Maternal Medical Disease and Stillbirth

Coletta, Jaclyn; Simpson, Lynn L.

doi:10.1097/grf.0b013e3181eb2ca0

Cited by 30 publications

(19 citation statements)

References 24 publications

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“…Raised BMI has been associated with a variety of endocrine and paracrine changes, which could impair embryonic development and fetoplacental function. These include disturbances in early hormonal milieu (29), altered trophoblastic invasion (30), diminished endometrial receptivity (31), impaired early embryonic development (32), increased insulin resistance (33), increased occurrence of apnea-hypoxia events (34), and hyperlipidemia (35). Pregnancy complications associated with obesity including gestational diabetes, hypertension, and preeclampsia may also mediate the relationship with stillbirth (36).…”

Section: Discussionmentioning

confidence: 99%

Prepregnancy and Early Adulthood Body Mass Index and Adult Weight Change in Relation to Fetal Loss

Gaskins

Rich‐Edwards

Colaci

et al. 2014

Obstetrics &Amp; Gynecology

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Objective To examine prospectively the relationships of prepregnancy body mass index (BMI), BMI at age 18, and weight change since age 18 with risk of fetal loss. Methods Our prospective cohort study included 25,719 pregnancies reported by 17,027 women in the Nurses’ Health Study II between 1990 and 2009. In 1989, height, current weight, and weight at age 18 were self-reported. Current weight was updated every 2 years thereafter. Pregnancies were self-reported, with case pregnancies lost spontaneously and comparison pregnancies ending in ectopic pregnancy, induced abortion, or live birth. Results Incident fetal loss was reported in 4,494 (17.5%) pregnancies. Compared to those of normal BMI, the multivariate relative risk (RR) (95% confidence interval [CI]) of fetal loss was 1.07 (1.00, 1.15) for overweight women, 1.10 (0.98, 1.23) for class I obese women, and 1.27 (1.11, 1.45) for class II & III obese women (P, trend=<0.001). BMI at age 18 was not associated with fetal loss (P, trend=0.59). Compared to women who maintained a stable weight (+/− 4 kg) between age 18 and before pregnancy, women who lost weight had a 20% (95% CI 9, 29%) lower risk of fetal loss. This association was stronger among women who were overweight at age 18. Conclusion Being overweight or obese prior to pregnancy was associated with higher risk of fetal loss. In women overweight or obese at age 18, losing 4 kg or more was associated with a lower risk of fetal loss.

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Section: Discussionmentioning

confidence: 99%

Prepregnancy and Early Adulthood Body Mass Index and Adult Weight Change in Relation to Fetal Loss

Gaskins

Rich‐Edwards

Colaci

et al. 2014

Obstetrics &Amp; Gynecology

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“…Although cholestasis is a pathologic condition of pregnancy due to maternal liver dysfunction precipitated by pregnancy in susceptible women, its association with PTB is not reported and is associated with stillbirth. [34][35][36] Figure 6 also details the bile acid metabolism in the liver.…”

Section: Bile Acidsmentioning

confidence: 99%

Amniotic Fluid Metabolomic Analysis in Spontaneous Preterm Birth

et al. 2014

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Objective: To identify metabolic changes associated with early spontaneous preterm birth (PTB; <34 weeks) and term births, using high-throughput metabolomics of amniotic fluid (AF) in African American population. Method: In this study, AF samples retrieved from spontaneous PTB (<34 weeks [n ¼ 25]) and normal term birth (n ¼ 25) by transvaginal amniocentesis at the time of labor prior to delivery were subjected to metabolomics analysis. Equal volumes of samples were subjected to a standard solvent extraction method and analyzed using gas chromatography/mass spectrometry (MS) and liquid chromatography/MS/MS. Biochemicals were identified through matching of ion features to a library of biochemical standards. After log transformation and imputation of minimum observed values for each compound, t test, correlation tests, and false discovery rate corrections were used to identify differentially regulated metabolites. Data were controlled for clinical/demographic variables and medication during pregnancy. Results: Of 348 metabolites measured in AF samples, 121 metabolites had a gestational age effect and 116 differed significantly between PTB and term births. A majority of significantly altered metabolites could be classified into 3 categories, namely, (1) liver function, (2) fatty acid and coenzyme A (CoA) metabolism, and (3) histidine metabolism. The signature of altered liver function was apparent in many cytochrome P450-related pathways including bile acids, steroids, xanthines, heme, and phase II detoxification of xenobiotics with the largest fold change seen with pantothenol, a CoA synthesis inhibitor that was 8-fold more abundant in PTB. Conclusion: Global metabolic profiling of AF revealed alteration in hepatic metabolites involving xenobiotic detoxification and CoA metabolism in PTB. Maternal and/or fetal hepatic function differences may be developmentally related and its contribution PTB as a cause or effect of PTB is still unclear.

