Pub Date : 2024-08-27DOI: 10.1007/s12072-024-10724-z
Dali Xiong, Jiaran Li, Shuanghu Yuan
{"title":"Is laparoscopic hepatectomy superior to radiofrequency ablation in treating small hepatocellular carcinoma?","authors":"Dali Xiong, Jiaran Li, Shuanghu Yuan","doi":"10.1007/s12072-024-10724-z","DOIUrl":"https://doi.org/10.1007/s12072-024-10724-z","url":null,"abstract":"","PeriodicalId":12901,"journal":{"name":"Hepatology International","volume":null,"pages":null},"PeriodicalIF":5.9,"publicationDate":"2024-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142072628","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background and aims: Metabolic dysfunction-associated steatohepatitis (MASH)-related fibrosis is reversible. However, the dynamic morphology change in fibrosis regression remains unclear. We aim to explore the morphological characteristics of fibrosis regression in advanced MASH patients.
Methods: Clinical and histological data of 79 biopsy-proved MASH patients with advanced fibrosis (F3-F4) were reviewed. The second harmonic generation/two-photon excitation fluorescence (SHG/TPEF) image technology was used to quantitatively identify the R (regressive) septa from P (progressive) septa and PS (perisinusoidal) fibrosis. Non-invasive tests were used to compare the fibrosis level with and without R septa groups. Transcriptomics was used to explore hub genes and the underlying mechanism of the formation of R septa.
Results: The R septa were different from the P septa and PS fibrosis in detail collagen quantitation identified by SHG/TPEF technology. The R septa were found in MASH fibrosis-regressed patients, which met the definition of the "Beijing classification". Therefore, patients were divided into two groups according to septa morphology: with R septa (n = 10, 12.7%), and without R septa (n = 69, 87.3%). Patients with R septa had lower values in most non-invasive tests, especially for liver stiffness assessed by TE (12.3 vs. 19.4 kPa, p = 0.010) and FAST (FibroScan®-AST) score (0.43 vs. 0.70, p = 0.003). Transcriptomics analysis showed that the expressions of five hub fibrogenic genes, including Col3A1, BGN, Col4A1, THBS2, and Col4A2 in the R septa group, were significantly lower.
Conclusions: The R septa can be differentiated from the P septa and PS fibrosis by quantitative assessment of SHG/TPEF, and it represents a tendency of fibrosis regression in MASH patients.
Trial registration: NCT03386890, 29/12/2017.
背景和目的:代谢功能障碍相关性脂肪性肝炎(MASH)相关的纤维化是可逆的。然而,纤维化消退过程中的动态形态变化仍不清楚。我们旨在探索晚期 MASH 患者纤维化消退的形态学特征:方法:回顾性分析 79 例经活检证实的晚期纤维化(F3-F4)MASH 患者的临床和组织学数据。采用二次谐波发生/双光子激发荧光(SHG/TPEF)图像技术,从P(进行性)隔和PS(窦周)纤维化中定量识别R(退行性)隔。采用非侵入性测试比较有R隔和无R隔组的纤维化水平。转录组学用于探索R隔形成的枢纽基因和内在机制:结果:通过SHG/TPEF技术确定的胶原蛋白定量细节显示,R隔与P隔和PS纤维化不同。在 MASH 纤维化衰退的患者中发现了 R 型隔,符合 "北京分型 "的定义。因此,根据隔膜形态将患者分为两组:有 R 型隔膜(10 人,占 12.7%)和无 R 型隔膜(69 人,占 87.3%)。有R型间隔的患者在大多数无创检测中的数值较低,尤其是通过TE评估的肝脏硬度(12.3对19.4 kPa,p = 0.010)和FAST(FibroScan®-AST)评分(0.43对0.70,p = 0.003)。转录组学分析表明,R隔组中Col3A1、BGN、Col4A1、THBS2和Col4A2等5个枢纽纤维化基因的表达量明显降低:R隔可通过SHG/TPEF的定量评估与P隔和PS纤维化区分开来,它代表了MASH患者纤维化消退的趋势:NCT03386890, 29/12/2017.
