Article(id=1317885672820691831, tenantId=1146029695717560320, journalId=1316781422847033486, issueId=1317885672153797495, articleNumber=null, orderNo=null, doi=10.12449/JCH260803, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1777996800000, receivedDateStr=2026-05-06, revisedDate=null, revisedDateStr=null, acceptedDate=1784822400000, acceptedDateStr=2026-07-24, onlineDate=1792138029532, onlineDateStr=2026-10-16, pubDate=1787587200000, pubDateStr=2026-08-25, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1792138029532, onlineIssueDateStr=2026-10-16, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1792138029532, creator=13701087609, updateTime=1792138029532, updator=13701087609, issue=Issue{id=1317885672153797495, tenantId=1146029695717560320, journalId=1316781422847033486, year='2026', volume='42', issue='8', pageStart='1745', pageEnd='2000', issueExtLink='null', onlineDate='null', pubDate='1787587200000', pubDateStr='2026-08-25', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=1, specialIssue=null, createTime=1792138029373, creator='13701087609', updateTime=1792138608261, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1317888100290900262, tenantId=1146029695717560320, journalId=1316781422847033486, issueId=1317885672153797495, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1317888100290900263, tenantId=1146029695717560320, journalId=1316781422847033486, issueId=1317885672153797495, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=1755, endPage=1760, ext={EN=ArticleExt(id=1317885673105904505, articleId=1317885672820691831, tenantId=1146029695717560320, journalId=1316781422847033486, language=EN, title=Alcohol-related liver disease-associated acute-on-chronic liver failure：Mechanisms，dynamic assessment，and precise management, columnId=1317885673009435512, journalTitle=Journal of Clinical Hepatology, columnName=Expert Forum, runingTitle=null, highlight=null, articleAbstract=

Acute-on-chronic liver failure （ACLF） is a high-mortality syndrome that develops during the acute deterioration of chronic liver disease and is characterized by multiple organ dysfunction driven by systemic inflammation. Due to gut microbiota dysbiosis，endotoxin translocation，and amplified inflammatory responses，alcohol-related liver disease-associated ACLF （ALD-ACLF） is more pronounced and is often accompanied by a high risk of secondary infection and extrahepatic organ involvement，thereby exhibiting distinct etiological and clinical characteristics. This article systematically reviews the advances in the definitional boundaries，pathophysiological mechanisms，dynamic early warning，and prognostic assessment of ALD-ACLF，elaborates on risk stratification and key issues in clinical management，and discusses the potential impact of the dual-hit phenotype of metabolic dysfunction and alcohol-related liver disease on risk stratification in ALD-ACLF. This article also highlights the need to further strengthen etiology-oriented early identification，dynamic stratification，control of predisposing factors，and earlier intervention，in order to provide a reference for the precise assessment and individualized intervention of these patients.

, authors=Na Ai^{1, 2, 3}, Huaining Cui^{1, 2, 3}, Xiaohui Fang^{1, 2, 3}, Tao Liu^{1, 2, 3}, Yanhang Gao^{1, 2, 3}, authorsList=Na Ai, Huaining Cui, Xiaohui Fang, Tao Liu, Yanhang Gao, authorCompany=null, correspAuthors=Yanhang Gao, authorNote=null, correspAuthorsNote=null, copyrightStatement=null, copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=null, magXml=null, pdfUrl=null, pdf=null, pdfFileSize=null, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=null, mapNumber=null, fund=null), CN=ArticleExt(id=1317885677765776256, articleId=1317885672820691831, tenantId=1146029695717560320, journalId=1316781422847033486, language=CN, title=酒精性肝病相关慢加急性肝衰竭：机制、动态评估与精准管理, columnId=1317885673185596282, journalTitle=临床肝胆病杂志, columnName=专家论坛, runingTitle=null, highlight=null, articleAbstract=

