Abstract
Patients receiving erythropoietin therapy require large quantities of iron to keep pace with the demands of the bone marrow during active erythropoiesis. If this iron supply to the marrow is not maintained, the response to erythropoietin is impaired, and indeed iron insufficiency is the most common cause of a poor response to this drug. Iron deficiency may be either absolute, which is defined as a reduction in total body iron stores, or functional, which implies adequate iron stores but a failure to supply available iron to the marrow or a failure in the utilization of this iron in the process of erythropoiesis. The detection of absolute or functional iron deficiency is difficult because there is no absolutely reliable marker of iron status, with the exception of an unequivocally low serum ferritin level. Measurement of serum ferritin and transferrin saturation are the most widely used methods, but both have drawbacks. Monitoring of the percentage of hypochromic erythrocytes in the circulation also seems promising, but the technology is of limited availability, and other methods (eg, monitoring erythrocyte ferritin, free erythrocyte protoporphyrin, and erythrocyte zinc protoporphyrin levels) lack widespread validation. Treatment of iron insufficiency is accomplished by intensifying iron supplementation either orally or intravenously, and in many instances the latter route becomes necessary. The high cost of erythropoietin demands that iron deficiency be screened for on a regular basis and treated to maximize the benefits of this drug.

This publication has 0 references indexed in Scilit: