[Anemia in malignant tumor diseases. VI. Secondary siderosis caused by the shift of iron, unused for hemoglobin synthesis, into iron stores].

Impaired utilization of iron by the heme synthesizing red cell precursors was investigated in 258 patients with malignant tumors of different histological types and different tumor spread. There was evidence, that impaired iron uptake by the erythropoietic cells results in an increased flow of iron to the reticuloendothelial iron stores. Investigations on bone marrow smears showed that sideroblast counts were significant lower than in healthy controls reflecting a deficient iron supply to the erythropoietic cells. In contrast, reticuloendothelial storage iron was increased paralleled by an increased serum ferritin concentration. Both abnormalities correlated with the malignancy and the stage of the tumor. It could be demonstrated that the degree of the hyperferritinemia paralleled very closely the severity of the anemia becoming more pronounced with increasing tumor mass. This parallelism indicates that the siderosis is pathophysiologically related to the defect of erythropoiesis observed in malignant disease. Since the iron uptake by the erythropoietic cells is mediated by transferrin in a further series of experiments the serum transferrin concentration was investigated in malignant diseases. There was found a close inverse correlation between serum transferrin concentration and serum ferritin concentration. This correlation supports the concept of a defect in erythropoiesis due to an impaired transferrin mediated iron supply caused by tumor induced hypotransferrinemia. This defect is responsible for a shift of iron to the iron stores and a secondary siderosis.