慢加急性肝衰竭（ACLF）是慢性肝病急性恶化期的高病死率综合征，以系统性炎症驱动的多器官功能障碍为核心特征。酒精性肝病相关慢加急性肝衰竭（ALD-ACLF）因肠道微生态失衡、内毒素易位及炎症反应放大更为突出，常伴随较高的继发感染风险和肝外器官受累，具有明显的病因学与临床特异性。本综述系统梳理ALD-ACLF的概念边界、病理生理机制、动态预警与预后评估进展，重点评述风险分层及临床管理决策要点，并探讨代谢功能障碍合并酒精相关肝病双重打击表型对ALD-ACLF风险分层的潜在影响。提示临床应进一步强化病因导向的早期识别、动态分层、诱因控制和干预前移，以期为该类患者的精准评估及个体化干预提供参考。

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注：ALD-ACLF，酒精性肝病相关慢加急性肝衰竭；LPS，脂多糖；PAMP，病原体相关分子模式；TLR4，Toll样受体4；MyD88，髓样分化因子88；NF-κB，核因子κB；IRF3，干扰素调节因子3；p38/ERK MAPK通路，p38/细胞外信号调节激酶丝裂原活化蛋白激酶通路；TNF-α，肿瘤坏死因子α；IL-6，白细胞介素6；IL-1β，白细胞介素1β；IL-8，白细胞介素8；CCL2，CC亚族趋化因子配体2；ROS，活性氧；DAMP，损伤相关分子模式；SIRS，全身炎症反应综合征；CARS，代偿性抗炎反应综合征；HLA-DR，人类白细胞抗原DR；MERTK，Mer受体酪氨酸激酶；CD163，白细胞分化抗原163；PD-L1，程序性死亡受体配体1。

, figureFileSmall=ei+tXO3xosWr5aKLcn8qWQ==, figureFileBig=XdoL/oz5F4lqXafRCiP4QA==, tableContent=null), ArticleFig(id=1317885683033822135, tenantId=1146029695717560320, journalId=1316781422847033486, articleId=1317885672820691831, language=EN, label=Table 1, caption=

Comparison of clinical characteristics among SAH，ALD-related acute decompensation，and ALD-ACLF

, figureFileSmall=null, figureFileBig=null, tableContent=

项目	SAH	ALD相关急性失代偿	ALD-ACLF
疾病特点	ALD最严重炎症表型，重症者常突发黄疸和肝衰竭	失代偿期并发症加重，但未进入ACLF	在SAH/ALD基础上由感染和/或系统性炎症触发的多器官衰竭综合征
发病机制	酒精毒性、氧化应激、肠-肝轴失衡及肝内炎症共同驱动	以长期肝纤维化/肝硬化、门静脉高压及肝合成功能减退为主	慢性肝损伤基础上叠加感染和/或系统性炎症，导致免疫失衡及器官衰竭
病理特点	脂肪变、胆汁淤积、肝细胞周围纤维化、中性粒细胞浸润、肝细胞气球样变及马洛里小体	以肝硬化结节形成、纤维间隔及门静脉高压相关结构改变为主	ALD病变基础上叠加系统性炎症和器官衰竭表型
临床表现	突发黄疸、肝衰竭，可伴凝血障碍、营养不良和感染风险升高	以腹水、肝性脑病及静脉曲张出血等失代偿表现为主	在黄疸和肝功能恶化基础上出现多系统受累，常伴感染及器官功能障碍
器官衰竭	以肝衰竭为主，重症时可进展为ACLF	一般无明确多器官衰竭	可导致多器官衰竭
短期预后	差	差	最差
治疗策略	戒酒、营养支持、纠正维生素缺乏，重症者可使用糖皮质激素，4 d或7 d以Lille评分评估反应，无应答者考虑早期肝移植	按照失代偿期肝硬化处理，控制并发症，并强化戒酒管理	在上述基础上强调器官支持、积极控制感染或炎症诱因，并尽早评估肝移植

