Fetal Growth Rate Research Articles

The impact of unemployment cycles on child and maternal health in Argentina.

The purpose of this study is to examine the effects of economic cycles in Argentina on infant and maternal health between 1994 and 2006, a period that spans the major economic crisis in 1999-2002. We evaluate the effects of province-level unemployment rates on several infant health outcomes, including birth weight, gestational age, fetal growth rate, and hospital discharge status after birth in a sample of 15,000 infants born in 13 provinces. Maternal health and healthcare outcomes include acute and chronic illnesses, infectious diseases, and use of prenatal visits and technology. Regression models control for hospital and year fixed effects and province-specific time trends. Unemployment rise reduces fetal growth rate particularly among high educated parents. Also, maternal poverty-related infectious diseases increase, although reporting of acute illnesses declines (an effect more pronounced among low educated parents). There is also some evidence for reduced access to prenatal care and technology among less educated parents with higher unemployment. Unemployment rise in Argentina has adversely affected certain infant and maternal health outcomes, but several measures show no evidence of significant change.

Relationship between placental surface area and fetal growth rate in artiodactyls and perissodactyls

Abstract Gestation periods in mammals are generally in line with scaling laws. There are several exceptions in which species of relatively similar size and degree of neonatal maturation show a significant difference in gestation length. For example the giraffids have a very long gestation period, compared to bovids of similar size. By using published data about the placental surface area at term, we show that in ungulates this surface area is more tightly correlated to the average fetal growth rate than to fetal and placenta weight. These data suggest that, within one type of placenta, gestation length and placental surface area are associated parameters.

Abstract 201: Maternal HDL-Cholesterol Levels in Women From the Gambia are Directly Related to Infant Birthweight

Babies born with low birthweight are often at a health disadvantage. Previous studies have shown direct relationships between maternal plasma cholesterol and infant birthweight in resource-rich countries. As plasma cholesterol levels are often decreased in resource-poor countries, the purpose of these studies was to evaluate the relationship between plasma cholesterol and birthweight in women enrolled in the ENID trial (ISRCTN49285450) in rural Gambia, West Africa. Plasma was obtained at enrolment (13.6±3.3 wk) and at 20 and 30 weeks of gestation; samples were obtained from women with term infants that weighed <2.75 kg or >3.25 kg at birth. Women with lower HDL-cholesterol (HDL-C) concentrations in mid-pregnancy had lower birthweight infants compared to women with higher HDL-C concentrations. There was no significant association between LDL-C or total cholesterol concentrations and birthweight. The relationship with HDL-C and birthweight was maintained when maternal BMI was included in the model. To begin to elucidate the processes involved in the regulation of fetal growth, placental function was examined in mice with increasing maternal HDL-C concentrations based on apoA-I levels; mice were lacking apoA-I (apoA-I -/- ), were wildtype (apoA-I +/+ ), or had excess apoA-I (apoA-I tg/tg ). HDL decreased in size as plasma apoA-I levels increased, and there were no statistical differences in the proteins carried by HDL, except for apoA-I, in pregnant mice of different genotypes. However, pregnancy alone led to changes in the HDL proteome. Importantly, fetuses of mice with lower concentrations of maternal HDL-C had reduced growth rates, not due to a lack of fetal apoA-I. The murine fetal growth rates were directly related to nutrient uptake by and transport across the placenta. This work suggests that maternal HDL affects placental function leading to enhanced nutrient supply and improved growth in utero, making HDL a potential biomarker for fetal growth and putative target for intervention.

Fetal Growth Restriction Is Associated With Malaria in Pregnancy: A Prospective Longitudinal Study in Benin.

Few studies have evaluated the effect of malaria on intrauterine growth restriction on the basis of the fetal growth rate, rather than just the small-for-gestational age z score. Here, we assessed the impact of malaria on IUGR, using data from a longitudinal, ultrasonography-based follow-up study of Beninese women. A total of 1016 women were followed up from gestational week 17 to delivery. Malaria was detected every month. Women underwent ultrasonography 4 times for gestational age determination and fetal biometry. We assessed the effect of malaria on birth weight-for-gestational age z score (n = 735 women) and fetal growth velocity (n = 664), defined as a change in fetal weight z score over time. Malaria was detected in 43% of women. Fetal growth velocity was negative overall, decreasing further at the end of the third trimester. Women with ≥2 malarial parasite infections tended to have lower z scores than uninfected women. Malaria both in early and late pregnancy was associated with a reduction in fetal growth velocity, which occurred either immediately or with a delay after infection. We confirmed the deleterious effect of malaria during both early and late pregnancy on fetal growth. This stresses the importance of starting preventive measures against malaria as early as possible during pregnancy.

