The Effect of Antenatal Steroids on Fetal Lung Maturation between the 34th and 36th Week of Pregnancy

2010 ◽  
Vol 70 (2) ◽  
pp. 95-99 ◽  
Author(s):  
Osman Balci ◽  
Suna Ozdemir ◽  
Alaa S. Mahmoud ◽  
Ali Acar ◽  
Mehmet C. Colakoglu
2021 ◽  
Vol 29 (2) ◽  
pp. 90-92
Author(s):  
Nashwa Eltaweel ◽  
Samuel Lockley ◽  
Irshad Ahmed ◽  
Bee K Tan

Immune system changes during pregnancy could make pregnant women more susceptible to SARS-Cov-2 infection. The use of corticosteroids within obstetrics has been shown to reduce the risks of respiratory distress syndrome, intraventricular haemorrhage, necrotizing enterocolitis and neonatal death in the baby associated with premature delivery. During the COVID-19 pandemic, corticosteroids have been trialled as a treatment to dampen the ‘cytokine storm’ and associated inflammatory processes. Corticosteroids have long been known to have immunosuppressive effects that could hinder the body's ability to mount a defence against COVID-19 and thereby delaying viral clearance. In this clinical case studies, antenatal steroids for fetal lung maturation appear to be of benefit and did not result in a deterioration of maternal disease. Our clinical case studies support the current recommendations from the Royal College of Obstetricians and Gynaecologists ie corticosteroids for fetal lung maturation is appropriate in patients who are suspected or have confirmed SARS-CoV-2 infection.


2005 ◽  
Vol 53 (12) ◽  
pp. 1469-1479 ◽  
Author(s):  
Zarah J. Pua ◽  
Barbara S. Stonestreet ◽  
Anne Cullen ◽  
Aliakbar Shahsafaei ◽  
Grazyna B. Sadowska ◽  
...  

A single course of antenatal steroids is widely used during preterm labor to promote fetal lung maturation. However, little is known regarding efficacy and safety of multiple courses of antenatal steroids. In animal models and clinical trials, treatment with glucocorticoids can inhibit growth. The present study of single- vs multiple-course steroids in pregnant ewes analyzes the effects of steroids vs placebo on fetal lung histopathology. Single-course groups received dexamethasone (Dex) 6 mg or normal saline every 12 hr for 48 hr at 104-106 days of gestation (term = 150 days). Multiple-course groups received the first course at 76-78 days; this was repeated weekly for 5 weeks. At 108 days, lungs were analyzed using immunohistochemistry for α-smooth muscle actin, a myofibroblast marker and proliferating cell nuclear antigen. Cell injury/death was evaluated using TdT-mediated dUTP digoxigenin nick end labeling (TUNEL) analysis. Although fetal growth was restricted by either single or multiple courses of Dex, alveolar development was accelerated as measured by mean linear intercepts. Alveolar walls were thinner, developing septa were longer, and septal myofibroblasts were increased for both Dex groups compared with controls. Cell proliferation increased following multiple steroid courses, especially in the distal parenchyma, with a corresponding decrease in apoptosis. These observations suggest that Dex promotes alveolarization, whether given in single or multiple courses.


2015 ◽  
Vol 8 (4) ◽  
pp. 172-176 ◽  
Author(s):  
Carolyn I Freeman ◽  
Natasha L Hezelgrave ◽  
Andrew H Shennan

Antenatal corticosteroids for fetal lung maturation have become mainstay treatment in women thought to be at high-risk of premature birth. To ensure treatment efficacy before delivery, the current practice is to administer steroids early to a woman considered at risk; however, neonatal benefit is lost after the seven-day treatment-to-delivery window. Over half of women who deliver before 34 weeks’ gestation do not receive antenatal corticosteroids within this timeframe, but many still deliver prematurely; however, clinicians are reluctant to administer repeated courses of steroids due to concerns, among others, of impaired fetal growth. However, evidence is mounting regarding the optimal timing for steroids, including substantive benefits close to delivery, and the benefits of repeated courses if delivery has not occurred. Better targeted treatment is required to allow for maximum benefit; reducing unnecessary treatment in low-risk women, while targeting therapy in the high-risk cohort and offering repeat courses if the seven-day window is exceeded. Novel tools to aid prediction may help implement this strategy.


