Omega-3 fatty acids and prenatal vitamins support fetal growth, but most studies assess omega-3 supplementation without accounting for baseline prenatal vitamin use during pregnancy. In this secondary analysis, we obtained data from the large, prospective Nulliparous Mother-to-be (nuMoM2b) cohort study of 9,461 nulliparous individuals. Participants were enrolled through eight clinical sites across the United States. We compared adverse birth outcomes between those taking additional omega-3 supplements beyond standard prenatal vitamin intake (PNV-OM) vs. prenatal vitamins alone (PNV). PNV-OM intake was associated with significantly lower rates of preterm birth (5.04 vs. 8.41%, P < 0.001) and SGA (2.84 vs. 4.48%, P = 0.004). After adjustment for demographic and clinical differences, PNV-OM use remained associated with reduced odds of preterm birth (aOR 0.64, 95% CI: 0.47-0.86, P = 0.004) and SGA (aOR 0.64, 95% CI: 0.42-0.95, P = 0.03). However, given substantial socioeconomic differences between groups and the potential for residual confounding, these findings should be interpreted with caution. Supplemental omega-3 intake during pregnancy may provide an additive benefit beyond prenatal vitamins alone, but randomized trials are needed to determine whether this relationship is causal.

Background:Differences in extracellular vesicles (EVs), bioactive nanoparticles involved in intercellular signaling, have been reported in those with autism. However, little is known about the association between maternal EVs during pregnancy and the likelihood of autism in offspring. This study evaluated the association of the concentration and cargo material of EVs in prenatal maternal plasma with childhood autism likelihood. Methods:Participants in the Nulliparous Pregnancy Outcomes Study provided maternal plasma at 15-23 weeks' gestational age. EVs were isolated by ultracentrifugation, and concentration, mean size, CD63 levels, and RNA cargo were assessed by nanoparticle tracking analysis, ELISA, and small RNA sequencing. At 4.5-6 years of age, parents completed the Social Communication Questionnaire. Thirty-one children at high-risk for autism were matched to 31 low-risk children on sex, age, and gestational age. Differential RNA transcript analysis and over representation analysis were performed. Results:There were no group differences in CD63 levels, mean particle size, or EV concentration (p>0.1). Nominal bin-level differences were observed at 280-290 nm and 430-440 nm before multiple-comparison correction. One hundred forty-five RNAs, including protein-coding RNAs, piRNAs, lncRNAs, miRNAs, snoRNAs, snRNAs, and tRNAs, were differentially contained, most of them downregulated in those at high risk of autism. These RNAs mapped to pathways involved in immune/inflammatory signaling, intracellular trafficking, protein turnover, and neurodevelopment. Six of the 62 (9.7%) differentially contained protein-coding RNAs overlapped with genes in the SFARI Gene database. Limitations:Large studies involving individuals diagnosed with autism are needed to evaluate the role of prenatal EVs in the pathogenesis of the condition. Additionally, prenatal sampling of EVs across multiple timepoints and subsequent deconvolution to determine the source of the EVs will strengthen interpretability and veracity of our findings. Conclusions:These findings provide preliminary evidence that maternal prenatal EV RNA cargo is associated with childhood autism likelihood.

Prenatal genomic sequencing can detect far more than clinicians conventionally report. Whether adult-onset conditions diagnosed in the fetus should be disclosed prenatally remains debated, and most laboratories and guidelines restrict reporting to childhood-onset disease. We argue that this restriction is not supported by available evidence. Prospective parents consistently elect to receive adult-onset findings, most often to plan for a child's future health. Pediatric and newborn sequencing studies have not demonstrated the psychological, relational, or developmental harms critics anticipated, and pregnancy offers an unmatched opportunity to reach an otherwise unscreened population. Policy should be guided by informed consent and patient autonomy.