Correlation between Maternal Characteristics during Early Pregnancy, Fetal Growth Rate and Newborn Weight in Healthy Pregnancies

Background: The objective of this study was to evaluate the association between maternal characteristics in early pregnancy and fetal growth (FG) and birth weight (BW). Methods: A prospective cohort study was performed in unselected pregnant women who attended an ultrasound evaluation at 11-14 weeks of pregnancy. Medical history, biochemical blood tests, biophysical variables and fetal weight at 20-25 and 30-36 weeks as well as the BW were assessed. Bivariate and multivariate linear models were constructed. Results: In all, 543 patients with normal pregnancy and labor were selected. The multiple regression analysis showed a statistically significant association between maternal body mass index (BMI) in early pregnancy and the uterine artery pulsatility index (UtAPI) in the first trimester with BW (p < 0.0008) and with the ratio of fetal growth between the second and third trimesters (p < 0.0001). No correlation was found between these variables and first trimester levels of hemoglobin or glycemia. Conclusion: Maternal first trimester BMI and UtAPI correlate with the rate of intrauterine FG and with the BW. This evidence highlights the influence of maternal first trimester variables on fetuses with normal growth and the potential role of these variables in fetal programming.

Assessment of in vivo fetal growth and placental vascular function in a novel intrauterine growth restriction model of progressive uterine artery occlusion in guinea pigs.

Intra-uterine growth restriction (IUGR) is associated with short and long-term metabolic and cardiovascular alterations. Mice and rats have been extensively used to study the effects of IUGR, but there are notable differences in fetal and placental physiology relative to those of humans that argue for alternative animal models. This study proposes that gradual occlusion of uterine arteries from mid-gestation in pregnant guinea pigs produces a novel model to better assess human IUGR. Fetal biometry and in vivo placental vascular function were followed by sonography and Doppler of control pregnant guinea pigs and sows submitted to surgical placement of ameroid constrictors in both uterine arteries (IUGR) at mid-gestation (35 days). The ameroid constrictors induced a reduction in the fetal abdominal circumference growth rate (0.205 cm day(-1) ) compared to control (0.241 cm day(-1) , P < 0.001) without affecting biparietal diameter growth. Umbilical artery pulsatility and resistance indexes at 10 and 20 days after surgery were significantly higher in IUGR animals than controls (P < 0.01). These effects were associated with a decrease in the relative luminal area of placental chorionic arteries (21.3 ± 2.2% vs. 33.2 ± 2.7%, P < 0.01) in IUGR sows at near term. Uterine artery intervention reduced fetal (∼30%), placental (∼20%) and liver (∼50%) weights (P < 0.05), with an increased brain to liver ratio (P < 0.001) relative to the control group. These data demonstrate that the ameroid constrictor implantations in uterine arteries in pregnant guinea pigs lead to placental vascular dysfunction and altered fetal growth that induces asymmetric IUGR.

Intrauterine Growth Restriction: Antenatal and Postnatal Aspects.

Intrauterine growth restriction (IUGR), a condition that occurs due to various reasons, is an important cause of fetal and neonatal morbidity and mortality. It has been defined as a rate of fetal growth that is less than normal in light of the growth potential of that specific infant. Usually, IUGR and small for gestational age (SGA) are used interchangeably in literature, even though there exist minute differences between them. SGA has been defined as having birth weight less than two standard deviations below the mean or less than the 10th percentile of a population-specific birth weight for specific gestational age. These infants have many acute neonatal problems that include perinatal asphyxia, hypothermia, hypoglycemia, and polycythemia. The likely long-term complications that are prone to develop when IUGR infants grow up includes growth retardation, major and subtle neurodevelopmental handicaps, and developmental origin of health and disease. In this review, we have covered various antenatal and postnatal aspects of IUGR.

Optimizing Early Protein Intake for Long-Term Health of Preterm Infants.

