Is self-management a burden? What are the experiences of women self-managing chronic conditions during pregnancy? A systematic review.

OBJECTIVE: This systematic review examines the qualitative literature on women's experiences of self-managing chronic conditions in pregnancy. DESIGN: Systematic review of qualitative literature. Searches were performed in PubMed and CINAHL from inception to February 2021. Critical interpretive synthesis informed the coding framework and the analysis of the data. The Burden of Treatment theory emerged during the initial analysis as having the most synergy with the included literature, themes were refined to consider key concepts from this theory. PARTICIPANTS: Pregnant women who are self-managing a chronic condition. RESULTS: A total of 2695 articles were screened and 25 were reviewed in detail. All 16 included studies concerned diabetes self-management in pregnancy. Common themes coalesced around motivations for, and barriers to, self-management. Women self-managed primarily for the health of their baby. Barriers identified were anxiety, lack of understanding and a lack of support from families and healthcare professionals. CONCLUSIONS: Pregnant women have different motivating factors for self-management than the general population and further research on a range of self-management of chronic conditions in pregnancy is needed. PROSPERO REGISTRATION NUMBER: CRD42019136681.

Fetal and trophoblast PI3K p110α have distinct roles in regulating resource supply to the growing fetus in mice.

Studies suggest that placental nutrient supply adapts according to fetal demands. However, signaling events underlying placental adaptations remain unknown. Here we demonstrate that phosphoinositide 3-kinase p110α in the fetus and the trophoblast interplay to regulate placental nutrient supply and fetal growth. Complete loss of fetal p110α caused embryonic death, whilst heterozygous loss resulted in fetal growth restriction and impaired placental formation and nutrient transport. Loss of trophoblast p110α resulted in viable fetuses, abnormal placental development and a failure of the placenta to transport sufficient nutrients to match fetal demands for growth. Using RNA-seq we identified genes downstream of p110α in the trophoblast that are important in adapting placental phenotype. Using CRISPR/Cas9 we showed loss of p110α differentially affects gene expression in trophoblast and embryonic stem cells. Our findings reveal important, but distinct roles for p110α in the different compartments of the conceptus, which control fetal resource acquisition and growth.