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Gestational age and infection are greater predictors of placental histopathology than maternal prepregnancy BMI.

Duffley, E.; Grynspan, D.; Scott, H.; Lafreniere, A.; Borba Vieira de Andrade, C.; Bloise, E.; Connor, K. L.

2021-12-27 pathology
10.1101/2021.12.21.21268133 medRxiv
Show abstract

The placenta undergoes morphological and functional adaptions to adverse exposures during pregnancy. The effects of suboptimal maternal body mass index (BMI), preterm birth, and infection on placental histopathological phenotypes remain unclear, despite the association between these conditions and poor offspring outcomes. We hypothesized that suboptimal maternal prepregnancy BMI and preterm birth (with and without infection) would associate with altered placental maturity and morphometry, and that altered placental maturity would associate with poor birth outcomes. Clinical data and human placentae were collected from 96 pregnancies where mothers were underweight, normal weight, overweight, or obese, without other major complications. Placental histopathological characteristics were scored with an anatomical pathologist. Associations between maternal BMI, placental pathology (immaturity and hypermaturity), placental morphometry, and infant outcomes were investigated at term and preterm, with and without infection. Fetal vascular endothelium volumetric proportion was decreased, whereas syncytial knot volumetric proportion was increased, in placentae from preterm pregnancies with chorioamnionitis compared to term placentae. At term and preterm, pregnancies with overweight and obesity had a high percentage increase in proportion of immature placentae compared to normal weight. Placental maturity did not associate with infant birth outcomes. We observed placental hypermaturity and altered placental morphometry among preterm pregnancies with chorioamnionitis, suggestive of altered placental development, which may inform about pregnancies susceptible to preterm birth and infection. Our data increase our understanding of how common metabolic exposures and preterm birth, in the absence of other comorbidities or perinatal events, potentially contribute to poor pregnancy outcomes and the programming of offspring development.

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