{"title":"Delicate and thin fibrous septa indicate a regression tendency in metabolic dysfunction-associated steatohepatitis patients with advanced fibrosis.","authors":"Xiaofei Tong, Yameng Sun, Qianyi Wang, Xinyan Zhao, Wei Chen, Mengyang Zhang, Yayun Ren, Xinyu Zhao, Xiaoning Wu, Jingjie Zhao, Chenglin Sun, Minghua Zheng, Hao Ren, Zhenghan Yang, Xiaojuan Ou, Jidong Jia, Hong You","doi":"10.1007/s12072-024-10719-w","DOIUrl":"https://doi.org/10.1007/s12072-024-10719-w","url":null,"abstract":"<p><strong>Background and aims: </strong>Metabolic dysfunction-associated steatohepatitis (MASH)-related fibrosis is reversible. However, the dynamic morphology change in fibrosis regression remains unclear. We aim to explore the morphological characteristics of fibrosis regression in advanced MASH patients.</p><p><strong>Methods: </strong>Clinical and histological data of 79 biopsy-proved MASH patients with advanced fibrosis (F3-F4) were reviewed. The second harmonic generation/two-photon excitation fluorescence (SHG/TPEF) image technology was used to quantitatively identify the R (regressive) septa from P (progressive) septa and PS (perisinusoidal) fibrosis. Non-invasive tests were used to compare the fibrosis level with and without R septa groups. Transcriptomics was used to explore hub genes and the underlying mechanism of the formation of R septa.</p><p><strong>Results: </strong>The R septa were different from the P septa and PS fibrosis in detail collagen quantitation identified by SHG/TPEF technology. The R septa were found in MASH fibrosis-regressed patients, which met the definition of the \"Beijing classification\". Therefore, patients were divided into two groups according to septa morphology: with R septa (n = 10, 12.7%), and without R septa (n = 69, 87.3%). Patients with R septa had lower values in most non-invasive tests, especially for liver stiffness assessed by TE (12.3 vs. 19.4 kPa, p = 0.010) and FAST (FibroScan®-AST) score (0.43 vs. 0.70, p = 0.003). Transcriptomics analysis showed that the expressions of five hub fibrogenic genes, including Col3A1, BGN, Col4A1, THBS2, and Col4A2 in the R septa group, were significantly lower.</p><p><strong>Conclusions: </strong>The R septa can be differentiated from the P septa and PS fibrosis by quantitative assessment of SHG/TPEF, and it represents a tendency of fibrosis regression in MASH patients.</p><p><strong>Trial registration: </strong>NCT03386890, 29/12/2017.</p>","PeriodicalId":12901,"journal":{"name":"Hepatology International","volume":null,"pages":null},"PeriodicalIF":5.9,"publicationDate":"2024-08-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141995651","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-13DOI: 10.1007/s12072-024-10717-y
Ruobin Zong, Yan Zheng, Yufei Yan, Wenao Sun, Liangyi Kong, Yating Huang, Yujie Liu, Chaochen Jiang, Jie Ping, Changyong Li
Background & aims: Despite increasing knowledge regarding the cellular and molecular mechanisms of liver fibrogenesis, there is currently no approved drug for the treatment of liver fibrosis. Mesenchymal stem cells (MSCs) are multipotent progenitor cells representing an attractive therapeutic tool for tissue damage and inflammation. This study was designed to determine the protective effect and underlying mechanism of human umbilical cord-derived MSCs (UC-MSCs) on thioacetamide-induced liver fibrosis.
Methods: Liver fibrosis was induced in mice by intraperitoneal injection of thioacetamide (TAA). Some mice were then given injection of UC-MSCs or UC-MSCs-derived exosomes (UC-MSCs-Exo) via the tail vein. Liver tissues were collected for histologic analysis.
Results: We found that administration of UC-MSCs significantly reduced serum alanine aminotransferase and aspartate aminotransferase levels, and attenuated hepatic inflammation and fibrosis. Moreover, the therapeutic effect of UC-MSCs-derived exosomes was similar to that of UC-MSCs. Intriguingly, UC-MSCs-Exo treatment downregulated the expression of smoothened (SMO), a fundamental component of Hedgehog signaling which plays a critical role in fibrogenesis, and subsequently inhibited the activation of hepatic stellate cells, a central driver of fibrosis in experimental and human liver injury. Furthermore, the anti-inflammatory and anti-fibrotic effects of UCMSCs- Exo was reversed by the SMO agonist SAG treatment in mice.
Conclusion: Our findings suggest that UC-MSCs-Exo exert therapeutic effects on liver fibrosis, at least in part, through inhibiting the Hedgehog/SMO signaling pathway.
{"title":"Mesenchymal stem cells-derived exosomes alleviate liver fibrosis by targeting Hedgehog/SMO signaling.","authors":"Ruobin Zong, Yan Zheng, Yufei Yan, Wenao Sun, Liangyi Kong, Yating Huang, Yujie Liu, Chaochen Jiang, Jie Ping, Changyong Li","doi":"10.1007/s12072-024-10717-y","DOIUrl":"https://doi.org/10.1007/s12072-024-10717-y","url":null,"abstract":"<p><strong>Background & aims: </strong>Despite increasing knowledge regarding the cellular and molecular mechanisms of liver fibrogenesis, there is currently no approved drug for the treatment of liver fibrosis. Mesenchymal stem cells (MSCs) are multipotent progenitor cells representing an attractive therapeutic tool for tissue damage and inflammation. This study was designed to determine the protective effect and underlying mechanism of human umbilical cord-derived MSCs (UC-MSCs) on thioacetamide-induced liver fibrosis.</p><p><strong>Methods: </strong>Liver fibrosis was induced in mice by intraperitoneal injection of thioacetamide (TAA). Some mice were then given injection of UC-MSCs or UC-MSCs-derived exosomes (UC-MSCs-Exo) via the tail vein. Liver tissues were collected for histologic analysis.</p><p><strong>Results: </strong>We found that administration of UC-MSCs significantly reduced serum alanine aminotransferase and aspartate aminotransferase levels, and attenuated hepatic inflammation and fibrosis. Moreover, the therapeutic effect of UC-MSCs-derived exosomes was similar to that of UC-MSCs. Intriguingly, UC-MSCs-Exo treatment downregulated the expression of smoothened (SMO), a fundamental component of Hedgehog signaling which plays a critical role in fibrogenesis, and subsequently inhibited the activation of hepatic stellate cells, a central driver of fibrosis in experimental and human liver injury. Furthermore, the anti-inflammatory and anti-fibrotic effects of UCMSCs- Exo was reversed by the SMO agonist SAG treatment in mice.</p><p><strong>Conclusion: </strong>Our findings suggest that UC-MSCs-Exo exert therapeutic effects on liver fibrosis, at least in part, through inhibiting the Hedgehog/SMO signaling pathway.</p>","PeriodicalId":12901,"journal":{"name":"Hepatology International","volume":null,"pages":null},"PeriodicalIF":5.9,"publicationDate":"2024-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141975575","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: CXCR6+CD8+T cells have been implicated in the pathogenesis of various liver and autoimmune diseases. However, their involvement in primary biliary cholangitis (PBC) has not been elucidated.
