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Review Article Open Access
Christopher J. Costa, Minh Thu T. Nguyen, Haleh Vaziri, George Y. Wu
Published online February 8, 2024
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Journal of Clinical and Translational Hepatology. doi:10.14218/JCTH.2023.00563
Abstract
Gallstone (GS) disease is common and arises from a combination of genetic and environmental factors. Although genetic abnormalities specifically leading to cholesterol GSs are rare, [...] Read more.

Gallstone (GS) disease is common and arises from a combination of genetic and environmental factors. Although genetic abnormalities specifically leading to cholesterol GSs are rare, there are clinically significant gene variants associated with cholesterol GSs. In contrast, most bilirubin GSs can be attributed to genetic defects. The pathogenesis of cholesterol and bilirubin GSs differs greatly. Cholesterol GSs are notably influenced by genetic variants within the ABC protein superfamily, including ABCG8, ABCG5, ABCB4, and ABCB11, as well as genes from the apolipoprotein family such as ApoB100 and ApoE (especially the E3/E3 and E3/E4 variants), and members of the MUC family. Conversely, bilirubin GSs are associated with genetic variants in highly expressed hepatic genes, notably UGT1A1, ABCC2 (MRP2), ABCC3 (MRP3), CFTR, and MUC, alongside genetic defects linked to hemolytic anemias and conditions impacting erythropoiesis. While genetic cases constitute a small portion of GS disease, recognizing genetic predisposition is essential for proper diagnosis, treatment, and genetic counseling.

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Guideline Open Access
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, Chinese Society of Hepatology, Chinese Medical Association
Published online November 4, 2024
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Journal of Clinical and Translational Hepatology. doi:10.14218/JCTH.2024.00311
Abstract
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 [...] Read more.

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.

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Original Article Open Access
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
Published online June 17, 2024
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Journal of Clinical and Translational Hepatology. doi:10.14218/JCTH.2024.00089
Abstract
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 [...] Read more.

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.

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.

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.

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%).

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Review Article Open Access
Zi-Xuan Qiu, Lin-Xiang Huang, Xiao-Xiao Wang, Zi-Long Wang, Xiao-He Li, Bo Feng
Published online May 28, 2024
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Journal of Clinical and Translational Hepatology. doi:10.14218/JCTH.2023.00531
Abstract
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, [...] Read more.

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.

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Original Article Open Access
Hua-Xiang Yang, Yang-Jie Li, Yang-Lan He, Ke-Ke Jin, Ling-Na Lyu, Hui-Guo Ding
Published online June 17, 2024
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Journal of Clinical and Translational Hepatology. doi:10.14218/JCTH.2024.00101
Abstract
The role of platelet autophagy in cirrhotic thrombocytopenia (CTP) remains unclear. This study aimed to investigate the impact of platelet autophagy in CTP and elucidate the regulatory [...] Read more.

The role of platelet autophagy in cirrhotic thrombocytopenia (CTP) remains unclear. This study aimed to investigate the impact of platelet autophagy in CTP and elucidate the regulatory mechanism of hydrogen sulfide (H2S) on platelet autophagy.

Platelets from 56 cirrhotic patients and 56 healthy individuals were isolated for in vitro analyses. Autophagy markers (ATG7, BECN1, LC3, and SQSTM1) were quantified using enzyme-linked immunosorbent assay, while autophagosomes were visualized through electron microscopy. Western blotting was used to assess the autophagy-related proteins and the PDGFR/PI3K/Akt/mTOR pathway following treatment with NaHS (an H2S donor), hydroxocobalamin (an H2S scavenger), or AG 1295 (a selective PDGFR-α inhibitor). A carbon tetrachloride-induced cirrhotic BALB/c mouse model was established. Cirrhotic mice with thrombocytopenia were randomly treated with normal saline, NaHS, or hydroxocobalamin for 15 days. Changes in platelet count and aggregation rate were observed every three days.

Cirrhotic patients with thrombocytopenia exhibited significantly decreased platelet autophagy markers and endogenous H2S levels, alongside increased platelet aggregation, compared to healthy controls. In vitro, NaHS treatment of platelets from severe CTP patients elevated LC3-II levels, reduced SQSTM1 levels, and decreased platelet aggregation in a dose-dependent manner. H2S treatment inhibited PDGFR, PI3K, Akt, and mTOR phosphorylation. In vivo, NaHS significantly increased LC3-II and decreased SQSTM1 expressions in platelets of cirrhotic mice, reducing platelet aggregation without affecting the platelet count.

Diminished platelet autophagy potentially contributes to thrombocytopenia in cirrhotic patients. H2S modulates platelet autophagy and functions possibly via the PDGFR-α/PI3K/Akt/mTOR signaling pathway.

Full article
Original Article Open Access
Anatoli D. Tahanovich, Mikalai M. Kauhanka, Elizabeth M. Barabanova, Oxana V. Gotko, Violetta I. Prokhorova
Published online June 18, 2024
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Cancer Screening and Prevention. doi:10.14218/CSP.2024.00004
Abstract
Despite efforts, tumor recurrence is diagnosed in 35–40% of patients with stage III squamous cell lung carcinoma (SCLC) during the first year after treatment. The purpose of the [...] Read more.

