PURPOSE: To test the hypothesis that the presence of bacteria and/or histologic inflammation in the placenta of infants born preterm is associated with an increased risk for severe retinopathy of prematurity (ROP). METHODS: This was a prospective cohort study. Exploratory and multivariable data analyses were used, including logistic regression models with interaction terms. Main outcomes were four definitions of severe ROP: stage 3 or higher, any ROP in zone I, prethreshold/threshold, and plus disease. RESULTS: Individually, placenta bacteria and histologic inflammation were not associated with severe ROP in univariable analyses among 1064 infants with gestational age <28 weeks or among 715 infants with gestational age <27 weeks (we excluded infants with a gestational age of 27 weeks because of the very small number of ROP cases). However, the co-occurrence of bacteria and inflammation was associated with an increased risk for ROP in zone I (odds ratio, 3.1; 95% confidence interval, 1.02-9.5). Among 339 infants with any placental bacteria, the co-occurrence of (1) inflammation and a gestational age of 23 to 24 weeks and (2) inflammation and hyperoxia were associated with prominent increases in risk for all definitions of severe ROP. CONCLUSIONS: While antenatal exposure to infection or inflammation alone does not appear to convey risk information for severe ROP, their co-occurrence does. This finding supports the hypothesis that a fetal inflammatory response to antenatal infection might be part of the etiology of severe ROP.
PURPOSE: To test the hypothesis that the presence of bacteria and/or histologic inflammation in the placenta of infants born preterm is associated with an increased risk for severe retinopathy of prematurity (ROP). METHODS: This was a prospective cohort study. Exploratory and multivariable data analyses were used, including logistic regression models with interaction terms. Main outcomes were four definitions of severe ROP: stage 3 or higher, any ROP in zone I, prethreshold/threshold, and plus disease. RESULTS: Individually, placenta bacteria and histologic inflammation were not associated with severe ROP in univariable analyses among 1064 infants with gestational age <28 weeks or among 715 infants with gestational age <27 weeks (we excluded infants with a gestational age of 27 weeks because of the very small number of ROP cases). However, the co-occurrence of bacteria and inflammation was associated with an increased risk for ROP in zone I (odds ratio, 3.1; 95% confidence interval, 1.02-9.5). Among 339 infants with any placental bacteria, the co-occurrence of (1) inflammation and a gestational age of 23 to 24 weeks and (2) inflammation and hyperoxia were associated with prominent increases in risk for all definitions of severe ROP. CONCLUSIONS: While antenatal exposure to infection or inflammation alone does not appear to convey risk information for severe ROP, their co-occurrence does. This finding supports the hypothesis that a fetal inflammatory response to antenatal infection might be part of the etiology of severe ROP.
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