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Loss of Mtarc1 Protects Against Steatotic Liver Disease in Mice 丢失Mtarc1可预防小鼠脂肪变性肝病。

IF 5.2 2区医学 Q1 GASTROENTEROLOGY & HEPATOLOGY

Liver International

Pub Date : 2026-01-13 DOI: 10.1111/liv.70507

Xiaofei Yin, Caroline Bickerton, Bryan MacDonald, Alessandro Arduini, Yunlong Shi, Mary Haas, Amy Deik, Mark Chaffin, Erika Kovacs-Bogdan, Julian Avila Pacheco, Maiwen Amegadjie, Bidur Bhandary, Shayan Sadre, Thomas Rathjen, Irinna Papangeli, Raymond T. Chung, Russell Goodman, Melina Claussnitzer, Clary Clish, Alexander Ehrmann, Alison Leed, Patrick T. Ellinor

Background & Aims

Metabolic dysfunction-associated steatotic liver disease (MASLD) spans from simple steatosis to metabolic dysfunction-associated steatohepatitis (MASH) and can progress to cirrhosis or hepatocellular carcinoma. Despite its prevalence, effective therapies are lacking. Recent genome-wide association studies identified a common missense variant (rs2642438) in the Mitochondrial Amidoxime Reducing Component 1 (MTARC1) gene that protects against liver cirrhosis without increasing cardiovascular disease risk. Biochemical and disease risk signatures associated with carriers of this missense variant also aligned with those of a known loss-of-function MTARC1 variant, suggesting mARC1 inhibition as a potential MASLD treatment.

Methods

To validate mARC1 loss-of-function as protective against MASLD, we generated Mtarc1 knockout (KO) mice and placed them on a choline-deficient, L-amino acid-defined, high-fat diet (CDAHFD). Effects of Mtarc1 KO on obesity and type 2 diabetes were explored using a high-fat diet. Hepatocytes from Mtarc1 KO mice were isolated to explore the molecular mechanisms by which Mtarc1 KO impacts lipid metabolism.

Results

Mtarc1 KO mice exhibited no vital growth or development defects. With a high-fat diet-induced obesity model, obese Mtarc1 KO mice exhibited reduced liver mass and lower cholesterol levels, with no effect on glucose homeostasis. In a CDAHFD-induced MASLD model, mARC1 deficiency significantly reduced liver steatosis, profibrosis, and inflammation. Untargeted metabolomics profiling further showed hepatic enrichment of phospholipids in Mtarc1 KO mice. Primary hepatocytes isolated from Mtarc1 KO mice exhibited reduced lipid droplet accumulation, decreased fatty acid uptake, and increased lipid secretion.

Conclusions

These findings support mARC1 inhibition as a promising therapeutic strategy for MASLD/MASH.

背景与目的：代谢功能障碍相关的脂肪性肝病（MASLD）涵盖从单纯的脂肪变性到代谢功能障碍相关的脂肪性肝炎（MASH），并可发展为肝硬化或肝细胞癌。尽管它很普遍，但缺乏有效的治疗方法。最近的全基因组关联研究发现，线粒体偕胺肟还原组分1 （MTARC1）基因中存在一种常见的错义变体（rs2642438），该基因可以预防肝硬化，但不会增加心血管疾病的风险。与该错意义变体携带者相关的生化和疾病风险特征也与已知功能丧失MTARC1变体的特征一致，表明抑制mARC1是潜在的MASLD治疗方法。方法：为了验证mARC1功能丧失对MASLD的保护作用，我们产生了Mtarc1敲除（KO）小鼠，并将它们置于缺乏胆碱、l -氨基酸定义的高脂肪饮食（CDAHFD）中。通过高脂饮食探讨Mtarc1 KO对肥胖和2型糖尿病的影响。分离Mtarc1 KO小鼠肝细胞，探讨Mtarc1 KO影响脂质代谢的分子机制。结果：Mtarc1 KO小鼠无明显生长发育缺陷。在高脂肪饮食诱导的肥胖模型中，肥胖的Mtarc1 KO小鼠表现出肝脏质量减少和胆固醇水平降低，对葡萄糖稳态没有影响。在cdahfd诱导的MASLD模型中，mARC1缺乏显著降低肝脏脂肪变性、纤维化和炎症。非靶向代谢组学分析进一步显示Mtarc1 KO小鼠的肝脏磷脂富集。从Mtarc1 KO小鼠分离的原代肝细胞显示脂滴积聚减少，脂肪酸摄取减少，脂质分泌增加。结论：这些发现支持mARC1抑制作为MASLD/MASH的一种有希望的治疗策略。

