Retinopathy of prematurity in infants without fetal growth restriction is decreased with the progression of acute histologic chorioamnionitis: New observation as a protective factor against retinopathy of prematurity. (15th January 2021)

• Record Type: Journal Article
• Authors: Park, Jee Yoon; Park, Chan-Wook; Moon, Kyung Chul; Park, Joong Shin; Jun, Jong Kwan; Lee, Seok Jae; Kim, Jeong Hun
• Is Part Of: Placenta. Volume 104(2021)
• Page Start: 161
• Page End: 167
• Publication Date: 2021-01-15
• Subjects: Retinopathy of prematurity -- Acute histologic chorioamnionitis -- Preterm birth; Placenta -- Periodicals; Reproduction -- Periodicals; Placenta -- Periodicals; Placenta -- Périodiques; Reproduction -- Périodiques; 612.63
• DOI: 10.1016/j.placenta.2020.12.007
• Languages: English
• ISSNs: 0143-4004

Abstract

Abstract: Introduction: IGF-1 deficiency in prenatal period is known to be a definite pathophysiology of retinopathy of prematurity(ROP), which is more frequent in infants with fetal growth restriction(FGR). Of note, recent reports demonstrated intra-amniotic inflammation(IAI) closely linked to acute histologic chorioamnionitis(acute-HCA) is associated with a decrease in intact-form of IGFBP-1, ultimately rising the probability of an increase in IGF-1. Therefore, we hypothesized ROP in preterm-infants without FGR would be decreased with the progression of acute-HCA. Methods: The frequency of ROP was examined in 85 singleton preterm-infants(24.5weeks ≤ gestational-age[GA] at delivery<30weeks) due to either preterm-labor and intact-membranes(PTL) or preterm premature rupture of membranes(preterm-PROM) without FGR(birth-weight<5th percentile for GA). Patients were divided according to the progression of inflammation in extra-placental membranes(EPM) and the progression of inflammation in chorionic-vessel(CV) and umbilical-cord(UC). Results: 1) ROP was present in 40%(34/85) of study-population; 2) Of note, there was a significant stepwise-decrease in ROP with the progression of inflammation in EPM(inflammation-free EPM vs. inflammation restricted to CD vs. amnionitis; 55.6%[15/27]vs.39.5%[17/43]vs.13.3%[2/15]) and the progression of inflammation in CV and UC(inflammation-free CV and UC vs. inflammation restricted to CV and umbilical vessels vs. inflammation in Wharton's jelly[WJ]; 49.2%[29/59]vs.25.0%[3/12]vs.14.3%[2/14])(each-for P < 0.05, Chi-square test and each-for P < 0.01, linear-by-linear association); 3) Multiple logistic-regression analysis demonstrated amnionitis(Odds-Ratio 0.120, 95%Confidence-Interval 0.022–0.654, P = 0.014) and inflammation in WJ(Odds-Ratio 0.124, 95%Confidence-Interval 0.022–0.694, P = 0.018) were independent protective-factors against ROP. Discussion: ROP in preterm-infants due to PTL or preterm-PROM without FGR is decreased with the progression of acute-HCA. This finding may be an evidence to suggest the progression of acute-HCA is closely associated with reducing the pathophysiology of ROP. Highlights: IGF-1 deficiency in prenatal period is known to be definite pathophysiology of ROP. FGR associated with IGF-1 deficiency is likely to be a confounding-factor for ROP. AF inflammation was associated with IGFBP-1 decrease, leading to IGF-1 increase. ROP in preterm infants without FGR is decreased with the progression of acute-HCA. Progression of acute-HCA is closely related to reducing the pathophysiology of ROP.