Fetal Growth Restriction and Asthma: Is the Damage Done?

Wang, Kimberley C. W.; Noble, Peter B.

doi:10.1152/physiol.00042.2020

Cited by 11 publications

(10 citation statements)

References 100 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The pathological mechanism is mainly placental dysfunction and uterine-placental insufficiency. This results in the lack of nutrients needed for fetal development, which is manifested as malnutrition [ 3 , 4 ]. The proportion of external symmetrical FGR is 14.55%, and adverse factors exist during the whole pregnancy because of the lack of important nutrients such as amino acids and folic acid.…”

Section: Introductionmentioning

confidence: 99%

[Retracted] Analysis of Causes and Results of Fetal Growth in Utero Caused by Genetic Factors Detected by Ultrasound

Liu

Wang

2022

Contrast Media & Molecular Imaging

View full text Add to dashboard Cite

In order to investigate the value of the ultrasonic monitoring of maternal and fetal vascular parameters, serum vitamin D, and placental growth factor (PLGF) in predicting fetal growth restriction (FGR), a method of ultrasonic detection of genetic factors causing fetal growth in utero was proposed. 125 pregnant women with FGR diagnosed in our hospital from June 2018 to June 2021 (the FGR group) and 125 pregnant women with a normal prenatal examination (the control group) were collected retrospectively. The systolic/diastolic blood flow ratio (S/D), pulsatile index (PI), and resistance index (RI) of the fetal umbilical artery (UA), middle cerebral artery (MCA), and maternal uterine artery (UtA) were monitored by ultrasound at 20 to 24 weeks of gestation, and the levels of serum vitamin D and PLGF were detected. The receiver operating characteristic curve (ROC curve) was used to evaluate the predictive value of FGR. The results showed that the S/D, PI, and RI of UA in the FGR group were higher than those in the control group, the areas under the curve (AUC) were 0.866, 0.817, and 0.849, and the sensitivity and specificity were (72.8%, 91.2%), (50.4%, 100%), and (72.8%, 91.2%), respectively. The S/D, PI, and RI of MCA were lower than those of the control group. The AUC was 0.882, 0.869, and 0.834, respectively; the sensitivity and specificity were (92.0%, 74.4%), (88.8%, 81.6%), and (90.4%, 72%), respectively. The S/D, PI, and RI of UtA were higher than those of the control group; the AUC was 0.768, 0.729, and 0.732; the sensitivity and specificity were (91.2%, 52%), (48%, 90.4%), and (48.8%, 90.4%), respectively. The serum levels of vitamin D and PLGF were lower than those of the control group (AUC 0.784 and 0.807), and the sensitivity and specificity were (54.4%, 91.2%) and (99.2%, 52%), respectively. It was concluded that the ultrasound monitoring of UA, MCA, and UtA in pregnant women in the middle of pregnancy and detection of serum vitamin D and PLGF levels had a certain predictive value for FGR. Moreover, the comprehensive evaluation could reduce the occurrence of FGR in high-risk pregnant women.

show abstract

Section: Introductionmentioning

confidence: 99%

[Retracted] Analysis of Causes and Results of Fetal Growth in Utero Caused by Genetic Factors Detected by Ultrasound

Liu

Wang

2022

Contrast Media & Molecular Imaging

View full text Add to dashboard Cite

show abstract

“…There is also a compelling argument that maternal health affects foetal lung growth and increases the susceptibility to airway disease. [28][29][30] Adverse foetal lung growth could certainly extend to the ASM layer. For example, maternal hypoxia in mice restricts foetal growth and increases ASM thickness.…”

Section: Discussionmentioning

confidence: 99%

“…Infants dying from SIDS have increased ASM compared with non‐SIDS infants 26 and were therefore not included in this study. There is also a compelling argument that maternal health affects foetal lung growth and increases the susceptibility to airway disease 28–30 . Adverse foetal lung growth could certainly extend to the ASM layer.…”

Section: Discussionmentioning

confidence: 99%

Growth of the airway smooth muscle layer from late gestation to childhood is mediated initially by hypertrophy and subsequently hyperplasia

et al. 2022

Self Cite

View full text Add to dashboard Cite

Background and objective: The airway smooth muscle (ASM) layer thickens during development. Identifying the mechanism(s) for normal structural maturation of the ASM reveals pathways susceptible to disease processes. This study characterized thickening of the ASM layer from foetal life to childhood and elucidated the underlying mechanism in terms of hypertrophy, hyperplasia and extracellular matrix (ECM) deposition. Methods: Airways from post-mortem cases were examined from seven different age groups: 22-24 weeks gestation, 25-31 weeks gestation, term (37-41 weeks gestation), <0.5 year, 0.5-1 year, 2-5 years and 6-10 years. The ASM layer area (thickness), the number and size of ASM cells and the volume fraction of ECM were assessed by planimetry and stereology. Results: From late gestation to the first year of life, normalized ASM thickness more than doubled as a result of ASM hypertrophy. Thereafter, until childhood, the ASM layer grew in proportion to airway size, which was mediated by ASM hyperplasia. Hypertrophy and hyperplasia of ASM were accompanied by a proportional change in ECM such that the broad composition of the ASM layer was constant across age groups. Conclusion: These data suggest that the mechanisms of ASM growth from late gestation to childhood are temporally decoupled, with early hypertrophy and subsequent proliferation. We speculate that the developing airway is highly susceptible to ASM thickening in the first year of life and that the timing of an adverse event will determine structural phenotype.

show abstract

“…3 Prenatal influences are associated with reduced lung function and increased risk of asthma in later life, which include maternal undernutrition and infections. 4 Many of these factors may also result in reduced fetal growth and/or intrauterine growth restriction (IUGR), which may be manifest as low birth weight or small for gestational age (SGA, defined as birth weight below 10th percentile). 5 In a recent publication in Respirology, Vellvé et al have examined the effects of SGA at term on subsequent lung function at around 35 years of age in a cohort of babies born between 1975 and 1995 at a single institution in Barcelona, Spain.…”

Section: Small For Gestational Age At Term and Adult Lung Functionmentioning

confidence: 99%

“…Deficits in lung function in adulthood may be the result of different trajectories, with different risk factors, determined early in life 3 . Prenatal influences are associated with reduced lung function and increased risk of asthma in later life, which include maternal undernutrition and infections 4 . Many of these factors may also result in reduced fetal growth and/or intrauterine growth restriction (IUGR), which may be manifest as low birth weight or small for gestational age (SGA, defined as birth weight below 10th percentile) 5 …”

mentioning

confidence: 99%