In this study, a single hepatitis C virus (HCV) RNA at 2-6 months was sensitive and specific (86.7% and 95% confidence interval [CI], 62.1%-96.3% and 100% and 95% CI, 98.8%-100%, respectively) in identifying perinatal transmission of HCV. No cases of perinatal infection requiring treatment were missed.

Skeletal dysplasias are a group of Mendelian disorders that variably alter the development of the musculoskeletal system and phenotypically range from mild short stature syndromes to severe perinatal or neonatal morbidity. Prenatal diagnosis of these conditions can be challenging due to the lack of precision with ultrasound imaging compared to postnatal radiographs as well as the known allelic heterogeneity and phenotypic variability underlying these conditions. Historically, the sonographic approach for phenotyping these conditions lacked genotypic specificity and counseling focused on predicting perinatal lethality. However, recent advances in genomic medicine and prenatal ultrasound resolution have enabled more precise diagnosis and individualized counseling. The following review provides a comprehensive overview of best practices for prenatal ultrasonography and molecular work-up for skeletal dysplasias and provides a standardized evidence-based framework for evaluation.

Introduction:Multiple studies have evaluated late second and third trimester values for soluble Fms-like tyrosine kinase 1 (sFlt-1), placental-like growth factor (PlGF), and sFlt-1:PlGF ratio for preeclampsia risk stratification, but few studies have assessed sFlt-1:PlGF ratio earlier in pregnancy. Objective:To investigate the utility of early pregnancy sFlt-1:PlGF ratio for predicting preeclampsia with severe features, and to compare its predictive ability with that of the United States Preventive Services Task Force (USPSTF) risk assessment algorithm. Methods:This was a secondary analysis of the Nulliparous Pregnancy Outcomes Study: Monitoring Mothers-to-be (nuMoM2b). Of 10,038 participants, 1977 (enriched for adverse outcomes) had blood, which had been drawn at the first (6w0d-13w6d) and second (16w0d-21w6d) visits, assayed for sFlt-1 and PlGF, allowing for the calculation of sFlt-1:PlGF ratios from both visits as well as the change between visits. The primary outcome for this analysis was preeclampsia with severe features. The predictive ability of the sFlt-1:PlGF ratio was compared to that of the USPSTF risk assessment algorithm using area under the receiver operating characteristic curves (AUROC). Youden indexes were used to identify optimal sFlt-1:PlGF ratio cut-points. The predictive characteristics of these cut-points were compared to those of a positive USPSTF risk assessment result. Results:Preeclampsia with severe features was diagnosed in 240 (12.1%) eligible participants, among whom the mean gestational age at delivery was 36w0d. The optimal sFlt-1:PlGF ratio for predicting this outcome was 19.1 at visit 1, 6.2 at visit 2, and a decrease of 15.0 between visits. The sFlt-1:PlGF ratio was inferior to the USPSTF risk assessment algorithm in predicting this diagnosis (AUROC: 0.51-0.60 vs. 0.60, p = 0.0014-0.048). At both visits and across visits, the sFLt-1:PlGF ratio and USPSTF risk assessment algorithm predicted preeclampsia with severe features with comparable sensitivity (visit 1: 63.0%, visit 2: 49.8%, between visits: 50.0% vs. USPSTF: 61.5%) and specificity (visit 1: 43.1%, visit 2: 68.6%, between visits: 53.3% vs. USPSTF: 58.0%). Conclusions:Early pregnancy sFLt-1:PlGF ratio is a poor risk assessment tool for preeclampsia with severe features.

