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Iliescu et al. Hepatoma Res 2018;4:3  I  http://dx.doi.org/10.20517/2394-5079.2017.48                                                 Page 7 of 10




















                           Figure 8. Abdominal MRI showing liver mass in the hepatic dome. MRI: magnetic resonance imaging

                                              Evolution of patients with higher AFP at SVR


                              Patient 3


                              Patient 2



                              Patient 1






                Figure 9. Evolution of patients with higher AFP at SVR. AFP: alpha-fetoprotein; SVR: sustained virological response; TACE: trans-arterial
                                              chemoembolization; EOT: end of treatment

               Notably, all patients acquired SVR. Overall, the risk of HCC in our study group was 1.51%. When reported
               to F4 patients, the risk of HCC increases to 6.35%.



               DISCUSSION
               It is acknowledged that patients with HCV compensated cirrhosis who achieved SVR due to IFN-based
                                                                   [13]
               therapy, were shown to be at a lower risk of developing HCC . It was also demonstrated that patients with
               HCV-induced chronic liver disease had a decrease of the fibrosis level, under DAA treatment . For the past
                                                                                             [14]
               several decades, pegylated interferon and ribavirin therapies were used to treat most of the patients with
               HCV associated liver disease, but they showed various side effects and toxicities.

               The use of DAA treatment regimens has opened a new era in the approach of HCV-induced liver disease,
               reducing the need for liver transplantation [15,16] . However, there is evidence of the occurrence or recurrence
               of HCC in patients with chronic HCV infection, who received DAA therapy, achieving SVR, as shown in
               a recent publication . Therefore, we consider that the association between IFN-free treatment and the
                                 [17]
               development of HCC in patients with chronic HCV infection, should be further investigated and discussed,
               as it represents a highly important issue in hepatology.


               There are several variables associated with an increased risk of developing HCC after SVR, such as advanced
               liver fibrosis, older age, alcohol abuse, metabolic diseases (especially diabetes mellitus) and the persistence
               of hepatic inflammation [18,19] . A variant in genotype 1b HCV core protein Gln70 (His 70) may also be
               incriminated in the increase of HCC incidence .
                                                       [20]
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