Definition and validation of recompensation in patients with primary biliary cholangitis-related decompensated cirrhosis treated with ursodeoxycholic acid: Based on the BAVENO VII criteria

Background and Objectives Few studies have provided real-world data on the biochemical response, risk assessment, and prognosis of patients with primary biliary cholangitis (PBC)-related decompensated cirrhosis undergoing ursodeoxycholic acid therapy. The objective of this study is to define recompensation in this patient population based on the BAVENO VII criteria. Methods This retrospective analysis included 170 patients with cirrhosis who presented with ascites, hepatic encephalopathy, and/or variceal bleeding as their initial decompensating events at Xijing Hospital from 2006 to 2023. Events of further decompensation, liver transplantation, and liver-related death were recorded. Results Alkaline phosphatase (ALP) had complex prognostic value in patients with PBC-related decompensated cirrhosis receiving ursodeoxycholic acid therapy. In patients with normal total bilirubin (TBIL) at the 1-year follow-up, elevated ALP was associated with poor prognosis (hazard ratio [HR]: 2.57, 95% confidence interval [CI]: 1.12-5.87, P = 0.025), whereas in those with elevated TBIL, decreased ALP was associated with poor prognosis (HR: 0.53, 95% CI: 0.26-1.08, P = 0.082). A Model for End-Stage Liver Disease score < 10 and the absence of decompensating events from the last decompensated state over the next 12 months were used to assess PBC recompensation. During follow-up, 26% (45/170) of patients experienced at least one episode of recompensation. Compared with observations in the non-recompensation group, the recompensation group exhibited a longer liver transplantation-free survival (HR: 16.48, 95% CI: 2.23-121.57, P = 0.006), lower rates of further decompensation (22% vs . 63%, P < 0.001), a significant reduction in high-risk patients ( P < 0.05, all), and notable improvements in serum indicators (platelet count, TBIL, albumin, and international normalized ratio). Baseline platelet and TBIL levels, the 1-year Rotterdam criteria, and severe interface hepatitis were associated with recompensation. Conclusions We defined PBC recompensation as a Model for End-Stage Liver Disease score < 10 and the absence of decompensating events from the last decompensated state for the next 12 months, aligned with the requirements of BAVENO VII for patients with PBC-related decompensated cirrhosis.