Background Preeclampsia is a complex syndrome that accounts for considerable maternal and perinatal morbidity and mortality. Despite its prevalence, no effective disease-modifying therapies are available. Maternal serum placenta-derived proteins have been in longstanding use as markers of risk for aneuploidy and placental dysfunction, but whether they have a causal contribution to preeclampsia is unknown. Objective We aimed to investigate the genetic regulation of serum placental proteins in early pregnancy and their potential causal links with preeclampsia and gestational hypertension. Study design This study used a nested case-control design with nulliparous women enrolled in the nuMoM2b study from eight clinical sites across the United States between 2010 and 2013. The first- and second-trimester serum samples were collected, and nine proteins were measured, including vascular endothelial growth factor (VEGF), placental growth factor, endoglin, soluble fms-like tyrosine kinase-1 (sFlt-1), a disintegrin and metalloproteinase domain-containing protein 12 (ADAM-12), pregnancy-associated plasma protein A, free beta-human chorionic gonadotropin, inhibin A, and alpha-fetoprotein. This study used genome-wide association studies to discern genetic influences on these protein levels, treating proteins as outcomes. Furthermore, Mendelian randomization was used to evaluate the causal effects of these proteins on preeclampsia and gestational hypertension, and their further causal relationship with long-term hypertension, treating proteins as exposures. Results A total of 2,352 participants were analyzed. We discovered significant associations between the pregnancy zone protein locus and concentrations of ADAM-12 (rs6487735, P= 3.03×10 -22 ), as well as between the vascular endothelial growth factor A locus and concentrations of both VEGF (rs6921438, P= 7.94×10 -30 ) and sFlt-1 (rs4349809, P= 2.89×10 -12 ). Our Mendelian randomization analyses suggested a potential causal association between first-trimester ADAM-12 levels and gestational hypertension (odds ratio=0.78, P= 8.6×10 -4 ). We also found evidence for a potential causal effect of preeclampsia (odds ratio=1.75, P =8.3×10 -3 ) and gestational hypertension (odds ratio=1.84, P =4.7×10 -3 ) during the index pregnancy on the onset of hypertension 2-7 years later. The additional mediation analysis indicated that the impact of ADAM-12 on postpartum hypertension could be explained in part by its indirect effect through gestational hypertension (mediated effect=-0.15, P= 0.03). Conclusions Our study discovered significant genetic associations with placental proteins ADAM-12, VEGF, and sFlt-1, offering insights into their regulation during pregnancy. Mendelian randomization analyses demonstrated evidence of potential causal relationships between the serum levels of placental proteins, particularly ADAM-12, and gestational hypertension, potentially informing future prevention and treatment investigations.

BACKGROUND: A major goal of contemporary obstetrical practice is to optimize fetal growth and development throughout pregnancy. To date, fetal growth during prenatal care is assessed by performing ultrasonographic measurement of 2-dimensional fetal biometry to calculate an estimated fetal weight. Our group previously established 2-dimensional fetal growth standards using sonographic data from a large cohort with multiple sonograms. A separate objective of that investigation involved the collection of fetal volumes from the same cohort. OBJECTIVE: The Fetal 3D Study was designed to establish standards for fetal soft tissue and organ volume measurements by 3-dimensional ultrasonography and compare growth trajectories with conventional 2dimensional measures where applicable. STUDY DESIGN: The National Institute of Child Health and Human Development Fetal 3D Study included research-quality images of singletons collected in a prospective, racially and ethnically diverse, low-risk cohort of pregnant individuals at 12 U.S. sites, with up to 5 scans per fetus (N1/41730 fetuses). Abdominal subcutaneous tissue thickness was measured from 2-dimensional images and fetal limb soft tissue parameters extracted from 3-dimensional multiplanar views. Cerebellar, lung, liver, and kidney volumes were measured using virtual organ computer aided analysis. Fractional arm and thigh total volumes, and fractional lean limb volumes were measured, with fractional limb fat volume calculated by subtracting lean from total. For each measure, weighted curves (fifth, 50th, 95th percentiles) were derived from 15 to 41 weeks' using linear mixed models for repeated measures with cubic splines. RESULTS: Subcutaneous thickness of the abdomen, arm, and thigh increased linearly, with slight acceleration around 27 to 29 weeks. Fractional volumes of the arm, thigh, and lean limb volumes increased along a quadratic curvature, with acceleration around 29 to 30 weeks. In contrast, growth patterns for 2-dimensional humerus and femur lengths demonstrated a logarithmic shape, with fastest growth in the second trimester. The mid-arm area curve was similar in shape to fractional arm volume, with an acceleration around 30 weeks, whereas the curve for the lean arm area was more gradual. The abdominal area curve was similar to the mid-arm area curve with an acceleration around 29 weeks. The mid- thigh and lean area curves differed from the arm areas by exhibiting a deceleration at 39 weeks. The growth curves for the mid-arm and thigh circumferences were more linear. Cerebellar 2-dimensional diameter increased linearly, whereas cerebellar 3-dimensional volume growth gradually accelerated until 32 weeks followed by a more linear growth. Lung, kidney, and liver volumes all demonstrated gradual early growth followed by a linear acceleration beginning at 25 weeks for lungs, 26 to 27 weeks for kidneys, and 29 weeks for liver. CONCLUSION: Growth patterns and timing of maximal growth for 3dimensional lean and fat measures, limb and organ volumes differed from patterns revealed by traditional 2-dimensional growth measures, suggesting these parameters reflect unique facets of fetal growth. Growth in these three-dimensional measures may be altered by genetic, nutritional, metabolic, or environmental influences and pregnancy complications, in ways not identifiable using corresponding 2-dimensional measures. Further investigation into the relationships of these 3dimensional standards to abnormal fetal growth, adverse perinatal outcomes, and health status in postnatal life is warranted.

