Liver International最新文献

{"title":"MASLD, At-Risk MASH and Increased Liver Stiffness Are Associated With Young Adulthood Obesity Without Residual Risk After Losing Obesity.","authors":"Laurens A van Kleef, Jesse Pustjens, Mesut Savas, Ibrahim Ayada, Pengfei Li, Qiuwei Pan, Elisabeth F C van Rossum, Harry L A Janssen, Willem P Brouwer","doi":"10.1111/liv.16169","DOIUrl":"https://doi.org/10.1111/liv.16169","url":null,"abstract":"<p><strong>Background: </strong>Obesity can result in persistent metabolic changes despite weight loss, which may affect liver health. We aimed to investigate associations between young adulthood obesity and metabolic dysfunction-associated steatotic liver disease (MASLD), at-risk steatohepatitis and increased liver stiffness measurement (LSM) in a general population setting.</p><p><strong>Methods: </strong>We studied NHANES 2017-2020 community-dwelling participants aged > 40 years with BMI ≥ 18.5 and no heart failure. Weight at age 25 was obtained through questionnaires and compared to current weight. Assessment included controlled attenuation parameter (CAP) and LSM. Associations between obesity status change with MASLD or at-risk metabolic dysfunction-associated steatohepatitis (MASH) and increased LSM were investigated and adjusted for demographics and metabolic health.</p><p><strong>Results: </strong>The cohort comprised 4,580 participants (57% stable non-obesity, 33% gained obesity, 2% lost obesity and 8% stable obesity). Compared to stable no-obesity, stable obesity was strongly associated with MASLD (odds ratio [OR]: 5.47, 95% confidence interval [95%CI]: 3.97-7.66) as was gained obesity (OR: 4.68, 95% CI: 3.93-5.59), whereas no increased risk was demonstrated for lost obesity (OR: 1.26, 95% CI: 0.76-2.10). Similar associations for stable obesity and gained obesity with at-risk MASH and LSM ≥ 8 kPa were demonstrated. No residual risk was found for lost obesity (MASH-OR: 1.05 95% CI: 0.36-2.49; LSM ≥ 8 kPa-OR: 0.85, 95% CI: 0.29-1.97). Results were consistent in sensitivity analysis where obesity change was calculated over the past 10 years and weight change was stratified in normal weight/overweight/obesity.</p><p><strong>Conclusion: </strong>Young adulthood obesity is an important risk factor for MASLD, at-risk MASH and increased LSM among the general population aged 40-80 years. Losing obesity resulted in normalisation of odds for MASLD, at-risk MASH and increased LSM. These findings underline the importance of preventing and treating young adulthood obesity to maintain liver health.</p>","PeriodicalId":18101,"journal":{"name":"Liver International","volume":" ","pages":""},"PeriodicalIF":6.0,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142687454","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}

{"title":"¹⁶⁶Ho-RadioEmbolizaTiOn Using personalized prediCtive dosimetry in patients with Hepatocellular carcinoma: A prospective, single-centre study (RETOUCH).","authors":"Ana-Maria Bucalau, Benoît Collette, Illario Tancredi, Irina Vierasu, Fadi Tannouri, Martina Pezzullo, Rodrigo Moreno-Reyes, Gontran Verset","doi":"10.1111/liv.15923","DOIUrl":"https://doi.org/10.1111/liv.15923","url":null,"abstract":"<p><strong>Background and aims: </strong>Holmium-166 (¹⁶⁶Ho) radioembolization could offer a more individualized approach in terms of imaging and dosimetry. We aim to evaluate the feasibility and safety of ¹⁶⁶Ho selective internal radiation therapy (SIRT) using a higher tumour dose than previously administered determined by ¹⁶⁶Ho-scout as a surrogate marker in HCC patients.</p><p><strong>Methods: </strong>This is an open-label, prospective, non-randomized, single-centre pilot study that included patients with HCC that received ¹⁶⁶Ho-SIRT if the work-up using ¹⁶⁶Ho-scout showed a tumour-absorbed dose ≥150 Gy, a non-tumoural liver absorbed dose less than 60 Gy and a lung absorbed dose less than 30 Gy. Primary endpoints were feasibility and safety-toxicity profiles at 24-48 h and 1 month. Overall response rates (ORR) at 3 months (mRECIST, RECIST 1.1 and metabolic response by FDG and choline PET CT) and time to progression (TTP) represented the secondary endpoints.</p><p><strong>Results: </strong>Fifteen patients with large tumours (mean diameter 55.67 ± 28.42 mm) received 17 ¹⁶⁶Ho-SIRT treatments between July 2020 and June 2022. All the attempted treatments were accomplished. Mean administered tumour dose was 183.18 ± 71.71 Gy, while non-tumour liver dose was 30.29 ± 14.56 Gy. Median time of follow-up was 12 months (IQR 9-16). Only grade 1-2 clinical and biological AEs were observed. There were no liver decompensations. At 3 months, objective response was achieved for all target lesions (CR 78.57%, PR 21.43% according to mRECIST). Median TTP was 18.8 (range 2.9; n.e.) months.</p><p><strong>Conclusion: </strong>Personalized ¹⁶⁶Ho-SIRT with a tumour delivered dose ≥150 Gy was feasible and safe for HCC patients with promising response rates.</p>","PeriodicalId":18101,"journal":{"name":"Liver International","volume":" ","pages":""},"PeriodicalIF":6.0,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142681649","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}