2020 ◽  
Vol 319 (3) ◽  
pp. L435-L443
Author(s):  
Cindy Lee ◽  
Reiko Sakurai ◽  
Eugene Shin ◽  
Ying Wang ◽  
Jie Liu ◽  
...  

Antenatal steroids (ANS) accelerate fetal lung maturation and reduce the incidence of respiratory distress syndrome. However, sex specificity, i.e., being less effective in males, and potential long-term neurodevelopmental sequelae, particularly with repeated courses, remain significant limitations. The differential sex response to ANS is likely mediated via the inhibitory effect of fetal androgens on steroid’s stimulatory effect on alveolar epithelial-mesenchymal interactions. Since peroxisome proliferator-activated receptor-γ (PPAR-γ) agonists accelerate lung maturation by stimulating alveolar epithelial-mesenchymal interactions, independent of fetal sex, we hypothesized that the effect of PPAR-γ agonist pioglitazone (PGZ) would be sex-independent. Pregnant Sprague-Dawley rat dams were intraperitoneally administered dexamethasone (DEX) or PGZ on embryonic day (e) 18 and e19. At e20, pups were delivered by cesarean section, and fetal lungs and brains were examined for markers of lung maturation and apoptosis, respectively. Mixed epithelial-fibroblast cell cultures were examined to gain mechanistic insights. Antenatal PGZ increased alveolar epithelial and mesenchymal maturation markers equally in males and females; in contrast, antenatal DEX had sex-specific effects. Additionally, unlike DEX, antenatal PGZ did not increase hippocampal apoptosis. We conclude that PPAR-γ agonist administration is an effective, and probably even a superior, alternative to ANS for accelerating fetal lung maturity equally in both males and females.


Author(s):  
Erin V. McGillick ◽  
Sandra Orgeig ◽  
Beth J. Allison ◽  
Kirsty L. Brain ◽  
Youguo Niu ◽  
...  

Abstract Background In the fetus, the appropriate balance of prooxidants and antioxidants is essential to negate the detrimental effects of oxidative stress on lung maturation. Antioxidants improve respiratory function in postnatal life and adulthood. However, the outcomes and biological mechanisms of antioxidant action in the fetal lung are unknown. Methods We investigated the effect of maternal daily vitamin C treatment (200 mg/kg, intravenously) for a month in late gestation (105–138 days gestation, term ~145 days) on molecular regulation of fetal lung maturation in sheep. Expression of genes and proteins regulating lung development was quantified in fetal lung tissue. The number of surfactant-producing cells was determined by immunohistochemistry. Results Maternal vitamin C treatment increased fetal lung gene expression of the antioxidant enzyme SOD-1, hypoxia signaling genes (HIF-2α, HIF-3α, ADM, and EGLN-3), genes regulating sodium movement (SCNN1-A, SCNN1-B, ATP1-A1, and ATP1-B1), surfactant maturation (SFTP-B and ABCA3), and airway remodeling (ELN). There was no effect of maternal vitamin C treatment on the expression of protein markers evaluated or on the number of surfactant protein-producing cells in fetal lung tissue. Conclusions Maternal vitamin C treatment in the last third of pregnancy in sheep acts at the molecular level to increase the expression of genes that are important for fetal lung maturation in a healthy pregnancy. Impact Maternal daily vitamin C treatment for a month in late gestation in sheep increases the expression of gene-regulating pathways that are essential for normal fetal lung development. Following late gestation vitamin C exposure in a healthy pregnancy, an increase in lung gene but not protein expression may act as a mechanism to aid in the preparation for exposure to the air-breathing environment after birth. In the future, the availability/development of compounds with greater antioxidant properties than vitamin C or more specific targets at the site of oxidative stress in vivo may translate clinically to improve respiratory outcomes in complicated pregnancies at birth.


Sign in / Sign up

Export Citation Format

Share Document