The idea that early protein intake may influence, or program, long-term health in preterm infants is strongly supported by decades of research starting from the early 1980s. At this time, it was recognized that preterm infants required a high protein intake to achieve postnatal growth closer to the intrauterine growth rate of a normal fetus of the same postconceptional age, a goal regarded optimal for short- and long-term health. Subsequently, follow-up of preterm infants randomized to different neonatal diets demonstrated that those receiving higher protein intakes that promoted growth had benefits for brain structure and function up to 16 years later, but also detrimental effects on cardiovascular risk factors such as insulin resistance and adiposity. These effects of early growth on risk of metabolic disease, termed the 'growth acceleration' hypothesis, have been demonstrated in randomized and observational studies in infants born preterm and at term. Nevertheless, on balance, current nutrition policy for preterm infants is based on the consensus that supporting optimal neurodevelopment is the neonatologist's highest priority. Therefore, this policy appropriately favors early administration of a high protein intake to benefit neurodevelopment, irrespective of any increase in cardiovascular risk. The current review will consider the evidence underlying this policy.

The relationship between human placental morphometry and ultrasonic measurements of utero-placental blood flow and fetal growth

IntroductionUltrasonic fetal biometry and arterial Doppler flow velocimetry are widely used to assess the risk of pregnancy complications. There is an extensive literature on the relationship between pregnancy outcomes and the size and shape of the placenta. However, ultrasonic fetal biometry and arterial Doppler flow velocimetry have not previously been studied in relation to postnatal placental morphometry in detail. MethodsWe conducted a prospective cohort study of nulliparous women in The Rosie Hospital, Cambridge (UK). We studied a group of 2120 women who had complete data on uterine and umbilical Doppler velocimetry and fetal biometry at 20, 28 and 36 weeks' gestational age, digital images of the placenta available, and delivered a liveborn infant at term. Associations were expressed as the difference in the standard deviation (SD) score of the gestational age adjusted ultrasound measurement (z-score) comparing the lowest and highest decile of the given placental morphometric measurement. ResultsThe lowest decile of placental surface area was associated with 0.87 SD higher uterine artery Doppler mean pulsatility index (PI) at 20 weeks (95% CI: 0.68 to 1.07, P < 0.001). The lowest decile of placental weight was associated with 0.73 SD higher umbilical artery Doppler PI at 36 weeks (95% CI: 0.54 to 0.93, P < 0.001). The lowest decile of both placental weight and placental area were associated with reduced growth velocity of the fetal abdominal circumference between 20 and 36 weeks (both P < 0.001). ConclusionPlacental area and weight are associated with uterine and umbilical blood flow, respectively, and both are associated with fetal growth rate.

Fetal growth and subsequent maternal risk of thyroid cancer

Thyroid cancer has peak incidence among women of reproductive age, and growth factors, which have procarcinogenic properties, may play an important etiologic role. However, the association between fetal growth rate during a woman's pregnancy and her subsequent risk of thyroid cancer has not been previously examined. We conducted a national cohort study of 1,837,634 mothers who had a total of 3,588,497 live-births in Sweden in 1973-2008, followed up for thyroid cancer incidence through 2009. There were 2,202 mothers subsequently diagnosed with thyroid cancer in 36.8 million person-years of follow-up. After adjusting for maternal age, height, weight, smoking, and sociodemographic factors, high fetal growth (birth weight standardized for gestational age and sex) was associated with a subsequent increased risk of thyroid cancer in the mother (incidence rate ratio [IRR] per additional 1 standard deviation, 1.05; 95% CI, 1.01-1.09; p = 0.02). Each 1,000 g increase in the infant's birth weight was associated with a 13% increase in the mother's subsequent risk of thyroid cancer (IRR, 1.13; 95% CI, 1.05-1.22; p = 0.001). These findings appeared to involve both papillary and follicular subtypes, and did not vary significantly by the mother's height, weight or smoking status. In this large national cohort study, high fetal growth during a woman's pregnancy was independently associated with a subsequent increased risk of her developing thyroid cancer. If confirmed, these findings suggest an important role of maternal growth factors in the development of thyroid cancer, and potentially may help facilitate the identification of high-risk subgroups of women.