{"title":"Effectiveness and Safety of Glecaprevir/Pibrentasvir in Italian Children and Adolescents With Chronic Hepatitis C: A Real-Word, Multicenter Study.","authors":"Mariangela Stinco, Chiara Rubino, Elisa Bartolini, Federica Nuti, Giulia Paolella, Gabriella Nebbia, Erika Silvestro, Silvia Garazzino, Emanuele Nicastro, Lorenzo D'Antiga, Chiara Zanchi, Laura Morra, Raffaele Iorio, Fabiola Di Dato, Giuseppe Maggiore, Maria Rita Sartorelli, Donatella Comparcola, Marta Stracuzzi, Vania Giacomet, Francesca Musto, Michele Pinon, Pierluigi Calvo, Ines Carloni, Federica Zallocco, Mara Cananzi, Sandra Trapani, Giuseppe Indolfi","doi":"10.1111/liv.16180","DOIUrl":"https://doi.org/10.1111/liv.16180","url":null,"abstract":"<p><strong>Background & aims: </strong>Glecaprevir/Pibrentasvir (GLE/PIB) has been approved by the European Medicine Agency (EMA) and by the US Food and Drug Administration (US-FDA) for the treatment of children and adolescents from 3 years of age with chronic hepatitis C virus (CHC) infection. The aim of this study was to confirm the real-world effectiveness and safety of GLE/PIB in children and adolescents (3 to < 18 years old) with CHC.</p><p><strong>Methods: </strong>This prospective, multicentre study involved 11 Italian centres. Children and adolescents (from 3 to < 18 years of age) received a weight-based dose (up to 300/120 mg) of GLE/PIB once daily for 8 weeks. The effectiveness endpoint was sustained virological response 12 weeks after the end of treatment (SVR12). Safety was assessed by adverse events (AE) and clinical/laboratory data.</p><p><strong>Results: </strong>Sixty-one patients (median age 12 years, interquartile range 5) were enrolled and treated between June 2020 and October 2023. Genotype distribution was as follows: 24/61 genotype 1 (39.4%), 13/61 genotype 2 (21.3%), 18/61 genotype 3 (29.5%) and 6/61 genotype 4 (9.8%). Sixty (98.4%) patients completed treatment and follow-up. SVR12 was obtained by 60/61 patients (98.4%). One patient died because of an oncological illness while on treatment. AE occurred in 13.1% of the patients, were mild and no patients prematurely stopped treatment.</p><p><strong>Conclusions: </strong>This study confirmed the real-life effectiveness and safety of the 8-week therapy with GLE/PIB for treatment of CHC in children and adolescents.</p>","PeriodicalId":18101,"journal":{"name":"Liver International","volume":" ","pages":""},"PeriodicalIF":6.0,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142681893","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}

