Background Multiple studies have shown that patients with hepatitis C show significant improvement in inflammatory grade and have reversal of fibrosis following hepatitis C therapy, particularly when a sustained virologic response (SVR) is attained. However, data on new direct acting antivirals (DAAs) in fibrosis regression are reported less frequently because of their recent introduction.

Purpose The aims of this study were:(i) to investigate the effect of new DAAs on the evolution of liver fibrosis; and(ii) to examine what conditions can influence this.

Material and methods A retrospective study was undertaken in all hepatitis C virus (HCV) infected patients with SVR treated with the new DAAs from May 2015 to May 2016 with at least one measurement of hepatic fibrosis by FibroScan before and after treatment. Fibrosis stage was defined as mild (Metavir F0–F1) if stiffness ≤7.1 kPa; moderate (F2) if 7.2–9.4 kPa; severe (F3) if 9.5–14 kPa and cirrhosis (F4) if >14 kPa. Data were collected from medical records, which also stored sociodemographic characteristics, HCV genotype, baseline viral load, coinfection with human immunodeficiency virus (HIV), pretreatment, HCV treatment, hepatic fibrosis and transaminases, bilirubin and platelet count before and after treatment.

Results We obtained data from 22 patients (age 51.2±16.8 years, 19 (86.3%) men), genotype 3=2 (9.1%), HCV-HIV coinfected patients=51.9%, stage F3 8 (36%) and stage 4 12 (55%) patients. After treatment, in 14 (63.6%) patients liver fibrosis was partially reversed (median kPa pretreatment 17.1 vs 13.8 post-treatment); 77% of all HCV monoinfected patients and 53.8% of HCV-HIV coinfected but none of genotype 3. There was equal fibrosis regression in patients with mild to moderate fibrosis (F1/F2/F3) compared with those with advanced stage of fibrosis (F4). Moreover, all patients with improved fibrosis regression also had improved bilirubin and transaminase levels. There was no relation between platelet count and fibrosis regression.

Conclusion It is likely that patients included here had a worse fibrosis stage at baseline. However, we can conclude that fibrosis regression in HCV patients can be reversed with the new DAAs, regardless of the stage but dependent on genotype. Moreover, patients with improved fibrosis regression also experience a decrease in transaminases.

No conflict of interest