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Article(id=1317885673269473642, tenantId=1146029695717560320, journalId=1316781422847033486, issueId=1317885672153797495, articleNumber=null, orderNo=null, doi=10.12449/JCH260802, 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=1792138029639, onlineDateStr=2026-10-16, pubDate=1787587200000, pubDateStr=2026-08-25, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1792138029639, onlineIssueDateStr=2026-10-16, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1792138029639, creator=13701087609, updateTime=1792138029639, 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=1749, endPage=1754, ext={EN=ArticleExt(id=1317885673458217323, articleId=1317885673269473642, tenantId=1146029695717560320, journalId=1316781422847033486, language=EN, title=Research advances in acute-on-chronic liver failure with infection, columnId=1317885673009435512, journalTitle=Journal of Clinical Hepatology, columnName=Expert Forum, runingTitle=null, highlight=null, articleAbstract=

Infection is not only a common predisposing factor for acute-on-chronic liver failure （ACLF），but also a critical complication of ACLF，and it is closely associated with multiple organ failure and high mortality. This article systematically reviews the recent advances in the epidemiology，clinical and etiological features，pathogenesis，and diagnosis and treatment strategies of ACLF with infection，in order to provide guidance for further optimizing clinical decision-making and exploring novel diagnostic and treatment methods for such patients.

, authors=Jiale Bian, Tao Han, authorsList=Jiale Bian, Tao Han, authorCompany=null, correspAuthors=Tao Han, 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=1317885677614772589, articleId=1317885673269473642, tenantId=1146029695717560320, journalId=1316781422847033486, language=CN, title=慢加急性肝衰竭合并感染的研究进展, columnId=1317885673185596282, journalTitle=临床肝胆病杂志, columnName=专家论坛, runingTitle=null, highlight=null, articleAbstract=

感染既是慢加急性肝衰竭的常见诱因，也是其重要的并发症，与患者多器官功能衰竭及高病死率密切相关。本文围绕慢加急性肝衰竭合并感染的流行病学、临床与病原学特征、发病机制以及诊断和治疗策略的新进展进行系统综述，旨在为进一步优化此类患者的临床决策、探索新型诊治方法提供参考。

, authors=卞佳乐, 韩涛, authorsList=卞佳乐, 韩涛, authorCompany=null, correspAuthors=韩涛, authorNote=

作者贡献声明

卞佳乐负责文献收集，起草撰写论文；韩涛负责设计论文框架，拟定写作思路，指导文章撰写、修改并定稿。

, correspAuthorsNote=
韩涛， （ORCID：0000-0003-4216-6968）
Han Tao， （ORCID：0000-0003-4216-6968）
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Diagnostic indicators and methods for acute-on-chronic liver failure complicated by infection

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类型指标或技术临床应用情况
经典指标
细菌感染C反应蛋白、降钙素原、白细胞计数及中性粒细胞比例等常规应用
血液、腹水、尿液、痰液等病原学培养及药敏试验常规应用
真菌感染G试验、GM试验、隐球菌荚膜多糖抗原、涂片镜检、染色和组织病理检查、分子生物学诊断技术等常规应用
新型标志物可溶性CD14亚型［38］、sTREM-1［38］、sPD-L1［35］、IL-1RA［36］、PGE2［20］、IL-6［39］、BTLA［23］等探索阶段
多指标联合模型IL-1RA联合模型［36］、GIC模型［39］、WBD模型［40］、整合蛋白质组学与临床变量联合模型［34］等探索阶段
其他新型技术mNGS［37］等选择性应用
MALDI-TOF MS选择性应用
多组学整合技术探索阶段
), ArticleFig(id=1317885679632232837, tenantId=1146029695717560320, journalId=1316781422847033486, articleId=1317885673269473642, language=CN, label=表1, caption=

