INTRODUCTION Placental thickness in the second trimester of pregnancy has been associated with risks of placenta-mediated complications of pregnancy. We aimed to estimate the association between first-trimester maximum placental thickness… Click to show full abstract
INTRODUCTION Placental thickness in the second trimester of pregnancy has been associated with risks of placenta-mediated complications of pregnancy. We aimed to estimate the association between first-trimester maximum placental thickness and the subsequent risk of preeclampsia and/or the delivery of small-for-gestational-age (SGA) neonate. METHODS Prospective cohort study of women recruited at 11-14 weeks gestation. Placental thickness was measured at its apparent center and reported in multiple of median (MoM) adjusted for gestational age. Participants were followed until delivery for pregnancy outcomes. Placental measurements of participants who developed preeclampsia and/or delivered SGA neonate (defined as birth weight below 10th percentile) were compared with those who did not using non-parametric statistical analyses. RESULTS We recruited 991 participants at a mean gestational age of 12.7 ± 0.7 weeks of gestation. SGA (n = 52) was associated with reduced 1st trimester placental thickness (median: 0.89 MoM; interquartile (IQ): 0.75-1.02 vs 0.98 MoM; IQ: 0.84-1.15; p < 0.01). Pregnancies that developed preeclampsia (n = 20) tended to have greater placental thickness (median: 1.10 MoM; IQ: 0.93-1.25 vs 0.97 MoM; IQ: 0.84-1.14; p = 0.06) with values > 1.2 MoM significantly increasing the risk for preeclampsia (relative risk: 3.6; 95%CI: 1.5-8.6, p < 0.01). Pregnancies complicated by both SGA and preeclampsia (n = 5) had similar placental thickness in the first-trimester in comparison with uncomplicated pregnancies (median: 1.03 MoM; IQ: 0.89-1.42 vs 0.98 MoM; IQ: 0.84-1.14; p = 0.33). CONCLUSION First-trimester placental thickness diverges in pregnancies at risk of preeclampsia (increased) or SGA (decreased), but remains within normal values in pregnancies at risk of both conditions, suggesting that the underlying pathologies have some opposing effects on early placental growth. The current findings should be validated in a larger cohort.
               
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