH.2024.00051","DOIUrl":"10.14218/JCTH.2024.00051","url":null,"abstract":"<p><strong>Background and aims: </strong>Hepatitis B virus (HBV) infection is a major risk factor for cirrhosis and liver cancer, and its treatment continues to be difficult. We previously demonstrated that a dopamine analog inhibited the packaging of pregenomic RNA into capsids. The present study aimed to determine the effect of dopamine on the expressions of hepatitis B virus surface and e antigens (HBsAg and HBeAg, respectively) and to elucidate the underlying mechanism.</p><p><strong>Methods: </strong>We used dopamine-treated HBV-infected HepG2.2.15 and NTCP-G2 cells to monitor HBsAg and HBeAg expression levels. We analyzed interferon-stimulated gene 15 (ISG15) expression in dopamine-treated cells. We knocked down ISG15 and then monitored HBsAg and HBeAg expression levels. We analyzed the expression of Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway factors in dopamine-treated cells. We used dopamine hydrochloride-treated adeno-associated virus/HBV-infected mouse model to evaluate HBV DNA, HBsAg, and HBeAg expression. HBV virus was collected from HepAD38.7 cell culture medium.</p><p><strong>Results: </strong>Dopamine inhibited HBsAg and HBeAg expression and upregulated ISG15 expression in HepG2.2.15 and HepG2-NTCP cell lines. ISG15 knockdown increased HBsAg and HBeAg expression in HepG2.2.15 cells. Dopamine-treated cells activated the JAK/STAT pathway, which upregulated ISG15 expression. In the adeno-associated virus-HBV murine infection model, dopamine downregulated HBsAg and HBeAg expression and activated the JAK-STAT/ISG15 axis.</p><p><strong>Conclusions: </strong>Dopamine inhibits the expression of HBsAg and HBeAg by activating the JAK/STAT pathway and upregulating ISG15 expression.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"12 5","pages":"443-456"},"PeriodicalIF":3.6,"publicationDate":"2024-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11106351/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141081605","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":"Ultrasonography of Hepatocellular Carcinoma: From Diagnosis to Prognosis.","authors":"Huisen Hu, Yonglei Zhao, Chengbin He, Lujie Qian, Pintong Huang","doi":"10.14218/JCTH.2024.00018","DOIUrl":"10.14218/JCTH.2024.00018","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is a prominent contributor to cancer-related mortality worldwide. Early detection and diagnosis of liver cancer can significantly improve its prognosis and patient survival. Ultrasound technology, serving has undergone substantial advances as the primary method of HCC surveillance and has broadened its scope in recent years for effective management of HCC. This article is a comprehensive overview of ultrasound technology in the treatment of HCC, encompassing early detection, diagnosis, staging, treatment evaluation, and prognostic assessment. In addition, the authors summarized the application of contrast-enhanced ultrasound in the diagnosis of HCC and assessment of prognosis. Finally, the authors discussed further directions in this field by emphasizing overcoming existing obstacles and integrating cutting-edge technologies.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"12 5","pages":"516-524"},"PeriodicalIF":3.6,"publicationDate":"2024-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11106354/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141081608","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":"A Revised Classification of Primary Iron Overload Syndromes.","authors":"Yasuaki Tatsumi, Motoyoshi Yano, Shinya Wakusawa, Hiroaki Miyajima, Tetsuya Ishikawa, Shinsaku Imashuku, Atsuko Takano, Wataru Nihei, Ayako Kato, Koichi Kato, Hisao Hayashi, Kentaro Yoshioka, Kazuhiko Hayashi","doi":"10.14218/JCTH.2023.00290","DOIUrl":"https://doi.org/10.14218/JCTH.2023.00290","url":null,"abstract":"<p><strong>Background and aims: </strong>The clinical introduction of hepcidin25 (Hep25) has led to a more detailed understanding of its relationship with ferroportin (FP) and divalent metal transporter1 in primary iron overload syndromes (PIOSs). In 2012, we proposed a classification of PIOSs based on the Hep25/FP system, which consists of prehepatic aceruloplasminemia, hepatic hemochromatosis (HC), and posthepatic FP disease (FP-D). However, in consideration of accumulated evidence on PIOSs, we aimed to renew the classification.</p><p><strong>Methods: </strong>We reviewed the 2012 classification and retrospectively renewed it according to new information on PIOSs.</p><p><strong>Results: </strong>Iron-loading anemia was included in PIOSs as a prehepatic form because of the newly discovered erythroferrone-induced suppression of Hep25, and the state of traditional FP-D was remodeled as the BIOIRON proposal. The key molecules responsible for prehepatic PIOSs are low transferrin saturation in aceruloplasminemia and increased erythroferrone production by erythroblasts in iron-loading anemia. Hepatic PIOSs comprise four genotypes of HC, in each of which the synthesis of Hep25 is inappropriately reduced in the liver. Hepatic Hep25 synthesis is adequate in posthepatic PIOSs; however, two mutant FP molecules may resist Hep25 differently, resulting in SLC40A1-HC and FP-D, respectively. PIOS phenotypes are diagnosed using laboratory tests, including circulating Hep25, followed by suitable treatments. Direct sequencing of the candidate genes may be outsourced to gene centers when needed. Laboratory kits for the prevalent mutations, such as C282Y, may be the first choice for a genetic analysis of HC in Caucasians.</p><p><strong>Conclusions: </strong>The revised classification may be useful worldwide.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"12 4","pages":"346-356"},"PeriodicalIF":3.6,"publicationDate":"2024-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11022062/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140855060","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}