Maternal Fetal Medicine Fellow Medstar Washington Hospital Center MedStar Washington Hospital Center District of Columbia, Washington, United States
Background: The placenta has critical endocrine functions to support the developing fetus, and molecular and pathologic studies have revealed important structural and functional placental changes in the setting of maternal diabetes mellitus (DM), yet little is known about the in vivo development in maternal DM.
Objective: We sought to examine fetal brain and placental response to maternal hyperoxia using blood oxygen level–dependent (BOLD) magnetic resonance imaging (MRI) in pregnancies complicated by DM.
Design/Methods: This is a single center prospective case control cohort study of women with singleton gestations, at least 18 weeks or greater. Cases include women diagnosed with either pre-gestational or gestational DM. Controls include healthy pregnancies without any comorbidities. Gradient-echo planar and fast spin-echo T2 weighted imaging was performed with a maternal hyperoxia paradigm of 2 minutes resting state baseline (RS), 6 minutes maternal hyperoxia (HO) of 100% oxygen via a non-rebreather and 5.6 minutes post oxygenation for return to resting state (RR). Analyses were performed at one minute time intervals to assess the change in R2* from baseline (DR2*). Student’s t-test was performed to compare outcomes between groups.
Results: 113 women were recruited in this study: 67 healthy controls with mean gestational age (GA) in weeks 30.9±4.3, and 45 cases, mean GA: 30.2±4.5. Of the cases: 13 had Type 1 DM mean GA 30.1±5.0; 15 Type 2 DM mean GA 29.4±4.5; 17 Gestational (G) DM, mean GA 31.2±6.7. Overall, results were similar between groups during HO. During RR minutes 4 and 5, the Delta R2 (difference in oxygen signal relative to baseline), was lower in the diabetic cohort compared to controls, with most significant decrease in T1DM (RR6) and T2DM (RR2, RR4) (Fig 1&2). Conclusion(s): Metabolic, inflammatory and vascular changes have been described in ex vivo placentas from diabetic pregnancies. Maternal hyperoxia during BOLD imaging reflects oxygen carrying capacity and transfer from the maternal circulation to the placenta and fetus. Decreased BOLD signaling suggests altered placenta function, reflecting either increased oxygen consumption of the diabetic placenta or continued oxygen transfer to the fetus. Additional studies to explore the clinical significance of these findings are underway.
Figure 1:
The BOLD response (DeltaR2*) during each phase of the maternal hyperoxia paradigm in pregnancies complicated by Diabetes Mellitus (DM) and healthy controls; RS = resting state (baseline); HO = hyperoxia (2 minute intervals); RR = return to rest (2 minute intervals); *p < 0.1, **p < 0.05.
Figure 2:
The BOLD response (DeltaR2*) during each phase of the maternal hyperoxia paradigm in pregnancies complicated by Type 1 Diabetes Mellitus (T1DM), Type 2 (T2DM) and gestational (GDM) and healthy controls; RS = resting state (baseline); HO = hyperoxia (2 minute intervals); RR = return to rest (2 minute intervals); *p < 0.1, **p < 0.05.
Authors/Institutions: Stacey L. Gold, MedStar Washington Hospital Center, Washington, District of Columbia, United States; Kushal J. Kapse, Childrens National Medical Center, Washington, District of Columbia, United States; Catherine A. Lopez, Childrens National Medical Center, Washington, District of Columbia, United States; Jessica Quistorff, Childrens National Medical Center, Washington, District of Columbia, United States; Sarah G. Downs, MedStar Washington Hospital Center, Washington, District of Columbia, United States; Sara N. Iqbal, MedStar Washington Hospital Center, Washington, District of Columbia, United States; Catherine Limperopoulos, Childrens National Medical Center, Washington, District of Columbia, United States; Nickie Andescavage, Children's National Health Systems, Washington, District of Columbia, United States
