The Pharmacokinetics of Tc^99m-Diethyl Ida in Hyperferremic Mice

Abstract

Iron excess may potentiate diseases affecting the liver. Hepatic cirrhosis of thalassaemia major is characterized by iron particles or aggregates deposition in parenchymal and reticuloendothelial cells especially in lysosome as haemosiderin or ferritin or in cellsap as ferritin (1,2). Most thalassaemic patients have however normal liver function tests until “end-stage disease” is reached (3). In idiopathic haemochromatosis, the enormous quantities of iron, in the order of 20–60 g, accumulate in the liver as a result of increased intestinal absorption and produce hepatic structural changes. In the early stages, portal zone fibrosis is observed with deposition of iron in the periportal liver cells and to a lesser extent in the Kupffer cells (4). Surprisingly, biochemical tests show little disturbance except for a positive BSP test (5). That would suggest a peculiar sensitivity to iron overload of the important bile excretory pathway including organic anions such as BSP, conjugated bilirubin, dyes and IDA derivatives. The purpose of the present study was to investigate the effect of hyperferremia on the pharmacokinetics of Tc ^99m-diethyl IDA.