), ArticleFig(id=1317885683109319608, tenantId=1146029695717560320, journalId=1316781422847033486, articleId=1317885672820691831, language=CN, label=表1, caption=

SAH、ALD相关急性失代偿与ALD-ACLF临床特征比较

, figureFileSmall=null, figureFileBig=null, tableContent=

项目	SAH	ALD相关急性失代偿	ALD-ACLF
疾病特点	ALD最严重炎症表型，重症者常突发黄疸和肝衰竭	失代偿期并发症加重，但未进入ACLF	在SAH/ALD基础上由感染和/或系统性炎症触发的多器官衰竭综合征
发病机制	酒精毒性、氧化应激、肠-肝轴失衡及肝内炎症共同驱动	以长期肝纤维化/肝硬化、门静脉高压及肝合成功能减退为主	慢性肝损伤基础上叠加感染和/或系统性炎症，导致免疫失衡及器官衰竭
病理特点	脂肪变、胆汁淤积、肝细胞周围纤维化、中性粒细胞浸润、肝细胞气球样变及马洛里小体	以肝硬化结节形成、纤维间隔及门静脉高压相关结构改变为主	ALD病变基础上叠加系统性炎症和器官衰竭表型
临床表现	突发黄疸、肝衰竭，可伴凝血障碍、营养不良和感染风险升高	以腹水、肝性脑病及静脉曲张出血等失代偿表现为主	在黄疸和肝功能恶化基础上出现多系统受累，常伴感染及器官功能障碍
器官衰竭	以肝衰竭为主，重症时可进展为ACLF	一般无明确多器官衰竭	可导致多器官衰竭
短期预后	差	差	最差
治疗策略	戒酒、营养支持、纠正维生素缺乏，重症者可使用糖皮质激素，4 d或7 d以Lille评分评估反应，无应答者考虑早期肝移植	按照失代偿期肝硬化处理，控制并发症，并强化戒酒管理	在上述基础上强调器官支持、积极控制感染或炎症诱因，并尽早评估肝移植

), ArticleFig(id=1317885683172234169, tenantId=1146029695717560320, journalId=1316781422847033486, articleId=1317885672820691831, language=EN, label=Table 2, caption=

Comparison of prognostic scoring systems for ALD-ACLF

, figureFileSmall=null, figureFileBig=null, tableContent=

模型名称	主要参数	适用人群	核心优势	主要局限性	近3年进展
MELD 3.0	胆红素、INR、肌酐、血钠、白蛋白和性别	终末期肝病、肝移植等待患者	计算简便，应用广泛，为肝移植分配基础	对系统性炎症反应及肝外器官衰竭反映不足	在酒精相关肝炎和酒精性肝硬化急性恶化队列中显示出较好的短期死亡预测效能
CLIF-C ACLF	基于6个器官系统衰竭评估，纳入年龄、白细胞计数	EASL定义下ACLF患者	可同时反映多器官功能衰竭和炎症负荷，适用于28 d/90 d死亡预测、ICU分层及移植决策	计算相对复杂，在极重症ICU患者中的预测效能有限	近年ICU验证研究进一步支持其临床分层价值；CLIF-C ACLF>70分提示极高短期死亡风险
AARC	胆红素、INR、肌酐、乳酸及肝性脑病	APASL定义下ACLF患者	具有肝衰竭起始表型及动态再评估价值，适用于住院早期连续风险分层	对呼吸、循环衰竭表征较弱；跨地区外推性有限	京都共识进一步强化AARC动态评估在治疗反应判断及短期预后分层中的应用价值

), ArticleFig(id=1317885683444863930, tenantId=1146029695717560320, journalId=1316781422847033486, articleId=1317885672820691831, language=CN, label=表2, caption=

