Response of Premature Anemic Infants to Subcutaneous Recombinant Erythropoietin

Abstract

Anemia of prematurity (AP) is a common complication in infants <32 weeks of gestation. It is more marked (Hb ⩽90 g/L in 50% of patients) and occurs earlier (4–8 weeks of life) than the physiologic anemia of term newborns [1, 2]. Although clearly of a multifactorial etiology, AP partly results from an abnormal or immature erythropoietin (EPO)-mediated regulation of erythropoiesis [3–6]. EPO is a glycoprotein normally secreted by peritubular renal cells in response to hypoxemia [7]. Its action is principally directed onto the marrow erythroid progenitor cells (CFU-E), the proliferation and maturation of which are entirely dependent on the presence of this hormone. While older children and adults promptly respond to even a mild degree of tissue hypoxia by increasing their endogenous production of EPO, premature infants are not capable of producing an adequate response until their red cell mass reaches critical values [3, 4, 6]. Thus, AP may have important clinical repercussions resulting from decreased O₂ availability, such as tachycardia, tachypnea, poor weight gain, and respiratory pauses [8, 9]. The most symptomatic of these premature infants are commonly transfused with packed red cells, despite current restrictive use of blood products. Therefore, unlike the anemia of infants born at term, AP cannot be considered as a simple physiologic, adaptive phenomenon.