Methods: We used immunohistochemistry and flow cytometry to quantify CXCR6+CD8+T cells in hepatic tissue and peripheral blood samples obtained from CXCR6+CD8+T cells obtained from PBC patients. Then, we performed comprehensive statistical analyses to access the correlation between the abundance of these cells and clinical as well as pathological data across different stages of PBC.
Results: Our research revealed that CXCR6+ cell frequencies in CD3+CD8+T cells from PBC patients significantly exceeded that of healthy controls (HCs) (2.24 vs. 0.61%, p < 0.01). A similar pattern emerged for hepatic CXCR6+CD8+T cell counts, which were notably higher in the PBC cohort compared to HCs. Our cohort consisted of 118 PBC patients, categorized into 62 early-stage (E-PBC) and 56 late-stage (L-PBC) cases. Notably, significant disparities existed between these groups in terms of liver enzyme and lipid profile levels (p < 0.05), with no notable differences observed in gender, age, blood counts, cholesterol levels, or autoantibodies (p > 0.05). Intriguingly, the quantity of hepatic CXCR6+CD8+T cells per high power field (HPF) was significantly elevated in both E-PBC and L-PBC patients as opposed to normal liver samples, indicating a substantial increase in these cells across all stages of PBC (p = 0.000). Spearman's rank correlation analysis showed a positive correlation between CXCR6+CD8+T cell counts and serum levels of Alkaline Phosphatase (AKP) and Gamma-Glutamyl Transferase (GGT), ANA, IgG and IgM, while revealing a negligible correlation with Alanine Aminotransferase (ALT) and Aspartate Aminotransferase (AST). Subsequent findings indicated significant variances in CXCR6+ cell numbers not only among different PBC stages but also across various degrees of inflammation and fibrosis (p ≤ 0.007). In a follow-up study post-Ursodeoxycholic Acid (UDCA) treatment, stark differences were identified in biochemical and immunohistochemical profiles between responder (31 patients) and non-responder (33 patients) groups (p < 0.05). A Wilcoxon rank-sum test further demonstrated a significant difference in the level of hepatic CXCR6+CD8+T cells between these two response groups (p = 0.002).
Conclusion: CXCR6+CD8+T cells play a vital role in the pathogenesis of PBC, exhibiting correlations with the extent of inflammation, staging of liver fibrosis, and response to pharmacological interventions in PBC patients.
{"title":"The relationship between CXCR6+CD8+T cells and clinicopathological parameters in patients with primary biliary cholangitis.","authors":"Huilian Shi, Xiangtao Xu, Shuangshuang Wang, Qinlei Chen, Fan Zhang, Haiyan Guo, Weiting Lu, Fei Qiao","doi":"10.1007/s12072-024-10715-0","DOIUrl":"https://doi.org/10.1007/s12072-024-10715-0","url":null,"abstract":"<p><strong>Background: </strong>CXCR6+CD8+T cells have been implicated in the pathogenesis of various liver and autoimmune diseases. However, their involvement in primary biliary cholangitis (PBC) has not been elucidated.</p><p><strong>Methods: </strong>We used immunohistochemistry and flow cytometry to quantify CXCR6+CD8+T cells in hepatic tissue and peripheral blood samples obtained from CXCR6+CD8+T cells obtained from PBC patients. Then, we performed comprehensive statistical analyses to access the correlation between the abundance of these cells and clinical as well as pathological data across different stages of PBC.</p><p><strong>Results: </strong>Our research revealed that CXCR6+ cell frequencies in CD3+CD8+T cells from PBC patients significantly exceeded that of healthy controls (HCs) (2.24 vs. 0.61%, p < 0.01). A similar pattern emerged for hepatic CXCR6+CD8+T cell counts, which were notably higher in the PBC cohort compared to HCs. Our cohort consisted of 118 PBC patients, categorized into 62 early-stage (E-PBC) and 56 late-stage (L-PBC) cases. Notably, significant disparities existed between these groups in terms of liver enzyme and lipid profile levels (p < 0.05), with no notable differences observed in gender, age, blood counts, cholesterol levels, or autoantibodies (p > 0.05). Intriguingly, the quantity of hepatic CXCR6+CD8+T cells per high power field (HPF) was significantly elevated in both E-PBC and L-PBC patients as opposed to normal liver samples, indicating a substantial increase in these cells across all stages of PBC (p = 0.000). Spearman's rank correlation analysis showed a positive correlation between CXCR6+CD8+T cell counts and serum levels of Alkaline Phosphatase (AKP) and Gamma-Glutamyl Transferase (GGT), ANA, IgG and IgM, while revealing a negligible correlation with Alanine Aminotransferase (ALT) and Aspartate Aminotransferase (AST). Subsequent findings indicated significant variances in CXCR6+ cell numbers not only among different PBC stages but also across various degrees of inflammation and fibrosis (p ≤ 0.007). In a follow-up study post-Ursodeoxycholic Acid (UDCA) treatment, stark differences were identified in biochemical and immunohistochemical profiles between responder (31 patients) and non-responder (33 patients) groups (p < 0.05). A Wilcoxon rank-sum test further demonstrated a significant difference in the level of hepatic CXCR6+CD8+T cells between these two response groups (p = 0.002).</p><p><strong>Conclusion: </strong>CXCR6+CD8+T cells play a vital role in the pathogenesis of PBC, exhibiting correlations with the extent of inflammation, staging of liver fibrosis, and response to pharmacological interventions in PBC patients.</p>","PeriodicalId":12901,"journal":{"name":"Hepatology International","volume":null,"pages":null},"PeriodicalIF":5.9,"publicationDate":"2024-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141970996","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-11DOI: 10.1007/s12072-024-10714-1
