Single Course Of Betamethasone Research Articles

Effects of Single-Course Betamethasone on the Outcomes of Late Preterm Neonates.

Background Prenatal glucocorticoids are commonly used in pregnancies before 34 weeks of gestation in women at risk of preterm delivery; however, the effects of these drugs on late preterm infants (those born after the 34th week of pregnancy) are controversial. As a result, we aimed to investigate the effect of a single course of betamethasone (two doses of betamethasone every 24 hours) on the neonatal outcome of late preterm births. Methods We retrospectively assessed all spontaneous late preterm births (34-36+6 weeks of gestation) at a tertiary hospital in Iran over a period of two and a half years. Exclusion criteria included multiple pregnancies, induced labor, and fetal malformations identified in sonograms. Neonatal outcome measures encompassed first and five-minute Apgar scores, respiratory distress syndrome, neonatal death, birth asphyxia, and the need for positive pressure ventilation, continuous positive airway pressure, tracheal intubation, and surfactant. Baseline characteristics, such as maternal age, parity, fetal gender, and high-risk pregnancy, were considered confounding variables. High-risk pregnancies were defined as any cases involving prolonged rupture of membranes or maternal comorbidities such as severe anemia, preeclampsia, diabetes, or COVID-19. Results During the study period, there were 830 spontaneous preterm births at our center. Of these, only 195 (23.5%) received complete doses of betamethasone. Low birth weight was more common in mothers who did not receive betamethasone compared to those who did (63.6% vs. 41.2%). The mean gestational age was lower in mothers who received betamethasone than in those who did not. Respiratory distress syndrome was more common in mothers who received betamethasone (P<0.001, RR 2.11, 95% CI (0.98-4.18)). However, after adjusting for confounding factors, such as gestational age and birth weight, betamethasone did not increase the risk of respiratory distress syndrome. Other adverse neonatal outcomes did not differ significantly. Conclusions There were no differences in neonatal outcomes between those who received betamethasone and those who did not.

Unresolved issues on the antenatal use of corticosteroids for fetal lung maturation

Antenatal corticosteroids (ACS) for fetal lung maturation is celebrating the 50th anniversary. The most recent Cochrane review concluded that there is robust evidence that a single course of ACS reduces the risk of perinatal death and respiratory distress syndrome. Some aspects of ACS remain unresolved, including variations in the steroids regimen, effectiveness in certain groups, long-term effects, optimal timing of ACS administration in elective cases. it is well established that a single course of betamethasone or dexamethasone is beneficial in cases of anticipated preterm birth and delivery eventually occurs between two and seven days from administration. The main focus for future research should be on limiting the unnecessary exposure in low-risk pregnancies and investigating the effect in specific groups, periviable and late preterm fetuses.

Neurocognitive sequelae of antenatal corticosteroids in a late preterm rabbit model

Late preterm birth is associated with short-term respiratory and adaptive problems. Although antenatal corticosteroids seem to reduce the respiratory burden, this may come at the cost of adverse neuropsychological outcomes later in life. This impact has not been investigated. Herein, we investigate what the short- and long-term neurodevelopmental effects of a single course of betamethasone in simulated late preterm birth. Time-mated pregnant does received 0.1 mg/kg betamethasone (n=8) or 1 mL saline intramuscular (n=6) at the postconceptional ages of 28 and 29 days. The antenatal corticosteroid dose and scheme were based on previous studies and were comparable with routine clinical use. Cesarean delivery was done on postconceptional age 30 days (term=31 days), and new-born rabbits were foster-cared for 28 days and were thereafter cared for in group housing. Neonatal lung function testing and short-term neurobehavioral testing was done. Open field, spontaneous alternation, and novel object recognition tests were subsequently performed at 4 and 8 weeks of age. On postnatal day 1 and at 8 weeks, a subgroup was euthanized and transcardially perfuse fixated. Exvivo high-resolution Magnetic Resonance Imaging was used to calculate the Diffusion Tensor Imaging-derived fractional anisotropy and mean diffusivity. Fixated brains underwent processing and were serial sectioned, and a set of 3 coronal sections underwent anti-NeuN, Ki67, and terminal deoxynucleotidyl transferase dUTP nick end labeling staining. Antenatal corticosteroid exposure was associated with improved neonatal lung function, yet resulted in a long-term growth deficit that coincided with a persistent neurobehavioral deficit. We demonstrated lower neonatal motor scores; a persistent anxious behavior in the open field test with more displacements, running, and self-grooming episodes; persistent lower alternation scores in the T-Maze test; and lower discriminatory indexes in the novel object recognition. On neuropathological assessment, antenatal corticosteroid exposure was observed to result in a persistent lower neuron density and fewer Ki67+ cells, particularly in the hippocampus and the corpus callosum. This coincided with lower diffusion tensor imaging-derived fractional anisotropy scores in the same key regions. Clinical equivalent antenatal corticosteroid exposure in this late preterm rabbit model resulted in improved neonatal lung function. However, it compromised neonatal and long-term neurocognition.

