Inositol During Perinatal Transition

Abstract

myo-Inositol (inositol) is a common micronutrient. Its content is high in breast milk, especially in colostrum. However, it is not included in parenteral nutrition of extremely preterm infants. On the basis of a meta-analysis of 2 trials, addition of inositol to parenteral nutrition or to enteral feeding decreased the risk of retinopathy of prematurity. During the presurfactant era, inositol additionally increased survival without serious pulmonary morbidity. Placenta is active in inositol synthesis, and the fetus reuses inositol secreted to amniotic fluid. As a result of loss of inositol to urine and inositol metabolism, the plasma half-life in very preterm infants shortly after birth is 5.5 hours. In the absence of inositol intake, 10% to 20% of total body inositol may be lost within 24 hours. Some preterm infants may be born with a deficient inositol pool (eg, prolonged rupture of fetal membranes). Mice that have a single-gene defect in inositol metabolism succumb at term birth despite apparently near-normal antenatal development. Pathologic features include dysfunction of the respiratory center, severe neuropathy, closure of pulmonary air spaces, defect in osteoblasts, and deformation of bones. All severe defects are preventable by antenatal and neonatal inositol supplementation. According to experimental results, inositol supplementation augments the efficacy of antenatal glucocorticoid for acceleration of lung maturity. The effect of inositol deficiency on the development of retina has not been studied in the experimental setting. Administration of inositol in small preterm infants shortly after birth appears to be safe. However, data are limited on the efficacy of inositol supplementation in the intensive care unit setting. Antenatal inositol supplementation in very high-risk pregnancies remains to be studied.