The placenta is the center of the chronic disease universe

Over the past quarter century it has become clear that adult onset chronic diseases like heart disease and type 2 diabetes have their roots in early development. The report by David Barker and colleagues showing an inverse relationship between birthweight and mortality from ischemic heart disease was the first clear-cut demonstration of fetal programming. Because fetal growth depends upon the placental capacity to transport nutrients from maternal blood, it has been a suspected causative agent since the original Barker reports. Epidemiological studies have shown that placental size and shape have powerful associations with offspring disease. More recent studies have shown that maternal phenotypic characteristics, such as body mass index and height, interact with placental size and shape to predict disease with much more precision than does birthweight alone. For example, among people in the Helsinki Birth Cohort, who were born during 1924–1944, the risk for acquiring colorectal cancer increased as the placental surface became longer and more oval. Among people in whom the difference between the length and breadth of the surface exceeded 6 cm, the hazard ratio for the cancer was 2.3 (95% CI 1.2–4.7, p=0.003) compared with those in whom there was no difference. Among Finnish men, the hazard ratio for coronary heart disease was 1.07 (1.02–1.13, P =0.01) per 1% increase in the placental weight/birthweight ratio. Thus, it appears that the ratio of birthweight to placental weight, known as placental efficiency, predicts cardiovascular risk as well. Babies born with placentas at the extremes of efficiency are more vulnerable for adult onset chronic diseases. Recent evidence suggests that placental growth patterns are sex specific. Boys’ placentas are, in general, more efficient than those made by girls. Another recent discovery is that the size, shape and efficiencies of the placenta can change over years of time with very narrow confidence limits. This suggests that the growth of the placenta within a population of women is strongly affected by their nutritional environment. Even though it is known that an individual placenta can expand to improve its nutrient acquisition capacity in the first 2/3rd of gestation, the mechanisms by which placentas grow in response to a specific nutritional environment are not known. Discovering those mechanisms is the task of the current generation of scientists. While it may seem obvious that good nutrition is highly important for women who are pregnant because it supports optimal placentation and fetal development, more research is needed to determine the mechanisms by which maternal nutrition, placenta growth and fetal health are related.

Fetal growth and maternal glomerular filtration rate: a systematic review

Objective: Glomerular filtration rate (GFR) may influence concentrations of biomarkers of exposure and their etiologic significance in observational studies of associations between environmental contaminants and fetal growth. It is unknown whether the size of a developing fetus affects maternal GFR such that a small fetus leads to reduced plasma volume expansion (PVE), reduced GFR and subsequent higher concentrations of biomarkers in maternal serum. Our objective was to answer the question: “Is there an association between fetal growth and maternal GFR in humans?”Methods: We adapted and applied the Navigation Guide systematic review methodology to assess the evidence of an association between fetal growth and GFR, either directly or indirectly via reduction in PVE.Results: We identified 35 relevant studies. We rated 31 human and two non-human observational studies as “low” quality and two experimental non-human studies as “very low” quality. We rated all three evidence streams as “inadequate”. The association between fetal growth and GFR was “not classifiable” according to pre-specified definitions.Conclusions: There is currently insufficient evidence to support the plausibility of a reverse causality hypothesis for associations between exposure to environmental chemicals during pregnancy and fetal growth. Further research would be needed to confirm or disprove this hypothesis.

Connecting proximate mechanisms and evolutionary patterns: pituitary gland size and mammalian life history.

At the proximate level, hormones are known to play a critical role in influencing the life history of mammals, including humans. The pituitary gland is directly responsible for producing several hormones, including those related to growth and reproduction. Although we have a basic understanding of how hormones affect life history characteristics, we still have little knowledge of this relationship in an evolutionary context. We used data from 129 mammal species representing 14 orders to investigate the relationship between pituitary gland size and life history variation. Because pituitary gland size should be related to hormone production and action, we predicted that species with relatively large pituitaries should be associated with fast life histories, especially increased foetal and post-natal growth rates. Phylogenetic analyses revealed that total pituitary size and the size of the anterior lobe of the pituitary significantly predicted a life history axis that was correlated with several traits including body mass, and foetal and post-natal growth rates. Additional models directly examining the association between relative pituitary size and growth rates produced concordant results. We also found that relative pituitary size variation across mammals was best explained by an Ornstein-Uhlenbeck model of evolution, suggesting an important role of stabilizing selection. Our results support the idea that the size of the pituitary is linked to life history variation through evolutionary time. This pattern is likely due to mediating hormone levels but additional work is needed. We suggest that future investigations incorporating endocrine gland size may be critical for understanding life history evolution.

Maternal adaptation to pregnancy is at least in part influenced by fetal gender.

