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Patterns of gestational weight gain and birthweight outcomes in the Eunice Kennedy Shriver National Institute of Child Health and Human Development Fetal Growth Studies-Singletons: a prospective study.

ABSTRACT:

SUBMITTER: Pugh SJ

PROVIDER: S-EPMC5581247 | biostudies-literature | 2017 Sep

REPOSITORIES: biostudies-literature

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Patterns of gestational weight gain and birthweight outcomes in the Eunice Kennedy Shriver National Institute of Child Health and Human Development Fetal Growth Studies-Singletons: a prospective study.

Pugh Sarah J SJ Albert Paul S PS Kim Sungduk S Grobman William W Hinkle Stefanie N SN Newman Roger B RB Wing Deborah A DA Grantz Katherine L KL

American journal of obstetrics and gynecology 20170511 3

<h4>Background</h4>Inadequate or excessive total gestational weight gain is associated with increased risks of small- and large-for-gestational-age births, respectively, but evidence is sparse regarding overall and trimester-specific patterns of gestational weight gain in relation to these risks. Characterizing the interrelationship between patterns of gestational weight gain across trimesters can reveal whether the trajectory of gestational weight gain in the first trimester sets the path for g ...[more]

PMID: 28502760

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Project description:Although much progress is being made in understanding the molecular pathways in the placenta that are involved in the pathophysiology of pregnancy-related disorders, a significant gap exists in the utilization of this information for the development of new drug therapies to improve pregnancy outcome. On March 5-6, 2015, the Eunice Kennedy Shriver National Institute of Child Health and Human Development of the National Institutes of Health sponsored a 2-day workshop titled Placental Origins of Adverse Pregnancy Outcomes: Potential Molecular Targets to begin to address this gap. Particular emphasis was given to the identification of important molecular pathways that could serve as drug targets and the advantages and disadvantages of targeting these particular pathways. This article is a summary of the proceedings of that workshop. A broad number of topics were covered that ranged from basic placental biology to clinical trials. This included research in the basic biology of placentation, such as trophoblast migration and spiral artery remodeling, and trophoblast sensing and response to infectious and noninfectious agents. Research findings in these areas will be critical for the formulation of the development of future treatments and the development of therapies for the prevention of a number of pregnancy disorders of placental origin that include preeclampsia, fetal growth restriction, and uterine inflammation. Research was also presented that summarized ongoing clinical efforts in the United States and in Europe that has tested novel interventions for preeclampsia and fetal growth restriction, including agents such as oral arginine supplementation, sildenafil, pravastatin, gene therapy with virally delivered vascular endothelial growth factor, and oxygen supplementation therapy. Strategies were also proposed to improve fetal growth by the enhancement of nutrient transport to the fetus by modulation of their placental transporters and the targeting of placental mitochondrial dysfunction and oxidative stress to improve placental health. The roles of microRNAs and placental-derived exosomes, as well as messenger RNAs, were also discussed in the context of their use for diagnostics and as drug targets. The workshop discussed the aspect of safety and pharmacokinetic profiles of potential existing and new therapeutics that will need to be determined, especially in the context of the unique pharmacokinetic properties of pregnancy and the hurdles and pitfalls of the translation of research findings into practice. The workshop also discussed novel methods of drug delivery and targeting during pregnancy with the use of macromolecular carriers, such as nanoparticles and biopolymers, to minimize placental drug transfer and hence fetal drug exposure. In closing, a major theme that developed from the workshop was that the scientific community must change their thinking of the pregnant woman and her fetus as a vulnerable patient population for which drug development should be avoided, but rather be thought of as a deprived population in need of more effective therapeutic interventions.

Project description:Pregnant individuals infected with SARS-CoV-2 have higher rates of intensive care unit admission, oxygen requirement, need for mechanical ventilation, and death than nonpregnant individuals. Increased COVID-19 disease severity may be associated with an increased risk of viremia and placental infection. Maternal SARS-CoV-2 infection is also associated with pregnancy complications such as preeclampsia and preterm birth, which can be either placentally mediated or reflected in the placenta. Maternal viremia followed by placental infection may lead to maternal-fetal transmission (vertical), which affects 1% to 3% of exposed newborns. However, there is no agreed-upon or standard definition of placental infection. The National Institutes of Health/Eunice Kennedy Shriver National Institute of Child Health and Human Development convened a group of experts to propose a working definition of placental infection to inform ongoing studies of SARS-CoV-2 during pregnancy. Experts recommended that placental infection be defined using techniques that allow virus detection and localization in placental tissue by one or more of the following methods: in situ hybridization with antisense probe (detects replication) or a sense probe (detects viral messenger RNA) or immunohistochemistry to detect viral nucleocapsid or spike proteins. If the abovementioned methods are not possible, reverse transcription polymerase chain reaction detection or quantification of viral RNA in placental homogenates, or electron microscopy are alternative approaches. A graded classification for the likelihood of placental infection as definitive, probable, possible, and unlikely was proposed. Manuscripts reporting placental infection should describe the sampling method (location and number of samples collected), method of preservation of tissue, and detection technique. Recommendations were made for the handling of the placenta, examination, and sampling and the use of validated reagents and sample protocols (included as appendices).

