Schistosomiasis is caused by blood flukes including all Schistosoma species. It affects about 207 million persons in 76 countries across the world, and is more prevalent in developing countries where about 800 million people are at the risk of schistosomiasis [1]. Following oviposition, schistosomes eggs that failed to exit with either urine or stools are carried back into the liver to be lodged in the pre-sinusoidal capillaries. The eggs are in intimate contact with the capillary endothelium before and during the generation of the granulomatous response [2]. Schistosoma miracidium inside the ovum secretes glycoprotein antigens that pass through microscopic pores within the egg shell, so are called SEA. These antigens elicit a vigorous immune response that encapsulates the ova in pre-granuloma collagen fibers and immune cells, predominantly eosinophils and macrophages. The granuloma formation presents a barrier to sequester egg toxicity and antigenicity. Fibrosis of granulation tissues leads to disturbance of hepatic parenchymal architecture including its vasculature [3]. Despite portal vascular impairment, it was found that the total hepatic blood flow remained within normal limits with normal parenchymal cell perfusion, accompanied by absent gross changes in hepatic function tests. This was attributed to hepatic neovascular formation in the