Atsushi Tanaka, Kenichi Harada
Acute presentation of autoimmune hepatitis (AIH) occurs in 22-43% of all AIH cases, and is not a rare condition. Rather than constituting a single disease entity, it represents a clinical spectrum characterized by considerable variability in severity and the presence of preexisting chronic AIH. This spectrum ranges from acute AIH and acute severe AIH to AIH presenting as acute liver failure (ALF) or as acute-on-chronic liver failure (ACLF), contingent upon factors such as coagulopathy, hepatic encephalopathy, and underlying liver disease. Diagnosing acute presentation of AIH can be particularly challenging due to the frequent absence of classical serologic signatures such as autoantibodies and elevated IgG levels. Histopathological examination remains essential for diagnosis, typically necessitating percutaneous or transjugular liver biopsy. Corticosteroids (CS) are recommended for the management of acute AIH and acute severe AIH with coagulopathy. However, the therapeutic response to CS should be meticulously monitored. If a poor response is anticipated, liver transplantation (LT) should be promptly considered. For AIH presenting as ALF with encephalopathy or ACLF with advanced underlying liver disease, LT is generally advised. Nonetheless, there is potential for a trial of CS therapy in cases of ALF with low MELD scores or ACLF without encephalopathy. This review provides an overview of the latest findings concerning the definition, diagnosis, and management of acute presentation of AIH.
{"title":"Acute presentation of autoimmune hepatitis -from acute hepatitis to ALF and ACLF.","authors":"Atsushi Tanaka, Kenichi Harada","doi":"10.1007/s12072-024-10714-1","DOIUrl":"https://doi.org/10.1007/s12072-024-10714-1","url":null,"abstract":"<p><p>Acute presentation of autoimmune hepatitis (AIH) occurs in 22-43% of all AIH cases, and is not a rare condition. Rather than constituting a single disease entity, it represents a clinical spectrum characterized by considerable variability in severity and the presence of preexisting chronic AIH. This spectrum ranges from acute AIH and acute severe AIH to AIH presenting as acute liver failure (ALF) or as acute-on-chronic liver failure (ACLF), contingent upon factors such as coagulopathy, hepatic encephalopathy, and underlying liver disease. Diagnosing acute presentation of AIH can be particularly challenging due to the frequent absence of classical serologic signatures such as autoantibodies and elevated IgG levels. Histopathological examination remains essential for diagnosis, typically necessitating percutaneous or transjugular liver biopsy. Corticosteroids (CS) are recommended for the management of acute AIH and acute severe AIH with coagulopathy. However, the therapeutic response to CS should be meticulously monitored. If a poor response is anticipated, liver transplantation (LT) should be promptly considered. For AIH presenting as ALF with encephalopathy or ACLF with advanced underlying liver disease, LT is generally advised. Nonetheless, there is potential for a trial of CS therapy in cases of ALF with low MELD scores or ACLF without encephalopathy. This review provides an overview of the latest findings concerning the definition, diagnosis, and management of acute presentation of AIH.</p>","PeriodicalId":12901,"journal":{"name":"Hepatology International","volume":null,"pages":null},"PeriodicalIF":5.9,"publicationDate":"2024-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141912438","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: This study conducted molecular subtyping of biliary tract cancer patients based on 19 PANoptosis-related gene signatures.
Methods: Through consensus clustering, patients were categorized into two subtypes, A and B. By integrating multi-omics data and clinical information from different cohorts, we elucidated the association between different subtypes of biliary tract cancer and patient prognosis, which correlated with the immune infiltration characteristics of patients.
Results: LASSO regression analysis was performed on the 19 gene signatures, and we constructed and validated a 9-gene risk score prognostic model that accurately predicts the overall survival rate of different biliary tract cancer patients. Additionally, we developed a predictive nomogram demonstrating the clinical utility and robustness of our model. Further analysis of the risk score-based immune landscape highlighted potential associations with immune cell infiltration, chemotherapy, and immune therapy response.
Conclusion: Our study provides valuable insights into personalized treatment strategies for biliary tract cancer, which are crucial for improving patient prognosis and guiding treatment decisions in clinical practice.
