Clinical outcomes after hepatitis C treatment in patients with advanced chronic liver disease


Fabio Pereira Correia, Gonçalo Alexandrino, Mariana Cardoso, Joana Branco, Mariana Costa, Rita Carvalho, Alexandra Martins

Hépatologie – 23/04/2023 – Communication orale

Background and Aims: Patients with advanced chronic liver disease (ACLD) and chronic hepatitis C are at high risk of developing clinically significant portal hypertension (CSPH) and its complications. Direct-acting antivirals have radically changed the outcomes of hepatitis C treatment. However, data on the impact of cured hepatitis C on the medium-term clinical evolution of patients with ACLD has only recently emerged. We aimed to evaluate the outcomes related to hepatic decompensation, hepatocellular carcinoma (HCC) and mortality in a cohort of patients with ACLD and cured hepatitis C with sustained virological response (SVR).

Method: Prospective, single-centre study, in patients with ACLD and chronic hepatitis C with SVR, treated since February 2015 and with a minimum follow-up (FU) of 2 years. The definition of ACLD was based on liver biopsy or Baveno VII’s concepts: liver stiffness measurement (LSM) > 10 kPa and/or clinical/imaging elements of CSPH. During FU, hepatic decompensation (ascites, variceal bleeding, and hepatic encephalopathy) unrelated to HCC, development of HCC and mortality were recorded. In decompensated ACLD, the recompensation rate was also evaluated.

Results: We included 147 patients (78.2% male, mean age of 59 years-old). At baseline, 84% (123/147) had compensated ACLD (cACLD), 16% (24/147) had decompensated ACLD (dACLD) and none had suspicious liver nodules. Among patients with cACLD with baseline LSM evaluation (97/123), 65% (63/97) had a LSM > 15 kPa. The median follow-up was 52 months. During follow-up, 13% (16/123) of cACLD patients developed complications: first decompensation in 5% (6/123) and HCC in 8% (10/123). All these 16 patients had LSM > 15 kPa or clinical/imaging elements of CSPH, and the majority (14/16) had platelet count < 150 x 109. The mortality rate was 3% (4/123). In dACLD patients, we observed
clinical recompensation in 21% (5/24), HCC in 17% (4/24), with a global mortality irate of 8% (2/24).

Conclusion: In this cohort of patients with ACLD and cured hepatitis C, the medium-term clinical evolution was globally favorable, with emphasis on clinical recompensation in about 25% of dACLD patients. However, HCC remains a major concern, especially in decompensated ACLD, but also in compensated patients. Adverse events occurred only in patients with pre-treatment LSM > 15 kPa, the majority with platelets count < 150 x 109). These cut-offs, with an established role in ACLD stratification, could perhaps redefine follow-up surveillance in compensated patients. The impact of other cofactors, such as alcohol and obesity, in the development of complications, needs to be further evaluated.