Liver fibrosis is an important prognostic factor in patients with hepatitis C virus (HCV) infection and most related complications arise in patients who subsequently develop advanced fibrosis and cirrhosis [1], [2]. Nearly 20 % of chronic HCV-infected patients develop liver cirrhosis within 20 to 30 years [3].

The primary endpoint of HCV treatment is viral eradication, which can prevent fibrosis progression and the development of liver- and non-liver-related complications [4], [5], [6]. Several studies have shown that achieving a sustained virological response is linked to regression in liver fibrosis and subsequent reduced risk of complications [7], [8], [9], [10]. In contrast, patients with ongoing infections are at increased risk for progression of liver fibrosis as results of persistent hepatic inflammation [11].

Long-term fibrosis progression has been studied in several cohorts. Women in Ireland who were infected with HCV through anti-D immunoglobulin injections were studied 17 years later, and the rate of fibrosis development and progression since the initial infection was determined [12]. The Trent hepatitis C study group evaluated repeat liver biopsies in a small number of patients with HCV infection in the Trent region of the UK, [13], [14]. A longitudinal study that evaluated data from the Veterans Administration (VA) database used fibrosis-4 (FIB-4) scores to study fibrosis progression over ten years [15]. Short-term fibrosis progression in a large number of patients in different stages of fibrosis and with ongoing infection has not been well studied.

The aim of the current study was to assess liver fibrosis changes in patients with known fibrosis stages who did not respond to previous interferon-based antiviral therapy and to determine the predictors of liver fibrosis progression.