Role of maternal, fetal and placental histopathology factors in the pathogenesis of retinopathy of prematurity

Abstract

AbstractPurposeTo investigate if maternal, fetal and placental vascular and/or molecular changes predict the risk for retinopathy of prematurity in preterm infants.MethodologyThe postnatal and antenatal data and placental histopathological changes; H&E staining of placental sections and molecular findings; gene expression analysis by qRT-PCR and protein expression by IHC at the maternal-fetal interface were collected from 20 placental samples and categorized into 3 groups: full-term (n=10), preterm without ROP (n=7) and preterm with ROP (n=6).ResultsThe correlation analysis indicated significant association of increased monocytes (p=0.042), fetal growth retardation (p=0.000), apnoeic spell (p=0.033), ventilation (p=0.009), length in hospital stay (p=0.001) and decreased RBC (p=0.02), Hb (p=0.048), PCV (p=0.010), gestational age (p=0.003), birth weight (p=0.000) with increased risk of ROP. Along with these factors, placental weight(p=0.001), diameter (p=0.019), Tenny-Parker changes (p=0.025), alternating area of small and short hyper mature villi (p=0.033) are also found to be significant determinants of the disease. Gene expression analysis revealed significant increase in hypoxia (HIF-1gene expression; p=0.007) and non-significant increase in the pro-inflammatory markerIL-6. The protein expression also showed the significantly increased activation of complement pathway (CFH) and NF- ΚB at maternal-fetal interface.ConclusionsOur preliminary results support the changes in the maternal-fetal factors, placental histopathology and molecular alterations related to hypoxia, inflammation and complement activation at maternal-fetal interface in preterm with ROP placentas. These changes have the potential to predict the risk of the disease but the results are required to be further validated in larger cohort.