Oral Propranolol Improve Retinopathy of Prematurity Outcomes in Very Preterm Infants
Status:
Unknown status
Trial end date:
2018-05-01
Target enrollment:
Participant gender:
Summary
Retinopathy of prematurity (ROP) is a major cause of blindness and visual impairment in
children in both developing and developed countries around the world. ROP is a multifactorial
disease characterized by perturbation of normal vascular development in the retina. The
pathogenesis of ROP is hypothesized to consist of two distinct phases of which the second
phase is characterized by hypoxia-induced up-regulation of vascular endothelial growth factor
(VEGF) and retinal neovascularization.
Recent studies have shown a relationship between the β-adrenergic system and angiogenesis.
This relationship has been observed in several diseases, like infantile hemangiomas, ROP, and
neoplasias. Studies in animal models have shown that norepinephrine stimulates VEGF
expression and secretion in retinal cells. In oxygen induced retinopathy, blockage of
β-adrenergic receptors (β-AR) can inhibit the angiogenic cascade and interfere with further
proliferation of retinal vasculature. Also, angiogenesis seems to be impaired in β-Argene
deficient mice, when exposed to hypoxia and other stimuli, but this function is restored
after gene therapy.
Assuming in human preterm newborns with ROP that VEGF overexpression and retinal
neovascularization in response to hypoxia might involve b-AR activation, we design
prospective randomized study to assess the effect of oral propranolol on the progression of
early stages of ROP in very low birth weight infants.