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引用次数: 0

Locoregional CAR-T Therapy for HCC: Potential and Pathways Forward 局部CAR-T治疗肝癌：潜力和未来途径。

IF 5.2 2区医学 Q1 GASTROENTEROLOGY & HEPATOLOGY

Liver International

Pub Date : 2026-01-11 DOI: 10.1111/liv.70513

Jue Wang, Jiale Qiu, Bo Feng

引用次数: 0

Genetic Information Enhances a Novel Non-Invasive Steatosis Index and Outperforms Existing Steatosis Indices 遗传信息增强了一种新的非侵入性脂肪变性指数，并优于现有的脂肪变性指数。

IF 5.2 2区医学 Q1 GASTROENTEROLOGY & HEPATOLOGY

Liver International

Pub Date : 2026-01-11 DOI: 10.1111/liv.70410

Yousif Alyousifi, Chinmay Raut, Vincent L. Chen, Antonino Oliveri, Yanhua Chen, Elizabeth K. Speliotes

<div> <section> <h3> Background and Aims</h3> <p>Early detection of individuals with metabolic dysfunction-associated steatotic liver disease (MASLD) is important as interventions to reduce steatosis can prevent progression to advanced liver disease. Identification of individuals with hepatic steatosis relies on imaging techniques, which are costly and often unavailable in large populations. Identifying hepatic steatosis through blood tests and demographics may serve as a cost-effective alternative to identifying hepatic steatosis. Here, we aim to identify demographic, serum and genetic variables that can help predict hepatic steatosis in two large population-based cohorts.</p> </section> <section> <h3> Methods</h3> <p>We analysed data from 32 008 participants in the UK Biobank (UKBB) with liver fat quantified using magnetic resonance proton density fat fraction (MRI-PDFF). We created non-invasive models to predict steatosis, the Enhanced Steatosis Indexes (ESIs), using logistic regression. Candidate predictors included variables from the literature and genetic markers. ESI-1 variables included demographic and serum values. ESI-2 included the ESI-1 variables plus the genetic markers. We trained and tested these models in UKBB and validated them in the Framingham Heart Study (FHS).</p> </section> <section> <h3> Results</h3> <p>In UKBB, ESI-1 and ESI-2 predicted ≥ 5% PDFF with AUC 0.844 and 0.858, respectively, outperforming DSI, HSI, FSI and FLI (AUC 0.818–0.834 vs. ESI-1 and AUC 0.830–0.844 vs. ESI-2). In FHS, ESI-1 and ESI-2 predicted CT-measured liver steatosis with AUC 0.803 and 0.808, respectively.</p> </section> <section> <h3> Conclusions</h3> <p>We developed a non-invasive model to diagnose steatosis that outperforms existing steatosis models. Including genetic information improved the performance of ESI-2. Deployment of our models can facilitate non-invasive screening of steatosis so that, with early intervention, disease progression can be prevented.</p> </section> <section> <h3> Impact and Implications</h3> <p>We developed a non-invasive model based on demographic, serum laboratory and genetic predictors that outperforms existing steatosis indices in identifying individuals with hepatic steatosis. This Enhanced Steatosis Index (ESI) enables more accurate and personalised early detection of hepatic steatosis, a highly prevalent yet underdiagnosed condition. By leveraging readily available clinical measures and genetic data, both ESI-1 and ESI-2 improve risk stratification and support large-scale screening and early intervention efforts. These

