169 - Effects of Using Reticulocyte Hemoglobin to Titrate Iron Supplementation in Neonates Receiving Erythropoietin

Publication Number: 2163.169

Alexandra Kinzer, UH Rainbow Babies & Children's Hospital, Cleveland, OH, United States; Rita M.. Ryan, UH Rainbow Babies & Children's Hospital, Cleveland, OH, United States; Eric Tano, Kidz Medical Services, Coral Gables, FL, United States; Jaime Marasch, UH Rainbow Babies & Children's Hospital, Cleveland, OH, United States; Mary Nock, UH Rainbow Babies & Children's Hospital, Case Western Reserve University School of Medicine, Cleveland, OH, United States

Background: Recombinant humanized erythropoietin (EPO) is used to treat anemia of prematurity (AOP) due to the role of erythropoietin in red blood cell production. Iron is necessary for both red blood cell production and neurodevelopment in developing infants. Reticulocyte hemoglobin (Ret-He) can assess iron sufficiency, and we previously noted a marked drop in Ret-He with EPO therapy. We hypothesized that using Ret-He to guide iron supplementation during EPO would reduce the drop in Ret-He and increase the EPO-induced rise in hematocrit (Hct).

Objective: To determine if a change in our neonatal intensive care unit (NICU) EPO protocol to increase iron dosing by 2mg/kg/day to a maximum of 12 mg/kg/day for a weekly Ret-He < 29 pg, results in a smaller drop in Ret-He while on EPO therapy. Secondary objectives of this study were to assess whether the change results in a higher rise in Hct, fewer blood transfusions, or more feeding intolerance.

Design/Methods: All NICU patients who received EPO for AOP were included. EPO is dosed at 300u/kg three times per week with a starting iron dose of 6 mg/kg/day. Data collected included adherence to the new protocol, Hct, weekly Ret-He, number of blood transfusions, and details about feeding tolerance.

Results: Data were previously collected for 172 EPO courses (cohort 1) and collected for 63 EPO treatment courses after the protocol change (cohort 2). Overall, there was a significant drop in Ret-He in each cohort (p < 0.0001 by Wilcoxon rank sum test) but no significant difference between the two groups (4.3±3.4 vs. 3.9±3.3) (Table). There was a trend toward a higher rise in Hct after the protocol change (5.1±4.3 vs. 6.2±3.3, p=0.07, by t-test). Overall, rise in Hct was significantly associated with the number of EPO doses received (p < 0.0001 by linear regression) and with iron dose at the start of EPO therapy (p=0.01). There was no significant difference in number of blood transfusions or in hematochezia, but percentage of patients with constipation requiring intervention (4.1% vs 12.7%, p=0.03) was increased after the protocol change. The new protocol was followed in 58.7% of EPO courses and improved over time.

Conclusion(s): Using Ret-He to titrate iron supplementation did not ameliorate the drop in Ret-He, but there was a trend toward a higher rise in Hct. Rise in Hct was significantly associated with the iron dose at the start of EPO therapy, suggesting that a larger initial iron dose at the start of therapy may produce a better EPO response. It is possible that, as time continues, the increase in iron dictated by the protocol may happen more consistently.

Hematocrit, Ret-He, and Iron Dosing on EPO
Table.pdf