{"title":"Recipient-Donor Sex Constellation in Liver Transplantation for Hepatocellular Carcinoma-An ELTR Study.","authors":"Christian Tibor Josef Magyar, Noah Free Arteaga, Giacomo Germani, Vincent Hassan Karam, Rene Adam, Renato Romagnoli, Paolo De Simone, Fabien Robin, Daniel Cherqui, Andrea Boscà, Vincenzo Mazzaferro, Yiliam Fundora, Michael Heneghan, Laura Llado, Mickael Lesurtel, Matteo Cescon, Darius Mirza, Andrea Cavelti, Lucienne Christen, Federico Storni, Corina Kim-Fuchs, Anja Lachenmayer, Guido Beldi, Daniel Candinas, Iuliana-Pompilia Radu, Birgit Schwacha-Eipper, Annalisa Berzigotti, Vanessa Banz","doi":"10.1111/liv.16178","DOIUrl":"https://doi.org/10.1111/liv.16178","url":null,"abstract":"<p><strong>Background & aims: </strong>Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related death worldwide. Liver transplantation (LT) is a curative treatment option. We investigated survival outcomes based on recipient-donor sex constellation (RDSC) following LT.</p><p><strong>Methods: </strong>We performed a European Liver Transplant Registry analysis, including patients from 1988 to December 2022. The cohort was split into four RDSC groups: female donor female recipient (FDFR), female donor male recipient (FDMR), male donor female recipient (MDFR) and male donor male recipient (MDMR). Survival analysis, including death with recurrence, was performed.</p><p><strong>Results: </strong>In 7601 LT for HCC with an overall median follow-up of 22.6 months (5.8, 60.7), death was registered in 25.1% and, as primary cause of death, HCC tumour recurrence in 26.0%. There was no statistically significant difference on crude survival estimates among the different RDSC groups (log-rank p = 0.66) with 10-year overall survival (OS) of 54.5% in FDFR, 54.6% in FDMR, 59.1% in MDFR and 56.9% in MDMR. On multivariable analysis, RDSC showed a significant effect on OS (FDFR as reference): MDFR (aHR 0.72, p = 0.023). No significant difference was found for FDMR (aHR 0.98, p = 0.821) and MDMR (aHR 0.90, p= 0.288). Regarding overall registered causes of death, differences between RDSC groups were found in rejection (p = 0.017) and cardiovascular (p = 0.046) associated deaths.</p><p><strong>Conclusions: </strong>In female recipients undergoing LT for HCC, male donor grafts were associated with a 28% reduction of mortality compared to female donor grafts.</p>","PeriodicalId":18101,"journal":{"name":"Liver International","volume":" ","pages":""},"PeriodicalIF":6.0,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142676358","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}

{"title":"PNPLA3 I148M Interacts With Environmental Triggers to Cause Human Disease.","authors":"Elizabeth K Speliotes, Carolin Victoria Schneider","doi":"10.1111/liv.16106","DOIUrl":"10.1111/liv.16106","url":null,"abstract":"<p><strong>Background: </strong>Metabolic dysfunction-associated steatotic liver disease (MASLD) affects up to 30% of Western populations. While obesity is a recognized risk factor, MASLD does not develop in all obese individuals, highlighting the need to understand genetic and environmental interactions. The PNPLA3 I148M variant has been identified as a key genetic risk factor, significantly increasing the likelihood of MASLD development and progression.</p><p><strong>Methods: </strong>We reviewed current literature on the role of PNPLA3 I148M in MASLD, focusing on gene-environment interactions involving diet, physical activity, obesity, and insulin resistance. We included studies analysing ethnic differences in PNPLA3 I148M prevalence and its association with MASLD. Additionally, we reviewed data on how PNPLA3 I148M influences the response to therapies, including lipid-lowering medications and GLP-1 agonists.</p><p><strong>Results: </strong>The PNPLA3 I148M variant markedly heightens MASLD risk, particularly in Hispanic populations, where a higher prevalence of MASLD is observed. Lifestyle factors such as high sugar intake, alcohol consumption, and physical inactivity exacerbate MASLD risk among I148M carriers. Evidence shows that insulin resistance amplifies MASLD risk associated with the I148M variant, especially in non-diabetic individuals. Moreover, the PNPLA3 I148M variant interacts with other genetic loci, further modifying MASLD risk and disease course. The variant also influences treatment response, with variability observed in effectiveness of lipid-lowering therapies and GLP-1 agonists among carriers.</p><p><strong>Conclusion: </strong>The interplay between PNPLA3 I148M and environmental factors underscores the need for personalized MASLD prevention and treatment strategies. Targeting both genetic and lifestyle contributors may enhance MASLD management, offering a tailored approach to reducing disease burden.</p>","PeriodicalId":18101,"journal":{"name":"Liver International","volume":" ","pages":""},"PeriodicalIF":6.0,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142667546","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}

