scholarly journals Alteration in 11 Beta-Hydroxysteroid Dehydrogenase Type-2 (HSD11B2) Gene as A Potential Candidate Parameter for Early Detection of Intrauterine Growth Restriction (IUGR) Events

2021 ◽  
Vol 5 (3) ◽  
pp. 98
Author(s):  
Louis Fabio Jonathan Jusni ◽  
Patricia Patricia ◽  
Brigitte Leonie Rosadi
Keyword(s):  
Early Detection ◽  
Doppler Ultrasound ◽  
Intrauterine Growth Restriction ◽  
Prenatal Testing ◽  
Hydroxysteroid Dehydrogenase ◽  
Growth Restriction ◽  
Diagnostic Parameter ◽  
Intrauterine Growth ◽  
Non Invasive

Intrauterine Growth Restriction (IUGR) incidence in Indonesia ranks in the top 10 of the highest in Asia. It is the main perinatal death cause. IUGR also impairs fetal neurodevelopment, which can affect the development of children until later ages. Lack of 11β-hydroxysteroid dehydrogenase type-2 (11β-HSD2) enzyme is influenced by changes in the coding gene, HSD11B2, one of IUGR's causes. The main diagnostic method of IUGR at this time is by using Doppler ultrasound. However, Doppler ultrasound has several limitations as many cases are not detected. Its clinical predictive value in various women is poor, as Doppler ultrasound is not recommended for use in the first trimester, detection of abnormalities in the second trimester seems to be too late for helpful interventions. The study aim is to present an overview concerning HSD11B2 gene alteration in an non-invasive prenatal testing (NIPT) as a possible diagnostic parameter for early detection in IUGR infants. This literature review is based on selected articles and studies taken from the Pubmed, Proquest, and EBSCO databases. A total of 4 studies reported the tendency for DNA methylation and decreased expression of the HSD11B2 gene in IUGR cases. Changes in the HSD11B2 gene have the potential to become a diagnostic parameter in the early detection of infants with IUGR. Further study and investigation of this possibility are needed.Keywords: intrauterine growth restriction, HSD11B2, early detection, diagnostic, non-invasive prenatal testing

scholarly journals Reduced Placental 11β-Hydroxysteroid Dehydrogenase Type 2 mRNA Levels in Human Pregnancies Complicated by Intrauterine Growth Restriction: An Analysis of Possible Mechanisms

2001 ◽  
Vol 86 (10) ◽  
pp. 4979-4983 ◽  
Author(s):  
C. L. McTernan ◽  
N. Draper ◽  
H. Nicholson ◽  
S. M. Chalder ◽  
P. Driver ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Intrauterine Growth Restriction ◽  
Subsequent Development ◽  
Hydroxysteroid Dehydrogenase ◽  
Underlying Mechanism ◽  
Growth Restriction ◽  
Mrna Levels ◽  
Intrauterine Growth ◽  
Apparent Mineralocorticoid Excess

11β-Hydroxysteroid dehydrogenase type 2 (11β-HSD2) inactivates cortisol to cortisone. In the placenta 11β-HSD2 activity is thought to protect the fetus from the deleterious effects of maternal glucocorticoids. Patients with apparent mineralocorticoid excess owing to mutations in the 11β-HSD2 gene invariably have reduced birth weight, and we have recently shown reduced placental 11β-HSD2 activity in pregnancies complicated by intrauterine growth restriction. This is reflected in the literature by evidence of hypercortisolemia in the fetal circulation of small babies. In this study we have determined the levels of placental 11β-HSD2 mRNA expression across normal gestation (n = 86 placentae) and in pregnancies complicated by intrauterine growth restriction (n = 19) and evaluated the underlying mechanism for any aberrant 11β-HSD2 mRNA expression in intrauterine growth restriction. 11β-HSD2 mRNA expression increased more than 50-fold across gestation, peaking at term. Placental 11β-HSD2 mRNA levels were significantly decreased in intrauterine growth restriction pregnancies when compared with gestationally matched, appropriately grown placentae [e.g. at termΔ Ct (11β-hydroxysteroid dehydrogenase type 2/18S) 12.8 ± 0.8 (mean ± se) vs. 10.2 ± 0.2, respectively, P < 0.001]. These differences were not attributable to changes in trophoblast mass in intrauterine growth restriction placentae, as assessed by parallel analyses of cytokeratin-8 mRNA expression. No mutations were found in the 11β-HSD2 gene in the intrauterine growth restriction cohort, and imprinting analysis revealed that the 11β-HSD2 gene was not imprinted. Although the underlying cause is unknown, 11β-HSD2 gene expression is reduced in intrauterine growth restriction pregnancies. These data highlight the important role of 11β-HSD2 in regulating fetal growth, a known factor in determining fetal morbidity but also the subsequent development of cardiovascular disease in adulthood.

scholarly journals 11Beta-hydroxysteroid dehydrogenase type 2 in human pregnancy and reduced expression in intrauterine growth restriction

