Effect Of Antenatal Dexamethasone Research Articles

Effect of Antenatal Dexamethasone in Late Preterm Period on Neonatal Hypoglycemia: A Prospective Cohort Study from a Developing Country.

This study compared the risk of hypoglycemia within 72 h of life in infants with and without exposure to antenatal dexamethasone in the late preterm period (34-366/7 week's gestational age). This prospective cohort study was conducted in a tertiary care neonatal unit of Eastern India from May 2021 to November 2021. Babies in the exposed group received at least one dose of antenatal dexamethasone in the late preterm period between 7 days before delivery and birth. 'Complete course' of antenatal steroid was defined as four doses of injection dexamethasone at 12 h intervals and <4 doses were considered as 'Partial course'. Primary outcome was incidence of hypoglycemia within 72 h of life, defined as whole blood glucose <45 mg/dl. Total 298 infants (98 in control, 134 in partial and 66 in complete group) were assessed for final outcome. No significant difference in outcomes were seen in the exposed group compared to unexposed group. However, incidence of hypoglycemia within 72 h (complete vs. partial p= 0.008, complete vs. control p=0.005) and 12 h of life (complete vs. partial p=0.013, complete vs. control p=0.013) was significantly less in complete steroid group. Logistic regression analysis revealed complete course of antenatal corticosteroid significantly decreased the risk of hypoglycemia [adjusted odds ratio, 95% confidence interval (CI) 0.15 (0.03-0.69), p=0.015]. Number needed to be exposed for one additional benefit was 7 (95% CI, 6.35-22.14). Complete course of dexamethasone administered to mothers at risk of late preterm delivery reduces risk of neonatal hypoglycemia within 72 h of life.

The Effect of Antenatal Dexamethasone to Improve Respiratory Neonatal Outcomes in Late Preterm Birth: A Randomized Controlled Trial

Objective: To evaluate the effect of dexamethasone on the rate of respiratory distress syndrome in late preterm infants Materials and Methods: One hundred ninety-four singleton pregnant women at risk for late preterm delivery were randomly allocated into two groups. Ninety-seven patients received 6 mg dexamethasone (group 1) and 97 patients received 1.5 mL normal saline (group 2), intramuscularly every 12 hours for four doses or until delivery. The primary outcome was the rate of neonatal respiratory distress syndrome. The secondary outcomes were the need for continuous positive airway pressure (CPAP), the neonatal intensive care unit admission, the Apgar scores at 1 minute and 5 minutes, the rate of transient tachypnea of the newborn (TTN), intraventricular hemorrhage, neonatal hypoglycemia, neonatal sepsis, and adverse effects. Results: The rate of neonatal respiratory distress syndrome was lower in group 1, five cases (5.2%), compared with group 2, six cases (6.2%) (p=0.756, relative risk 0.83, 95% CI 0.26 to 2.64). The need for CPAP, NICU admission, rate of TTN, and intraventricular hemorrhage were not significantly different. Group1 had significantly higher Apgar scores at 1 minute and 5 minutes (p=0.021 and 0.043, respectively). No adverse effects were reported. Conclusion: Administration of dexamethasone in late preterm birth did not decrease the rate of neonatal respiratory distress and the need for CPAP and NICU admission but statistically significantly improved the Apgar scores at 1 minute and 5 minutes. More research in the future is needed to correct the limitation in the present study. Keywords: Late preterm, Dexamethasone, Respiratory distress syndrome, Apgar scores

