An update of the Swedish reference standards for weight, length, and head circumference at birth, for each week of gestational age, is presented. It is based on the total Swedish cohorts of infants born 1977-1981 (n = 475,588). A "healthy population" (79%) was extracted, using prospectively collected data. Weekly (28-42 weeks) grouped data for length and head circumference were well approximated by the normal distribution, but the distributions for birthweight were positively skewed. The original skewed distributions for birthweight were transformed, using the square root, resulting in distributions close to the Gaussian. For smoothing purposes, the weakly values for the mean and the standard deviation were both fitted by a third degree polynomial function. These functions also make possible the calculation of the continuous variable, standard deviation score, for individual newborn infants as well as a comparison of distributions between groups of infants. The reference values and charts presented here have two major advantages over the current Swedish ones: the sample size used is now sufficiently large at the lower gestational ages, so that empirically found variations can be used, and the skewness of the birth weight distribution has been taken into account. The use of the reference standards presented here improves and facilitates evaluation of size deviation at birth.
Retinopathy of prematurity is a blinding disease, initiated by lack of retinal vascular growth after premature birth. We show that lack of insulin-like growth factor I (IGF-I) in knockout mice prevents normal retinal vascular growth, despite the presence of vascular endothelial growth factor, important to vessel development. In vitro, low levels of IGF-I prevent vascular endothelial growth factor-induced activation of protein kinase B (Akt), a kinase critical for endothelial cell survival. Our results from studies in premature infants suggest that if the IGF-I level is sufficient after birth, normal vessel development occurs and retinopathy of prematurity does not develop. When IGF-I is persistently low, vessels cease to grow, maturing avascular retina becomes hypoxic and vascular endothelial growth factor accumulates in the vitreous. As IGF-I increases to a critical level, retinal neovascularization is triggered. These data indicate that serum IGF-I levels in premature infants can predict which infants will develop retinopathy of prematurity and further suggests that early restoration of IGF-I in premature infants to normal levels could prevent this disease.
These results indicate that persistent low serum concentrations of IGF-I after premature birth are associated with later development of ROP and other complications of prematurity. IGF-I is at least as strong a determinant of risk for ROP as postmenstrual age at birth and birth weight.
Background: Growth charts and child growth assessment have become prime global instruments in child health practice over the 30 years. An updated, continuous growth standard that bridges size at birth values with postnatal growth values can improve child growth screening and monitoring.
The weight, insulin-like growth factor, neonatal retinopathy of prematurity algorithm detected early 100% of infants who developed retinopathy of prematurity requiring treatment and correctly predicted the majority who did not require treatment. With this simple postnatal evaluation, costly stressful eye examinations can be markedly reduced (approximately 75% of infants). In addition, early identification of children at risk may lead to the initiation of interventions and possibly prevent sight-threatening retinopathy of prematurity.
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