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Abstract

Purpose: Evaluation of hepatic stellate cell (HSC) activation due to viral hepatitis in various stages of cirrhosis and fibrosis. We aimed to determine portal hypertension development by examining neoangiogenesis and fibrosis in the vascular epithelium. Materials and Methods: A total of 80 patients with chronic viral hepatitis before treatment and 40 hepatocirrhotic transplant patients were consented for this study. A modified histology activity index was used for fibrosis and necroinflammatory activity. 40 samples from all groups: The fibrosis 0-1 group, the fibrosis 2-3-4 group, and the cirrhosis group were taken. Samples embedded in paraffin were subjected to immunohistochemistry and stained for alpha smooth muscle actin (SMA). For microvascular counting, the Chalkley method was used, and an average of three different areas was taken. Results: A significant difference in SMA staining was detected in the three different groups (P < 0.001). Interestingly, fibrosis 2-3-4 was significantly higher compared to the fibrosis 0-1 group (P = 0.007). The cirrhosis group was higher compared to the fibrosis 0-1 group (P < 0.001) and the fibrosis 2-3-4 group (P < 0.001). Neoangiogenesis was significantly different between groups (P < 0.001), and neoangiogenesis was the highest in the cirrhosis group. Discussion: In conclusion, hepatic neoangiogenesis and fibrosis development are associated with each other. We show that neovascularization and HSC activation were augmented in the more progressive disease states. Future work should be focused on developing therapies targeting the activation of vascular endothelial growth factor or HSC activation may help prevent chronic hepatic diseases.

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	JPR Solutions

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