While a number of studies investigated iron and copper storage or alpha 1-antitrypsin (A1AT) deficiency in the liver of patients with cirrhosis, we did not find any similar study in schistosomotic patients reported in literature. We investigated the storage of both metals and the A1AT deficiency in the liver of 72 cirrhotic and 27 schistosomotic patients (5 with the hepatointestinal and 22 with the hepatoesplenic form of the disease). Forty-four patients with cirrhosis were also alcoholic, and 28 were not. Iron storage was detected in 23 patients with cirrhosis (31.9%); among these 16 (36.3%) were alcoholic and 7 (25.0%) non-alcoholic (the difference was not statistically significant). Thirteen (56.5%), 5 (21.7%) and 5 (21.7%) patients presented I-grade, II-grade, and III-grade iron storage, respectively. Copperstorage was detected in 24 cirrhotic patients (33.3%), 15 being alcoholic (34.0%) in contrast with 9 non-alcoholic patients (32.1%), a statistically non-significant difference. A1AT deficiency was observed in 2 patients with cirrhosis (2.8%), one with history of alcoholism. HBsAg and HBcAg in hepatic tissue were detected in 5 cirrhotic patients (6.9%), three of them with a history of alcoholism. Iron and copper storage and A1AT deficiency were observed in 3 patients with cirrhosis (12.5%), while iron storage and A1AT deficiency were found in 2 additional patients with cirrhosis (2.8%). The authors underline that neither iron nor copper storage nor A1AT deficiency was found in any schistosomotic patient. The authors discuss the possible importance of these data.