Clinical Removal of Iron

Abstract

Iron is of primary biologic significance because of its role in oxidation­ reduction reactions. Its ability to facilitate electron exchange is also respon­ sible for much of the toxicity associated with acute iron poisoning (1) and probably with chronic iron overload (2) as well. It is fortunate, therefore, that the amount of iron gaining access to the body is tightly controlled. The average North American diet contains 10-20 mg of iron (3), 90% of which is not contained in heme (4). Only about 1-2 mg of dietary iron is heme iron, half of which is absorbed. The total absorption must normally com­ pensate for the obligatory losses from passive desquamation of epithelial cells from the skin, gastrointestinal and genitourinary tracts. Since most of the excess iron in food is nonheme iron, this is the pool that is under regulatory control and that accounts for the increased gastrointestinal (GI) absorption of iron occurring when daily losses exceed 1-2 mg. If insufficient bioavailable iron is presented to the GI tract, or if iron losses become excessive, iron deficiency, the common state of iron imbalance, results. Except for red cell transfusion, iron overload is an unusual event that is due to continued excessive absorption of dietary or medicinal iron. The condition occurs in the chronic hyperplastic anemias associated with a significant degree of ineffective erythropoiesis (5), in idiopathic hemo­ chromatosis (6)-a genetic disorder of iron metabolism-and in certain dietary iron overload states as exhibited by the Bantu population of South Africa (7). Iatrogenic iron overload is much more common than any of the naturally occurring disorders and is the result of chronic parenteral admin­ istration of iron in the form of red cell transfusion or oral administration of medicinal iron to patients heterozygous for thalassemia genes in the mistaken belief that these people suffer from iron deficiency.