Antenatal betamethasone and the risk of neonatal hypoglycemia: it's all about timing.

Our objective was to evaluate whether there is a relationship between the "time during the day" of maternal betamethasone administration between 24 and 34weeks' gestation and the risk for neonatal hypoglycemia. A retrospective study included cases between 2008 and 2018. Eligible cases were pregnant women with singleton pregnancies who received a single course of betamethasone between 24 and 34weeks' gestation. Each woman was allocated into one of four pre-defined groups based on the time when intramuscular betamethasone was administered. Group 1 (23:00-04:59) represents the lowest daily natural corticosteroids' activity, group 2 (05:00-10:59) represents the peak daily natural corticosteroids' activity, whereas group 3 (11:00-16:59) and group 4 (17:00-22:59) present an intermediate natural state of steady corticosteroids' secretion and activity. The primary outcome of the study was the incidence of neonatal hypoglycemia (glucose level of less than 40mg/dL). We have identified 868 women who received a single complete course of betamethasone, of which 353 women (40.7%) had a steroid treatment latency to delivery up to 14days. The incidence of neonatal hypoglycemia was significantly higher in group 2 (39.5%, 30/76, p = 0.0063), compared to group 1, who had the lowest incidence of neonatal hypoglycemia (16.9%, 12/71), and to group 3 and group 4. The "time during the day" when betamethasone administered is important when considering the risk for neonatal hypoglycemia. The risk was significantly higher when betamethasone was administered during the peak time and significantly lower when administered at the nadir time of maternal endogenous corticosteroid activity.

Antenatal corticosteroids for women at risk of preterm delivery: the “Emperor’s New Clothes” tale in medical practice

Objective To introduce the effect of a single course of betamethasone for pregnant women at risk of preterm delivery (PTD). Materials and methods In this study, a single course of 12 mg Bethamethasone was administered twice in 24 h (between 24–34 gestational weeks) for antenatal corticosteroid prophylaxis. Four hundred ninety-three neonates fulfilled the inclusion criteria and they were categorized (259 singletons, 192 twins and 42 triplets who met the inclusion criteria) into two groups according to the utilization of antenatal corticosteroid as control (n = 202) and study (n = 291) groups. We used respiratory distress syndrome (RDS), congenital pneumonia, intraventricular hemorrhage (IVH), neonatal sepsis, and bronchopulmonary dysplasia (BPD) as primary outcomes for the evaluation of neonatal morbidity. Results Study and control groups were similar in terms of clinical characteristics. RDS, congenital pneumonia, neonatal sepsis, and BPD rates were significantly higher in the study group (betamethasone) (p = .05, p = .007, 0.003, and 0.004, respectively) between 24–34 gestational weeks (when the neonates of multiple pregnancies were excluded from the analysis, we have demonstrated that congenital pneumonia (p = .033) and neonatal sepsis (p = .030) were still significantly higher in the betamethasone group). The neonates of 24–28 gestational weeks were compared separately and we demonstrated that RDS (p = .012), congenital pneumonia (p = .022), IVH (p = .044), neonatal sepsis (p = .023), and BPD (0.001) were also more frequent in the study group. When the 28–32 gestational week data were compared, IVH (p = .020) and neonatal sepsis (p = .017) were more frequent in the single course betamethasone users. However, we could not demonstrate a significant difference between the control and study groups between 32–34 gestational weeks in terms of the primary neonatal outcomes used in this study. Conclusion Single course antenatal betamethasone administration may be ineffective on the respiratory complications of preterm and very preterm infants while it may be unfavorable for extremely preterm infants. What is new about the paper, what could add to the current knowledge Pregnant women at risk for preterm labor must be under intensive antenatal care programs, and if possible, necessary precautions must be undertaken to prevent fetal hypoxia together with etiology specific treatments. This approach might contribute to better perinatal outcomes than just administering antenatal corticosteroid therapy.

