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. 2016 Jul 11;11(7):e0158807.
doi: 10.1371/journal.pone.0158807. eCollection 2016.

Sexual Dimorphism in Adverse Pregnancy Outcomes - A Retrospective Australian Population Study 1981-2011

Petra E Verburg  1   2   3 , Graeme Tucker  3   4 , Wendy Scheil  3   4 , Jan Jaap H M Erwich  2 , Gus A Dekker  1   5 , Claire Trelford Roberts  1
Affiliations

Sexual Dimorphism in Adverse Pregnancy Outcomes - A Retrospective Australian Population Study 1981-2011

Petra E Verburg et al. PLoS One. .

Abstract

Objectives: Sexual inequality starts in utero. The contribution of biological sex to the developmental origins of health and disease is increasingly recognized. The aim of this study was to assess and interpret sexual dimorphisms for three major adverse pregnancy outcomes which affect the health of the neonate, child and potentially adult.

Methods: Retrospective population-based study of 574,358 South Australian singleton live births during 1981-2011. The incidence of three major adverse pregnancy outcomes [preterm birth (PTB), pregnancy induced hypertensive disorders (PIHD) and gestational diabetes mellitus (GDM)] in relation to fetal sex was compared according to traditional and fetus-at-risk (FAR) approaches.

Results: The traditional approach showed male predominance for PTB [20-24 weeks: Relative Risk (RR) M/F 1.351, 95%-CI 1.274-1.445], spontaneous PTB [25-29 weeks: RR M/F 1.118, 95%-CI 1.044-1.197%], GDM [RR M/F 1.042, 95%-CI 1.011-1.074], overall PIHD [RR M/F 1.053, 95%-CI 1.034-1.072] and PIHD with term birth [RR M/F 1.074, 95%-CI 1.044-1.105]. The FAR approach showed that males were at increased risk for PTB [20-24 weeks: RR M/F 1.273, 95%-CI 1.087-1.490], for spontaneous PTB [25-29 weeks: RR M/F 1.269, 95%-CI 1.143-1.410] and PIHD with term birth [RR M/F 1.074, 95%-CI 1.044-1.105%]. The traditional approach demonstrated female predominance for iatrogenic PTB [25-29 weeks: RR M/F 0.857, 95%-CI 0.780-0.941] and PIHD associated with PTB [25-29 weeks: RR M/F 0.686, 95%-CI 0.581-0.811]. The FAR approach showed that females were at increased risk for PIHD with PTB [25-29 weeks: RR M/F 0.779, 95%-CI 0.648-0.937].

Conclusions: This study confirms the presence of sexual dimorphisms and presents a coherent framework based on two analytical approaches to assess and interpret the sexual dimorphisms for major adverse pregnancy outcomes. The mechanisms by which these occur remain elusive, but sex differences in placental gene expression and function are likely to play a key role. Further research on sex differences in placental function and maternal adaptation to pregnancy is required to delineate the causal molecular mechanisms in sex-specific pregnancy outcome. Identifying these mechanisms may inform fetal sex specific tailored antenatal and neonatal care.

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Conflict of interest statement

Competing Interests: The authors have declared that no competing interests exist.

Figures

Fig 1
Fig 1. Schematic depiction of pregnancy course and options for calculating the gestational age-specific disease rate in 10 hypothetical pregnancies.
Traditional approach: Number of affected births in a gestational group divided by the number of total births within that gestation group = 1/3. Fetuses at risk approach: Number of affected births at gestational group divided by the number of fetuses at risk for a disease at that gestation group = 1/5. Modified after Joseph et al(24).
Fig 2
Fig 2. Sexual dimorphism for length of gestation in categories.
Births in South Australia 1981–2011. Marked points represent significant RR M/F.
Fig 3
Fig 3. Sexual dimorphism for spontaneous birth by length of gestation.
Births in South Australia 1981–2011. Marked points represent significant RR M/F.
Fig 4
Fig 4. Sexual dimorphism for iatrogenic birth by length of gestation.
Births in South Australia 1981–2011. Marked points represent significant RR M/F.
Fig 5
Fig 5. Sexual dimorphism for PIHD by length of gestation in categories.
Births in South Australia 1981–2011. Marked points represent significant RR M/F.
See this image and copyright information in PMC

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