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“…In humans, stillbirth is frequently associated with maternal hypertension or diabetes (3,6,21,32) but is also increased in women with Cushing's disease (17,26,34,35) and maternal stress or depression (8,10,16,37), in which maternal cortisol would be chronically increased. Our study suggests that the adverse outcomes in ovine pregnancy with hypercortisolemia may be related to the metabolic effects of cortisol in the mother and/or fetus.…”

Section: Perspectives and Significancementioning

confidence: 99%

Elevated maternal cortisol leads to relative maternal hyperglycemia and increased stillbirth in ovine pregnancy

Keller‐Wood

Feng

Wood

et al. 2014

American Journal of Physiology-Regulatory, Integrative and Comp

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Keller-Wood M, Feng X, Wood CE, Richards E, Anthony RV, Dahl GE, Tao S. Elevated maternal cortisol leads to relative maternal hyperglycemia and increased stillbirth in ovine pregnancy. Am J Physiol Regul Integr Comp Physiol 307: R405-R413, 2014. First published June 11, 2014 doi:10.1152/ajpregu.00530.2013.-In normal pregnancy, cortisol increases; however, further pathological increases in cortisol are associated with maternal and fetal morbidities. These experiments were designed to test the hypothesis that increased maternal cortisol would increase maternal glucose concentrations, suppress fetal growth, and impair neonatal glucose homeostasis. Ewes were infused with cortisol (1 mg·kg Ϫ1 ·day Ϫ1 ) from day 115 of gestation to term; maternal glucose, insulin, ovine placental lactogen, estrone, progesterone, nonesterified free fatty acids (NEFA), ␤-hydroxybutyrate (BHB), and electrolytes were measured. Infusion of cortisol increased maternal glucose concentration and slowed the glucose disappearance after injection of glucose; maternal infusion of cortisol also increased the incidence of fetal death at or near parturition. The design of the study was altered to terminate the study prior to delivery, and post hoc analysis of the data was performed to test the hypothesis that maternal metabolic factors predict the fetal outcome. In cortisol-infused ewes that had stillborn lambs, plasma insulin was increased relative to control ewes or cortisol-infused ewes with live lambs. Maternal cortisol infusion did not alter maternal food intake or plasma NEFA, BHB, estrone, progesterone or placental lactogen concentrations, and it did not alter fetal body weight, ponderal index, or fetal organ weights. Our study suggests that the adverse effect of elevated maternal cortisol on pregnancy outcome may be related to the effects of cortisol on maternal glucose homeostasis, and that chronic maternal stress or adrenal hypersecretion of cortisol may create fetal pathophysiology paralleling some aspects of maternal gestational diabetes. glucose; insulin; cortisol; pregnancy MATERNAL CORTISOL IS INCREASED in normal human pregnancy and is thought to contribute to the increase in maternal glucose concentration, as well as supporting increases in maternal plasma volume and cardiac output. In studies done in our laboratory, we have found that increasing maternal cortisol beyond the normal doubling in ovine pregnancy led to increased uterine blood flow and maternal and fetal glucose and lactate concentrations, whereas decreasing maternal cortisol to concentrations similar to those of nonpregnant ewes resulted in reduced uterine blood flow as gestation advanced (12, 13). Either increased or decreased maternal cortisol concentrations slowed the rate of fetal growth between 115 and 130 days of gestation. In women with Cushing's disease or Cushing's syndrome in pregnancy, there is also an increased incidence of small-for-gestational-age babies, as well as an increased risk of adverse pregnancy outcomes (26, 34). Maternal glucocorticoid treatme...

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Maternal Medical Disease and Stillbirth

Cited by 30 publications

References 24 publications

Prepregnancy and Early Adulthood Body Mass Index and Adult Weight Change in Relation to Fetal Loss

Prepregnancy and Early Adulthood Body Mass Index and Adult Weight Change in Relation to Fetal Loss

Amniotic Fluid Metabolomic Analysis in Spontaneous Preterm Birth

Elevated maternal cortisol leads to relative maternal hyperglycemia and increased stillbirth in ovine pregnancy

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