Erythropoiesis after exchange transfusion in hemolytic anemia.

I HE CONTROL of red cell productiomi is undoubtedly geared toward maintaining the red cell mass at a functionally optimal size. Since the primary function of the red cell mass is to transport oxygen to the tissues, it is generally assumed that the control is triggered by the tissue tension of oxygen. Recent studies indicate that the oxygen tension in one target area, the kidney, is inversely proportional to the production or release of the hormone erythropoietin, and that the rate of red cell production is influenced by the amount or concentration of this hormone in circulating blood. However, it is not known if this system provides the sole control of red cell production. The red cells do have other functions than that of carrying oxygen. They participate in CO2 transport and they provide important bulk and viscosity to circulating blood, making it possible that other parameters play a role in the regulation of red cell production. The possibility of dual or even multiple control mechanisms is usually invoked whenever clinical or experimental observations do not seem to fit the tissue-hypoxia control mechanism. One such observation was reported by Stohiman in 19621 and used to support the hypothesis of a dual control of red cell production. Stohiman in a review mentioned that the rate of red cell production was reduced in a patient with hereditary spherocytosis after a 40 per cent exchange transfusion. Since the hemoglobin concentration was kept constant, he felt that the reduction in red cell production could not be related to a change in tissue tension of oxygen but must have been caused by some other regulatory mechanisms. The present study was made in order to confirm this interesting observation, using reticulocytes, bone marrow differential and serum iron turnover in patients with hemolytic anemia before and after exchange transfusion. MATERIALS AND METHODS Three adult patients with hereditary spherocytosis and splenomegaly, and one adult patient with acquired hemolytic anemia, were admitted to the Clinical Research Center for exchange transfusion. Complete hematologic workup in the patients with hereditary spherocytosis revealed the classical picture of chronic mild anemia, spherocytosis, negative From the Cardeza