ALD-ACLF预后评分体系对比

, figureFileSmall=null, figureFileBig=null, tableContent=

模型名称	主要参数	适用人群	核心优势	主要局限性	近3年进展
MELD 3.0	胆红素、INR、肌酐、血钠、白蛋白和性别	终末期肝病、肝移植等待患者	计算简便，应用广泛，为肝移植分配基础	对系统性炎症反应及肝外器官衰竭反映不足	在酒精相关肝炎和酒精性肝硬化急性恶化队列中显示出较好的短期死亡预测效能
CLIF-C ACLF	基于6个器官系统衰竭评估，纳入年龄、白细胞计数	EASL定义下ACLF患者	可同时反映多器官功能衰竭和炎症负荷，适用于28 d/90 d死亡预测、ICU分层及移植决策	计算相对复杂，在极重症ICU患者中的预测效能有限	近年ICU验证研究进一步支持其临床分层价值；CLIF-C ACLF>70分提示极高短期死亡风险
AARC	胆红素、INR、肌酐、乳酸及肝性脑病	APASL定义下ACLF患者	具有肝衰竭起始表型及动态再评估价值，适用于住院早期连续风险分层	对呼吸、循环衰竭表征较弱；跨地区外推性有限	京都共识进一步强化AARC动态评估在治疗反应判断及短期预后分层中的应用价值

), ArticleFig(id=1317885683524555708, tenantId=1146029695717560320, journalId=1316781422847033486, articleId=1317885672820691831, language=EN, label=Table 3, caption=

Comparison of the clinical characteristics of ACLF associated with different etiologies

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项目	ALD-ACLF	HBV-ACLF	HCV-ACLF	AIH-ACLF
常见诱因	持续饮酒或复饮、SAH、细菌感染	HBV再激活、停药、病毒学反弹后免疫暴发	感染、出血或药物打击	免疫暴发、减停免疫抑制后反跳
炎症特点	中性粒细胞主导，高炎症负荷	肝内免疫损伤和肝细胞坏死突出	多与失代偿基础上的继发打击有关	自身免疫攻击介导
器官衰竭	肝外器官衰竭突出	以肝衰竭为主	肝衰竭或多器官功能障碍并见	可迅速进展为重度肝衰竭
治疗重点	戒酒、抗感染、营养支持、AKI/HRS管理	尽早启动抗病毒治疗、肝支持、移植评估	去除诱因、器官支持、活动性HCV评估抗病毒时机	评估糖皮质激素反应，移植评估
预后关键	感染控制、AKI进展、肝外器官衰竭负荷	肝细胞残存功能、胆红素及INR变化	肝功能储备、诱因可逆性、器官衰竭程度	激素反应性、肝衰竭进展程度及移植时机

), ArticleFig(id=1317885683616830397, tenantId=1146029695717560320, journalId=1316781422847033486, articleId=1317885672820691831, language=CN, label=表3, caption=

不同病因相关ACLF的临床特征比较

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项目	ALD-ACLF	HBV-ACLF	HCV-ACLF	AIH-ACLF
常见诱因	持续饮酒或复饮、SAH、细菌感染	HBV再激活、停药、病毒学反弹后免疫暴发	感染、出血或药物打击	免疫暴发、减停免疫抑制后反跳
炎症特点	中性粒细胞主导，高炎症负荷	肝内免疫损伤和肝细胞坏死突出	多与失代偿基础上的继发打击有关	自身免疫攻击介导
器官衰竭	肝外器官衰竭突出	以肝衰竭为主	肝衰竭或多器官功能障碍并见	可迅速进展为重度肝衰竭
治疗重点	戒酒、抗感染、营养支持、AKI/HRS管理	尽早启动抗病毒治疗、肝支持、移植评估	去除诱因、器官支持、活动性HCV评估抗病毒时机	评估糖皮质激素反应，移植评估
预后关键	感染控制、AKI进展、肝外器官衰竭负荷	肝细胞残存功能、胆红素及INR变化	肝功能储备、诱因可逆性、器官衰竭程度	激素反应性、肝衰竭进展程度及移植时机

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