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预防肝硬化进展至失代偿期和死亡。

Preventing the progression of cirrhosis to decompensation and death.

作者信息

Villanueva Càndid, Tripathi Dhiraj, Bosch Jaume

机构信息

Department of Gastroenterology, Hospital de la Santa Creu i Sant Pau, Biomedical Research Institute Sant Pau (IIB Sant Pau), Barcelona, Spain.

Department of Medicine, Universitat Autònoma de Barcelona, Bellaterra, Spain.

出版信息

Nat Rev Gastroenterol Hepatol. 2025 Apr;22(4):265-280. doi: 10.1038/s41575-024-01031-x. Epub 2025 Jan 27.

DOI:10.1038/s41575-024-01031-x
PMID:39870944
Abstract

Two main stages are differentiated in patients with advanced chronic liver disease (ACLD), one compensated (cACLD) with an excellent prognosis, and the other decompensated (dACLD), defined by the appearance of complications (ascites, variceal bleeding and hepatic encephalopathy) and associated with high mortality. Preventing the progression to dACLD might dramatically improve prognosis and reduce the burden of care associated with ACLD. Portal hypertension is a major driver of the transition from cACLD to dACLD, and a portal pressure of ≥10 mmHg defines clinically significant portal hypertension (CSPH) as the threshold from which decompensating events may occur. In recent years, innovative studies have provided evidence supporting new strategies to prevent decompensation in cACLD. These studies have yielded major advances, including the development of noninvasive tests (NITs) to identify patients with CSPH with reasonable confidence, the demonstration that aetiological therapies can prevent disease progression and even achieve regression of cirrhosis, and the finding that non-selective β-blockers can effectively prevent decompensation in patients with cACLD and CSPH, mainly by reducing the risk of ascites, the most frequent decompensating event. Here, we review the evidence supporting new strategies to manage cACLD to prevent decompensation and the caveats for their implementation, from patient selection using NITs to ancillary therapies.

摘要

晚期慢性肝病(ACLD)患者可分为两个主要阶段,一个是代偿期(cACLD),预后良好,另一个是失代偿期(dACLD),其定义为出现并发症(腹水、静脉曲张出血和肝性脑病),且死亡率高。预防进展至dACLD可能会显著改善预后并减轻与ACLD相关的护理负担。门静脉高压是从cACLD转变为dACLD的主要驱动因素,门静脉压力≥10 mmHg定义为临床显著性门静脉高压(CSPH),这是可能发生失代偿事件的阈值。近年来,创新性研究提供了证据支持预防cACLD失代偿的新策略。这些研究取得了重大进展,包括开发出非侵入性检测(NITs)以合理可靠地识别CSPH患者,证明病因治疗可预防疾病进展甚至实现肝硬化逆转,以及发现非选择性β受体阻滞剂可有效预防cACLD和CSPH患者失代偿,主要是通过降低腹水这一最常见失代偿事件的风险。在此,我们综述支持管理cACLD以预防失代偿的新策略的证据及其实施时的注意事项,从使用NITs进行患者选择到辅助治疗。

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JHEP Rep. 2024 Oct 10;6(12):101233. doi: 10.1016/j.jhepr.2024.101233. eCollection 2024 Dec.
2
Metabolic phenotyping of patients with advanced chronic liver disease for better characterization of cirrhosis regression.对晚期慢性肝病患者进行代谢表型分析,以更好地描述肝硬化逆转。
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Tirzepatide for Metabolic Dysfunction-Associated Steatohepatitis with Liver Fibrosis.
替尔泊肽治疗代谢相关脂肪性肝炎伴肝纤维化
N Engl J Med. 2024 Jul 25;391(4):299-310. doi: 10.1056/NEJMoa2401943. Epub 2024 Jun 8.
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A Phase 2 Randomized Trial of Survodutide in MASH and Fibrosis.MASH 和纤维化中苏沃杜肽的 2 期随机试验。
N Engl J Med. 2024 Jul 25;391(4):311-319. doi: 10.1056/NEJMoa2401755. Epub 2024 Jun 7.
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Enhanced liver fibrosis (ELF) score predicts hepatic decompensation and mortality.增强型肝纤维化(ELF)评分可预测肝失代偿和死亡率。
JHEP Rep. 2024 Mar 11;6(6):101062. doi: 10.1016/j.jhepr.2024.101062. eCollection 2024 Jun.
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Pathophysiology and therapeutic options for cirrhotic portal hypertension.肝硬化门静脉高压症的病理生理学和治疗选择。
Lancet Gastroenterol Hepatol. 2024 Jul;9(7):646-663. doi: 10.1016/S2468-1253(23)00438-7. Epub 2024 Apr 17.
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