Anemia of prematurity and indications for erythropoietin therapy

doi:10.1017/CBO9780511545306.006

4 - Anemia of prematurity and indications for erythropoietin therapy

Published online by Cambridge University Press: 10 August 2009

Pamela J. Kling

Edited by

Pedro A. de Alarcón and

Eric J. Werner

Foreword by

J. Lawrence Naiman

Show author details

Pamela J. Kling: Affiliation:
M.D. University of Wisconsin, Madison, WI, USA
Pedro A. de Alarcón: Affiliation:
University of Tennessee
Eric J. Werner: Affiliation:
Eastern Virginia Medical School
J. Lawrence Naiman: Affiliation:
Stanford University School of Medicine, California

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Summary

Introduction

Anemia of prematurity is a multifactorial anemia characterized by relatively low plasma erythropoietin (EPO) levels, iatrogenic blood loss, low circulating blood volumes, and insufficient erythropoiesis. This anemia has been long characterized as nutritionally insensitive, but nutrition may influence its clinical course. Anemia of prematurity is treated with erythrocyte transfusions, and many published studies have examined the potential of recombinant human erythropoietin (rhEPO) therapy. Although rhEPO therapy is associated with a statistically lower number of transfusions, it does not eliminate transfusions in most premature infants. In addition, optimal dosage, route of administration, and timing of rhEPO therapy in prematurity remain under study. Of concern, rhEPO therapy is associated with both functional iron deficiency and depleted iron stores in other populations. In prematurity, rhEPO is given in conjunction with supplemental iron, but long-term iron status of premature infants after rhEPO therapy has been studied poorly.

Physiology of anemia of prematurity

EPO, the primary hormone regulating erythropoiesis, is measurable throughout fetal gestation [1]. In the fetus and newborn, EPO is produced primarily by the liver, which may be relatively insensitive to hypoxia compared with the kidney [1, 2]. After term birth, erythropoiesis is suppressed by markedly improved postnatal oxygen delivery and a relatively depressed plasma EPO level; consequently, a fall in hemoglobin occurs, which reaches physiologic nadir in the first months postpartum [3]. This response is exaggerated in premature infants [4].

Type: Chapter
Information: Neonatal Hematology , pp. 58 - 67

DOI: https://doi.org/10.1017/CBO9780511545306.006 [Opens in a new window]

Publisher: Cambridge University Press

Print publication year: 2005

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