Radioactive Iron Metabolism and Erythrocyte Survival Studies of the Mechanism of the Anemia Associated with Rheumatoid Arthritis1

Abstract
The physiology of red cell production, destruction and survival was studied in 42 rheumatoid arthritis patients and 10 controls. Studies of Fe metabolism utilizing Fe59 revealed a decreased serum Fe concentration and more rapid removal of injected transferrin bound Fe59 from the plasma in the patients. The red cell incorporation of injected Fe59 was normal and unimpaired, while the ferrokinetic pattern determined by external body monitoring over organ sites was normal. Hypoferremia seem to result from impaired release of Fe from the tissues to the plasma, coupled with unimpaired removal of Fe from the plasma by the bone marrow. Computation of plasma and red cell Fe turnover rates indicated a normal quantity of hemoglobin production, but when related to red cell mass, an increased rate of red cell renewal. Studies of fecal urobilinogen excretion indicated normal quantities of hemoglobin destruction. Studies of red cell survival utilizing the differential agglutination technique revealed increased random destruction of transfused red cells, while red cells from arthritic patients showed normal survival in normal recipients. Thus the hemolytic mechanism is based on some factor associated with the red cell environment rather than on a defective quality of the red cell. Anemia results from failure of the bone marrow to respond to the increased need for red cell production. The patients showed a moderate hypochromia of their red cells. Moreover the degree of hypoferremia was directly related to the degree of anemia, indicating that a diminished supply of Fe for red cell production contributes to the impaired capacity of the marrow for red cell production.