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Review
. 2018 Jul;61(1):R61-R73.
doi: 10.1530/JME-18-0077. Epub 2018 May 2.

Glucocorticoids, antenatal corticosteroid therapy and fetal heart maturation

Affiliations
Review

Glucocorticoids, antenatal corticosteroid therapy and fetal heart maturation

Emma J Agnew et al. J Mol Endocrinol. 2018 Jul.

Abstract

Glucocorticoids are essential in mammals to mature fetal organs and tissues in order to survive after birth. Hence, antenatal glucocorticoid treatment (termed antenatal corticosteroid therapy) can be life-saving in preterm babies and is commonly used in women at risk of preterm birth. While the effects of glucocorticoids on lung maturation have been well described, the effects on the fetal heart remain less clear. Experiments in mice have shown that endogenous glucocorticoid action is required to mature the fetal heart. However, whether the potent synthetic glucocorticoids used in antenatal corticosteroid therapy have similar maturational effects on the fetal heart is less clear. Moreover, antenatal corticosteroid therapy may increase the risk of cardiovascular disease in adulthood. Here, we present a narrative review of the evidence relating to the effects of antenatal glucocorticoid action on the fetal heart and discuss the implications for antenatal corticosteroid therapy.

Keywords: 11β-HSD; HPA axis; antenatal corticosteroid; fetal origins; glucocorticoid; heart; lung; preterm birth; programming; steroid.

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References

    1. Adler CP, Friedburg H, Herget GW, Neuburger M, Schwalb H. 1996. Variability of cardiomyocyte DNA content, ploidy level and nuclear number in mammalian hearts. Virchows Archiv 429 159–164. - PubMed
    1. Adler A, Camm EJ, Hansell JA, Richter HG, Giussani DA. 2010. Investigation of the use of antioxidants to diminish the adverse effects of postnatal glucocorticoid treatment on mortality and cardiac development. Neonatology 98 73–83. (10.1159/000275561) - DOI - PubMed
    1. Alkass K, Panula J, Westman M, Wu TD, Guerquin-Kern JL, Bergmann O. 2015. No evidence for cardiomyocyte number expansion in preadolescent mice. Cell 163 1026–1036. (10.1016/j.cell.2015.10.035) - DOI - PubMed
    1. Althabe F, Belizan JM, McClure EM, Hemingway-Foday J, Berrueta M, Mazzoni A, Ciganda A, Goudar SS, Kodkany BS, Mahantshetti NS, et al 2015. A population-based, multifaceted strategy to implement antenatal corticosteroid treatment versus standard care for the reduction of neonatal mortality due to preterm birth in low-income and middle-income countries: the ACT cluster-randomised trial. Lancet 385 629–639. (10.1016/S0140-6736(14)61651-2) - DOI - PMC - PubMed
    1. Anatskaya OV, Sidorenko NV, Beyer TV, Vinogradov AE. 2009. Neonatal cardiomyocyte ploidy reveals critical windows of heart development. International Journal of Cardiology 141 81–91. (10.1016/j.ijcard.2008.11.158) - DOI - PubMed

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