The Mechanism of the Anemia Associated with Hodgkin’s Disease

1. The survival of autotransfused Cr⁵¹-tagged erythrocytes was shortened in a group of five patients with the anemia of Hodgkin’s disease, but since the normal marrow is believed to be capable of compensating for destruction rates of six to eight times greater than normal, it is felt that the increased rate of hemolysis was not sufficient to account for the development of anemia in any of these patients.

2. There was evidence of an increased rate of erythropoiesis in all of the patients with Hodgkin’s disease. This was manifested by normoblastic hyperplasia of the marrow, a moderate reticulocytosis and increased plasma iron clearance rates. The shortened red cell survival times were associated with the increased plasma iron clearance rates. However, in view of the fact that all of the patients were anemic, it is evident that these patients were incapable of increasing the rate of red cell production sufficiently to compensate for the increased rate of destruction.

3. Intravenously injected Fe⁵⁹ citrate was incorporated more rapidly into the circulating red cell mass in the patients with Hodgkin’s disease than in the normal subjects.

4. The tissue iron stores of the liver and spleen were greatly increased, but no iron was demonstrated in the marrow of a group of seven patients with Hodgkin’s disease.

5. The plasma iron was low and the UIBC normal in a group of 12 patients with active Hodgkin’s disease.

6. It is suggested that one of the factors which limits the ability of the marrow to produce hemoglobin in the anemia of Hodgkin’s disease may be a relative hypoferremia caused by a defect in the mobilization of iron from tissue stores.