Angiogenic output in viral hepatitis, C and B, and HCV-associated hepatocellular carcinoma

Angiogenesis is known to play a pivotal role in most of malignancy, including HCC, and in chronic inflammation. To investigate the angiogenic output in HCV and HBV infection and its implication in the development of HCV associated HCC. Blood samples were collected and grouped as; HS healthy subjects control group; HCC–HCV; chronic HCV infected patient group (HCV+ve) who are positive for serum anti-HCV antibodies and HCV–RNA; anti-HCV antibody positive and HCV–RNA negative patient group (HCV−ve); patients with positive HBsAg and HBV-DNA group (HBV+ve); and HBsAg positive and HBV-DNA negative patient group (HBV−ve). Serum levels of vascular endothelial growth factor, angiopoietin-2, endostatin and angiostatin were assessed in different studied groups. The level of sVEGF was insignificantly elevated in both HCV+ve and HCV−ve groups when compared with controls, while Ang-2, sES and sAS were significantly elevated in both groups as compared with healthy controls. The studied parameters were significantly elevated in HBV-+ve patients when compared with the control. However, HBV−ve patients showed significantly elevated levels in sAng-2, sES and sAS when compared with the control while the level of sVEGF was equal to that of controls. In patients with HCC, the studied parameters showed a significant elevation when compared with healthy controls and patients either with HBV or HCV infection except for sAS in the case of HCV-+ve patients and VEGF for HBV-+ve patients who were also higher but not significant. The increased hepatic angiogenesis in chronic HCV and HBV could provide the molecular basis for liver carcinogenesis and contribute to the increased risk of HCC in patients with cirrhosis due to HCV and/or HBV.