This cohort study examines the association of adverse pregnancy outcomes and N-terminal pro-brain natriuretic peptide levels years after delivery.

Objective:Resistance to blood flow in the maternal uterine artery (UtA) has been associated with both preeclampsia (PE) and small-for-gestational age (SGA). Our objective was to assess the association of increased maternal UtA resistance with child neurodevelopmental and behavioral outcomes in low-risk pregnancies. Study Design:Serial ultrasound exams were prospectively performed in 2334 racial and ethnically diverse, healthy patients with low-risk singleton pregnancies (July 2009 to Jan 2013) as part of the NICHD-Fetal Growth Studies. Maternal UtA Dopplers were performed between 18w0d and 25w6d and pregnancy outcomes were collected at delivery including the occurrence of PE and SGA birthweight. Mother-child pairs from the original study were re-recruited to the NIH-Environmental Influences on Child Health Outcomes (ECHO) Study (May 2017 to April 2019). Analysis of neurodevelopment was performed using age-appropriate versions of the NIH Toolbox for children including executive (inhibitory control/attention, cognitive flexibility, and working memory) and motor domains (dexterity, grip strength, and standing balance). Assessment of behavioral problems was obtained by parent report using the Child Behavioral Checklist. Multivariable adjusted general linear and logistic regression models were used to determine the mean difference in standardized test scores of observed child executive and motor functions and parent-reported child behaviors associated with a 1-standard deviation (SD) increment in UtA pulsatility index (PI). Results:A total of 675 patients had both interrogation of mid-pregnancy UtA Dopplers and at least one measure of executive or motor domain function or parent-reported behavior between the ages of 4 and 8 years. Each 1-SD increase in UtA PI was associated with a significant reduction in cognitive flexibility in children aged 4-7 years (n = 457; adjusted mean difference[aMD] -0.97; 95% CI -1.8, -0.14). There were no associations between motor function and increased UtA resistance. A 1-SD increase in UtA PI was not associated with any increased parent report of child behavioral problems. A 1-SD increase in UtA PI was associated with a 1.5-fold increased risk of PE. In mediation analyses, differences in executive function domains associated with increased UtA PI Doppler findings were not explained by either maternal PE, SGA, or birthweight z-scores. Conclusion:Increased maternal mid-pregnancy UtA resistance appears to be associated with small decreases in executive domain function (cognitive flexibility) but not motor domain function. In this exploratory study, the observed effect sizes were modest and the clinical implications are uncertain, but they suggest the possibility of long-term neurodevelopmental effects of subclinical placental dysfunction in low-risk pregnancies. The findings, however, are biologically plausible and contribute to a growing body of literature exploring antenatal predictors of child neurodevelopment. Larger confirmatory studies will be needed to determine if maternal UtA resistance can contribute to the early identification of at-risk children. Trial Registration:Clinicaltrials.gov identifiers: NCT00912132, NCT03266198.

