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.