Erythropoietin is not a risk factor for severe retinopathy of prematurity among high risk preterm infants.

BACKGROUND: Retinopathy of prematurity (ROP) is a developmental retinal vaso-proliferative disease and a leading cause of blindness in children. Early gestational age, low birth weight and unregulated oxygen exposure are the main risk factors for the development of ROP. There are conflicting reports of a possible association between recombinant Erythropoietin (rhEPO) use and an increased risk for the development of ROP. OBJECTIVE: To determine whether rhEPO is an independent risk factor for the development of severe ROP among preterm infants with a gestational age of 23 to 32 weeks and a birth weight <1500 g. METHODS: We performed a retrospective study of risk factors for ROP on a cohort of 1762 premature infants born between 2009 and 2014, half of whom received rhEPO. To examine the association between treated ROP and rhEPO, a propensity score (PS) analysis was performed using the inverse probability of treatment weighted (IPTW) approach. RESULTS: The incidence of treated ROP was 7.3% (129/1762). PS analysis did not show an association between rhEPO and severe ROP needing treatment or ROP stage 2 or higher, in either the whole population or in the subgroup of babies born at 23 to 28 weeks gestation, in whom the incidence of severe ROP was the highest. Of 117 patients treated for Type 1 or worsening stage 3 ROP, 17 were first diagnosed after NICU discharge. CONCLUSION: Our study showed no association between Erythropoietin use and severe ROP and highlights the importance of Ophthalmology follow up after hospital discharge.

Erythropoietin treatment is associated with a reduction in moderate to severe bronchopulmonary dysplasia in preterm infants. A regional retrospective study.

Erythropoietin treatment is associated with a reduction in moderate to severe bronchopulmonary dysplasia in preterm infants. A regional retrospective study. OBJECTIVE: To determine whether premature infants treated with erythropoietin (Epo) in the neonatal period for anemia had a lower incidence of bronchopulmonary dysplasia (BPD), defined as oxygen need at 36 weeks postmenstrual age, and lower rehospitalization rates in the first year of life than infants not exposed. METHODS: Retrospective study of a population of infants born at 23 to 32 weeks gestational age, between January 2009 and December 2014, with birthweight ≤1500 g. Patient characteristics, and risk factors for BPD were compared between patients who received erythropoietin, and those not exposed. To examine the association between the outcomes of BPD at 36 weeks PMA, rehospitalization, and erythropoietin treatment, we performed a propensity score (PS) analysis using inverse probability of treatment weighted (IPTW) approach. For comparison, we conducted a logistic regression adjusting for the same covariates used to generate PS using the original population. RESULTS: The study population included 1821 preterm infants: 928 received Epo and 893 did not. Epo treatment was associated with a reduction in BPD (18.8% versus 25.9%, p < 0.01) at 36 weeks PMA and reduced median length of stay with lowest BPD rate with Epo initiation before 2 weeks of age. There was no difference in rehospitalization rates in the first year of life. CONCLUSION: Erythropoietin treatment was associated with a reduction in BPD but not in rehospitalization rate in the first year of life.

Myocardial macronutrient transporter adaptations in the adult pregestational female intrauterine and postnatal growth-restricted offspring.

Associations between exponential childhood growth superimposed on low birth weight and adult onset cardiovascular disease with glucose intolerance/type 2 diabetes mellitus exist in epidemiological investigations. To determine the metabolic adaptations that guard against myocardial failure on subsequent exposure to hypoxia, we compared with controls (CON), the effect of intrauterine (IUGR), postnatal (PNGR), and intrauterine and postnatal (IPGR) calorie and growth restriction (n = 6/group) on myocardial macronutrient transporter (fatty acid and glucose) -mediated uptake in pregestational young female adult rat offspring. A higher myocardial FAT/CD36 protein expression in IUGR, PNGR, and IPGR, with higher FATP1 in IUGR, FATP6 in PNGR, FABP-c in PNGR and IPGR, and no change in GLUT4 of all groups was observed. These adaptive macronutrient transporter protein changes were associated with no change in myocardial [(3)H]bromopalmitate accumulation but a diminution in 2-deoxy-[(14)C]glucose uptake. Examination of the sarcolemmal subfraction revealed higher basal concentrations of FAT/CD36 in PNGR and FATP1 and GLUT4 in IUGR, PNGR, and IPGR vs. CON. Exogenous insulin uniformly further enhanced sarcolemmal association of these macronutrient transporter proteins above that of basal, with the exception of insulin resistance of FATP1 and GLUT4 in IUGR and FAT/CD36 in PNGR. The basal sarcolemmal macronutrient transporter adaptations proved protective against subsequent chronic hypoxic exposure (7 days) only in IUGR and PNGR, with notable deterioration in IPGR and CON of the echocardiographic ejection fraction. We conclude that the IUGR and PNGR pregestational adult female offspring displayed a resistance to insulin-induced translocation of FATP1, GLUT4, or FAT/CD36 to the myocardial sarcolemma due to preexistent higher basal concentrations. This basal adaptation of myocardial macronutrient transporters ensured adequate fatty acid uptake, thereby proving protective against chronic hypoxia-induced myocardial compromise.

Postnatal rosiglitazone administration to neonatal rat pups does not alter the young adult metabolic phenotype.

BACKGROUND: Rosiglitazone (RGZ), a peroxisome proliferator-activated receptor-γ (PPARγ) agonist, significantly enhances lung maturation without affecting blood biochemical and metabolic profiles in the newborn period. However, whether this exposure to RGZ in neonatal life alters the adult metabolic phenotype is not known. OBJECTIVE: To determine the effects of early postnatal administration of RGZ on the young adult metabolic phenotype. METHODS: Newborn rat pups were administered either saline or RGZ for the first 7 days of life. At 11-14 weeks, glucose and insulin tolerance tests and deuterium labeling were performed. Blood and tissues were analyzed for various metabolic parameters. RESULTS: Overall, there was no effect of early postnatal RGZ administration on young adult body weight, glucose and insulin tolerance, plasma cholesterol and triglyceride profiles, insulin, glucagon, cardiac troponin, fatty acid synthesis, or tissue adipogenic differentiation. CONCLUSIONS: Treatment with RGZ in early neonatal life does not alter later developmental metabolic programming or lead to an altered metabolic phenotype in the young adult, further re-enforcing the safety of PPARγ agonists as a novel lung-protective strategy.