Blood, 1959, Vol. 14, No. 7, pp. 856-869.
© 1959 American Society of Hematology, Inc.
The Mechanism of the Anemia Associated
with Hodgkin’s Disease
P. PIKOULI GIANNOPOULOS 1 and
DANIEL E. BERGSAGEL 1
1 Department of Medicine, The University of Texas M. D. Anderson Hospital and
Tumor Institute, Houston, Tex.
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.
Submitted on April 17, 1958
Accepted on February 2, 1959