背景和目的：早期发现代谢功能障碍相关的脂肪变性肝病（MASLD）非常重要，因为减少脂肪变性的干预措施可以预防进展为晚期肝病。肝脂肪变性个体的识别依赖于成像技术，这是昂贵的，往往无法在大量人群。通过血液检查和人口统计学来识别肝脏脂肪变性可能是一种具有成本效益的替代方法。在这里，我们的目的是确定人口统计学，血清和遗传变量，可以帮助预测肝脂肪变性在两个大型人群为基础的队列。方法：我们分析了来自英国生物银行（UKBB）的32008名参与者的数据，他们的肝脏脂肪使用磁共振质子密度脂肪分数（MRI-PDFF）进行量化。我们使用逻辑回归建立了非侵入性模型来预测脂肪变性，即增强脂肪变性指数（Enhanced steatosis Indexes, ESIs）。候选预测因子包括来自文献和遗传标记的变量。ESI-1变量包括人口统计学和血清值。ESI-2包括ESI-1变量和遗传标记。我们在UKBB中训练和测试了这些模型，并在弗雷明汉心脏研究（FHS）中对它们进行了验证。结果：在UKBB中，ESI-1和ESI-2预测PDFF≥5%，AUC分别为0.844和0.858，优于DSI、HSI、FSI和FLI （AUC分别为0.818-0.834与ESI-1和0.830-0.844与ESI-2）。在FHS中，ESI-1和ESI-2预测ct测量的肝脏脂肪变性，AUC分别为0.803和0.808。结论：我们开发了一种非侵入性的脂肪变性诊断模型，优于现有的脂肪变性模型。遗传信息的加入提高了ESI-2的性能。我们的模型的部署可以促进脂肪变性的非侵入性筛查，因此，通过早期干预，可以预防疾病进展。影响和意义：我们开发了一种基于人口统计学、血清实验室和遗传预测因子的无创模型，在识别肝脏脂肪变性个体方面优于现有的脂肪变性指数。这种增强脂肪变性指数（ESI）能够更准确和个性化地早期检测肝脏脂肪变性，这是一种非常普遍但未被诊断的疾病。通过利用现成的临床措施和遗传数据，ESI-1和ESI-2都改善了风险分层，支持大规模筛查和早期干预工作。这些进展有可能提供更实惠、更准确和更有针对性的筛查，促进早期治疗，减轻代谢性肝病的负担，并有助于解决肝脂肪变性诊断和管理方面的差异。

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引用次数: 0

Breaking Barriers: Equitable Treatment Access Achieves Survival Parity in HCC for People With HIV 打破障碍：公平的治疗机会实现艾滋病毒感染者HCC的生存均等。

IF 5.2 2区医学 Q1 GASTROENTEROLOGY & HEPATOLOGY

Liver International

Pub Date : 2026-01-10 DOI: 10.1111/liv.70498

Massimo Iavarone, Eleonora Alimenti, Alessandro Soria

引用次数: 0

Reassessing the Use of Nivolumab Plus Ipilimumab After Atezolizumab Plus Bevacizumab in Advanced HCC 在Atezolizumab + Bevacizumab治疗晚期HCC后，重新评估Nivolumab + Ipilimumab的使用。

IF 5.2 2区医学 Q1 GASTROENTEROLOGY & HEPATOLOGY

Liver International

Pub Date : 2026-01-09 DOI: 10.1111/liv.70512

Xin Xiang, Yang Yu

引用次数: 0

Evaluation of Pathogenic Variants Associated With Monogenic Disorders of Dyslipidemia in Patients With Well Characterised MASLD 与特征明确的MASLD患者血脂异常单基因疾病相关的致病变异评估

IF 5.2 2区医学 Q1 GASTROENTEROLOGY & HEPATOLOGY

Liver International

Pub Date : 2026-01-09 DOI: 10.1111/liv.70486

Tae-Hwi Schwantes-An, Marco A. Abreu, Brent A. Neuschwander-Tetri, Jian Wang, Xiuqing Guo, Jingyi Tan, Robert A. Hegele, Nicholas O. Davidson, Luca Lotta, Niek Verweij, Katherine P. Yates, Jerome I. Rotter, Naga Chalasani

Background and Aims

Dyslipidemia is common in patients with MASLD, but the frequency and significance of inherited disorders of dyslipidemia are unclear. We investigated the prevalence and significance of pathogenic variants associated with selected monogenic disorders of dyslipidemia in 3358 patients with well-characterised MASLD.