Sex-specific and lasting effects of a single course of antenatal betamethasone treatment on human placental 11β-HSD2

IntroductionWe have previously shown that even a single course of antenatal betamethasone (BET) as an inductor for lung maturity reduces birth weight and head circumference. Moreover, animal studies link BET administration to alterations of the hypothalamic-pituitary-adrenal-gland-axis (HPA). The unhindered development of the fetal HPA axis is dependent on the function and activity of 11β-hydroxysteroiddehydrogenase type 2 (11β-HSD2), a transplacental cortisol barrier. Therefore, we investigated the effects of BET on this transplacental barrier and fetal growth. MethodsPregnant women treated with a single course of BET between 23 + 5 to 34 + 0 weeks of gestation were compared to gestational-age-matched controls. Placental size and neonatal anthropometrics were taken. Cortisol and ACTH levels were measured in maternal and umbilical cord blood samples. Placental 11β-hydroxysteroiddehydrogenase type 1 (11β-HSD1) protein levels and 11β-HSD2 protein and activity levels were determined. Parameters were analyzed independent of sex, and in subgroups divided by gender and gestational age. ResultsIn term born females, BET administration was associated with reduced head circumference and decreased 11β-HSD2 protein levels and enzyme activity. Males treated with BET, especially those born prematurely, showed increased 11β-HSD2 protein levels. ConclusionA single course of BET alters placental glucocorticoid metabolism in a sex-specific manner. Decreased 11β-HSD2 levels in term born females may lead to an increased placental transfer of maternal cortisol and therefore result in a reduced head circumference and a higher risk for altered stress response in adulthood. Further research is needed to conclude the significance of increased 11β-HSD2 levels in males.

Effect of antenatal betamethasone administration on rat cerebellar expression of type 1a metabotropic glutamate receptors (mGluR1a) and anxiety-like behavior in the elevated plus maze

Preclinical studies indicate that endogenous or exogenous glucocorticoids acting during the pre- or postnatal periods produce a significant Purkinje cell dendritic atrophy, especially during late postnatal ages. The present authors hypothesized that the underlying substrate that may contribute in part to this morphological change is the under-expression of the metabotropic glutamate 1a receptor (mGluR1a) because its expression is correlated with Purkinje cell dendritic outgrowth. Therefore, in the current study, they analyzed the impact of antenatal betamethasone on the immunoreactive expression of the mGluR1a and on anxiety-like behavior in the elevated plus maze (EPM). Pregnant rats were randomly divided into two experimental groups: control (CONT) and betamethasone-treated (BET). At gestational day 20 (G20), BET rats were subcutaneously injected with a solution of 170 &#x03BC;g.kg-1 of betamethasone, and CONT animals received a similar volume of saline. At postnatal days 22 (P22) and P52, BET and CONT offspring were evaluated behaviorally in the EPM, and their cerebella were immunohistochemically processed. Contrary to the uthors’ expected results, animals that were prenatally treated with a single course of betamethasone did not exhibit under-expression of mGluR1a or behavioral changes consistent with anxiety-like behaviors.

Antenatal betamethasone produces protracted changes in anxiety-like behaviors and in the expression of microtubule-associated protein 2, brain-derived neurotrophic factor and the tyrosine kinase B receptor in the rat cerebellar cortex

Using classic Golgi staining methods, we previously showed that the administration of synthetic glucocorticoid betamethasone in equivalent doses to those given in cases of human premature birth generates long-term alterations in Purkinje cell dendritic development in the cerebellar cortex. In the present study, we evaluated whether betamethasone alters the immunohistochemical expression of proteins that participate in cerebellar Purkinje cell dendritic development and maintenance, including microtubule-associated protein 2 (MAP2), brain-derived neurotrophic factor (BDNF) and the tyrosine kinase B receptor (TrkB), which are located predominantly in the cerebellar molecular layer where Purkinje cell dendritogenesis occurs. Consistent with our previous Golgi stain studies, we observed that animals prenatally exposed to a single course of betamethasone showed long-term alterations in the expression of MAP2, BDNF and TrkB. Additionally, these protracted molecular changes were accompanied by anxiety-like behaviors in the elevated plus maze and marble burying tests.

Single course of antenatal betamethasone produces delayed changes in morphology and calbindin-D28k expression in a rat's cerebellar Purkinje cells.