(Abstracted from Am J Obstet Gynecol 2025;232:402.e1–402.e16) Amniocentesis, introduced in 1970, is the most common method for obtaining fetal samples for genetic testing. It is usually performed between 15 and 22 weeks’ gestation but can be done later if clinically indicated.

Pregnancy orchestrates a rare physiological transformation across vascular, immune, and metabolic systems. When this dynamic balance is disrupted - as in hypertensive disorders of pregnancy - the consequences can be life-threatening, spanning maternal mortality, fetal growth restriction, and elevated long-term cardiovascular risk. Despite clear links to early placental dysfunction and systemic endothelial disruption, current screening remains clinically imprecise, biologically opaque, and logistically challenging. A shift is urgently needed - from detecting maternal complications late in gestation to understanding how pregnancy reshapes vascular physiology systemically and how this remodeling may go awry. Here we present Visionary AI, an artificial intelligence platform that integrates ultra-widefield retinal imaging (200°) with biologically grounded vascular modeling to predict hypertensive disorders of pregnancy early in gestation. Unlike prior approaches that rely on generic deep learning models and clinical inputs, Visionary AI constructs an interpretable, graph-based representation of the maternal retinal vasculature and applies topological and geometric analysis to identify condition-specific microvascular signatures. In a prospective multiethnic U.S. cohort of 1,267 pregnancies, Visionary AI achieved high predictive performance for preeclampsia (AUC = 0.90), early-onset (AUC = 0.93), and severe preeclampsia (AUC = 0.89), outperforming current clinical paradigms. It also generalized to predict gestational hypertension (AUC = 0.91) and chronic hypertension (AUC = 0.90). Topological and geometric analyses of the vasculature revealed distinct and interpretable remodeling patterns across subtypes of hypertensive disorders of pregnancy, offering mechanistic insight into their divergent pathophysiology. These results position the maternal retina as a minimally invasive, high-fidelity biosensor of early systemic vascular health and establish Visionary AI as a clinically actionable, biologically grounded diagnostic framework with potential for broad global scalability.

Small for gestational age (SGA) infants face increased morbidity, mortality, and long-term health risks, yet causes of SGA remain unclear. While placental insufficiency and environmental factors contribute, genetic disorders play a significant role. Syndromes like Silver-Russell and Noonan are linked to SGA, but the overall genetic contribution remains uncertain. We reviewed literature on genomic sequencing in SGA and fetal growth restriction (which often precedes SGA) and identified 161 single-gene disorders. The top ten genes explained one-third of cases, but half were attributable to unique genes. Genetic disorders were frequently accompanied by congenital anomalies (often skeletal dysplasia) and developmental delays. Current guidelines for genetic evaluation of SGA are limited. Our findings support consideration of exome or genome sequencing, particularly in the setting of congenital anomalies or developmental delays. Early identification of genetic disorders can enable tailored therapy. Given the complexity of the SGA genetic landscape, prospective genomic studies are urgently needed.

