The effect of erythroid hyperplasia on iron balance

Abstract

Measurements of erythropoiesis and iron balance were made in eight normal and 32 anemic subjects. The latter consisted of 12 individuals with ineffective erythropoiesis (beta-thalassemia/hemoglobin E), 13 subjects with ineffective erythropoiesis and hemolytic anemia (hemoglobin H), and seven subjects with hemolytic anemia (hereditary spherocytosis). A consistent relationship within each group existed between the degree of erythropoiesis and radioiron absorption. Although the effect of erythropoiesis on iron absorption was of similar magnitude in the two thalassemia groups, the effect in hereditary spherocytosis was much less. There was agreement between absorption and ferritin or magnetic susceptibility (SQUID) measurements of iron stores in thalassemia, but in hereditary spherocytosis a discrepancy existed between absorption and ferritin. It is concluded that, although increased erythropoiesis is associated with increased iron absorption, some additional factor associated with red cell breakdown is more directly responsible for the positive iron balance in thalassemia.

Serum erythropoietin and its relation with soluble transferrin receptor in patients with different types of anaemia in a locally defined reference population

“…The patients with simple iron-de®ciency anaemia showed a predicted physiological Epo response to anaemia. The remaining patients had haemolytic anaemias, characterized by effective erythropoiesis (Pootrakul et al, 1988) or a combination of effective and variable degrees of ineffective erythropoieis, as reported in thalassaemic patients by Camaschella et al (1996).…”

Disparity in the management of iron overload between patients with sickle cell disease and thalassemia who received transfusions

“…By contrast, iron absorption is on average three times that of healthy controls in anemic patients with Thal syndromes. 29 Increased iron absorption in Thal is most likely due to ineffective erythropoiesis leading to inhibition of hepcidin synthesis in the liver. 30 Given this, even patients with Thal who did not receive transfusions should be monitored on a regular basis and treated when necessary to avoid iron-related organ dysfunction ( Table 4).…”

Markers of inflammation in children with severe malarial anaemia

“…Also, that white blood cell and platelet counts were not lower in the children with severe anaemia indicates that generalized bone marrow suppression was not the cause but that a suppression or dysfunction of erythropoiesis may have played a role. The higher transferrin saturations in the children with severe anaemia are also compatible with an interruption in erythropoiesis (Gordeuk et al 1986;Pootrakul et al 1988).…”