SFEBES2018 Poster Presentations Adrenal and steroids (38 abstracts)
1University of Edinburgh, Edinburgh, UK; 2UC Irvine, Irvine, California, USA; 3Charité Universitätsmedizin Berlin, Berlin, Germany.
Background: Both excess and insufficient glucocorticoid exposure in utero is associated with adverse fetal outcomes. Characterising the maternal hypothalamic-pituitary-adrenal (HPA) axis is challenging with large intra-individual variations in plasma and saliva. We hypothesised that 24-hour total urinary glucocorticoid (TUG) is a marker of maternal HPA axis during pregnancy. We tested associations of TUG with maternal BMI and birthweight.
Methods: TUG was measured by GC-MS/MS in 24-hour urine samples collected at mean 17.3 (S.D.=2.4) weeks gestation from 153 women aged 30.3 (S.D.=5.1) years, body mass index (BMI) 27.9 (S.D.=7.5) kg/m2, participating in a longitudinal cohort pregnancy study. Birth outcomes were available for 145 infants with mean birthweight 3470 (S.D.=495) grams, gestational age 39.4 (S.D.=1.5) weeks. Differences in TUG according to maternal BMI were tested. Regression analysis tested associations between TUG and birthweight adjusting for confounding factors.
Results: TUG was higher in women with higher BMI (r=0.413, P<0.001). In adjusted models, increased TUG was associated with increased birthweight. This was most marked in obese women (BMI≥30 kg/m2) (Table 1).
Model 1: TUG, gestational age
Model 2: TUG, gestational age, infant sex, ethnicity, maternal age, smoking status, gestational hypertension, pre-eclampsia, diabetes, maternal BMI, TUG gestation
Univariate | Multivariate Model 1 | Multivariate Model 2 | |
All participants | β=0.148 | β=0.187 | β=0.161, |
P-value=0.074 | P-value=0.007 | P-value=0.041 | |
BMI<30 | β=0.130 | β=0.150 | β=0.022 |
P-value=0.190 | P-value=0.077 | P-value=0.813 | |
BMI>30 | β=0.254 | β=0.233 | β=0.423 |
P-value=0.105 | P-value=0.051 | P-value=0.002 |
Conclusions: Obese pregnancy is associated with raised second trimester TUG. This increased peripheral clearance of maternal cortisol likely contributes to the low plasma cortisol levels in obese compared to lean pregnant women. The positive association of increased TUG with increased birthweight in obese women suggests a mechanism whereby increased peripheral clearance reduces fetal glucocorticoid exposure, contributing to macrosomia in infants of mothers with high BMI.