In the current study, we analyzed the impact of antenatal betamethasone on macroscopic cerebellar development, Purkinje cell morphology and the expression of the neuroprotective protein calbindin-D28k. Pregnant rats (Sprague-Dawley) were randomly divided into two experimental groups: control (CONT) and betamethasone-treated (BET). At gestational day 20 (G20), BET dams were subcutaneously injected with a solution of 0.17 mg kg⁻¹ of betamethasone, while CONT animals received a similar volume of saline. At postnatal days 22 (P22) and P52, BET and CONT offspring were behaviorally evaluated, and the cerebella were histologically and immunohistochemically processed. Animals that were prenatally treated with a single course of betamethasone exhibited long-lasting behavioral changes consistent with anxiety-like behavior in the open-field test, together with (1) reduced cerebellar weight and volume, (2) Purkinje cell dendritic atrophy, and (3) an overexpression of calbindin-D28k. The current results indicate that an experimental single course of betamethasone in pregnant rats produces long-lasting anxiety-like behaviors, together with macroscopic and microscopic cerebellar alterations.

Effects of a single course of prenatal betamethasone on dendritic development in dentate gyrus granular neurons and on spatial memory in rat offspring.

Preterm babies treated with synthetic glucocorticoids (sGC) in utero exhibit behavioral alterations and disturbances in brain maturation during infancy. However, the effects on dentate granule cell morphology and spatial memory in rats that were given clinically equivalent doses of antenatal betamethasone remain unclear. Pregnant rats were randomly divided into the following two experimental groups: control (CON) and betamethasone-treated (BET) groups. At gestational day 20 (G20), BET dams were subcutaneously injected with a 0.17 mg/kg betamethasone solution, and CON animals received a similar volume of saline. At postnatal days 22 (P22) and P52, BET and CON offsprings were behaviorally evaluated in the Y-Maze test, and the dentate gyrus granular neurons were histologically analyzed. Animals prenatally treated with a single course of betamethasone exhibit a significant decrement in the dendritic outgrowth of dentate granule cells along with impaired spatial memory when evaluated at P52. Moreover, the body and brain weight of the BET group was significantly lower than the CON group at P0, P22, and P52. The current results indicate that a single course of betamethasone in pregnant rats produces significant neuronal and behavioral impairments of the offspring at adolescence along with a decrement in somatic and brain weights at each of the three ages evaluated.

Growth restricting effects of a single course of antenatal betamethasone treatment and the role of human placental lactogen

Betamethasone (BET) is a widely used treatment for women who are at high risk of preterm delivery. In sheep, BET-induced growth restriction was found to be associated with reduced placenta lactogen (PL), a key regulator of fetal growth. We therefore hypothesized that also in humans a single course of BET administration is associated with a reduction of PL, associated with a deceleration in fetal growth. ObjectiveTo investigate effects of a single course of antenatal BET in humans on birth weight and PL. MethodsWomen exposed to BET (2 × 12 mg; n = 44) with normally grown fetuses between 23 + 5 and 34 + 0 wks (weeks + days of gestation) who delivered between 23 + 5 to 42 + 0 wks were compared to gestational age-matched controls (n = 49). Maternal gestational blood samples were obtained before, during and after BET treatment and at the time of birth. Main outcome measuresBET effects on fetal anthropometrics, placental morphometry and placental PL-protein and maternal plasma levels. ResultsThe mean duration of days between BET administration and birth was 52 days. BET treatment was associated with decreased birth weight (−18.2%), head circumference (−8.6%), body length (−6.0%), and placental width (−5.5%), as compared to controls. These changes were irrespective of possible maternal confounders (gestational age at birth, maternal age, maternal BMI gain during pregnancy, smoking etc.). However, neither PL-plasma levels within 48 h after BET treatment nor placental PL-protein levels and maternal plasma levels at birth were changed after BET treatment. In central regions of the placenta, BET treatment increased the circumference of syncytiotrophoblast nuclei by +4.7% and nucleus surface area by +9.4% compared to controls, but these changes were not related to placental PL-protein or maternal PL-plasma levels at birth. ConclusionA single course of BET treatment was accompanied with reduced fetal growth, but this growth restricting effect was not associated with altered placental or maternal plasma PL levels. Altered expression of PL appears not to be causal for BET-induced fetal growth restriction in the human.

