1.
Effect of enteral erythropoietin on feeding-related complications in preterm newborns: A pilot randomized controlled study.
Omar, OM, Massoud, MN, Ghazal, H, Hassouna, H, Somaa, MF
Arab journal of gastroenterology : the official publication of the Pan-Arab Association of Gastroenterology. 2020;(1):37-42
Abstract
BACKGROUND AND STUDY AIMS To evaluate the effects of enteral administration of recombinant human erythropoietin (rhEPO) on feeding-related complications in preterm infants. PATIENTS AND METHODS This double-blind, randomized controlled pilot study enrolled 120 preterm infants born ≤ 32 weeks' gestation who were admitted to the neonatal intensive care unit in a tertiary hospital; 60 patients randomly received recombinant human erythropoietin while the other 60 received placebo. Newborns who underwent cardiopulmonary resuscitation, infants with genetic syndromes, infants with inborn errors of metabolism, infants with major congenital or acquired gastrointestinal tract malformations, infants with previous use of parenteral growth factors such as recombinant human erythropoietin and granulocyte-macrophage colony-stimuating factor (GM-CSF) and infants previously treated with intravenous immunoglobulin were excluded. Overall, 48 patients withdrew from the study because of intravenous haematopoietic growth factor intake or death before treatment was completed. A total of 72 preterm infants remained in the study: 36 preterm infants in the erythropoietin (EPO) group, and 36 preterm infants in the placebo group. The day that enteral feeding was successfully started, the time to establishing one-half, two-thirds, and full enteral feedings (reaching at least 150 mL/kg/day), the number of episodes of feeding intolerance, the time to regain birth weight and the incidence of necrotizing enterocolitis (NEC) were recorded. RESULTS Both groups showed no significant difference in the time to achieve one-half, two-thirds, or full enteral feeding, no signs of feeding intolerance, and no cases of NEC were recorded. CONCLUSION Enteral erythropoietin does not appear to affect feeding intolerance or NEC incidence.
2.
Iron and the anemia of chronic disease.
Spivak, JL
Oncology (Williston Park, N.Y.). 2002;(9 Suppl 10):25-33
Abstract
The anemia of chronic disease traditionally is defined as a hypoproliferative anemia of no apparent cause that occurs in association with an inflammatory, infectious, or neoplastic disorder, and resolves when the underlying disorder is corrected. Disordered iron metabolism as manifested by a low serum iron, decreased serum transferrin, decreased transferrin saturation, increased serum ferritin, increased reticuloendothelial iron stores, increased erythrocyte-free protoporphyrin, and reduced iron absorption, is a characteristic feature of the anemia of chronic disease and has been thought to be a major factor contributing to the syndrome. A mild shortening of red cell life span also occurs. However, we now know that impaired erythropoietin production and impaired responsiveness of erythroid progenitor cells to this hormone are also important abnormalities contributing to the anemia of chronic disease, and appear to be due to the effects of inflammatory cytokines. Increased intracellular iron may also have a role in the inhibition of erythropoietin production, since the oxygen sensor is a hemoprotein. While the role of inflammatory cytokines in the pathogenesis of anemia of chronic disease appears unequivocal, it has become apparent that disordered iron metabolism, while characteristic of this form of anemia, may not be central to its pathogenesis. It is undisputed that iron absorption is reduced, and that iron administered intravenously is rapidly sequestered in the reticuloendothelial system; however, iron delivery to the bone marrow is not impaired, and erythroid iron utilization is not markedly depressed in anemia of chronic disease. Importantly, recombinant erythropoietin therapy can correct the anemia of chronic disease, but it cannot correct the anemia due to iron deficiency. This refutes the concept that the lack of available iron is central to the pathogenesis of the syndrome. Indeed, it is highly likely that abnormalities such as reduced iron absorption and decreased erythroblast transferrin-receptor expression largely result from decreased erythropoietin production and inhibition of its activity by inflammatory cytokines.