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Higgins LE, Rey de Castro N, Addo N, et al. Placental Features of Late-Onset Adverse Pregnancy Outcome. PLoS One. 2015;10(6):e0129117doi: 10.1371/journal.pone.0129117.
Higgins, L. E., Rey de Castro, N., Addo, N., Wareing, M., Greenwood, S. L., Jones, R. L., Sibley, C. P., Johnstone, E. D., & Heazell, A. E. (2015). Placental Features of Late-Onset Adverse Pregnancy Outcome. PloS one, 10(6), e0129117. https://doi.org/10.1371/journal.pone.0129117
Higgins, Lucy E, et al. "Placental Features of Late-Onset Adverse Pregnancy Outcome." PloS one vol. 10,6 (2015): e0129117. doi: https://doi.org/10.1371/journal.pone.0129117
Higgins LE, Rey de Castro N, Addo N, Wareing M, Greenwood SL, Jones RL, Sibley CP, Johnstone ED, Heazell AE. Placental Features of Late-Onset Adverse Pregnancy Outcome. PLoS One. 2015 Jun 29;10(6):e0129117. doi: 10.1371/journal.pone.0129117. eCollection 2015. PMID: 26120838; PMCID: PMC4488264.
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PLoS One. 2015 Jun 29;10(6):e0129117. doi: 10.1371/journal.pone.0129117. eCollection 2015.

Placental Features of Late-Onset Adverse Pregnancy Outcome.

PloS one

Lucy E Higgins, Nicolas Rey de Castro, Naa Addo, Mark Wareing, Susan L Greenwood, Rebecca L Jones, Colin P Sibley, Edward D Johnstone, Alexander E P Heazell

Affiliations

  1. Maternal and Fetal Health Research Centre, Institute of Human Development, University of Manchester, Manchester, M13 9WL, United Kingdom; Maternal and Fetal Health Research Centre, St. Mary's Hospital, Central Manchester University Hospitals NHS Foundation Trust, Manchester Academic Health Science Centre, Manchester, M13 9WL, United Kingdom.

PMID: 26120838 PMCID: PMC4488264 DOI: 10.1371/journal.pone.0129117

Abstract

OBJECTIVE: Currently, no investigations reliably identify placental dysfunction in late pregnancy. To facilitate the development of such investigations we aimed to identify placental features that differ between normal and adverse outcome in late pregnancy in a group of pregnancies with reduced fetal movement.

METHODS: Following third trimester presentation with reduced fetal movement (N = 100), placental structure ex vivo was measured. Placental function was then assessed in terms of (i) chorionic plate artery agonist responses and length-tension characteristics using wire myography and (ii) production and release of placentally derived hormones (by quantitative polymerase chain reaction and enzyme linked immunosorbant assay of villous tissue and explant conditioned culture medium).

RESULTS: Placentas from pregnancies ending in adverse outcome (N = 23) were ~25% smaller in weight, volume, length, width and disc area (all p<0.0001) compared with those from normal outcome pregnancies. Villous and trophoblast areas were unchanged, but villous vascularity was reduced (median (interquartile range): adverse outcome 10 (10-12) vessels/mm2 vs. normal outcome 13 (12-15), p = 0.002). Adverse outcome pregnancy placental arteries were relatively insensitive to nitric oxide donated by sodium nitroprusside compared to normal outcome pregnancy placental arteries (50% Effective Concentration 30 (19-50) nM vs. 12 (6-24), p = 0.02). Adverse outcome pregnancy placental tissue contained less human chorionic gonadotrophin (20 (11-50) vs. 55 (24-102) mIU/mg, p = 0.007) and human placental lactogen (11 (6-14) vs. 27 (9-50) mg/mg, p = 0.006) and released more soluble fms-like tyrosine kinase-1 (21 (13-29) vs. 5 (2-15) ng/mg, p = 0.01) compared with normal outcome pregnancy placental tissue.

CONCLUSION: These data provide a description of the placental phenotype of adverse outcome in late pregnancy. Antenatal tests that accurately reflect elements of this phenotype may improve its prediction.

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