Human recombinant erythropoietin in the prevention and treatment of anemia of prematurity

被引:17
作者
Ohls R.K. [1 ]
机构
[1] Division of Neonatology, University of New Mexico, Albuquerque, NM
关键词
Preterm Infant; Erythropoietin; Oral Iron; Human Recombinant Erythropoietin; Iron Sucrose;
D O I
10.2165/00128072-200204020-00004
中图分类号
学科分类号
摘要
Human recombinant erythropoietin has been studied extensively as treatment for a variety of anemias. Since in vitro studies showed the primary etiology of the anemia of prematurity to be insufficient serum erythropoietin concentrations, clinical trials have evaluated the administration of human recombinant erythropoietin to preterm infants to treat this indication. These studies were followed by pharmacokinetic determinations in animal models and preterm infants, which revealed that preterm infants required greater doses of human recombinant erythropoietin because of a more rapid clearance and greater volume of distribution. Recent studies have focused on the administration of human recombinant erythropoietin in the first weeks of life to alleviate the anemia caused by excessive phlebotomy losses, and to prevent the anemia of prematurity. In addition, human recombinant erythropoietin has been tried clinically in a variety of neonatal populations in an attempt to decrease or eliminate transfusions. Although much information has been accumulated about the clinical use of human recombinant erythropoietin in preterm infants over the last 15 years, many questions remain unanswered. The evolution of clinical practice in the care of extremely low birthweight infants continues to affect the number of transfusions. It is likely that human recombinant erythropoietin administration in combination with instituting rigorous transfusion guidelines and decreasing phlebotomy losses will have the greatest impact in decreasing transfusion requirements in all preterm and term neonates, regardless of the etiology of their anemia.
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页码:111 / 121
页数:10
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共 72 条
[1]  
Malek A., Sager R., Eckardt K.U., Et al., Lack of transport of erythropoietin across the human placenta as studied by an in vitro perfusion system, Pflugers Arch, 427, pp. 157-161, (1994)
[2]  
Widness J.A., Sawyer S.T., Schmidt R.L., Et al., Lack of maternal to fetal transfer of 1251-labelled erythropoietin in sheep, J Devel Physiol, 15, pp. 139-143, (1991)
[3]  
Zanjani E.D., Pixley J.S., Slotnick N., Et al., Erythropoietin does not cross the placenta into the fetus, Pathobiology, 61, pp. 211-215, (1993)
[4]  
Jacobsen L.O., The effect of transfusion-induced polycythemia in the mother of the fetus, Blood, 4, (1959)
[5]  
Ebert B.L., Bunn H.F., Regulation of the erythropoietin gene, Blood, 94, 6, pp. 1864-1877, (1999)
[6]  
Erslev A.J., Caro J., Kansu E., Et al., Renal and extrarenal erythropoietin production in anemic rats, Br J Haematol, 45, pp. 65-72, (1980)
[7]  
Fried W., The liver as a source of extrarenal erythropoietin production, Blood, 40, pp. 671-677, (1972)
[8]  
Zanjani E.D., Poster J., Burlington H., Et al., Liver as primary site of erythropoietin formation in the fetus, J Lab Clin Med, 89, pp. 640-644, (1977)
[9]  
Ohls R.K., Kerbleski J.F., The effect of hypoxia on quantitative erythropoietin and HIF-1a mRNA expression in mid-gestation human fetal kidney and liver, Pediatr Res, 47, (2000)
[10]  
Dame C., Fahnenstich H., Freitag P., Et al., Erythropoietin mRNA expression in human fetal and neonatal tissue, Blood, 92, 9, pp. 3218-3225, (1998)