Despite efforts, tumor recurrence is diagnosed in 35–40% of patients with stage III squamous cell lung carcinoma (SCLC) during the first year after treatment. The purpose of the present investigation was to determine the levels of cytokeratin-fragment 19 (CYFRA 21-1) in blood serum, the percentages of lymphocytes containing chemokine receptor 1 (CXCR1, %, lymphocytes), and the percentages of monocytes containing chemokine receptor 2 (CXCR2, %, monocytes), as well as their combined model before and after treatment for the early detection of recurrence.

Forty-eight patients (29 men and 19 women) with newly diagnosed stage III SCLC were examined. Serum levels of CYFRA 21-1, CXCR1, %, lymphocytes, and CXCR2, %, monocytes in peripheral blood were measured before treatment and at three weeks, three months, and six months after treatment using a chemiluminescence immunoassay analyzer and a flow cytometer, respectively.

The levels of all determined indicators, which were elevated before treatment, decreased sharply three weeks after treatment. Subsequently, three months and six months after treatment, the levels steadily increased in patients with diagnosed tumor recurrence. The differences in these indicators in three weeks to three months, three months to six months, and three weeks to six months after treatment, when included in a regression equation, corresponded to the presence of recurrence with accuracies of 83.3%, 91.7%, and 95.8%, respectively.

Determining the combination of CYFRA 21-1 levels, CXCR1, %, lymphocytes, and CXCR2, %, monocytes in the blood of patients with stage III SCLC is important for assessing the probability of recurrence after treatment.

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Review Article Open Access
Hongbin Wei, Chunlu Dong, Xun Li
Published online February 28, 2024
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Journal of Clinical and Translational Hepatology. doi:10.14218/JCTH.2023.00462
Abstract
Hepatocellular carcinoma (HCC) is a common cancer, and the body’s immune responses greatly affect its progression and the prognosis of patients. Immunological suppression and the [...] Read more.

Hepatocellular carcinoma (HCC) is a common cancer, and the body’s immune responses greatly affect its progression and the prognosis of patients. Immunological suppression and the maintenance of self-tolerance in the tumor microenvironment are essential responses, and these form part of the theoretical foundations of immunotherapy. In this review, we first discuss the tumor microenvironment of HCC, describe immunosuppression in HCC, and review the major biomarkers used to track HCC progression and response to treatment. We then examine antibody-based therapies, with a focus on immune checkpoint inhibitors (ICIs), monoclonal antibodies that target key proteins in the immune response (programmed cell death protein 1, anti-cytotoxic T-lymphocyte associated protein 4, and programmed death-ligand 1) which have transformed the treatment of HCC and other cancers. ICIs may be used alone or in conjunction with various targeted therapies for patients with advanced HCC who are receiving first-line treatments or subsequent treatments. We also discuss the use of different cellular immunotherapies, including T cell receptor (TCR) T cell therapy and chimeric antigen receptor (CAR) T cell therapy. We then review the use of HCC vaccines, adjuvant immunotherapy, and oncolytic virotherapy, and describe the goals of future research in the development of treatments for HCC.

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Review Article Open Access
Zhaoyu Xu, Xiuding Zhang, Jiyang Chen, Yu Shi, Shangwei Ji
Published online June 20, 2024
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Journal of Clinical and Translational Hepatology. doi:10.14218/JCTH.2024.00137
Abstract
Acute-on-chronic liver failure (ACLF) is a distinct condition characterized by the abrupt exacerbation of pre-existing chronic liver disease, often leading to multi-organ failures [...] Read more.

Acute-on-chronic liver failure (ACLF) is a distinct condition characterized by the abrupt exacerbation of pre-existing chronic liver disease, often leading to multi-organ failures and significant short-term mortalities. Bacterial infection is one of the most frequent triggers for ACLF and a common complication following its onset. The impact of bacterial infections on the clinical course and outcome of ACLF underscores their critical role in the pathogenesis of systemic inflammation and organ failures. In addition, the evolving epidemiology and increasing prevalence of multidrug-resistant bacteria in cirrhosis and ACLF highlight the importance of appropriate empirical antibiotic use, as well as accurate and prompt microbiological diagnosis. This review provided an update on recent advances in the epidemiology, diagnosis, pathogenesis, and management of bacterial infections in ACLF.

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Original Article Open Access
Kingsley R. Oranuka, Calvin Chama, Ibrahim O. Adogu, Chigozie G. Okafor, George U. Eleje, Emmanuel O. Ugwu, Olumide P. Adeleke, Palmer H. Obakpororo, Kenneth O. Nnabuchi, Abdulazeez Yusuf, Nnaemeka P. Ugwu, Josephat C. Akabuike, Ahizechukwu C. Eke
Published online June 20, 2024
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Exploratory Research and Hypothesis in Medicine. doi:10.14218/ERHM.2023.00015
Abstract
Malaria can be fatal during pregnancy, posing a serious risk to both mothers and fetuses, especially in sub-Saharan Africa. Primigravidae are particularly susceptible to placental [...] Read more.