{"title":"All Children With NAFLD Meet the Criteria for MAFLD and MASLD: Evidence From a Chinese Longitudinal Cohort.","authors":"Lili Yang, Yanan Qiao, Xin'nan Zong, Min Zhao, Bo Xi","doi":"10.1111/liv.16172","DOIUrl":"https://doi.org/10.1111/liv.16172","url":null,"abstract":"","PeriodicalId":18101,"journal":{"name":"Liver International","volume":" ","pages":""},"PeriodicalIF":6.0,"publicationDate":"2024-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142648378","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}

{"title":"Overall Mortality and Cardiovascular Mortality Associated With MAFLD+/NAFLD- Versus MAFLD-/NAFLD+: A Secondary Analysis.","authors":"Guiying Gao, Ai-Jia Guan, Guo-Fu Li, Guo Yu","doi":"10.1111/liv.16118","DOIUrl":"https://doi.org/10.1111/liv.16118","url":null,"abstract":"","PeriodicalId":18101,"journal":{"name":"Liver International","volume":" ","pages":""},"PeriodicalIF":6.0,"publicationDate":"2024-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142648398","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}

{"title":"Characterisation and Clinical Relevance of Tertiary Lymphoid Structures in Primary Biliary Cholangitis.","authors":"Hongyu Chu, Yanni Li, Hui Yang, Yuhang Liu, Rongrong Zheng, Xue Zhang, Xiaoyi Wang, Jingwen Zhao, Yujie Zhang, Quan Wang, Ying Ran, Liping Guo, Simin Zhou, Man Liu, Wenjing Song, Bangmao Wang, Long Li, Lu Zhou","doi":"10.1111/liv.16157","DOIUrl":"https://doi.org/10.1111/liv.16157","url":null,"abstract":"<p><strong>Background and aims: </strong>The pathological characteristics of lymphocyte infiltration in the hepatic portal tracts of patients with primary biliary cholangitis (PBC) remain unclear. Tertiary lymphoid structures (TLSs) are ectopic lymphoid tissues associated with the exacerbation of autoimmune reactions. Here, we evaluate the role of TLSs in PBC and investigate their potential therapeutic value.</p><p><strong>Methods: </strong>We recruited 75 patients with PBC and 53 control patients with liver biopsies who were followed more than 2 years. TLSs and their maturity were identified by the amount and spatial distribution of immune cells. Bulk RNA sequencing of liver was performed in PBC patients with different TLS maturity. The sphingosine-1-phosphate receptor (S1PRs) modulator FTY720 was administered to dnTGFβRII mice to assess the role of TLSs on cholangitis.</p><p><strong>Results: </strong>TLSs presented in 61.3% (46/75) of liver tissues from patients with PBC, including 26 patients with mature TLS (mTLS) and 20 patients with immature TLS (imTLS). The proportion of mTLS was higher in PBC compared with chronic hepatitis B and autoimmune hepatitis. PBC patients with mTLS exhibited the highest serum levels of biochemical indicators, immune globulin and proportions of liver cirrhosis. Gene sets for lymphocyte migration and chemokine signalling pathways were enriched in patients with PBC presenting with TLS. FTY720 inhibited TLS formation and relieved cholangitis and fibrosis in dnTGFβRII mice.</p><p><strong>Conclusion: </strong>TLSs are characteristics of lymphocyte accumulation in the portal tracts of PBC, of which the maturity of TLSs correlates with the inflammation and fibrosis of PBC. Targeting TLSs formation is a potential treatment of PBC.</p>","PeriodicalId":18101,"journal":{"name":"Liver International","volume":" ","pages":""},"PeriodicalIF":6.0,"publicationDate":"2024-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142648395","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}