Fetal acid–base balance after betamethasone administration: relation to fetal heart rate variability

To explore whether the known decrease in fetal heart rate variability, which follows antenatal betamethasone administration is related to fetal acid-base changes. A retrospective study of 42 women with premature delivery following a single course of betamethasone. The study group consisted of 21 women who delivered within 48 h following first injection of betamethasone. The 21 women who delivered later than 48 h formed the control group. Fetal heart rate variability measurements and cord acid-base values were compared. The mean fetal heart rate variability (beats per minute) before the administration of betamethasone was significantly higher than at 24 h [8.05 (SD 3.15) vs. 5.32 (SD 2.27); p<0.001]. This was evident in both the groups, with no significant difference between them. In the control group, the mean variability before betamethasone administration and the variability prior to delivery were not significantly different [8.48 (SD 3.46) vs. 7.26 (SD 3.03); p=0.36]. There were no significant differences between study and control groups regarding the arterial cord acid-base values at delivery [pH 7.29 (SD 0.15) vs. 7.31 (SD 0.1); p=0.38]. Assuming that the fetal heart rate and the acid-base status prior to delivery would be a reflection of the effects of betamethasone as evident by reduced fetal heart rate variability, our data does not support acid-base changes as a pathophysiological mechanism.

Blood glucose level in preterm infants after antenatal exposure to glucocorticoid

To determine the impact of antenatal glucocorticoid on neonatal glucose homeostasis. This is a retrospective gestationally paired survey followed by a randomized study. On the basis of the interval between last antenatal dexamethasone and birth, 228 preterm infants born before 34 weeks were divided into Short (< 24 h), Intermediate (1-6 days), and Long (> or = 7 days) exposure groups and compared their gestationally paired controls. After a single course of betamethasone, the parturients remaining undelivered for one week were randomized to receive either one dose of betamethasone (n = 52) or placebo (n = 53). Glucose values were recorded at 11 time points in the first 3 days of life. Hypoglycaemic and hyperglycaemic values were counted. There were no overall differences in mean glucose levels between the antenatal glucocorticoid and the control groups. However, the long exposure time to antenatal glucocorticoid was associated with increased risk of hyperglycaemia (OR 4.1; 2.2-7.6). Antenatal glucocorticoid administration was associated with subtle disturbances of glucose homeostasis in preterm infants. These differences were dependent on the length of drug-delivery interval so that long exposition time seemed to increase the incidence of hyperglycaemia during the first days of life.

Randomized Trial of a Single Repeat Dose of Prenatal Betamethasone Treatment in Imminent Preterm Birth

A single dose of prenatal betamethasone treatment decreases neonatal morbidity rates when administered within 7 days before preterm delivery. A single repeat dose or booster dose of betamethasone before delivery has been proposed to be effective, but its efficacy has not been subjected to a randomized, blinded trial. Women with imminent delivery before 34.0 gestational weeks were eligible if they remained without delivery for >7 days after a single course of betamethasone. After stratification, a single repeat dose of betamethasone (12 mg) or placebo was administered. The primary outcome was survival without respiratory distress syndrome or severe intraventricular hemorrhage (grade 3 or 4). A total of 249 mothers had been enrolled by the time the study was discontinued. All of the 159 infants in the betamethasone group and 167 in the placebo group were born before 36 weeks of gestation. The intact survival rate was unaffected and was lower than anticipated, because the gestational age-adjusted incidence of respiratory distress syndrome was higher than the population incidence. The requirement for surfactant therapy in respiratory distress syndrome was increased in the betamethasone group. According to posthoc analysis of the data for 206 infants who were delivered within 1 to 24 hours, the betamethasone booster tended to increase the risk of respiratory distress syndrome and to decrease intact survival rates. According to this study, a single booster dose of betamethasone just before preterm birth may perturb respiratory adaptation. These results caution against uncontrolled use of a repeat dose of glucocorticoid in high-risk pregnancies.

Effects of Antenatal Betamethasone on Maternal and Fetoplacental Matrix Metalloproteinases 2 and 9 Activities in Human Singleton Pregnancies

BackgroundA single course of antenatal betamethasone is administered to women at risk of preterm labor to advance fetal lung maturation. Matrix metalloproteinases (MMPs) are collagen-degrading enzymes that remodel extracellular matrix...

Lowering the dose of antenatal steroids: The effects of a single course of betamethasone on somatic growth and brain cell proliferation in the rat

We investigated the effects of a single course of antenatal betamethasone on neonatal somatic and brain development. On day 20 of gestation, pregnant rats were injected with either with 170 microg kg(-1) body weight of betamethasone ("clinically-equivalent dose," equivalent to 12 mg twice, 24 hours apart) or half this dose or vehicle. Pups (8-11 animals per experimental group per timepoint per gender) were analyzed at 1 (P1), 2, and 21 days after birth. We report that betamethasone induced a significant dose-dependent decrease of somatic measurements in both genders. At P1 cell proliferation was affected by the "clinically equivalent dose" only in the subventricular zone in both genders and in the hippocampus in males. In summary, we show for the first time that a lower dose (equivalent to 6 mg) induces fewer and less severe effects on somatic growth, whereas it does not affect cell proliferation within the brain.