慢加急性肝衰竭合并感染的诊断指标与方法

, figureFileSmall=null, figureFileBig=null, tableContent=
类型指标或技术临床应用情况
经典指标
细菌感染C反应蛋白、降钙素原、白细胞计数及中性粒细胞比例等常规应用
血液、腹水、尿液、痰液等病原学培养及药敏试验常规应用
真菌感染G试验、GM试验、隐球菌荚膜多糖抗原、涂片镜检、染色和组织病理检查、分子生物学诊断技术等常规应用
新型标志物可溶性CD14亚型［38］、sTREM-1［38］、sPD-L1［35］、IL-1RA［36］、PGE2［20］、IL-6［39］、BTLA［23］等探索阶段
多指标联合模型IL-1RA联合模型［36］、GIC模型［39］、WBD模型［40］、整合蛋白质组学与临床变量联合模型［34］等探索阶段
其他新型技术mNGS［37］等选择性应用
MALDI-TOF MS选择性应用
多组学整合技术探索阶段
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慢加急性肝衰竭合并感染的研究进展
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卞佳乐 , 韩涛
临床肝胆病杂志 | 专家论坛 2026,42(8): 1749-1754
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临床肝胆病杂志 |专家论坛 2026 , 42 (8) : 1749 -1754
慢加急性肝衰竭合并感染的研究进展
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卞佳乐, 韩涛
作者信息
  • 南开大学第一附属医院/天津市人民医院消化（肝病）科，天津 300121
通讯作者:
韩涛， （ORCID：0000-0003-4216-6968）
Han Tao， （ORCID：0000-0003-4216-6968）
作者简介:

作者贡献声明

卞佳乐负责文献收集，起草撰写论文；韩涛负责设计论文框架，拟定写作思路，指导文章撰写、修改并定稿。

Research advances in acute-on-chronic liver failure with infection
Jiale Bian, Tao Han
Affiliations
  • Department of Gastroenterology and Hepatology，The First Affiliated Hospital of Nankai University/Tianjin People’s Hospital，Tianjin 300121，China
出版时间: 2026-08-25 doi: 10.12449/JCH260802
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摘要
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感染既是慢加急性肝衰竭的常见诱因，也是其重要的并发症，与患者多器官功能衰竭及高病死率密切相关。本文围绕慢加急性肝衰竭合并感染的流行病学、临床与病原学特征、发病机制以及诊断和治疗策略的新进展进行系统综述，旨在为进一步优化此类患者的临床决策、探索新型诊治方法提供参考。

慢加急性肝功能衰竭  /  感染  /  诊断  /  治疗学

Infection is not only a common predisposing factor for acute-on-chronic liver failure （ACLF），but also a critical complication of ACLF，and it is closely associated with multiple organ failure and high mortality. This article systematically reviews the recent advances in the epidemiology，clinical and etiological features，pathogenesis，and diagnosis and treatment strategies of ACLF with infection，in order to provide guidance for further optimizing clinical decision-making and exploring novel diagnostic and treatment methods for such patients.

