Ramírez-Quesada Wagner, Alvarado-Tapias Edilmar, Shalaby Sarah, Hernández-Gea Virginia
Barcelona Hepatic Hemodynamic Laboratory, Liver Unit, Hospital Clínic, Institut de Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain.
Departament de Medicina i Ciències de la Salut, Fundació de Recerca Clínic Barcelona (FRCB-IDIBAPS), Health Care Provider of the European Reference Network on Rare Liver Disorders (ERN-RareLiver), Universitat de Barcelona, Barcelona, Spain.
Semin Liver Dis. 2025 Mar;45(1):129-143. doi: 10.1055/a-2542-9930. Epub 2025 Apr 3.
The onset of decompensation in advanced chronic liver disease (ACLD) is a hallmark in natural history, with a poor prognosis and a significantly increased liver-related mortality. Etiological treatments for viral hepatitis or abstinence in cirrhosis due to alcohol abuse have demonstrated that some patients experience partial to complete clinical and analytical improvement, a stage termed "recompensation." Although recompensation is primarily defined clinically based on treatable etiologies, it is still evolving for conditions like metabolic dysfunction-associated steatotic liver disease (MASLD). Despite the need for specific biomarkers in hepatic recompensation, no biomarkers have been thoroughly studied in this context. Biomarkers identified in compensated ACLD (cACLD) following etiological treatment might be explored for recompensation. Although the pathophysiology mechanisms underlying the hepatic recompensation remain unclear, understanding the mechanism involved in cirrhosis decompensation could help identify potential targets for recompensation. This review provides an update on the hepatic recompensation concept, examines the existing data on invasive and non-invasive biomarkers, mainly in cACLD after cure, that could be raised in recompensation, and explores future therapeutic targets for the hepatic recompensation process.
晚期慢性肝病（ACLD）失代偿的发生是自然病程中的一个标志，预后较差，肝脏相关死亡率显著增加。针对病毒性肝炎的病因治疗或酒精性肝硬化患者的戒酒已表明，一些患者会出现部分至完全的临床和分析改善，这一阶段称为“再代偿”。尽管再代偿主要基于可治疗的病因进行临床定义，但对于代谢功能障碍相关脂肪性肝病（MASLD）等疾病，其定义仍在不断发展。尽管肝脏再代偿需要特定的生物标志物，但目前尚未在此背景下对生物标志物进行深入研究。在病因治疗后的代偿期ACLD（cACLD）中确定的生物标志物可能有助于探索再代偿情况。尽管肝脏再代偿的病理生理机制尚不清楚，但了解肝硬化失代偿所涉及的机制有助于确定再代偿的潜在靶点。本综述提供了肝脏再代偿概念的最新进展，研究了主要在治愈后的cACLD中有关有创和无创生物标志物的现有数据，这些生物标志物可能与再代偿有关，并探讨了肝脏再代偿过程未来的治疗靶点。
