Factors associated with recompensation and criteria for etiological suppression in patients with primary biliary cholangitis.

BACKGROUND AND AIMS: The potential for recompensation and its defining criteria in patients with decompensated cirrhosis due to primary biliary cholangitis (PBC) remain poorly defined. Therefore, our study aimed to explore the criteria for etiological suppression and provide preliminary insights into PBC recompensation.

METHODS

In this retrospective-prospective study, we enrolled hospitalized patients with PBC cirrhosis from January 2014 to June 2023. Recompensation was defined according to the Baveno VII criteria. In addition, expanded recompensation criteria were evaluated for patients on low-dose diuretics and/or lactulose/rifaximin with resolution of decompensation and stable improvement of liver function. We explored whether the biochemical responses to UDCA could serve as surrogates for etiological suppression.

RESULTS

We enrolled 240 patients with PBC cirrhosis (122 compensated and 118 decompensated). With a median follow-up of 50.0 (31.0, 72.0) months, 18 (15.3%) out of 118 decompensated patients achieved recompensation and 31 (26.3%) achieved the expanded recompensation. Both recompensated and expanded recompensated patients showed similar long-term outcomes to compensated patients (recompensation: hazard ratio [HR]: 0.70, p = 0.735; expanded recompensation: HR: 0.83, p = 0.814). Patients with variceal hemorrhage as index decompensation had higher potential of recompensation. Fulfillment of the Paris II and Momah/Lindor criteria was linked to better further decompensation-free survival and long-term stabilization of liver function reserve.

CONCLUSION

Regression to a recompensated stage is possible in PBC patients with decompensated cirrhosis, especially when portal hypertension is the main driver of index decompensation. The Paris II and Momah/Lindor criteria are potentially useful as surrogate indicators for etiological suppression.