Recompensation and Further Decompensation After Index Decompensation in Patients with Autoimmune Hepatitis: A...

There are limited data on hepatic recompensation in autoimmune hepatitis (AIH)-related decompensated cirrhosis. We evaluated incidence and predictors of recompensation and further decompensation, and assessed the impact of recompensation on survival.

In this retrospective analysis of a prospectively maintained database, we included patients with AIH-related decompensated cirrhosis, confirmed by liver biopsy, who were treated with immunosuppression. Recompensation, defined by Baveno VII criteria (including etiological suppression), was analyzed using Fine and Gray competing-risk model with death as competing events. Secondary outcomes were all-cause mortality and further decompensation.

Among 112 patients (71% women; mean age 41 ± 13 years), 75% had ascites, 26% had variceal bleeding, and 13% had hepatic encephalopathy; median MELD-Na and CTP scores were 15.7 and 7, respectively. Prednisolone, azathioprine, and mycophenolate mofetil were used in 89%, 62% and 21% of patients, respectively. Over a median follow-up of 29 months, 60 (54%) patients achieved recompensation. Younger age, lower CTP score, and biochemical response at 6 months independently predicted recompensation, with biochemical response being the strongest predictor (sHR 1.75, 95% CI 1.02-2.88). After recompensation, 9 (15%) patients developed further decompensation (1- and 2-year incidence of 3.4% and 8.5%), whereas among 52 non-recompensated patients, 36 (69%) developed further decompensation and 16 (31%) remained in a stable decompensated state. Recompensation was associated with reduced mortality (HR 0.22, 95% CI 0.05-0.90) compared with non-recompensated patients.

Over half of treated AIH-related decompensated cirrhosis can achieve recompensation with immunosuppression, which is associated with reduced mortality. Younger age, lower CTP score, and biochemical response predict recompensation.