Evaluation of neoangiogenesis and hepatic stellate cell activation in hepatic fibrosis and cirrhosis due ti chronic viral hepatitis

Backround and aim: Evaluation of hepatic stellate cell (HSC) activation determinant alpha Smooth Muscle Actin (a-SMA) expression in different stages of fibrosis and cirrhosis due to viral hepatitis. It is aimed to determine neoangiogenesis and fibrosis in vascular epitel with Factor 8 dye and couting microvascularity with Chalkley method in order to investigate portal hypertension development.Materials and Method: 80 patients before treatment of chronic viral hepatitis with hepatic biopsy and 40 hepatic transplant patient due to cirrhosis are attended for study. Modified HAİ index is used for fibrosis and necroenflamatuary activity. 40 samples for fibrosis 0-1 group, 40 samples for fibrosis 2-3-4 group and 40 samples for cirrhosis group are taken. Samples in parafine are dyed with SMA antibody (1: 100) and Factor 8 (1: 50) immunochemistry techniques. For microvascular counting Chalkley Eyepiece Graticule Microscope attachment is used by average of three different areas.Results: There is significant difference detected in three different groups by SMA antibody dye (p<0,001). Fibrosis 2-3-4 is significantly higher compared with fibrosis 0-1 group (p=0,007). Cirrhosis group is higher compared with fibrosis 0-1 group (p<0,001). Cirrhosis group is higher compared with fibrosis 2-3-4 (p<0,001). Neoangiogenesis is significantly different in groups (p<0,001). Noeangiogenesis is highest in cirrhosis group.Discussion: In conclusion, development of hepatic neoangiogenesis and fibrosis are related with each other. In our study we established that HSC activation and neoangiogenesis is higher in progressed disease. The studies for agents for blocking the activation for VEGF or HSC activation would stop developing chronic hepatic diseases. Advanced studies are needed for this purpose.Key Words: Hepatic Fibrosis, Viral Hepatitis, Hepatic Stellate Cell, Angiogenesis