Differentially methylated regions (DMRs) in certain areas of the genome are subject to genomic imprinting. DMRs at chromosome 11p15.5 are associated with Beckwith-Wiedemann syndrome (BWS) and Russell-Silver Syndrome (RSS), two growth disorders with opposite phenotypes. We identified a maternally inherited duplication containing part of the 11p15 DMR in a non-anomalous fetus in first trimester using genome sequencing (GS). The ∼281kb duplication at 11p15.5 contains the entire imprinting control region 1 (ICR1) and the H19 gene but lacks the IGF2 gene and the imprinting control region 2 (ICR2). Methylation studies revealed hypomethylation of ICR1 in fetal cells as well as in the mother (leukocytes), who had a history of feeding difficulties in infancy and short stature. The duplication was inherited from the asymptomatic maternal grandmother of the fetus, who showed hypermethylation of ICR1 in leukocytes suggesting paternal inheritance. The fetus developed decelerating growth in late gestation and phenotypes overlapping those of RSS were noted in infancy. This study adds to the limited literature on partial duplications of the 11p15.5 region and their associated phenotypes, underscoring the efficacy of GS in cases involving DMRs associated with imprinting disorders.

Objective: To examine the association between elective induction of labor (EIOL) start time and labor duration among nulliparous women Methods: The ARRIVE trial was a multi-center randomized controlled trial of induction of labor at 39 weeks 0 days to 39 weeks 4 days versus expectant management in low-risk nulliparous women. In this secondary analysis, we included participants randomized to the induction group who had an EIOL without spontaneous labor or rupture of membranes prior to the induction start. Start time of EIOL was categorized as: early AM (midnight to 5:59 AM), late AM (6 AM-11:59 AM), early PM (noon-5:59 PM), or late PM (6 PM-11:59 PM). The primary outcome was labor duration. Cesarean delivery rates by induction start time were also examined. Multivariable analysis was conducted controlling for age, body mass index, insurance status, and modified Bishop score on admission (< 5 or ≥5). Results: Of 3,062 women randomized to EIOL, 2,197 were included in this analysis. EIOL occurred in the early AM in 13%, in late AM in 28%, in early PM in 13%, and in late PM in 45%. Participants induced in the late AM had the shortest mean labor durations (21.5 ±11.3 hours) and the highest frequency of delivery at < 24 hours (68%). In adjusted analyses, induction in the late AM (vs. grouped other time periods) remained significantly associated with shorter labor duration (-1.5 hrs, 95% CI -2.5, -0.4, p=0.006), and there was no interaction between Bishop score and time of EIOL. Cesarean delivery rates did not differ by start time. Conclusions: Induction of labor starting between 6AM and 11:59 AM was associated with shorter labor durations, independent of baseline maternal characteristics including cervical status on admission.

BACKGROUND:Genetic disorders are recognized as key contributors to morbidity, mortality, and congenital anomalies in term infants. However, the rates of diagnosis and association with morbidity, mortality, and congenital anomalies in preterm infants are poorly characterized. We sought to determine rates of diagnosis of genetic disorders in preterm infants and to define the association of genetic disorders with morbidity, mortality, and congenital anomalies. METHODS:This was a multicenter observational cohort study conducted in neonatal intensive care units in the Pediatrix Clinical Data Warehouse. Infants born from 23 to 0/7 to 33 and 6/7 weeks of gestation, admitted to 374 U.S. community and academic neonatal intensive care units from 2000 to 2020 were included. Infants transferred after birth or prior to discharge were excluded. We analyzed diagnosis of genetic disorders; predischarge morbidity (including acute kidney injury, bronchopulmonary dysplasia, necrotizing enterocolitis, sepsis, shock, severe retinopathy, and intracranial hemorrhage); mortality; and presence of congenital anomalies. RESULTS:Among 323,770 early preterm infants analyzed, 4,196 (1.3%) were diagnosed with one of twenty genetic disorders. Single gene disorders were identified in 2,250 (0.7%) infants, copy number variants in 88 (0.03%) infants, and aneuploidies in 1,885 (0.6%) infants. Morbidity, mortality, and congenital anomalies occurred in 1,319 (31.4%), 566 (13.5%), and 1,041 (24.8%) infants with genetic disorders compared to 77,957 (24.5%), 15,240 (4.7%), and 9,455 (3.0%) infants without genetic disorders. Common aneuploidies accounted for most of these associations. However, morbidity, mortality, and congenital anomalies were also significantly more common in early preterm infants with single gene disorders and pathogenic copy number variants. We did not detect meaningful differences in diagnostic rates of genetic disorders over the study period. CONCLUSIONS:1.3% of early preterm infants were diagnosed with genetic disorders. Genetic disorders were strongly associated with morbidity, mortality, and congenital anomalies. Clinicians should strongly consider genetic evaluation in early preterm infants with morbidity, mortality, or congenital anomalies. Prospective research is needed to determine the true prevalence of genetic disorders in this high-risk population.