Project description:ObjectiveTo describe the natural history of fibroids in pregnancy in a racially diverse cohort and explore whether fibroid changes were associated with participant characteristics.DesignProspective cohort study.SettingTwelve clinical sites.Patient(s)Pregnant women (n = 2774; 27% non-Hispanic White, 28% non-Hispanic Black, 29% Hispanic, 17% Asian/Pacific Islander) who had up to 6 obstetric ultrasounds in gestational weeks 10-41.Intervention(s)Sonographers recorded fibroid number and volume of the 3 largest fibroids at each visit. Generalized linear mixed models estimated the trajectories of fibroid number and total volume (overall and stratified by total volume at first visualization: equivalent to a fibroid of <1 cm [small], 1 to <3 cm [medium], or ≥3 cm [large] in diameter). We tested the interactions between the trajectories and race/ethnicity, age (<26, 26-30, 31-34, and ≥35 years), body mass index (<25, 25-29.9, and ≥30 kg/m2), previous miscarriage, parity, and fetal sex, adjusted for total volume at first visualization.Main outcome measure(s)Average change in total fibroid volume during pregnancy.Result(s)Overall, 9.6% (266/2,774) of women had a visualized fibroid at any time during pregnancy, including 9% (67/745) of non-Hispanic White women, 14% (106/770) of non-Hispanic Black women, 6% (47/794) of Hispanic women, and 10% (46/465) of Asian or Pacific Islander women. The mean total fibroid volume decreased by 1.0% (95% confidence interval [CI], -1.9%, -0.2%) per week, with a variation in starting total volume. On average, the total volume increased by 2.0% (95% CI, -0.3%, 4.5%) per week among women with small volume; decreased by 0.5% (95% CI, -2.0%, 1.0%) per week among women with medium volume; and decreased by 2.2% (95% CI, -3.4%, -1.0%) per week among women with large volume at first visualization. The volume change also varied by race or ethnicity, parity, age, and miscarriage history. For example, non-Hispanic Black women's total fibroid volume decreased more than those of non-Hispanic White, Hispanic and Asian/Pacific Islander women (-2.6%, 0.1%, 0.5%, and 0.9% average change per week, respectively). The visualized fibroid number declined on an average by 1.2% per week (95% CI, -1.9%, -0.5%) without significant variation by demographic characteristics.Conclusion(s)The total fibroid volume declined on average throughout pregnancy. However, summarizing across all fibroids disguises substantial heterogeneity by starting total fibroid volume and maternal characteristics. The findings may be a useful reference for clinicians to anticipate how fibroids may change in obstetric patients.Clinical trial registration numberNCT00912132.

Project description:BackgroundClinical recommendations to limit gestational weight gain (GWG) imply high GWG is causally related to adverse outcomes in mother or offspring, but GWG is the sum of several inter-related complex phenotypes (maternal fat deposition and vascular expansion, placenta, amniotic fluid and fetal growth). Understanding the genetic contribution to GWG could help clarify the potential effect of its different components on maternal and offspring health. Here we explore the genetic contribution to total, early and late GWG.Participants and methodsA genome-wide association study was used to identify maternal and fetal variants contributing to GWG in up to 10 543 mothers and 16 317 offspring of European origin, with replication in 10 660 mothers and 7561 offspring. Additional analyses determined the proportion of variability in GWG from maternal and fetal common genetic variants and the overlap of established genome-wide significant variants for phenotypes relevant to GWG (for example, maternal body mass index (BMI) and glucose, birth weight).ResultsApproximately 20% of the variability in GWG was tagged by common maternal genetic variants, and the fetal genome made a surprisingly minor contribution to explain variation in GWG. Variants near the pregnancy-specific beta-1 glycoprotein 5 (PSG5) gene reached genome-wide significance (P=1.71 × 10-8) for total GWG in the offspring genome, but did not replicate. Some established variants associated with increased BMI, fasting glucose and type 2 diabetes were associated with lower early, and higher later GWG. Maternal variants related to higher systolic blood pressure were related to lower late GWG. Established maternal and fetal birth weight variants were largely unrelated to GWG.ConclusionsWe found a modest contribution of maternal common variants to GWG and some overlap of maternal BMI, glucose and type 2 diabetes variants with GWG. These findings suggest that associations between GWG and later offspring/maternal outcomes may be due to the relationship of maternal BMI and diabetes with GWG.

Dataset Information

Patterns of gestational weight gain and birthweight outcomes in the Eunice Kennedy Shriver National Institute of Child Health and Human Development Fetal Growth Studies-Singletons: a prospective study.

Publications

Patterns of gestational weight gain and birthweight outcomes in the Eunice Kennedy Shriver National Institute of Child Health and Human Development Fetal Growth Studies-Singletons: a prospective study.

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