Impact of antenatal steroid treatment on external morphological feature of newly born rats. Examine antenatal steroid effects (dexamethasone, hydrocortisone) on newborn rats. Dexamethasone causes severe growth retardation and teratogenic effects, emphasizing crucial timing for treatment.
This paper is about the application of Steroid treatment during pregnancy as practiced in common in practice, in rheumatological and autoimmune diseases, its prolonged use has an adverse effect on fetal growth. The study aimed to assess the effect of prenatal dexamethasone and hydrocortisone treatment on rats' offspring concerning growth parameters, congenital malformation, and survival rate. Sixty pregnant rats were allocated into 12 groups, and administered intraperitoneally either dexamethasone (1mg/kg/day) or hydrocortisone (9 mg/kg/day), and a control group that received normal saline. These were administered in the first week or last week of gestation. Neonatal body weight, length, and gross morphological anomalies were evaluated postnatal at 1 and 15 days. Prenatal dexamethasone treatment in late pregnancy resulted in 27 % neonatal mortality on day 3. Dexamethasone and hydrocortisone significantly reduced body weight and length of neonates compared to the control group, which is more prominent in dexamethasone treatment. However, both glucocorticoids resulted in profound developmental deficits when given in late pregnancy, especially dexamethasone, which causes profound growth retardation and teratogenic effects in neonates. At the same time hydrocortisone has a less severe impact on postnatal malformations and growth retardation. This sheds more light on the timing of steroid administration during the prenatal period, which should be taken into consideration for risk-benefit assessment.
This paper, "Impact of Antenatal Steroid Treatment on External Morphological Feature of Newly Born Rats," investigates a clinically pertinent issue: the adverse effects of antenatal steroid treatment on fetal development. Given the common use of steroids in managing rheumatological and autoimmune conditions during pregnancy, understanding their impact, especially with prolonged use, is crucial. The study's clear aim was to meticulously assess the effects of prenatal dexamethasone and hydrocortisone administration on rat offspring, focusing on key growth parameters, the incidence of congenital malformations, and survival rates. The researchers employed a robust design, allocating sixty pregnant rats into twelve groups, comparing two different glucocorticoids administered at two distinct gestational timings (first or last week), against a saline control. The findings presented are significant and demonstrate a clear differential impact based on the type of steroid and the timing of its administration. A critical observation was the pronounced neonatal mortality rate of 27% by day 3 when dexamethasone was administered in late pregnancy. Both dexamethasone and hydrocortisone significantly reduced neonatal body weight and length compared to controls, with dexamethasone showing a more severe effect. Crucially, the study elucidates that glucocorticoid treatment, particularly dexamethasone in late pregnancy, led to profound developmental deficits, including severe growth retardation and teratogenic effects. Hydrocortisone, while still impacting growth, showed a less severe incidence of postnatal malformations and growth retardation, suggesting a potentially safer profile or a dose-dependent difference in its developmental toxicity. Overall, this research provides valuable insights into the embryotoxic and teratogenic potential of antenatal glucocorticoids, underscoring the importance of careful consideration regarding their therapeutic use during pregnancy. The differential effects observed between dexamethasone and hydrocortisone, and critically, the timing of administration, directly inform the clinical risk-benefit assessment for pregnant patients. The study highlights that the choice of steroid and the specific gestational window for its application are vital factors in mitigating adverse outcomes on fetal development. While conducted in a rat model, these findings lay important groundwork for further investigations into the mechanisms of steroid-induced developmental toxicity and could influence future guidelines for managing maternal conditions requiring steroid treatment.
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