An age-old question, ‘is it a boy or a girl?’ may be of greater significance than we have assumed! Differences in fetal growth rates by gender have been recognised for decades; however, the reasons why such differences exist remain poorly understood. Constitutional, genetic, metabolic, and many other factors have been proposed as affecting fetal growth and gender-related growth differences. The importance of placental function in fetal growth is unquestionable. Although each fetus has its own phenotype, it has typically been assumed that it is maternal factors that exhibit the greatest influence on placental function, and thereby upon fetal development. Examples include the patterns of fetal growth seen in mothers with medical issues such as diabetes, hypertension, or those with a pro-thrombotic disposition; however, recent data highlight the importance of maternal–fetal interactions, and furthermore what role fetal gender may have to play in these. Differential responses in fetal growth have been observed between genders with respect to maternal height and weight (Lampl et al. Am J Hum Biol 2010;22:431–443). Rather than the expected (that fetal weight would correlate directly with maternal height and weight), this study showed contrasting, gender-specific, growth patterns that varied not only with time but also with maternal height and weight independent of each other. Recent publications have demonstrated more direct associations between fetal gender and placental function. It appears that male fetuses are better able to maintain placental growth than females in the presence of maternal pre-eclampsia (Roland et al. Pregnancy Hypertension 2013;3:95). Prior data from the current authors suggest that fetal gender is associated with differences in placental function from early pregnancy, as demonstrated by observed differences in first-trimester placental biomarkers in uncomplicated pregnancies (Brown Placenta 2014;35:359–64). Although these differences may be superseded in pathological states, important gender influences persist nonetheless, with maternal blood pressures in complicated pregnancies (including pre-eclampsia) being higher in pregnancies with female fetuses (Brown et al. Pregnancy Hypertension 2015;5:31–2). In this present study (Brown et al. BJOG 2016; 123:1087–95) the authors have evaluated maternal vascular adaptation to pregnancy through the assessment of uterine artery Doppler and blood pressure, and have shown that pregnancies with male fetuses were more frequently associated with evidence of poor maternal vascular adaptation. Offering an important insight into the function of the fetoplacental unit, these data represents another piece in an as yet incomplete puzzle. The interactions between mother and fetus appear even more complex than was previously thought, and the balances and interplays that exist between the two appear themselves subject to modification by disease states. Further studies may highlight the roles that not only fetal gender but other fetal characteristics play. An understanding of how these might interact with various parental factors may provide further insights into the regulation of placental function and subsequent fetal development in both normal and complicated pregnancies. An improved understanding of these interrelationships is required in order for us to be better able to influence higher risk pregnancies and improve outcomes. None declared. Completed disclosure of interests form available to view online as supporting information.

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Impact of Childhood Anthropometry Trends on Adult Lung Function

BACKGROUND:Poor fetal growth rate is associated with lower respiratory function; however, there is limited understanding of the impact of growth trends and BMI during childhood on adult respiratory function.METHODS:The current study data are from the Mater-University of Queensland Study of Pregnancy birth cohort. Prospective data were available from 1,740 young adults who performed standard spirometry at 21 years of age and whose birth weight and weight, height, and BMI at 5, 14, and 21 years of age were available. Catch-up growth was defined as an increase of 0.67Zscore in weight between measurements. The impact of catch-up growth on adult lung function and the relationship between childhood BMI trends and adult lung function were assessed using regression analyses.RESULTS:Lung function was higher at 21 years in those demonstrating catch-up growth from birth to 5 years (FVC, men: 5.33 L vs 5.54 L; women: 3.78 L vs 4.03 L; and FEV1, men: 4.52 L/s vs 4.64 L/s; women: 3.31 L/s vs 3.45 L/s). Subjects in the lowest quintile of birth (intrauterine growth retardation) also showed improved lung function if they had catch-up growth in the first 5 years of life. There was a positive correlation between increasing BMI and lung function at 5 years of age. However, in the later measurements when BMI increased into the obese category, a drop in lung function was observed.CONCLUSIONS:These data show evidence for a positive contribution of catch-up growth in early life to adult lung function. However, if weight gain or onset of obesity occurs after 5 years of age, an adverse impact on adult lung function is noted.

Epigenetic regulation of histone modifications and Gata6 gene expression induced by maternal diet in mouse embryoid bodies in a model of developmental programming.