{"title":"Impact of Metabolic Syndrome Traits on Kidney Disease Risk in Individuals with MASLD: A UK Biobank Study.","authors":"Josh Bilson, Theresa J Hydes, Declan McDonnell, Ryan M Buchanan, Eleonora Scorletti, Alessandro Mantovani, Giovanni Targher, Christopher D Byrne","doi":"10.1111/liv.16159","DOIUrl":"https://doi.org/10.1111/liv.16159","url":null,"abstract":"<p><strong>Background and aims: </strong>The impact of metabolic syndrome (MetS) traits on chronic kidney disease (CKD) risk in metabolic dysfunction-associated steatotic liver disease (MASLD) is unknown. We investigated the impact of type and number of MetS traits and liver fibrosis on prevalent CKD and incident end-stage renal disease (ESRD) risk in SLD.</p><p><strong>Methods: </strong>234 488 UK Biobank participants' were analysed. Hepatic steatosis index (> 36 for SLD, < 30 for no SLD) and MRI-proton density fat fraction (≥ 5.56%) were used to identify SLD. MetS traits were identified using MASLD criteria. Advanced fibrosis (FIB-4 score > 2.67) was determined using FIB-4 scores. eGFR < 60 mL/min/1.73 m² or albuminuria > 3 mg/mmol identified prevalent CKD. A validated algorithm identified incident ESRD. Binary logistic and Cox regressions were used to test associations with prevalent CKD ([adjusted odds ratios (ORs)]) and incident ESRD (adjusted hazard ratios [HRs]) respectively.</p><p><strong>Results: </strong>102 410 participants (41.2%) had SLD. 64.4% had MetS. 1.3% had FIB-4 score > 2.67. With SLD and only one MetS trait, hypertension (OR 1.35, 95% CI 1.35-1.72) or type 2 diabetes (T2D) (OR 1.89, 95% CI 1.06-3.38) increased risk of prevalent CKD. MetS (≥ 3 traits) increased prevalent CKD risk (OR 1.94, 95% CI 1.75-2.15), which was further increased by advanced liver fibrosis (OR 4.29, 95% CI 3.36-5.47). CKD prevalence increased with increasing MetS traits. Over 13.6 years (median follow-up), MetS was associated with increased risk of developing ESRD (HR 1.70, 95% CI 1.19-2.43).</p><p><strong>Conclusions: </strong>In MASLD, hypertension, and T2D, number of MetS traits and liver fibrosis increased risk of prevalent CKD and presence of MetS increased the risk of incident ESRD.</p>","PeriodicalId":18101,"journal":{"name":"Liver International","volume":" ","pages":""},"PeriodicalIF":6.0,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142644393","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}

{"title":"Novel Emerging Mechanisms in Acetaminophen (APAP) Hepatotoxicity.","authors":"Alejandro Hionides-Gutierrez, Naroa Goikoetxea-Usandizaga, Carlos Sanz-García, María L Martínez-Chantar, Francisco Javier Cubero","doi":"10.1111/liv.16167","DOIUrl":"https://doi.org/10.1111/liv.16167","url":null,"abstract":"<p><strong>Background: </strong>Drug-induced liver injury represents a critical public health issue, marked by unpredictable and potentially severe adverse reactions to medications, herbal products or dietary supplements.</p><p><strong>Aims: </strong>Acetaminophen is notably a leading cause of hepatotoxicity, impacting over one million individuals worldwide.</p><p><strong>Materials & methods: </strong>Extensive research has elucidated the intricate mechanisms driving APAP-induced liver injury, emphasising the significant roles of endoplasmic reticulum stress, oxidative stress, mitochondrial dysfunction and cell death.</p><p><strong>Results: </strong>These insights pave the way for innovative therapeutic strategies, including the use of magnesium, bile acids, microbiota modulation and mesenchymal stem cells.</p><p><strong>Discussion & conclusion: </strong>This review explores into these pathological mechanisms, proposing viable therapeutic interventions for patients suffering from APAP-induced liver injury.</p>","PeriodicalId":18101,"journal":{"name":"Liver International","volume":" ","pages":""},"PeriodicalIF":6.0,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142644395","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}