Iron and the Reticuloendothelial System

Abstract

The anemia of defective iron reutilization that complicates chronic disorders is at present the most common type of anemia (10). It is usually mild and not progressive, but can produce symptoms. This type of anemia complicates such chronic inflammatory states as rheumatoid arthritis and subacute bacterial endocarditis as well as malignant disorders such as Hodgkin’s disease. It is occasionally seen in chronic renal disease and severe tissue injury (4,10,11,26,29,36). A similar type of anemia has also been described as a primary disorder (30,39). Although its exact cause is unknown, it has been considered that the host, in its own defense, may withhold iron not only from hemoglobin synthesis (an innocent bystander) but primarily from microbes, other invasive organisms and possibly tumor cells (45,61). The ability of the host to withhold iron in this fashion has been called “nutritional immunity” (10). Certain bacteria, for their own growth, can produce compounds called siderophores by which they can extract iron from transferrin if this protein is at least 30% saturated with iron [for an excellent review, see Weinberg (61)]. The anemia is characterized by decreased plasma iron, decreased total iron binding capacity (TIBC) in most instances, increased serum haptoglobin (50), decreased bone marrow sideroblasts, and normal or increased reticuloendothelial system (RES) iron. Of the above features, the triad of low plasma iron, decreased TIBC and increased RES iron are distinctive and occur in no other condition.