Abstract / Summary
ABSTRACT Decompensated cirrhosis was traditionally regarded as an irreversible “point of no return.” However, effective etiological therapy has made this progression potentially reversible in a subset of patients. These observations led to the formalization of recompensation within the Baveno VII consensus framework. In this perspective, we propose reframing recompensation as a distinct treatment‐related disease state. Current evidence shows that reported rates of recompensation vary substantially across etiologies, cohort characteristics, and follow‐up design. Although recompensation improves prognosis compared with persistent decompensation, outcomes do not fully normalize to those with compensated cirrhosis. Moreover, we outline a subclassification of recompensation into stable and unstable recompensation, as some patients experience recurrent decompensation after recovery, highlighting the need for continued cirrhosis‐specific surveillance. Durable etiological control is the primary prerequisite for recompensation. Nevertheless, residual hepatic reserve, portal hypertensive burden, baseline decompensation phenotype, and dynamic on‐treatment changes also influence the likelihood of recompensation. Future studies should validate study‐specific expanded criteria, identify earlier non‐invasive markers, and elucidate the structural and hemodynamic mechanisms underlying recompensation.