ABSTRACT
Retinopathy of prematurity (ROP) is one of the leading yet preventable causes of childhood blindness worldwide. The purpose of this review is to provide a practical template for observational and treatment methods in order to reduce the overall incidence of any ROP and to improve both short-term and long-term outcomes once Type 1 ROP (treatable ROP) develops.
Subject(s)
Retinopathy of Prematurity , Blindness/epidemiology , Blindness/etiology , Blindness/prevention & control , Humans , Infant, Newborn , Retinopathy of Prematurity/complications , Retinopathy of Prematurity/epidemiology , Retinopathy of Prematurity/prevention & controlABSTRACT
BACKGROUND: Transient neonatal hyperglycemia (HG) has been reported in up to 80% of extremely preterm human infants. We hypothesize that severe HG is associated with increased morbidity and mortality in preterm baboons. METHODS: Sixty-six baboons born at 67% of gestation were studied. HG was defined as serum glucose level ≥150 mg/dl during the first week of life. Animals were stratified into two groups: severe HG (≥8 events) and nonsevere HG (<8 events). RESULTS: HG developed in 65 of the 66 (98%) baboons that were included. A total of 3,386 glucose measurements were obtained. The mean serum glucose level was 159 ± 69 mg/dl for the severe HG group and 130 ± 48 mg/dl for the nonsevere HG group during the first week of life. No differences were found in gender, birth weight, sepsis, patent ductus arteriosus, or oxygenation/ventilation indexes between groups. Severe HG was associated with early death even after controlling for sepsis, postnatal steroid exposure, and catecholamine utilization. CONCLUSION: HG is common in preterm baboons and is not associated with short-term morbidity. Severe HG occurring in the first week of life is associated with early death in preterm baboons.
Subject(s)
Disease Models, Animal , Hyperglycemia/mortality , Hyperglycemia/physiopathology , Animals , Animals, Newborn , Birth Weight , Blood Glucose , Female , Humans , Infant, Extremely Premature , Infant, Newborn , Logistic Models , Male , Papio , Sex FactorsABSTRACT
Erratic regulation of glucose metabolism including hyperglycemia is a common condition in premature infants and is associated with increased morbidity and mortality. The objective of this study was to examine histological and ultrastructural differences in the endocrine pancreas in fetal (throughout gestation) and neonatal baboons. Twelve fetal baboons were delivered at 125 days (d) gestational age (GA), 140d GA, or 175d GA. Eight animals were delivered at term (185d GA); half were fed for 5 days. Seventy-three nondiabetic adult baboons were used for comparison. Pancreatic tissue was studied using light microscopy, confocal imaging, and electron microscopy. The fetal and neonatal endocrine pancreas islet architecture became more organized as GA advanced. The percent areas of α-ß-δ-cell type were similar within each fetal and newborn GA (NS) but were higher than the adults (P<0.05) regardless of GA. The ratio of ß cells within the islet (whole and core) increased with gestation (P<0.01). Neonatal baboons, which survived for 5 days (feeding), had a 2.5-fold increase in pancreas weight compared with their counterparts killed at birth (P=0.01). Endocrine cells were also found in exocrine ductal and acinar cells in 125, 140 and 175d GA fetuses. Subpopulation of tissue that coexpressed trypsin and glucagon/insulin shows the presence of cells with mixed endo-exocrine lineage in fetuses. In summary, the fetal endocrine pancreas has no prevalence of a α-ß-δ-cell type with larger endocrine cell percent areas than adults. Cells with mixed endocrine/exocrine phenotype occur during fetal development. Developmental differences may play a role in glucose homeostasis during the neonatal period and may have long-term implications.
