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Chapter 8 - Anemia of Prematurity and Indications for Erythropoietin Therapy
- from Section III - Erythrocyte Disorders
- Edited by Pedro A. de Alarcón, Eric J. Werner, Robert D. Christensen, University of Utah, Martha C. Sola-Visner, Harvard University, Massachusetts
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- Neonatal Hematology
- Published online:
- 30 January 2021
- Print publication:
- 18 February 2021, pp 120-132
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Summary
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. However, delaying umbilical cord clamping may increase initial hematocrit percentages, improve infant iron status, prevent erythrocyte transfusions, decrease necrotizing enterocolitis (NEC), and decrease intraventricular hemorrhage (IVH). Many published studies have examined the potential of therapy with recombinant human EPO or other erythropoietic stimulating agent (ESA). Although EPO therapy is associated with statistically lower number of total erythrocyte transfusions, most early transfusions are not eliminated. However, early erythropoietic EPO dosing may also decrease NEC and IVH as well as improve neurocognitive outcomes. A recent systematic review refuted previous concerns that early administration of EPO was associated with increased retinopathy of prematurity (ROP). Early high dose EPO regimens are currently being studied for neuroprotection in premature infants. Iron deficiency in EPO treatment is also of potential concern, but long-term iron status of EPO treated premature infants is similar to controls.
4 - Anemia of prematurity and erythropoietin therapy
- from Section II - Erythrocyte disorders
- Edited by Pedro de Alarcón, Eric Werner, Robert D. Christensen
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- Book:
- Neonatal Hematology
- Published online:
- 05 February 2013
- Print publication:
- 10 January 2013, pp 37-46
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Summary
Physiology of anemia of prematurity
Erythropoietin (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 to the kidneys (1, 2). During the first postpartum months after term birth, erythropoiesis is suppressed by markedly improved postnatal oxygen delivery and a relatively depressed plasma EPO levels, resulting in a “physiologic nadir” in hemoglobin (Hb) (3). This response is exaggerated in premature infants (4). The anemia of prematurity reflects not only insufficient EPO production (4), but also small circulating blood volume, iatrogenic blood loss, hemorrhage, hemolysis and shortened red blood cell (RBC) survival (summarized by Ohls) (5). Anemia of prematurity is traditionally described as nutritionally “insensitive,” although iron contributes to the recovery of Hb (6, 7). Iron status is critical, in that insufficient iron supplementation may inhibit the efficacy of EPO in prematurity (7, 8).
Therapy for anemia of prematurity
Minimizing blood loss
Blood loss impacts the clinical course of the anemia of prematurity. In a typical 800 gram birthweight premature infant, with red cell mass at birth of 27 mL, avoidance of blood transfusions depends on avoidance of blood loss (9). In the presence or absence of EPO, phlebotomy volume clearly correlates to erythrocyte volume transfused (9–17). This observation is most evident when precise transfusion criteria are employed (13). Some centers report relatively lower phlebotomy loss on even the smallest children (18, 19). Using inline and microsampling point-of-care testing may contribute to less blood loss in unstable infants (16, 20, 21). With such small circulating blood volumes, phlebotomy volume, as well as phlebotomist overdraw volumes relate to volume transfused (9, 22, 23). It is logical that advances in perinatal care which may decrease patient acuity would also decrease transfusions (11), but inter-institutional transfusion practices on infants with similar acuity vary widely (13–15).
4 - Anemia of prematurity and indications for erythropoietin therapy
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- By Pamela J. Kling, M.D. University of Wisconsin, Madison, WI, USA
- Edited by Pedro A. de Alarcón, University of Tennessee, Eric J. Werner
- Foreword by J. Lawrence Naiman, Stanford University School of Medicine, California
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- Book:
- Neonatal Hematology
- Published online:
- 10 August 2009
- Print publication:
- 18 August 2005, pp 58-67
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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].