BackgroundDietary interventions during pregnancy alter offspring fitness. We have shown mouse maternal low protein diet fed exclusively for the preimplantation period (Emb-LPD) before return to normal protein diet (NPD) for the rest of gestation, is sufficient to cause adult offspring cardiovascular and metabolic disease. Moreover, Emb-LPD blastocysts sense altered nutrition within the uterus and activate compensatory cellular responses including stimulated endocytosis within extra-embryonic trophectoderm and primitive endoderm (PE) lineages to protect fetal growth rate. However, these responses associate with later disease. Here, we investigate epigenetic mechanisms underlying nutritional programming of PE that may contribute to its altered phenotype, stabilised during subsequent development. We use embryonic stem (ES) cell lines established previously from Emb-LPD and NPD blastocysts that were differentiated into embryoid bodies (EBs) with outer PE-like layer.ResultsEmb-LPD EBs grow to a larger size than NPD EBs and express reduced Gata6 transcription factor (regulator of PE differentiation) at mRNA and protein levels, similar to Emb-LPD PE derivative visceral yolk sac tissue in vivo in later gestation. We analysed histone modifications at the Gata6 promoter in Emb-LPD EBs using chromatin immunoprecipitation assay. We found significant reduction in histone H3 and H4 acetylation and RNA polymerase II binding compared with NPD EBs, all markers of reduced transcription. Other histone modifications, H3K4Me2, H3K9Me3 and H3K27Me3, were unaltered. A similar but generally non-significant histone modification pattern was found on the Gata4 promoter. Consistent with these changes, histone deacetylase Hdac-1, but not Hdac-3, gene expression was upregulated in Emb-LPD EBs.ConclusionsFirst, these data demonstrate ES cells and EBs retain and propagate nutritional programming adaptations in vitro, suitable for molecular analysis of mechanisms, reducing animal use. Second, they reveal maternal diet induces persistent changes in histone modifications to regulate Gata6 expression and PE growth and differentiation that may affect lifetime health.

Disparities in birth weight and gestational age by ethnic ancestry in South American countries.

We examine disparities in birth weight and gestational age by ethnic ancestry in 2000-2011 in eight South American countries. The sample included 60,480 singleton live births. Regression models were estimated to evaluate differences in birth outcomes by ethnic ancestry controlling for time trends. Significant disparities were found in seven countries. In four countries-Brazil, Ecuador, Uruguay, and Venezuela-we found significant disparities in both low birth weight and preterm birth. Disparities in preterm birth alone were observed in Argentina, Bolivia, and Colombia. Several differences in continuous birth weight, gestational age, and fetal growth rate were also observed. There were no systematic patterns of disparities between the evaluated ethnic ancestry groups across the study countries, in that no racial/ethnic group consistently had the best or worst outcomes in all countries. Racial/ethnic disparities in infant health are common in several South American countries. Differences across countries suggest that racial/ethnic disparities are driven by social and economic mechanisms. Researchers and policymakers should acknowledge these disparities and develop research and policy programs to effectively target them.

Fetal lung growth represented by longitudinal changes in MRI-derived fetal lung volume parameters predicts survival in isolated left-sided congenital diaphragmatic hernia.

The aim of this study was to evaluate fetal lung growth rate for isolated left-sided congenital diaphragmatic hernia (CDH) using serial magnetic resonance imaging (MRI)-based volumetric measures. Early and late gestational (22-30 and >30 weeks' gestation) lung volumetry was obtained by fetal MRI in 47 cases of isolated left-sided CDH. At both of these time points, lung volume indices, including total lung volume (TLV), observed to expected TLV (o/e TLV), and percentage of predicted lung volume (PPLV) as well as their change rates (Δ) and relative Δ during gestation were calculated and analyzed in regard to their capacity to predict neonatal survival. TLV, o/e TLV, and PPLV had various changes during gestation. Late TLV, early and late o/e TLV, and late PPLV were predictive of neonatal survival. Non-survivors had lower ΔTLV and more negative relative ΔPPLV than survivors (1.18 vs 1.85 mL/week, P = 0.004 and -4.15%/week vs -1.95%/week, P = 0.002, respectively). The severity of pulmonary hypoplasia is dynamic and can worsen in the third trimester. MRI lung volumetry repeated in late gestation can provide additional information on individual lung growth that may facilitate prenatal counseling and focus perinatal management.