Acute-On-Chronic Liver Failure  /  Infections  /  Diagnosis  /  Therapeutics
卞佳乐, 韩涛. 慢加急性肝衰竭合并感染的研究进展. 临床肝胆病杂志, 2026 , 42 (8) : 1749 -1754 . DOI: 10.12449/JCH260802
Jiale Bian, Tao Han. Research advances in acute-on-chronic liver failure with infection[J]. Journal of Clinical Hepatology, 2026 , 42 (8) : 1749 -1754 . DOI: 10.12449/JCH260802
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慢加急性肝衰竭（acute-on-chronic liver failure，ACLF）是发生在慢性肝病基础上的急性肝衰竭，伴或不伴肝外器官功能衰竭，短期病死率较高，是造成慢性肝病患者死亡的主要原因之一［1］。感染既是ACLF的常见诱因，也是ACLF发生、发展过程中重要的并发症；慢性肝病合并感染会加速病情进展，显著增加病死率［2］。因此，重视ACLF患者感染的早期识别与积极防治，对于改善患者预后具有重要临床意义。本文旨在系统梳理近年来ACLF合并感染的研究进展，以期为优化此类患者的临床实践决策与开展科学研究提供参考。
1　ACLF合并感染的流行病学、临床与病原学特征
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1.1　ACLF合并感染的流行病学
一项纳入全球6个地区共1 175例因肝硬化失代偿合并感染住院患者的研究发现，333例患者在感染确诊时已存在ACLF，另有230例患者在发生感染后进展为ACLF，细菌感染相关ACLF的总体发生率为48%［3］。一项多中心前瞻性临床研究也发现，ACLF患者合并感染的比例显著高于入院时无ACLF的患者；且无ACLF的患者在病情进展为ACLF的过程中，细菌感染比例明显升高［4］。Wang等［5］纳入1 124例乙型肝炎病毒（hepatitis B virus，HBV）相关ACLF患者的分析显示，细菌感染发生率为58.48%。除细菌感染外，病毒、真菌感染亦不容忽视。Thiyagarajah等［6］研究发现，ACLF患者中人巨细胞病毒和EB病毒的检出率均高于非ACLF患者。在急性失代偿肝硬化患者中，人巨细胞病毒再激活发生率为4.8%，并与进展为ACLF相关［7］。Liu等［8］研究纳入835例ACLF患者，其中侵袭性肺曲霉病的临床诊断率为6.6%。
1.2　ACLF合并感染的临床与病原学特征
Wong等［3］研究发现，自发性细菌性腹膜炎是ACLF患者细菌感染最为常见的临床表现，其次是尿路感染、肺炎和皮肤软组织感染；但临床感染的类型在不同地区和年代可能存在一定差异。尽管目前革兰氏阴性菌仍是主要病原体，但革兰氏阳性菌与多重耐药菌占比呈现逐渐上升趋势。最常见的革兰氏阴性杆菌是大肠埃希菌和肺炎克雷伯菌；最常见的革兰氏阳性球菌是粪肠球菌、屎肠球菌和金黄色葡萄球菌。值得注意的是，相当比例的患者病原体培养结果为阴性［9］。
除细菌感染外，真菌和病毒感染也是ACLF重要的致病因素。Liu等［8］对835例ACLF患者的回顾性分析表明，侵袭性肺曲霉病的发生与ACLF的高病死率密切相关，尤其是在ACLF确诊后14 d内出现侵袭性肺曲霉病的患者，其短期死亡风险极高。ACLF合并真菌感染时，最常见的致病真菌为念珠菌属和曲霉属，同时，隐球菌、肺孢子菌等感染亦呈增加趋势；肺是最常见的感染部位［10-11］。Hong等［7］研究显示，人巨细胞病毒再激活者更易进展为ACLF，且90 d病死率更高。Yao等［12］研究发现，感染新型冠状病毒的ACLF患者，血小板减少更为显著，炎症反应更为强烈，入院1周内病情进展更快。
