학술논문

Influence of further decompensation on survival across clinical stages of decompensated cirrhosis: The role of portal hypertension and HVPG changes.
Document Type
Article
Source
Liver International. Apr2024, p1. 19p. 3 Illustrations, 5 Charts.
Subject
Language
ISSN
1478-3223
Abstract
Background and Aims Methods Results Conclusions Decompensated‐cirrhosis encompasses several stages with different prognosis, such as bleeding, ascites and bleeding‐plus‐ascites. Development of further‐decompensation worsens survival, while non‐selective β‐blockers (NSBBs) can modify the risk. However, how this applies to each stage is uncertain. We aimed to investigate, in each stage of decompensated‐cirrhosis, the influence of further‐decompensation on mortality and whether changes in portal‐pressure (HVPG) under NSBBs influence these outcomes.Patients with variceal bleeding were consecutively included differentiating those with bleeding‐alone from those who also had ascites. Patients with ascites and high‐risk varices referred for primary‐prophylaxis were also investigated. A baseline haemodynamic study was performed and was repeated after 1‐3‐months under NSBBs. Outcomes were investigated by competing‐risk.Totally 103 patients had bleeding‐alone, 186 bleeding‐plus‐ascites and 187 ascites‐alone. Mean follow‐up was 32‐months (IQR, 12–60). Patients with bleeding‐plus‐ascites had higher HVPG and were more hyperdynamic than patients with ascites‐alone and these than those with bleeding‐alone. At each stage, the mortality risk was more than twice in patients developing further‐decompensation vs. those without (p < .001). In each stage, HVPG‐decrease under NSBBs showed better discrimination to predict further‐decompensation than the baseline MELD, Child–Pugh or HVPG, by time‐dependent ROC‐curves (c‐statistic >70%). At each stage, patients without HVPG‐decreases, either ≥10% or ≥20% from the baseline, had higher risk of further‐decompensation (sHR from 2.43 to 6.73, p < .01) and worse survival.In each stage of decompensated cirrhosis, mortality risk significantly and very markedly increase with further‐decompensation. HVPG‐non‐response to NSBBs may adequately stratify the risk of further decompensation and death, in each stage. This suggests potential benefit with pre‐emptive therapies in HVPG‐non‐responders at each‐stage. [ABSTRACT FROM AUTHOR]