The progression of cirrhosis with clinically significant portal hypertension towards decompensated cirrhosis remains clinically challenging and the evolution towards acute-on-chronic liver failure (ACLF), with one or more extrahepatic organ failures, is associated with very high mortality. In the last decade, significant progress has been made in the understanding of the mechanisms leading to decompensation and ACLF. As portal hypertension advances, bacterial translocation across an impaired gut barrier culminates in endotoxaemia, systemic inflammation and cirrhosis-associated immune dysfunction (CAID). Gut-derived systemic inflammation and CAID have become the logical targets for innovative therapies that prevent hepatic decompensation episodes and the progression to ACLF. Furthermore, classification of disease and biomarker discovery to personalise care have advanced in the field. This review discusses progress in biomarker discovery and personalisation of treatment in decompensated cirrhosis and ACLF.

中文翻译：

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失代偿性肝硬化和慢加急性肝衰竭（ACLF）预防和治疗的最新进展以及生物标志物的作用

具有临床意义的门静脉高压的肝硬化向失代偿性肝硬化的进展在临床上仍然具有挑战性，并且向慢加急性肝衰竭（ACLF）的演变（伴有一种或多种肝外器官衰竭）与非常高的死亡率相关。在过去的十年中，对导致失代偿和 ACLF 的机制的理解取得了重大进展。随着门脉高压的进展，细菌穿过受损的肠道屏障易位，最终导致内毒素血症、全身炎症和肝硬化相关的免疫功能障碍（CAID）。肠源性全身炎症和 CAID 已成为预防肝功能失代偿发作和 ACLF 进展的创新疗法的逻辑目标。此外，疾病分类和个性化护理的生物标志物发现在该领域取得了进展。本综述讨论了失代偿性肝硬化和 ACLF 生物标志物发现和个性化治疗的进展。