{"title":"Identification of PANoptosis-relevant subgroups and predicting signature to evaluate the prognosis and immune landscape of patients with biliary tract cancer.","authors":"Dongming Liu, Wenshuai Chen, Zhiqiang Han, Yu Wang, Wei Liu, Aomei Ling, Qiang Wu, Huikai Li, Hua Guo","doi":"10.1007/s12072-024-10718-x","DOIUrl":"https://doi.org/10.1007/s12072-024-10718-x","url":null,"abstract":"<p><strong>Background: </strong>This study conducted molecular subtyping of biliary tract cancer patients based on 19 PANoptosis-related gene signatures.</p><p><strong>Methods: </strong>Through consensus clustering, patients were categorized into two subtypes, A and B. By integrating multi-omics data and clinical information from different cohorts, we elucidated the association between different subtypes of biliary tract cancer and patient prognosis, which correlated with the immune infiltration characteristics of patients.</p><p><strong>Results: </strong>LASSO regression analysis was performed on the 19 gene signatures, and we constructed and validated a 9-gene risk score prognostic model that accurately predicts the overall survival rate of different biliary tract cancer patients. Additionally, we developed a predictive nomogram demonstrating the clinical utility and robustness of our model. Further analysis of the risk score-based immune landscape highlighted potential associations with immune cell infiltration, chemotherapy, and immune therapy response.</p><p><strong>Conclusion: </strong>Our study provides valuable insights into personalized treatment strategies for biliary tract cancer, which are crucial for improving patient prognosis and guiding treatment decisions in clinical practice.</p>","PeriodicalId":12901,"journal":{"name":"Hepatology International","volume":null,"pages":null},"PeriodicalIF":5.9,"publicationDate":"2024-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141912439","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-08DOI: 10.1007/s12072-024-10716-z
Matheus Souza, Ivanna Diaz, Lubna Al-Sharif
Background and aims: Non-alcoholic fatty liver disease (NAFLD) is present in lean people. However, the magnitude of the prognostic hepatic and cardiovascular risk in these patients compared to non-lean counterparts remains unclear. We aimed to investigate this topic, and to explore whether these risks change based on factors related to NAFLD severity.
Methods: PubMed and Embase databases were searched for cohort studies (published through April 2024) that evaluated liver and cardiovascular (CV) outcomes in lean and non-lean individuals with NAFLD and reported unadjusted or adjusted data. We pooled risk ratios (RRs) or hazard ratios (HRs) using a random-effects modeling and performed subgroup and meta-regressions analyses.
Results: We identified 22 studies with over 1 million NAFLD patients (13.0% were lean). Lean NAFLD showed a similar risk of liver-related events in unadjusted analysis (RR 1.08, 95% CI 0.79-1.49, I2 = 31%), but a higher risk in adjusted analysis (HR 1.66, 95% CI 1.17-2.36, I2 = 83%) compared to non-lean NAFLD. Lean NAFLD had a higher risk of liver-related mortality (RR 2.22, 95% CI 1.57-3.15, I2 = 0%; HR 2.26, 95% CI 1.14-4.51, I2 = 0%). For CV outcomes, lean NAFLD had a lower risk of any cardiovascular disease in unadjusted analysis (RR = 0.82, 95% CI 0.70-0.95, I2 = 88%), but similar risk in adjusted analysis (HR 0.89, 95% CI 0.77-1.02, I2 = 78%), and similar risk of cardiovascular mortality (RR 1.09, 95% CI 0.71-1.66, I2 = 85%; HR 1.26, 95% CI 0.89-1.78, I2 = 46%) compared to non-lean NAFLD.
Conclusions: Lean NAFLD patients have worse liver outcomes, but similar CV outcomes compared to non-lean NAFLD patients, highlighting the importance of monitoring both groups closely.
背景和目的:非酒精性脂肪肝(NAFLD)存在于体型偏瘦的人群中。然而,与非瘦人相比,这些患者的肝脏和心血管预后风险的大小仍不清楚。我们旨在研究这一课题,并探讨这些风险是否会因非酒精性脂肪肝严重程度的相关因素而发生变化:我们在 PubMed 和 Embase 数据库中检索了对患有非酒精性脂肪肝的瘦弱和非瘦弱患者的肝脏和心血管 (CV) 结果进行评估的队列研究(发表至 2024 年 4 月),并报告了未调整或调整后的数据。我们采用随机效应模型对风险比(RRs)或危险比(HRs)进行了汇总,并进行了亚组和元回归分析:我们确定了 22 项研究,涉及超过 100 万名非酒精性脂肪肝患者(13.0% 为瘦型)。在未调整分析中,瘦型非酒精性脂肪肝发生肝脏相关事件的风险相似(RR 1.08,95% CI 0.79-1.49,I2 = 31%),但在调整分析中,与非瘦型非酒精性脂肪肝相比,瘦型非酒精性脂肪肝发生肝脏相关事件的风险更高(HR 1.66,95% CI 1.17-2.36,I2 = 83%)。瘦型非酒精性脂肪肝的肝脏相关死亡风险更高(RR 2.22,95% CI 1.57-3.15,I2 = 0%;HR 2.26,95% CI 1.14-4.51,I2 = 0%)。对于心血管疾病的结局,在未调整分析中,非酒精性脂肪肝瘦患者罹患任何心血管疾病的风险较低(RR = 0.82,95% CI 0.70-0.95,I2 = 88%),但在调整分析中风险相似(HR 0.89,95% CI 0.77-1.02,I2 = 78%),与非瘦型非酒精性脂肪肝相比,心血管死亡风险相似(RR 1.09,95% CI 0.71-1.66,I2 = 85%;HR 1.26,95% CI 0.89-1.78,I2 = 46%):瘦型非酒精性脂肪肝患者的肝脏预后较差,但与非瘦型非酒精性脂肪肝患者的心血管预后相似,这凸显了密切监测这两类患者的重要性。