1.3　ACLF合并耐药菌感染
耐药菌感染已成为全球肝硬化患者面临的严峻挑战，其与ACLF的发生及不良预后密切相关［13］。常见的多重耐药菌以产超广谱β-内酰胺酶及产Amp C酶的大肠埃希菌为主，其次为耐甲氧西林金黄色葡萄球菌，耐万古霉素肠球菌、耐碳青霉烯铜绿假单胞菌和鲍曼不动杆菌也较为常见［14］。Hernández-Tejero等［15］通过一项纳入408例肝硬化失代偿患者的前瞻性研究发现，多重耐药菌定植普遍存在，发生同源菌株感染的风险显著增加，近期发生ACLF的患者预后更差。耐药菌感染不仅增加了经验性抗感染治疗的难度，且感染控制率较低，更易发生严重脓毒症或脓毒性休克，28 d病死率更高［2］。
1.4　不同类型ACLF合并感染的差异
目前全球范围内尚缺乏统一的ACLF定义和诊断标准，这不仅与不同定义和诊断标准源自的研究队列特点存在差异有关，而且体现了ACLF复杂的病理生理学机制与临床异质性。HBV感染是亚太地区最常见的基础肝病病因之一，尽管近年来酒精相关性肝病的占比持续上升，亚太肝病学会对ACLF的定义更关注非肝硬化及代偿期肝硬化基础上发生的急性肝衰竭，并将感染归为ACLF的并发症［16］。而欧美地区ACLF定义对应的研究队列中酒精性肝病占比最高，将代偿期和失代偿期肝硬化均纳入基础慢性肝病范畴，更关注肝外器官衰竭的发生，感染被认为是ACLF的重要诱因或并发症［13］。Zhang等［17］利用多中心临床队列，依据世界胃肠病学组织ACLF A/B/C分型，阐明HBV与酒精相关ACLF临床表型的异同。在HBV相关ACLF队列中，A型占18.51%，B型占33.54%，C型占47.95%；相比之下，在酒精相关ACLF队列中，A型仅占6.75%，B型占23.99%，C型占69.26%，C型所占比例显著高于其他类型。与HBV相关ACLF相比，酒精相关ACLF更易合并细菌感染，肝外器官衰竭更为常见。细菌感染从A型至C型逐渐增多，C型较A、B型更常由细菌感染诱发，且该趋势在酒精相关ACLF中更为突出。上述研究表明，不同病因、不同慢性肝病基础上发生的ACLF，其临床特征不尽相同。因此，对ACLF进行合理分型具有重要临床意义。我国ACLF诊治指南将ACLF分为Ⅰ型与Ⅱ型，有利于制定包括感染防治在内的精准分层管理策略［1］。
2　ACLF合并感染的发病机制
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ACLF合并感染的发病机制极为复杂，除致病因素、肝脏储备功能及门静脉高压外，目前研究主要聚焦于宿主免疫功能障碍、系统性炎症反应、肠-肝轴功能障碍及胆汁酸代谢异常等方面。
2.1　免疫系统功能障碍与免疫麻痹
ACLF状态下强烈的系统性炎症反应可导致机体免疫系统功能障碍及免疫麻痹，宿主免疫系统功能障碍与感染发生、器官功能障碍及患者预后密切相关［18］。在先天免疫方面，中性粒细胞和单核细胞等可出现明显的免疫抑制性改变。例如，Liang等［19］研究发现，ACLF进展过程中CXC亚族趋化因子受体2阳性的中性粒细胞具有免疫抑制作用，可诱导细胞毒性T细胞耗竭。Maini等［20］研究发现，失代偿期肝硬化患者存在以单核细胞功能障碍为特征的免疫功能障碍，前列腺素E2作为关键介质，可通过EP4受体抑制单核细胞功能。在肝硬化急性失代偿患者中，免疫抑制性CD52低表达的单核细胞占据优势，且与感染发生和较低的无移植生存率相关［21］。除先天免疫受损外，ACLF患者还存在显著的适应性免疫功能障碍。Yu等［22］研究发现，ACLF患者的淋巴细胞呈现明显功能障碍，自然杀伤细胞数量减少、T细胞毒性/促炎细胞因子分泌能力减弱。此外，研究还发现，HBV相关ACLF患者存在以CD4⁺ T细胞耗竭为特征的适应性免疫障碍，B细胞和T细胞衰减因子（B- and T-lymphocyte attenuator，BTLA）水平显著升高，且与疾病严重程度、感染并发症和不良预后呈正相关。BTLA可抑制CD4⁺ T细胞活化与增殖，并促进细胞凋亡，从而导致CD4⁺ T细胞耗竭；动物实验表明，给予中和性抗BTLA抗体可降低肺炎克雷伯菌负荷和ACLF小鼠死亡率［23］。
