Vascular endothelial growth factor in relation to the development of hepatocellular carcinoma in hepatitis C virus patients treated by direct-acting antivirals

Abstract

Abstract Background Hepatocellular carcinoma (HCC) comprises 5.6% of all cancers worldwide representing the sixth most common cancer. It is also the fourth most common cause of cancer-related mortality. Angiogenesis is a main factor in the development of HCC. Vascular endothelial growth factor (VEGF) is considered as the force for physiological and pathological angiogenesis, and overexpression of VEGF is prominent in HCC. We aimed to study the effect of direct-acting antivirals (DAAs) on VEGF considered as the key regulator of angiogenesis in HCC. This cross-sectional study involved fifty patients who were divided into two groups: group I—twenty-five chronic hepatitis C virus (HCV) patients as (cases) subjected to treatment with direct-acting antiviral drugs for 3 months; group II—twenty-five chronic HCV patients developed HCC as (controls). Serum VEGF level was measured in of group I at baseline, at end of treatment, and 3 months after the end of treatment by sofosbuvir 400 mg plus daclatasvir 60 mg for 3 months in the HCV patient group, also VEGF was assessed in group II with HCC. Results Serum VEGF was high in both groups, but it was higher in the HCC group with a statistically significant difference (p < 0.001), also serum VEGF in the HCV group decreased after 3 months at the end of DAA treatment from 209.5 ± 137.6 to 44.1 (31.8–55.3) mg/ml, and all patients who received DAAs achieved sustained virologic response (SVR). Conclusion We found that change in serum VEGF in HCV patients treated with DAAs in this study cannot explain the risk of HCC after treatment by DAAs.

Keywords

• Vascular endothelial growth factor A
• HCV
• DAAs
• HCC