Approach

We identified clinically relevant variants in APOB, MTTP, PCSK9, ANGPTL3, LDLR and LDLRAP1 genes which can cause hypobetalipoproteinemia (HBL) and familial hypercholesterolemia (FH). Using ClinVar annotations as initial variant selection, we identified 2027 variants in those 6 genes which are reported as ‘pathogenic’ or ‘likely pathogenic’ (P/LP). We first assessed for the presence of P/LP variants in the study cohort and then investigated the effect of carrying P/LP variants on liver histology, by comparing ~4 matched controls for each APOB and LDLR carrier. As interpretative analyses, we also looked at the difference between liver enzymes, lipid measures and outcomes between the carriers and matched controls.

Results

Twenty-two variants among these 2027 P/LP variants were present in 24 out of 3358 patients (12 ApoB, 10 LDLR, 1 ANGPTL3 and 1 MTTP variant carriers). Compared to controls, APOB carriers had higher steatosis grade (2.4 vs. 1.7, p-value 0.0028), higher NAFLD activity score (NAS) (4.9 vs. 3.8, p-value 0.04), and numerically higher but statistically not significant fibrosis stage (1.2 vs. 1.1, p-value 0.75) and ALT (87.4 vs. 58.1 U/L, p-value 0.06). Their LDL-c (51 vs. 147.8 mg/dL, p-value 6.1E-09) and triglycerides (91.5 vs. 160.6 mg/dL, p-value 2.8E-03) were significantly lower. Compared to controls, LDLR carriers had numerically higher steatosis grade, NAS, fibrosis stage and LDL-c levels, but these were not statistically different.

Conclusions

Monogenic disorders of dyslipidemia are rarely present in patients with MASLD and are sometimes associated with worse liver histology. Testing for these conditions may be considered on a case-by-case basis.

背景与目的：血脂异常在MASLD患者中很常见，但血脂异常遗传性疾病的发生频率和意义尚不清楚。我们调查了3358例特征明确的MASLD患者中与选定的血脂异常单基因疾病相关的致病变异的患病率和意义。方法：我们鉴定了APOB、MTTP、PCSK9、ANGPTL3、LDLR和LDLRAP1基因的临床相关变异，这些基因可导致低脂蛋白血症（HBL）和家族性高胆固醇血症（FH）。使用ClinVar注释作为初始变异选择，我们在这6个基因中确定了2027个被报道为“致病”或“可能致病”（P/LP）的变异。我们首先评估了研究队列中P/LP变异的存在，然后通过比较每个APOB和LDLR携带者约4个匹配的对照，研究了携带P/LP变异对肝脏组织学的影响。作为解释性分析，我们还研究了携带者和匹配对照组之间肝酶、脂质测量和结果的差异。结果：在3358例患者中，24例患者（12例ApoB携带者，10例LDLR携带者，1例ANGPTL3携带者和1例MTTP携带者）存在这2027种P/LP变体中的22种变体。与对照组相比，APOB携带者具有更高的脂肪变性等级（2.4 vs. 1.7， p值0.0028），更高的NAFLD活性评分（NAS）（4.9 vs. 3.8， p值0.04），纤维化阶段（1.2 vs. 1.1， p值0.75）和ALT （87.4 vs. 58.1 U/L， p值0.06）更高，但在统计学上不显著。他们的LDL-c（51比147.8 mg/dL， p值6.1E-09）和甘油三酯（91.5比160.6 mg/dL， p值2.8E-03）显著降低。与对照组相比，LDLR携带者的脂肪变性等级、NAS、纤维化分期和LDL-c水平在数值上更高，但这些没有统计学差异。结论：血脂异常的单基因疾病在MASLD患者中很少出现，有时与较差的肝脏组织学相关。对这些条件的测试可以根据具体情况进行考虑。