2.2　系统性炎症反应
ACLF患者由于肝功能严重受损、门静脉高压、肝脏结构重塑及肝内网状内皮系统清除功能下降，同时叠加肠屏障受损、菌群失衡等因素，使机体长期暴露于病原相关分子模式和损伤相关分子模式刺激之下，从而导致系统性炎症反应［24-25］。Cao等［26］研究显示，肝硬化急性失代偿患者的炎症细胞因子水平变化、中性粒细胞增多以及淋巴细胞减少，均与进展为ACLF的风险增加相关。ACLF肝组织内中性粒细胞，尤其是CC亚族趋化因子配体4⁺亚群显著富集，可募集更多中性粒细胞及炎症性单核细胞，从而进一步驱动炎症进展［22］。
2.3　肠-肝轴功能障碍
肠道微生态失衡可导致肠道菌群多样性下降、条件致病菌增多，并伴随肠屏障功能受损与通透性升高，使细菌、真菌等病原体及其代谢产物易从肠腔易位至肠系膜淋巴结、门静脉系统、腹水或体循环，从而导致感染［27］。近年来，口-肠-肝轴在肝病发病中的作用日益受到关注。口腔菌群向肠道的异常易位，可能是ACLF患者肠道菌群持续失衡的重要原因之一。Lee等［28］通过对患者的唾液和粪便配对样本进行宏基因组测序，发现失代偿期肝硬化和ACLF患者的口腔与肠道菌群重叠程度增加，肠道致病菌群富集更加明显，毒力因子和抗生素耐药基因的检出频率也显著升高。Jin等［29］进一步揭示了进展期慢性肝病患者口腔和肠道菌群易位的潜在致病机制，发现进展期慢性肝病患者肠道中口腔来源菌株，尤其是韦荣球菌和链球菌的丰度显著升高，并与疾病严重程度及肠屏障损伤相关；口腔和肠道易位菌共同携带编码胶原酶样蛋白的prtC基因；携带prtC基因的韦荣球菌和链球菌可加重肠屏障破坏和肝纤维化。Bajaj等［30］纳入8 359例代偿期肝硬化患者，发现规律性的牙科预防及牙周护理与2年内新发腹水、肝性脑病、肝细胞癌、全因住院及肝病相关住院风险的降低相关，该保护作用可能与改善口-肠-肝轴相关炎症、免疫和微生态异常有关。
2.4　胆汁酸代谢异常
胆汁酸除参与脂质消化吸收外，在维持肠道菌群稳态、抑制细菌过度生长及维持肠黏膜屏障完整性方面也发挥重要作用。ACLF患者存在肠道菌群失衡和血清胆汁酸谱异常；伴有亚大块肝坏死的ACLF患者粪便胆汁酸组成发生显著改变，提示胆汁酸和肠道菌群紊乱共同参与ACLF的疾病进展［31］。另有研究发现，微生物来源代谢物尤其是次级胆汁酸，与ACLF的发生及短期死亡风险升高相关［32］。
3　ACLF合并感染的诊断及评估指标
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ACLF合并感染的诊断需要对危险因素、临床表现、实验室检查、影像学检查及病原学检查结果进行全面评估［33］。除经典的诊断指标外，近年来新型生物标志物与检测技术不断涌现。例如，Xiong等［34］通过前瞻性多中心研究构建并验证了整合蛋白质组学与临床变量的HBV相关ACLF继发性感染预测模型，该模型包含溶菌酶、钙调蛋白1、丝氨酸蛋白酶抑制剂家族D成员1、皮肤桥蛋白、总胆红素、天冬氨酸氨基转移酶等指标，不仅对ACLF继发感染具有较高的预测效能，且对28 d死亡的预测效能也优于传统模型，有助于ACLF感染高危人群的早期识别。Juanola等［35］通过检测995例慢性肝病患者的血浆可溶性程序性死亡受体配体1水平，发现其与细菌感染发生风险及病死率增加相关。Konstantis等［36］通过分析肝硬化急性失代偿及ACLF患者的炎症反应特征，发现白细胞介素1受体拮抗剂可作为细菌感染的重要生物标志物。其所构建的包含白细胞介素1受体拮抗剂及相关临床参数的模型，有助于提高细菌感染的识别效能。上述新型感染风险预测或辅助识别指标多处于研究阶段，其临床价值尚需进一步验证。