Adiponectin is a hormone that modulates glucose regulation and fatty acid oxidation. Low adiponectin concentration has been associated with increased insulin resistance. Studies show a beneficial effect of vitamin E supplementation on insulin sensitivity. We aimed to investigate the association of prenatal antioxidant supplementation with increased adiponectin concentrations in pregnant participants and their newborn infants.Secondary analysis of a randomized control trial of prenatal vitamin C and E supplementation to prevent preeclampsia in low-risk nulliparous participants. Plasma of participants at time of randomization (9-16 weeks gestation) and delivery, and neonatal cord blood were analyzed by specific enzyme-linked immunosorbent assay for adiponectin concentration. Multivariable analysis was adjusted for confounders.A total of 198 (98 vitamin, 100 placebo) maternal-neonatal dyad samples were analyzed. Maternal and neonatal characteristics were similar between the vitamin and placebo groups, with the exception of race/ethnicity, with Whites more common in the placebo group (80 vs. 66.3%, p = 0.02). In bivariable analyses, adiponectin concentrations at delivery were higher in the vitamin group compared with the placebo group (29.4 vs. 27.5 µg/mL, p = 0.04), whereas cord blood adiponectin concentrations were similar (26.6 . vs. 27.4 µg/mL, p = 0.47) between the two groups. There was a significant interaction between treatment group and maternal baseline adiponectin level on the adiponectin concentrations at delivery (p = 0.04) and cord blood adiponectin (p < 0.05). For participants whose baseline adiponectin concentrations were in the highest tertile, vitamin supplementation was associated with higher adiponectin concentrations at delivery. However, for participants whose baseline adiponectin concentration were in the lowest tertile, vitamin supplementation was associated with lower cord blood adiponectin concentrations.For participants with high baseline adiponectin concentration, vitamin C and E supplementation is associated with higher adiponectin concentration at delivery. Conversely, vitamin supplementation is associated with lower cord adiponectin concentration among participants with low baseline adiponectin concentration. · Vitamin E is an antioxidant with metabolic properties.. · Adiponectin is a cytokine with metabolic properties.. · Vitamin E is associated with higher pregnancy adiponectin.. · Vitamin E is associated with lower neonatal adiponectin.. · Vitamin E correlated with positive pregnancy and neonatal adiponectin trends..

Our objective was to develop a prediction model for hepatitis C virus (HCV) infection perinatal transmission to improve triage for neonatal follow-up. This was a secondary analysis of HCV antibody-positive participants who were enrolled in the Eunice Kennedy Shriver National Institute of Child Health and Human Development Maternal-Fetal Medicine Units Network multicenter observational study of HCV infection in pregnancy. Among 432 participants, the perinatal transmission rate was 6.0% (95% CI, 4.0-8.7%). The prediction model was developed and included two factors: maternal HCV RNA titer greater than 10 6 international units/mL and having had any antepartum bleeding. Using this model, the area under the curve for perinatal transmission was 0.76 (95% CI, 0.67-0.86). Probabilities of perinatal transmission of HCV infection ranged from 1.5% (a pregnant individual with HCV RNA 10 6 international units/mL or less and no antepartum bleeding) to 28.5% (a pregnant individual with an HCV RNA titer greater than 10 6 international units/mL and antepartum bleeding). Our results provide data to aid in clinical counseling of pregnant individuals with positive HCV antibodies. Additional research is needed to externally validate this prediction model.