{"title":"Evaluation of Pathogenic Variants Associated With Monogenic Disorders of Dyslipidemia in Patients With Well Characterised MASLD","authors":"Tae-Hwi Schwantes-An, Marco A. Abreu, Brent A. Neuschwander-Tetri, Jian Wang, Xiuqing Guo, Jingyi Tan, Robert A. Hegele, Nicholas O. Davidson, Luca Lotta, Niek Verweij, Katherine P. Yates, Jerome I. Rotter, Naga Chalasani","doi":"10.1111/liv.70486","DOIUrl":"10.1111/liv.70486","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background and Aims</h3>\u0000 \u0000 <p>Dyslipidemia is common in patients with MASLD, but the frequency and significance of inherited disorders of dyslipidemia are unclear. We investigated the prevalence and significance of pathogenic variants associated with selected monogenic disorders of dyslipidemia in 3358 patients with well-characterised MASLD.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Approach</h3>\u0000 \u0000 <p>We identified clinically relevant variants in <i>APOB</i>, <i>MTTP</i>, <i>PCSK9</i>, <i>ANGPTL3</i>, <i>LDLR</i> and <i>LDLRAP1</i> genes which can cause hypobetalipoproteinemia (HBL) and familial hypercholesterolemia (FH). Using ClinVar annotations as initial variant selection, we identified 2027 variants in those 6 genes which are reported as ‘pathogenic’ or ‘likely pathogenic’ (P/LP). We first assessed for the presence of P/LP variants in the study cohort and then investigated the effect of carrying P/LP variants on liver histology, by comparing ~4 matched controls for each <i>APOB</i> and <i>LDLR</i> carrier. As interpretative analyses, we also looked at the difference between liver enzymes, lipid measures and outcomes between the carriers and matched controls.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Twenty-two variants among these 2027 P/LP variants were present in 24 out of 3358 patients (12 <i>ApoB</i>, 10 <i>LDLR</i>, 1 <i>ANGPTL3</i> and 1 <i>MTTP</i> variant carriers). Compared to controls, <i>APOB</i> carriers had higher steatosis grade (2.4 vs. 1.7, <i>p</i>-value 0.0028), higher NAFLD activity score (NAS) (4.9 vs. 3.8, <i>p</i>-value 0.04), and numerically higher but statistically not significant fibrosis stage (1.2 vs. 1.1, <i>p</i>-value 0.75) and ALT (87.4 vs. 58.1 U/L, <i>p</i>-value 0.06). Their LDL-c (51 vs. 147.8 mg/dL, <i>p</i>-value 6.1E-09) and triglycerides (91.5 vs. 160.6 mg/dL, <i>p</i>-value 2.8E-03) were significantly lower. Compared to controls, <i>LDLR</i> carriers had numerically higher steatosis grade, NAS, fibrosis stage and LDL-c levels, but these were not statistically different.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Monogenic disorders of dyslipidemia are rarely present in patients with MASLD and are sometimes associated with worse liver histology. Testing for these conditions may be considered on a case-by-case basis.</p>\u0000 </section>\u0000 </div>","PeriodicalId":18101,"journal":{"name":"Liver International","volume":"46 2","pages":""},"PeriodicalIF":5.2,"publicationDate":"2026-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12789714/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145944856","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Risk of Extrahepatic Cancer for Metabolic Dysfunction-Associated Steatohepatitis (MASH) in the United States Medicare Population 美国医疗保险人群中代谢功能障碍相关脂肪性肝炎（MASH）的肝外癌风险

IF 5.2 2区医学 Q1 GASTROENTEROLOGY & HEPATOLOGY

Liver International

Pub Date : 2026-01-08 DOI: 10.1111/liv.70508

Yestle Kim, Dominic Nunag, Matthew Davis, Robert Gish

This retrospective observational cohort study was conducted using 100% Medicare fee-for-service claims data (10/01/2015–12/31/2021) to characterise risk of incident extrahepatic cancer in patients with non-cirrhotic metabolic dysfunction-associated steatohepatitis (MASH) and for patients with MASH who progressed to more advanced liver disease (compensated cirrhosis, decompensated cirrhosis, hepatocellular carcinoma, liver transplant). For patients with non-cirrhotic MASH, 5-year cumulative incidence was 3.1% for breast cancer, 2.8% for lymphoma/leukaemia, 2.6% for prostate cancer and 1.4% for lung cancer. The greatest hazard of cancer incidence was observed for bladder (hazard ratio [HR] = 2.36), kidney (HR = 2.15), liver (HR = 2.48) and stomach cancers (HR = 3.38; all p < 0.05), each relative to control individuals without MASH/metabolic dysfunction-associated steatotic liver disease. Additionally, patients who progressed to advanced liver disease experienced a significantly increased hazard of several extrahepatic cancers. This study provides some of the first evidence on the incidence and risk of extrahepatic cancer among patients with MASH in the United States.