{"title":"Liver and cardiovascular outcomes in lean non-alcoholic fatty liver disease: an updated systematic review and meta-analysis of about 1 million individuals.","authors":"Matheus Souza, Ivanna Diaz, Lubna Al-Sharif","doi":"10.1007/s12072-024-10716-z","DOIUrl":"https://doi.org/10.1007/s12072-024-10716-z","url":null,"abstract":"<p><strong>Background and aims: </strong>Non-alcoholic fatty liver disease (NAFLD) is present in lean people. However, the magnitude of the prognostic hepatic and cardiovascular risk in these patients compared to non-lean counterparts remains unclear. We aimed to investigate this topic, and to explore whether these risks change based on factors related to NAFLD severity.</p><p><strong>Methods: </strong>PubMed and Embase databases were searched for cohort studies (published through April 2024) that evaluated liver and cardiovascular (CV) outcomes in lean and non-lean individuals with NAFLD and reported unadjusted or adjusted data. We pooled risk ratios (RRs) or hazard ratios (HRs) using a random-effects modeling and performed subgroup and meta-regressions analyses.</p><p><strong>Results: </strong>We identified 22 studies with over 1 million NAFLD patients (13.0% were lean). Lean NAFLD showed a similar risk of liver-related events in unadjusted analysis (RR 1.08, 95% CI 0.79-1.49, I<sup>2</sup> = 31%), but a higher risk in adjusted analysis (HR 1.66, 95% CI 1.17-2.36, I<sup>2</sup> = 83%) compared to non-lean NAFLD. Lean NAFLD had a higher risk of liver-related mortality (RR 2.22, 95% CI 1.57-3.15, I<sup>2</sup> = 0%; HR 2.26, 95% CI 1.14-4.51, I<sup>2</sup> = 0%). For CV outcomes, lean NAFLD had a lower risk of any cardiovascular disease in unadjusted analysis (RR = 0.82, 95% CI 0.70-0.95, I<sup>2</sup> = 88%), but similar risk in adjusted analysis (HR 0.89, 95% CI 0.77-1.02, I<sup>2</sup> = 78%), and similar risk of cardiovascular mortality (RR 1.09, 95% CI 0.71-1.66, I<sup>2</sup> = 85%; HR 1.26, 95% CI 0.89-1.78, I<sup>2</sup> = 46%) compared to non-lean NAFLD.</p><p><strong>Conclusions: </strong>Lean NAFLD patients have worse liver outcomes, but similar CV outcomes compared to non-lean NAFLD patients, highlighting the importance of monitoring both groups closely.</p>","PeriodicalId":12901,"journal":{"name":"Hepatology International","volume":null,"pages":null},"PeriodicalIF":5.9,"publicationDate":"2024-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141906360","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-01Epub Date: 2024-06-15DOI: 10.1007/s12072-024-10702-5
Huai Zhang, Giovanni Targher, Christopher D Byrne, Seung Up Kim, Vincent Wai-Sun Wong, Luca Valenti, Myer Glickman, Jaime Ponce, Christos S Mantzoros, Javier Crespo, Henning Gronbaek, Wah Yang, Mohammed Eslam, Robert J Wong, Mariana Verdelho Machado, Ming-Lung Yu, Omar M Ghanem, Takeshi Okanoue, Jun-Feng Liu, Yong-Ho Lee, Xiao-Yuan Xu, Qiuwei Pan, Meili Sui, Amedeo Lonardo, Yusuf Yilmaz, Li-Yong Zhu, Christophe Moreno, Luca Miele, Monica Lupsor-Platon, Lei Zhao, Teresa LeAnn LaMasters, Robert G Gish, Huijie Zhang, Marius Nedelcu, Wah Kheong Chan, Ming-Feng Xia, Fernando Bril, Jun-Ping Shi, Christian Datz, Stefano Romeo, Jian Sun, Dan Liu, Silvia Sookoian, Yi-Min Mao, Nahum Méndez-Sánchez, Xiao-Yan Wang, Nikolaos T Pyrsopoulos, Jian-Gao Fan, Yasser Fouad, Dan-Qin Sun, Cosimo Giannini, Jin Chai, Ze-Feng Xia, Dae Won Jun, Guo-Jing Li, Sombat Treeprasertsuk, Ying-Xu Li, Tan To Cheung, Faming Zhang, George Boon-Bee Goh, Masato Furuhashi, Wai-Kay Seto, Hui Huang, Anna Di Sessa, Qing-Hong Li, Evangelos Cholongitas, Le Zhang, Themis Reverbel Silveira, Giada Sebastiani, Leon A Adams, Wei Chen, Xiaolong Qi, Ivan Rankovic, Victor De Ledinghen, Wen-Jie Lv, Masahide Hamaguchi, Radwan Kassir, Dirk Müller-Wieland, Manuel Romero-Gomez, Ying Xu, Yi-Cong Xu, Shi-Yao Chen, Mohammad Kermansaravi, Mohammad Shafi Kuchay, Sander Lefere, Chetan Parmar, Gregory Y H Lip, Chun-Jen Liu, Fredrik Åberg, George Lau, Jacob George, Shiv Kumar Sarin, Jing-Ya Zhou, Ming-Hua Zheng
Background: With the implementation of the 11th edition of the International Classification of Diseases (ICD-11) and the publication of the metabolic dysfunction-associated fatty liver disease (MAFLD) nomenclature in 2020, it is important to establish consensus for the coding of MAFLD in ICD-11. This will inform subsequent revisions of ICD-11.
