الفهرس 
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Abstract
Alphal antitrypsin is the moat important antiprote- { aae in the body, it is responsible for about 90% of the total serum trypsin inhibitory capacity. It is a glycoprotein of molecular weight approximately 50.000 and is only synthetized in the liver (Crawford, 1973). About 28 variants of alphal antitrypsin had been recognized, collectively they are known as the Pi (Protease inhibitor) system; the most frequent gene is PiM and is associated with normal alphal antitrypsin in blood while PiZ phenotype is the commonest allele associated with severe deficiency (Hug et al,1981). Post-schistosomal hepatic fibrosis, which is a common complication of intestinal schistosomiasis, develops in some individuals infested with schistosoma mansoni and not in others (5asazuki et al., 1977). This suggestes the existence of host factors as well as parasitic factors in the pathogenesis of bilharzial liver fibrosis. Patients with alphal antitrypsin deficiency may be predisposed to liver cirrhosis (Talamo, 1975). So, the aim of this work is to prove the possibility that alphal antitrypsin deficiency may be a factor in the pathogenesis of bilharzial hepatic fibrosis with the object of finding a relation between its level and the presence of liver fibrosis.