这项回顾性观察性队列研究使用100%医疗保险按服务收费索赔数据（2015年10月1日- 2021年12月31日）进行，以表征非肝硬化代谢功能障碍相关脂肪性肝炎（MASH）患者和进展为更晚期肝病（代偿性肝硬化、失代偿性肝硬化、肝细胞癌、肝移植）的患者发生肝外癌的风险。对于非肝硬化MASH患者，5年累积发病率为乳腺癌3.1%，淋巴瘤/白血病2.8%，前列腺癌2.6%，肺癌1.4%。膀胱癌（危险比[HR] = 2.36）、肾癌（危险比[HR] = 2.15）、肝癌（危险比[HR] = 2.48）和胃癌（危险比[HR] = 3.38）的发生率最高

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引用次数: 0

Sex Hormones and the Liver: Implications for Disease Progression and Hormonal Therapy 性激素和肝脏：疾病进展和激素治疗的意义。

IF 5.2 2区医学 Q1 GASTROENTEROLOGY & HEPATOLOGY

Liver International

Pub Date : 2026-01-06 DOI: 10.1111/liv.70509

Nora Cazzagon, Martina Gambato, Maurizia Rossana Brunetto, Erica Villa, Patrizia Burra, Annarosa Floreani, Special Interest Group Gender in Hepatology of the Italian Association for the Study of the Liver (AISF)

The liver is central to sex hormone metabolism, and sex hormones in turn modulate hepatic physiology and disease processes. Oestrogens are often protective, while androgens tend to worsen disease progression. The clinical implications of hormonal therapies in patients with liver disease remain an area of active investigation. To review current evidence on the interplay between sex hormones and liver disease, with a focus on the safety and impact of hormonal therapies, including contraception, hormone replacement therapy, assisted reproductive technology and gender-affirming treatments. Prolonged or high-dose oestrogen exposure, particularly via oral contraceptives, has been associated with intrahepatic cholestasis and hepatocellular adenoma (HCA), especially in predisposed individuals. In contrast, hormone replacement therapy in postmenopausal women is generally safe and may confer metabolic and hepatic benefits. Oestrogens appear to slow fibrosis progression and reduce hepatocellular carcinoma risk, whereas androgens can promote steatosis and HBV-related oncogenesis. Hormonal therapies are safe in most patients with compensated chronic liver disease but require caution in settings such as in polycystic liver disease, where oestrogens can accelerate cyst growth. Emerging data also indicate a role of sex hormones in autoimmune and cholestatic diseases, as well as in outcomes of assisted reproduction and gender-affirming therapy. Hormonal therapies are feasible in most liver disease contexts, but individualised assessment, awareness of genetic predisposition, and disease-specific risks are essential to optimise safety and therapeutic benefit.

肝脏是性激素代谢的中心，性激素反过来调节肝脏生理和疾病过程。雌激素通常具有保护作用，而雄激素往往会使疾病恶化。肝脏疾病患者激素治疗的临床意义仍然是一个积极研究的领域。回顾性激素与肝脏疾病之间相互作用的现有证据，重点关注激素疗法的安全性和影响，包括避孕、激素替代疗法、辅助生殖技术和性别肯定疗法。长期或高剂量雌激素暴露，特别是通过口服避孕药，与肝内胆汁淤积和肝细胞腺瘤（HCA）有关，特别是在易感个体中。相比之下，绝经后妇女的激素替代疗法通常是安全的，并可能带来代谢和肝脏方面的益处。雌激素似乎可以减缓纤维化进展并降低肝细胞癌的风险，而雄激素可以促进脂肪变性和hbv相关的肿瘤发生。激素治疗对大多数代偿性慢性肝病患者是安全的，但在多囊性肝病等情况下需要谨慎，因为雌激素会加速囊肿的生长。新出现的数据还表明，性激素在自身免疫性疾病和胆汁淤积症以及辅助生殖和性别肯定疗法的结果中发挥作用。激素治疗在大多数肝病中是可行的，但个体化评估、遗传易感性的认识和疾病特异性风险对于优化安全性和治疗效益至关重要。