Methods: Using the Qualtrics XM and WJX platforms, questionnaires were sent online to MAFLD-ICD-11 coding collaborators, authors of papers, and relevant association members.
Results: A total of 890 international experts in various fields from 61 countries responded to the survey. We also achieved full coverage of provincial-level administrative regions in China. 77.1% of respondents agreed that MAFLD should be represented in ICD-11 by updating NAFLD, with no significant regional differences (77.3% in Asia and 76.6% in non-Asia, p = 0.819). Over 80% of respondents agreed or somewhat agreed with the need to assign specific codes for progressive stages of MAFLD (i.e. steatohepatitis) (92.2%), MAFLD combined with comorbidities (84.1%), or MAFLD subtypes (i.e., lean, overweight/obese, and diabetic) (86.1%).
Conclusions: This global survey by a collaborative panel of clinical, coding, health management and policy experts, indicates agreement that MAFLD should be coded in ICD-11. The data serves as a foundation for corresponding adjustments in the ICD-11 revision.
{"title":"A global survey on the use of the international classification of diseases codes for metabolic dysfunction-associated fatty liver disease.","authors":"Huai Zhang, Giovanni Targher, Christopher D Byrne, Seung Up Kim, Vincent Wai-Sun Wong, Luca Valenti, Myer Glickman, Jaime Ponce, Christos S Mantzoros, Javier Crespo, Henning Gronbaek, Wah Yang, Mohammed Eslam, Robert J Wong, Mariana Verdelho Machado, Ming-Lung Yu, Omar M Ghanem, Takeshi Okanoue, Jun-Feng Liu, Yong-Ho Lee, Xiao-Yuan Xu, Qiuwei Pan, Meili Sui, Amedeo Lonardo, Yusuf Yilmaz, Li-Yong Zhu, Christophe Moreno, Luca Miele, Monica Lupsor-Platon, Lei Zhao, Teresa LeAnn LaMasters, Robert G Gish, Huijie Zhang, Marius Nedelcu, Wah Kheong Chan, Ming-Feng Xia, Fernando Bril, Jun-Ping Shi, Christian Datz, Stefano Romeo, Jian Sun, Dan Liu, Silvia Sookoian, Yi-Min Mao, Nahum Méndez-Sánchez, Xiao-Yan Wang, Nikolaos T Pyrsopoulos, Jian-Gao Fan, Yasser Fouad, Dan-Qin Sun, Cosimo Giannini, Jin Chai, Ze-Feng Xia, Dae Won Jun, Guo-Jing Li, Sombat Treeprasertsuk, Ying-Xu Li, Tan To Cheung, Faming Zhang, George Boon-Bee Goh, Masato Furuhashi, Wai-Kay Seto, Hui Huang, Anna Di Sessa, Qing-Hong Li, Evangelos Cholongitas, Le Zhang, Themis Reverbel Silveira, Giada Sebastiani, Leon A Adams, Wei Chen, Xiaolong Qi, Ivan Rankovic, Victor De Ledinghen, Wen-Jie Lv, Masahide Hamaguchi, Radwan Kassir, Dirk Müller-Wieland, Manuel Romero-Gomez, Ying Xu, Yi-Cong Xu, Shi-Yao Chen, Mohammad Kermansaravi, Mohammad Shafi Kuchay, Sander Lefere, Chetan Parmar, Gregory Y H Lip, Chun-Jen Liu, Fredrik Åberg, George Lau, Jacob George, Shiv Kumar Sarin, Jing-Ya Zhou, Ming-Hua Zheng","doi":"10.1007/s12072-024-10702-5","DOIUrl":"10.1007/s12072-024-10702-5","url":null,"abstract":"<p><strong>Background: </strong>With the implementation of the 11th edition of the International Classification of Diseases (ICD-11) and the publication of the metabolic dysfunction-associated fatty liver disease (MAFLD) nomenclature in 2020, it is important to establish consensus for the coding of MAFLD in ICD-11. This will inform subsequent revisions of ICD-11.</p><p><strong>Methods: </strong>Using the Qualtrics XM and WJX platforms, questionnaires were sent online to MAFLD-ICD-11 coding collaborators, authors of papers, and relevant association members.</p><p><strong>Results: </strong>A total of 890 international experts in various fields from 61 countries responded to the survey. We also achieved full coverage of provincial-level administrative regions in China. 77.1% of respondents agreed that MAFLD should be represented in ICD-11 by updating NAFLD, with no significant regional differences (77.3% in Asia and 76.6% in non-Asia, p = 0.819). Over 80% of respondents agreed or somewhat agreed with the need to assign specific codes for progressive stages of MAFLD (i.e. steatohepatitis) (92.2%), MAFLD combined with comorbidities (84.1%), or MAFLD subtypes (i.e., lean, overweight/obese, and diabetic) (86.1%).</p><p><strong>Conclusions: </strong>This global survey by a collaborative panel of clinical, coding, health management and policy experts, indicates agreement that MAFLD should be coded in ICD-11. The data serves as a foundation for corresponding adjustments in the ICD-11 revision.</p>","PeriodicalId":12901,"journal":{"name":"Hepatology International","volume":null,"pages":null},"PeriodicalIF":5.9,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141327437","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-01Epub Date: 2024-05-13DOI: 10.1007/s12072-024-10658-6
He Li, Lingzhan Meng, Simiao Yu, Haocheng Zheng, Lingxiang Yu, Hongbo Wang, Hui Ren, Hu Li, Xiaofeng Zhang, Zizheng Wang, Peng Yu, Xiongwei Hu, Muyi Yang, Jin Yan, Yanling Shao, Li Cao, Xia Ding, Zhixian Hong, Zhenyu Zhu
Background: Evidence concerning long-term outcome of robotic liver resection (RLR) and laparoscopic liver resection (LLR) for hepatocellular carcinoma (HCC) patients is scarce.