Malaria can be fatal during pregnancy, posing a serious risk to both mothers and fetuses, especially in sub-Saharan Africa. Primigravidae are particularly susceptible to placental malaria in areas with high rates of transmission due to insufficient immunity. This study aimed to determine the prevalence of placental malaria infection, risk factors, types of Plasmodium causing malaria during pregnancy, and its relationship with neonatal birth weight among primigravidae.

This was an analytical cross-sectional study involving 357 primigravidae who delivered at Abubakar Tafawa Balewa University Teaching Hospital, Bauchi, Nigeria. Placental blocks were taken from the pericentric area of the maternal surface of the placenta, and the birth weights of the neonates were recorded. The samples were fixed in 10% neutral-buffered formalin, and histopathological analysis was performed. The primary outcome measure was to determine the relationship between placental malaria and neonatal birth weight. Demographics and outcomes were analyzed using standard statistical tests. Multivariable regression models accounting for potential confounders were created for the primary and secondary outcomes with adjusted odds ratios as the measures of effect.

The prevalence of placental malaria was 38.4%. Among the participants with positive placenta malaria parasitemia, 49.6%, 36.5%, and 13.9% had chronic, acute, and past placental malaria infections, respectively. Only Plasmodium falciparum was found in the placenta. According to the bivariate analysis, unbooked status (p = 0.001), non-use of intermittent preventive therapy for malaria (p < 0.001), and village dwelling (p = 0.020) were significantly associated with placental malaria. However, on multivariable logistic regression, only non-uptake of intermittent preventive therapy for malaria was independently associated with placental malaria (adjusted odds ratio, 2.2, 95% confidence interval: 1.20, 4.1, p = 0.011). There was a significant difference in the mean birth weight between those with placental malaria and those without placental malaria (2.8 ± 0.5 kg vs. 3.2 ± 0.4 kg, p = 0.001). Additionally, placental malaria was significantly associated with low birth weight among the primigravidae (p < 0.001).

In Nigeria, there is a strong correlation between low birth weight and placental malaria in Primidravidae. Placental malaria was found to be independently correlated with non-uptake of intermittent preventive therapy for malaria.

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Original Article Open Access
Xiaoli Huang, Xiaofan Wang, Yanhong Wang, Shuangjun Shen, Wei Chen, Tianhui Liu, Ping Wang, Xu Fan, Lin Liu, Jidong Jia, Min Cong
Published online June 11, 2024
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Journal of Clinical and Translational Hepatology. doi:10.14218/JCTH.2023.00514
Abstract
Tissue inhibitor of metalloproteinase-1 (TIMP-1) plays a role in the excessive generation of extracellular matrix in liver fibrosis. This study aimed to explore the pathways through [...] Read more.

Tissue inhibitor of metalloproteinase-1 (TIMP-1) plays a role in the excessive generation of extracellular matrix in liver fibrosis. This study aimed to explore the pathways through which TIMP-1 controls monocyte chemoattractant protein-1 (MCP-1) expression and promotes hepatic macrophage recruitment.

Liver fibrosis was triggered through carbon tetrachloride, and an adeno-associated virus containing small interfering RNA targeting TIMP-1 (siRNA-TIMP-1) was administered to both rats and mice. We assessed the extent of fibrosis and macrophage recruitment. The molecular mechanisms regulating macrophage recruitment by TIMP-1 were investigated through transwell migration assays, luciferase reporter assays, the use of pharmacological modulators, and an analysis of extracellular vesicles (EVs).

siRNA-TIMP-1 alleviated carbon tetrachloride-induced liver fibrosis, reducing macrophage migration and MCP-1 expression. Co-culturing macrophages with hepatic stellate cells (HSCs) post-TIMP-1 downregulation inhibited macrophage migration. In siRNA-TIMP-1-treated HSCs, microRNA-145 (miRNA-145) expression increased, while the expression of Friend leukemia virus integration-1 (Fli-1) and MCP-1 was inhibited. Downregulation of Fli-1 led to decreased MCP-1 expression, whereas Fli-1 overexpression increased MCP-1 expression within HSCs. Transfection with miRNA-145 mimics reduced the expression of both Fli-1 and MCP-1, while miRNA-145 inhibitors elevated the expression of both Fli-1 and MCP-1 in HSCs. miRNA-145 bound directly to the 3′-UTR of Fli-1, and miRNA-145-enriched EVs secreted by HSCs after TIMP-1 downregulation influenced macrophage recruitment.

TIMP-1 induces Fli-1 expression through miRNA-145, subsequently increasing MCP-1 expression and macrophage recruitment. MiRNA-145-enriched EVs from HSCs can transmit biological information and magnify the function of TIMP-1.

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