新型检测技术的应用与探索日益增多，其中宏基因组二代测序已经进入临床应用阶段，目前多用于疑难、重症、混合或疑似特殊病原体感染患者的病原学诊断。Liu等［37］纳入275例疑似或确诊感染的ACLF患者，发现宏基因组二代测序的总体病原体阳性率显著高于传统检测方法，病原学确诊时间明显提前，尤其在病毒和真菌检测方面具有显著优势。ACLF合并感染相关的经典诊断指标、新型生物标志物、联合预测模型及新型检测技术总结见表1。
4　ACLF合并感染的治疗策略
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ACLF合并感染的治疗涉及多个方面，需通过积极治疗原发病、早期识别与及时控制感染、加强营养支持等综合治疗措施，降低感染相关并发症及器官衰竭风险，从而改善患者预后。
4.1　病因治疗
病因及诱因的治疗是改善ACLF患者预后的关键举措［1］。鉴于HBV感染仍是目前我国ACLF的常见病因，对于HBV感染者，无论HBV DNA检测结果是否为阳性，均建议立即启动强效低耐药的核苷（酸）类似物抗病毒治疗［41］。对于已接受抗病毒治疗的慢性HBV感染者，擅自停药导致的病毒反弹可能诱发ACLF，且预后较差［42］。
4.2　抗感染类药物的应用
对于肝硬化及ACLF合并严重细菌感染的患者，及时给予适当充分的经验性抗感染治疗至关重要。对于炎症程度高、血白蛋白水平低及肝功能严重受损的患者，及时应用广谱抗菌药物等综合治疗有助于改善预后［43］。延迟使用抗菌药物会显著增加患者死亡风险，当患者合并感染尤其是可能存在脓毒症或脓毒性休克时，应尽早启动抗菌药物治疗［44］。Maiwall等［43］研究发现，在因肝硬化合并细菌或真菌感染住院的1 302例患者中，仅61%的患者获得临床应答；对经验性抗菌治疗无临床应答的独立预测因素包括C反应蛋白、血白细胞计数、血白蛋白水平、医院获得性感染、肺炎以及药敏试验显示治疗无效。因此，ACLF的抗感染治疗应采取综合举措，一旦获得病原学及药敏结果，应尽早调整为目标性治疗。关于额外使用利福昔明是否与广谱抗生素具有协同效应，目前尚不明确。Kulkarni等［45］通过一项随机双盲对照临床研究发现，ACLF伴显性肝性脑病的患者入住重症监护室并接受广谱抗菌药物治疗，追加利福昔明并未带来额外获益。
Verma等［46］研究显示，对于ACLF合并或疑似侵袭性真菌感染的高危患者，采用阿尼芬净等经验性抗真菌治疗可提高28 d生存率。对于发生人巨细胞病毒再激活的患者，给予更昔洛韦治疗有助于改善其90 d无移植存活率［7］。
4.3　合并脓毒症的管理
近期，美国重症医学会与欧洲重症医学会联合发布了《拯救脓毒症运动：脓毒症与感染性休克国际指南（2026年版）》［47］，为脓毒症和感染性休克的管理提供了较为全面的推荐意见和建议，该指南仍然强调“1 h内尽早启动抗菌药物治疗，6 h内控制感染源，3 h内完成30 mL/kg晶体液复苏和收入重症监护室救治”等核心观点，同时指出，需根据患者个体情况和当地医疗条件实施具体措施。此版指南对ACLF合并感染，尤其是合并脓毒症和感染性休克的临床诊治具有重要的参考与指导价值。
4.4　新兴辅助治疗策略
近年来，靶向肠-肝轴及微生态调节已成为ACLF防治领域的重要研究方向之一。Li等［48］发现，伴有细菌感染的肝硬化失代偿患者以及ACLF小鼠的粪便潘糖水平低于未感染的对照组。潘糖通过抑制氧化应激反应，减轻肠道屏障损伤；通过与溶质载体家族7成员11蛋白的相互作用，提高肠上皮细胞谷胱甘肽水平，提示潘糖具有预防细菌感染的潜力。此外，粪菌移植等微生态调节也处于探索阶段。
针对系统性炎症反应与免疫代谢功能障碍等潜在干预靶点的研究，正日益受到学界重视。白蛋白具有包括免疫调节在内的多种生物学效能，尽管其在除自发性细菌性腹膜炎防治之外的感染治疗中获益仍存在争议，但白蛋白在ACLF防治中的作用受到越来越多关注。Trebicka等［49］提出，靶向Toll样受体、MER酪氨酸激酶等可减轻系统性炎症反应、改善宿主免疫功能。蛋氨酸亚砜酰亚胺作为谷氨酰胺合成酶抑制剂，有助于恢复ACLF患者单核细胞的杀菌能力［50］。白细胞介素22Fc可促进肝再生，提高感染诱发的ACLF小鼠模型的生存率［51］。