Methods: This study enrolled all patients who underwent RLR and LLR for resectable HCC between July 2016 and July 2021. Propensity score matching (PSM) was employed to create a 1:3 match between the RLR and LLR groups. A comprehensive collection and analysis of patient data regarding efficacy and safety have been conducted, along with the evaluation of the learning curve for RLR.
Results: Following PSM, a total of 341 patients were included, with 97 in the RLR group and 244 in the LLR group. RLR group demonstrated a significantly longer operative time (median [IQR], 210 [152.0-298.0] min vs. 183.5 [132.3-263.5] min; p = 0.04), with no significant differences in other perioperative and short-term postoperative outcomes. Overall survival (OS) was similar between the two groups (p = 0.43), but RLR group exhibited improved recurrence-free survival (RFS) (median of 65 months vs. 56 months, p = 0.006). The estimated 5-year OS for RLR and LLR were 74.8% (95% CI: 65.4-85.6%) and 80.7% (95% CI: 74.0-88.1%), respectively. The estimated 5-year RFS for RLR and LLR were 58.6% (95% CI: 48.6-70.6%) and 38.3% (95% CI: 26.4-55.9%), respectively. In the multivariate Cox regression analysis, RLR (HR: 0.586, 95% CI (0.393-0.874), p = 0.008) emerged as an independent predictor of reducing recurrence rates and enhanced RFS. The operative learning curve indicates that approximately after the 11th case, the learning curve of RLR stabilized and entered a proficient phase.
Conclusions: OS was comparable between RLR and LLR, and while RFS was improved in the RLR group. RLR demonstrates oncological effectiveness and safety for resectable HCC.
{"title":"Efficacy and safety of robotic versus laparoscopic liver resection for hepatocellular carcinoma: a propensity score-matched retrospective cohort study.","authors":"He Li, Lingzhan Meng, Simiao Yu, Haocheng Zheng, Lingxiang Yu, Hongbo Wang, Hui Ren, Hu Li, Xiaofeng Zhang, Zizheng Wang, Peng Yu, Xiongwei Hu, Muyi Yang, Jin Yan, Yanling Shao, Li Cao, Xia Ding, Zhixian Hong, Zhenyu Zhu","doi":"10.1007/s12072-024-10658-6","DOIUrl":"10.1007/s12072-024-10658-6","url":null,"abstract":"<p><strong>Background: </strong>Evidence concerning long-term outcome of robotic liver resection (RLR) and laparoscopic liver resection (LLR) for hepatocellular carcinoma (HCC) patients is scarce.</p><p><strong>Methods: </strong>This study enrolled all patients who underwent RLR and LLR for resectable HCC between July 2016 and July 2021. Propensity score matching (PSM) was employed to create a 1:3 match between the RLR and LLR groups. A comprehensive collection and analysis of patient data regarding efficacy and safety have been conducted, along with the evaluation of the learning curve for RLR.</p><p><strong>Results: </strong>Following PSM, a total of 341 patients were included, with 97 in the RLR group and 244 in the LLR group. RLR group demonstrated a significantly longer operative time (median [IQR], 210 [152.0-298.0] min vs. 183.5 [132.3-263.5] min; p = 0.04), with no significant differences in other perioperative and short-term postoperative outcomes. Overall survival (OS) was similar between the two groups (p = 0.43), but RLR group exhibited improved recurrence-free survival (RFS) (median of 65 months vs. 56 months, p = 0.006). The estimated 5-year OS for RLR and LLR were 74.8% (95% CI: 65.4-85.6%) and 80.7% (95% CI: 74.0-88.1%), respectively. The estimated 5-year RFS for RLR and LLR were 58.6% (95% CI: 48.6-70.6%) and 38.3% (95% CI: 26.4-55.9%), respectively. In the multivariate Cox regression analysis, RLR (HR: 0.586, 95% CI (0.393-0.874), p = 0.008) emerged as an independent predictor of reducing recurrence rates and enhanced RFS. The operative learning curve indicates that approximately after the 11th case, the learning curve of RLR stabilized and entered a proficient phase.</p><p><strong>Conclusions: </strong>OS was comparable between RLR and LLR, and while RFS was improved in the RLR group. RLR demonstrates oncological effectiveness and safety for resectable HCC.</p>","PeriodicalId":12901,"journal":{"name":"Hepatology International","volume":null,"pages":null},"PeriodicalIF":5.9,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140916326","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}