Perinatal corticosteroid effect on amygdala and hippocampus volume during brain development in the rat model

Exposure of the fetus to corticosteroid during brain development has been suggested to cause permanent change in brain structure and has been associated with long term cognitive, behavioral and emotional impairment. We evaluated the effect of perinatal corticosteroid, at a dose similar to that which human fetuses are exposed, on cerebral cortex, corpus collosum, hippocampus, dentate gyrus and amygdala in a rat model. Rat pups were given betamethasone at day 1 (P1). Brain sections from the rat pups at postnatal day 45 (P45) were then analyzed. No differences were noted in the volumes of cerebral cortex, corpus collosum, hippocampus, dentate gyrus, or three nuclei of the amygdala compared to the control and sham groups. We concluded that a single course of betamethasone, at a comparable dose to that which the human fetus is exposed in clinical practice, had no effect on these regional brain volumes at this stage of development.

Antenatal exposure to betamethasone: psychological functioning and health related quality of life 31 years after inclusion in randomised controlled trial

Objectives To determine if antenatal exposure to betamethasone for the prevention of neonatal respiratory distress syndrome alters psychological functioning and health related quality of life in adulthood.Design Follow-up of the...

288 The Effect of Second Course of Antenatal Betamethasone (BM) on Neonatal Morbidity in Preterm Infants: A Randomized Trial

Background: Single course of BM decreases neonatal morbidity when administrated within 7 days before preterm delivery. The benefits of second course of BM are unknown.Aims: To evaluate the efficacy of second course of BM in increasing the intact survival of preterm infants.Methods: In this randomized, blinded trial, pregnant women (before 34.0 gestational weeks) were eligible if they had remained undelivered more than 7 days after antenatal BM. Single dose of BM (12 mg) or placebo was given, when the preterm delivery was anticipated. Primary outcome was intact survival without respiratory distress syndrome and/or intracerebral hemorrhage (grade 3–4).Results: 251 mothers participated the study. All infants were delivered prior to 35 weeks of gestation. At present the outcome of 285 infants has been analyzed. The intact survival was 48% in BM and 58% in placebo groups (P=0.1). The intact survival was non-significantly higher in BM group (58% vs. 41%, P=0.3), when the study drug was administered more than 24 h before birth (group 1). The incidence of intact survival was lower in BM group (44% vs. 61%, P=0.01), when the intervention took place less than 24 h before birth (group 2). In group 1, the risk of patent ductus arteriosus was 16% in BM and 41% in placebo group (P=0.04), vs. 29% and 27% in group 2. In group 2, systolic and diastolic blood pressures were increased in BM arm (P=0.02 and P=0.03). In group 1, blood pressure levels were similar between study groups. The second course of BM did not influence the acute outcome of preterm infants. The preterm infants benefited from antenatal BM, when treatment was given more than 24 h before delivery. BM given less than 24 hours before delivery was associated with increased blood pressure after birth and with a decrease in intact survival.

The effect of a single course of antenatal corticosteroids on maternal adrenal function at term

Objective: To determine if one course of antenatal corticosteroids at 32 weeks produces maternal adrenal suppression at term.Methods: The adrenocorticotropic hormone (ACTH) stimulation test was administered at 38 weeks to 11 pregnant women who had received a single course of antenatal betamethasone prior to 33 weeks and to six control subjects.Results: There was no difference in basal cortisol levels (mean ± standard deviation) between the two groups: 41.6 ± 6.9 μg/dl for controls versus 36.0 ± 7.8 μg/dl for the steroid group, p = 0.16. Peak cortisol levels at 45 min following ACTH stimulation were not different: 61.6 ± 3.5 μg/dl for controls versus 55.0 ± 2.6 μg/dl for the steroid group, p = 0.16. The power of the study to detect a statistical difference in the observed peak cortisol levels was greater than 95%. None of the study subjects had laboratory criteria or clinical signs of adrenal suppression.Conclusions: A single course of betamethasone for women at risk for preterm delivery does not produce adrenal insufficiency at term and stress dose steroids are not recommended.