此外，脓毒症领域的研究为ACLF合并感染治疗新方法的探索提供了值得借鉴的新思路。Xiang等［52］制备的复合纳米药物通过改善肝巨噬细胞功能，增强其对细菌的捕获与杀灭能力，从而改善脓毒症小鼠的预后。Ma等［53］构建的肝巨噬细胞膜仿生纳米颗粒可减少炎症因子释放，减轻脓毒症相关肝损伤。Chaudhary等［54］构建了由间充质基质细胞与载二甲双胍微球组成的生物工程杂化球状体，实验表明其具有抗炎、抗氧化、免疫调节及促进再生的作用，可显著改善脓毒症相关的肝、肾、肺等器官功能障碍。
5　小结与展望
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感染是贯穿ACLF疾病发生、进展和转归全过程的关键事件，需要引起高度关注。早期识别与控制、密切监测、动态评估以及多学科协作下的综合干预，是改善ACLF合并感染者预后的关键。尽管目前ACLF合并感染的诊治已取得一定进展，但仍存在诸多尚未解决的问题。未来仍需进一步加强临床与基础研究，深入探讨肝硬化及ACLF相关感染的发病机制，探索新的诊治靶点；基于临床队列、多组学技术与人工智能手段，建立涵盖感染风险早期预警、快速诊断、精准分层和个体化临床决策的防治体系；同时，研发适用于重症肝病的新型抗感染及免疫调节药物，积极应对多重耐药菌感染带来的挑战，从而进一步降低ACLF合并感染患者的病死率。

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2026年第42卷第8期
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doi: 10.12449/JCH260802
  • 接收时间：2026-05-06
  • 首发时间：2026-10-16
  • 出版时间：2026-08-25
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  • 收稿日期：2026-05-06
  • 录用日期：2026-07-24
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    南开大学第一附属医院/天津市人民医院消化（肝病）科，天津 300121

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韩涛， （ORCID：0000-0003-4216-6968）
Han Tao， （ORCID：0000-0003-4216-6968）
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Number of
species		 占总种数比例
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total species (%)		 属
Genus		 种数
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鹅膏菌科Amanitaceae 2 11 5.26 鹅膏菌属 Amanita 10 4.78
小菇科 Mycenaceae 2 12 5.74 丝盖伞属 Inocybe 5 2.39
多孔菌科 Polyporaceae 8 14 6.70 蜡蘑属 Laccaria 5 2.39
红菇科 Russulaceae 3 23 11.00 小皮伞属 Marasmius 6 2.87
小菇属 Mycena 11 5.26
光柄菇属 Pluteus 5 2.39
红菇属 Russula 17 8.13
栓菌属 Trametes 5 2.39
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