IGF-I in the clinics: Use in retinopathy of prematurity

Abstract

Retinopathy of prematurity is a potentially blinding disease, which is associated with low neonatal IGF-I serum concentrations and poor growth. In severe cases impaired retinal vessel growth is followed by pathologic neovascularization, which may lead to retinal detachment. IGF-I may promote growth even in catabolic states. Treating preterm infants with recombinant human (rh) IGF-I to concentrations normally found during gestation has been suggested to have a preventative effect on ROP. A recent phase 2 study treating infants (gestational age between 23 weeks+ 0 days and 27 weeks + 6 days) with rhIGF-I/IGF binding protein-3 until 30 postmenstrual weeks showed no effect on ROP but a 53% reduction in severe bronchopulmonary dysplasia and 44% reduction in severe intraventricular hemorrhage. Oxygen is a major risk factor for ROP and during the phase 2 study oxygen saturation targets were increased to 90–95%, due to national guidelines, which might have affected ROP rate and severity making increased IGF-I a weaker preventative factor for ROP.

Severe retinopathy of prematurity is associated with reduced cerebellar and brainstem volumes at term and neurodevelopmental deficits at 2 years

“…Insulin-like growth factor-1 (IGF-1) and vascular endothelial growth factor (VEGF) are two essential growth factors that need to be in balance for normal retinal vessel growth (4). Peri-and postnatal infections, postnatal undernutrition, and fluctuating oxygen levels-as a result of an immature respiratory system and neonatal illness-may impede IGF-1 production in the preterm infant (5). Concomitantly, VEGF is relatively suppressed by higher oxygen levels present in the extrauterine environment.…”

Current evidence and outcomes for retinopathy of prematurity prevention: insight into novel maternal and placental contributions

“…This necessitates an understanding of early ROP risk and disease mechanisms, occurring prior to and within the first phase of ROP. While overall these are incompletely understood, there has been a significant effort to better delineate early ROP pathological mechanisms [10,11,[14][15][16]. Work from our group and others substantiates that only low BW, prematurity and post-natal oxygen exposure confer independent ROP risk [9-11, 15, 17-19].…”

Retracted: Effects of apelin on retinal microglial cells in a rat model of oxygen‐induced retinopathy of prematurity

“…It exclusively occurs in new born preterm infants, which may result in severe visual impairment or childhood blindness, and ROP has inevitably become the major cause of blindness in children all over the world as the mortality rate in preterm infants has decreased over the last few years . Each year, over 20 000 infants globally become blind or suffer from severe visual impairment owing to ROP, and a part of the blindness can be prevented by means of advanced care . ROP affects especially preterm infants born before 28 weeks, while there are more and more blind infants with ROP receiving no appropriate neonatal care .…”