What are the Pathophysiologic Processes Leading to ACD?
In ACD, a modest decrease in RBC survival creates a demand for increased red cell production which cannot be met (because of impaired mobilization and utilization of reticuloendothelial iron) and an impaired erythropoietic response. The impaired erythropoietic response has two components a blunted erythropoietin increment in response to anemia and a relative resistance of erythroid progenitors to erythropoietin. All of these processes are induced by the cytokines that mediate the inflammatory response cytokine activation is the feature linking the syndromes associated with ACD. Shortened RBC survival in ACD may result from selective hemolysis of young RBC induced by erythropoietin deficiency (neocytolysis). The iron abnormalities of ACD are due to the cytokine-induced peptide hepcidin. Hepcidin binding causes degradation of the iron export protein ferroportin; iron is then retained in reticuloendothelial cells where it is unavailable for erythropoiesis. What are the Diagnostic Difficul