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引用次数: 0

Reconsidering the Impacts of Steatotic Liver Disease on Adverse Pregnancy Outcomes 重新考虑脂肪变性肝病对不良妊娠结局的影响。

IF 5.2 2区医学 Q1 GASTROENTEROLOGY & HEPATOLOGY

Liver International

Pub Date : 2026-01-06 DOI: 10.1111/liv.70499

Rumeng Tang, Dongsen Hu, Lili Zhang

引用次数: 0

MyWayUp: A Digital Intervention for Alcohol Use Disorder in Patients With Alcohol-Related Liver Disease—Results From an RCT MyWayUp：酒精相关性肝病患者酒精使用障碍的数字干预——来自一项随机对照试验

IF 5.2 2区医学 Q1 GASTROENTEROLOGY & HEPATOLOGY

Liver International

Pub Date : 2026-01-05 DOI: 10.1111/liv.70506

Clara Oliveras, Mercè Balcells-Oliveró, Ramón Bataller, Pol Bruguera, Noel Cabrera, Cristina Calomarde-Gomez, Elsa Caballeria, Neus Freixa, Óscar Garcia-Pañella, Jordi Gratacós-Ginès, Pablo Guzman, Anna Hernández-Rubio, Anna Lligoña, Lluisa Ortega, Martina Pérez-Guasch, María Teresa Pons-Cabrera, Elisa Pose, Paola Zuluaga, Hugo López-Pelayo

Background

Alcohol-related liver disease (ArLD) is a public health concern that requires multidisciplinary interventions. Digital health tools may improve retention in alcohol use disorder (AUD) treatment and enhance health outcomes. This study explores a blended intervention (brief intervention plus a serious game (SG) based on motivational interviewing and cognitive-behavioural therapy) on AUD in patients with ArLD.

Methods

Randomised, single-blinded controlled trial on patients with recent-onset ArLD and AUD. Brief intervention plus the SG was compared to standard addiction therapy. Primary outcomes were AUD treatment retention and adherence at 6 months. Secondary outcomes included liver disease progression, alcohol use patterns, quality of life, functionality, motivational changes and usability.

Results

Seventy-nine patients (mean age 56, MELD-Na 14) were included. Participants in the intervention arm were three times more likely to remain in treatment at month six than those in the control arm (adjusted odds ratio (aOR) 3.24; 82.9% vs. 47.4% of engagement respectively) and attended 50% more appointments. Effect sizes (Cohen's D) were moderate for adherence at months three and six (0.51–0.64). At 6 months, Model for End-Stage Liver Disease Sodium (MELD-Na) scores were lower in the experimental group (12 vs. 16, p < 0.001). Among baseline drinkers, alcohol consumption decreased more in the intervention group at month one (11 vs. 6 Standard Drink Units (SDU)/day, p = 0.031).

Conclusion

The blended intervention increases engagement with AUD treatment, reduces the amount of consumed alcohol and improves MELD-Na scores. These results support the use of digital tailored interventions for AUD in these patients.

背景：酒精相关性肝病（ArLD）是一个需要多学科干预的公共卫生问题。数字健康工具可以提高酒精使用障碍（AUD）治疗的保留率，并提高健康结果。本研究探讨了一种混合干预（简短干预加基于动机访谈和认知行为治疗的严肃游戏）对ArLD患者AUD的影响。方法：随机、单盲对照试验，纳入新近发病的ArLD和AUD患者。将短暂干预加SG与标准成瘾治疗进行比较。主要结果是6个月时AUD治疗的保留和依从性。次要结局包括肝病进展、酒精使用模式、生活质量、功能、动机变化和可用性。结果：纳入79例患者，平均年龄56岁，MELD-Na 14岁。干预组的参与者在第六个月继续接受治疗的可能性是对照组的三倍(调整后的优势比（aOR） 3.24；（82.9% vs. 47.4%），赴约率高出50%。在第3个月和第6个月，依从性的效应量（Cohen's D）为中等（0.51-0.64）。6个月时，实验组的终末期肝病模型钠（MELD-Na）评分较低（12比16，p）。结论：混合干预增加了AUD治疗的参与程度，减少了饮酒量，提高了MELD-Na评分。这些结果支持在这些患者中使用数字定制的AUD干预措施。

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引用次数: 0