The effect of maternal obstructive sleep apnea on the placenta.


Journal

Sleep
ISSN: 1550-9109
Titre abrégé: Sleep
Pays: United States
ID NLM: 7809084

Informations de publication

Date de publication:
11 06 2019
Historique:
received: 22 08 2018
revised: 07 02 2019
accepted: 14 03 2019
pubmed: 25 3 2019
medline: 31 3 2020
entrez: 24 3 2019
Statut: ppublish

Résumé

Obstructive sleep apnea (OSA) during pregnancy has been associated with adverse maternal outcomes. However, the effect of maternal OSA on fetal growth is less clear. The placenta is a critical organ for fetal growth and development and the principal determinant of birthweight. We aimed to investigate the effect of maternal OSA on placental growth and function. Placentas of women recruited to a prospective longitudinal study were consecutively obtained immediately after delivery. Each placenta was measured for length, width, and thickness. Total RNA was isolated for gene expression analysis of VEGF, VEGF receptor, PIGF, and leptin. Histological and morphometric evaluations of the placenta were performed. A total of 53 placentas were investigated. Ten women (19%) had OSA, and the weight of their placentas was significantly higher compared with the placentas of the controls (526.1 ± 83.9 vs. 425.7 ± 95.5 g, p = 0.004). There was a significant positive correlation between placental weight and the log apnea-hypopnea index even after controlling for maternal body mass index (BMI; r = 0.31, p = 0.04). The birthweight/placental weight ratio was significantly lower in women with OSA compared with controls (p = 0.03). Placental weight and newborn triceps adiposity thickness correlated positively after controlling for maternal BMI (r = 0.29, p = 0.04). Leptin expression was 1.8-fold higher in placentas of women with OSA compared with controls (p = 0.02). No histological differences were found between the groups. Maternal OSA is associated with increased placental weight that correlated with OSA severity and neonatal adiposity independently of maternal BMI. Placental leptin overexpression may mediate/underlie the above findings.Trial Registration: Clinical Trials NCT00931099.

Identifiants

pubmed: 30903184
pii: 5418772
doi: 10.1093/sleep/zsz072
pii:
doi:

Substances chimiques

Leptin 0

Banques de données

ClinicalTrials.gov
['NCT00931099']

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

© Sleep Research Society 2019. Published by Oxford University Press on behalf of the Sleep Research Society. All rights reserved. For permissions, please e-mail journals.permissions@oup.com.

Auteurs

Debora Kidron (D)

The Pathology Department, Meir Medical Center, Kfar Saba.
Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.

Yamit Bar-Lev (Y)

Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.
Department of Clinical Microbiology and Immunology, Lis Maternity Hospital, Tel Aviv, Israel.

Ilan Tsarfaty (I)

Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.
Department of Clinical Microbiology and Immunology, Lis Maternity Hospital, Tel Aviv, Israel.

Ariel Many (A)

Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.
Department of Obstetrics and Gynceology, Lis Maternity Hospital, Tel Aviv, Israel.

Riva Tauman (R)

Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.
The Sleep Disorders Center, Tel Aviv Medical Center, all affiliated to Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.

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Classifications MeSH