1998 ◽  
Vol 13 (4) ◽  
pp. 799-804 ◽  
Author(s):  
M. Shams ◽  
M. D. Kilby ◽  
D. A. Somerset ◽  
A. J. Howie ◽  
A. Gupta ◽  
...  
Keyword(s):  
Intrauterine Growth Restriction ◽  
Hydroxysteroid Dehydrogenase ◽  
Growth Restriction ◽  
Human Pregnancy ◽  
Intrauterine Growth

Values of T/QRS ratio in pregnancies complicated by intrauterine growth restriction

2016 ◽  
Vol 44 (7) ◽  
Author(s):  
Tomasz Fuchs
Keyword(s):  
Intrauterine Growth Restriction ◽  
Well Being ◽  
Study Groups ◽  
Growth Restriction ◽  
Healthy Controls ◽  
Value Differences ◽  
Intrauterine Growth ◽  
Non Invasive ◽  
Invasive Method ◽  
Ratio Variables

AbstractAims:To evaluate values of T/QRS ratio in normal pregnancies and those complicated by intrauterine growth restriction (IUGR) using non-invasive method with transabdominal electrodes. Assessment of fetal well-being in IUGR pregnancies.Methods:Fetal electrocardiograms were recorded and analyzed by KOMPOREL software from ITAM (Zabrze, Poland) and T/QRS ratios were automatically calculated. Doppler velocimetry of the middle cerebral artery and umbilical artery was carried out. The study group consisted of IUGR pregnancies with normal cerebroplacental ratios (CPRs) (n=110), IUGR pregnancies with decreased CPRs (n=29), and healthy controls (n=549). Analyses were performed between the study groups and by gestational age. T/QRS ratio variables and CPRs were calculated. Analysis of variance and linear regression were performed.Results:Maximum values, maximum minimal value differences, and standard deviations of T/QRS ratio were significantly different between the IUGR group with reduced CPRs and normal CPRs (P=0.0009, P=0.0000, P=0.0034, respectively) as well as between the IUGR group with reduced CPRs and healthy controls (P=0.0000, P=0.0001, P=0.0009, respectively). Mean maximum values in the IUGR group with reduced CPRs exceeded normal values.Conclusions:T/QRS ratio may be useful in assessing fetal well-being in IUGR pregnancies; however, future studies are needed to determine typical ranges of T/QRS ratio in pregnancies complicated by IUGR.

Novel Polymorphisms in the Angiotensin II type 2 Receptor Gene: Common Haplotypes and Implications for Intrauterine Growth Restriction (IUGR)

2002 ◽  
Vol 103 (s47) ◽  
pp. 60P-61P
Author(s):  
Clare Tower ◽  
Sally Plummer ◽  
Pedro Alonso ◽  
Linda Morgan ◽  
Philip Baker ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Intrauterine Growth Restriction ◽  
Receptor Gene ◽  
Growth Restriction ◽  
Intrauterine Growth

scholarly journals Diethylstilbestrol inhibits human and rat 11β-hydroxysteroid dehydrogenase 2

2019 ◽  
Vol 8 (7) ◽  
pp. 1061-1069
Author(s):  
Yiyan Wang ◽  
Yaoyao Dong ◽  
Yinghui Fang ◽  
Yao Lv ◽  
Qiqi Zhu ◽  
...  
Keyword(s):  
Mode Of Action ◽  
Intrauterine Growth Restriction ◽  
Area Under The Curve ◽  
Hydroxysteroid Dehydrogenase ◽  
Competitive Inhibitor ◽  
Growth Restriction ◽  
Sprague Dawley ◽  
Intrauterine Growth ◽  
Cortisol Metabolism ◽  
Metabolizing Enzyme

Glucocorticoid hormone might cause intrauterine growth restriction. The glucocorticoid-metabolizing enzyme 11β-hydroxysteroid dehydrogenase 2 (HSD11B2) in the placenta eliminates excess levels of glucocorticoids during pregnancy. The aim of the current study was to define the effects of diethylstilbestrol (DES) on HSD11B2 activity in the mammalian placentas and identify its mode of action. Rat and human placental microsomal HSD11B2 were incubated with different concentrations of DES, and IC50 values were determined. The mode of action was analyzed by incubation of DES together with substrates, glucocorticoid and NAD+. DES suppressed rat and human HSD11B2 with IC50 values of 5.33 and 12.62 μM, respectively. DES was a competitive inhibitor of rat and human HSD11B2 when steroid substrates were added, while it was an uncompetitive inhibitor when cofactor NAD+ was exposed. Oral administration of DES (0.5 mg/kg) to the rat delayed the cortisol metabolism in adult female Sprague–Dawley rats, as indicated by the increases in cortisol’s elimination half-life, maximum concentration and area under the curve. In conclusion, DES is a potent HSD11B2 inhibitor, possibly contributing to the intrauterine growth restriction.

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