ANTENATAL BETAMETHASONE COMPARED WITH DEXAMETHASONE IN TERMS OF FETAL HEART RATE VARIABILITY AND FETAL BODY MOVEMENTS

Introduction: Preterm labor occurs between 20th and 37th gestational week which is regardless of the birth weight. The incidence of preterm birth is increasing and continues to be the leading cause of neonatal mortality and morbidity. Antenatal corticosteroids are used for pregnant women at risk of preterm labor to reduce fetal mortality and morbidity by increasing fetal lung maturation and preventing the fetus from respiratory distress syndrome. In this study, we aimed to evaluate the effects of antenatal dexamethasone and betamethasone on fetal heart rate variability and fetal body movements. Material and method: The pregnant women applied to clinic due to the risk of preterm labor between November 2003 and May 2004 hospitalised due to the risk of preterm labor and tocolytic treatment. The glucocorticoids to be initiated and to provide lung maturation were included in the study. Included in the study pregnant women were randomly divided into two groups. 24 hours for 20 pregnant women in the first group, 12 mg betamethasone was administered intramuscularly. 20 in the second group 6 mg dexamethasone was administered intramuscularly every 12 hours. NSTs for later evaluation of fetal well-being and baby movements were compared. Results: Pregnant women in betamethasone and dexamethasone groups compared in terms of age, gravida, parity and gestational week, there was no significant difference between the two groups (p&gt; 0.05). At the time of first glucocorticoid application (onset) and 24 hours after the last dose of betamethasone/dexamethasone therapy, fetal heart rate, acceleration, deceleration and fetal movement counts were calculated for 3 days in the morning and evening. A significant increase was observed at heart rate in the betamethasone group after treatment, but there was no change in basal heart rate in the dexamethasone group. In the number of acceleration; significant increase was observed in betamethasone group while there was no statistically significant change was observed in the dexamethasone group. Fetal body movements were changed significantly in both groups compared with the basal movements. Conclusion: Antenatal glucocorticoid application (especially betamethasone) caused a temporary suppression in the NST and fetal movements that were used to determine fetal well-being. It should be kept in mind that these temporary changes may be misdiagnosed as fetal distress. Both dexamethasone and betamethasone can be applied in preterm delivery as a safe manner.

Effects of antenatal dexamethasone and hyperglycemia on cardiovascular adaptation to asphyxia in preterm fetal sheep.

Antenatal glucocorticoids improve outcomes among premature infants but are associated with hyperglycemia, which can exacerbate hypoxic-ischemic injury. It is still unclear how antenatal glucocorticoids or hyperglycemia modulate fetal cardiovascular adaptations to severe asphyxia. In this study, preterm fetal sheep received either saline or 12 mg im maternal dexamethasone, followed 4 h later by complete umbilical cord occlusion (UCO) for 25 min. An additional cohort of fetuses received titrated glucose infusions followed 4 h later by UCO to control for the possibility that hyperglycemia contributed to the cardiovascular effects of dexamethasone. Fetuses were studied for 7 days after UCO. Maternal dexamethasone was associated with fetal hyperglycemia (P < 0.001), increased arterial pressure (P < 0.001), and reduced femoral (P < 0.005) and carotid (P < 0.05) vascular conductance before UCO. UCO was associated with bradycardia, femoral vasoconstriction, and transient hypertension. For the first 5 min of UCO, fetal blood pressure in the dexamethasone-asphyxia group was greater than saline-asphyxia (P < 0.001). However, the relative increase in arterial pressure was not different from saline-asphyxia. Fetal heart rate and femoral vascular conductance fell to similar nadirs in both saline and dexamethasone-asphyxia groups. Dexamethasone did not affect the progressive decline in femoral vascular tone or arterial pressure during continuing UCO. By contrast, there were no effects of glucose infusions on the response to UCO. In summary, maternal dexamethasone but not fetal hyperglycemia increased fetal arterial pressure before and for the first 5 min of prolonged UCO but did not augment the cardiovascular adaptations to acute asphyxia.

Effects of Antenatal Dexamethasone on Antioxidant Enzymes and Nitric Oxide Synthase in the Rat Lung

We investigated the effects of prenatal dexamethasone (DEX) administration on antioxidant enzymes (AOEs) and nitric oxide synthase (NOS) in fetal and neonatal rat lungs. DEX (1 mg/kg, s.c., for 2 days) or vehicle alone was administered to pregnant rats, and the lungs of fetuses on days 19 and 21 of gestation and of 1- and 3-day-old neonates were examined. We measured protein levels of the AOEs manganese superoxide dismutase and copper-zinc super-oxide dismutase (Mn SOD and Cu-Zn SOD), glutathione peroxidase (GSH-Px), catalase (CAT), and inducible and endothelial nitric oxide synthase (i-NOS and e-NOS). Mn SOD, GSH-Px, and e-NOS expression gradually increased with increasing gestational and postnatal age in the lungs of the control groups. Cu-Zn SOD, CAT, and i-NOS expression did not change with increasing gestational and postnatal age in the lungs of the control groups. DEX administration had significant effects on i-NOS and e-NOS protein and mRNA expression. The increased Mn SOD, GSH-Px, and e-NOS expressions during the perinatal period suggests that antenatal developmental changes in AOEs in the lungs of premature fetuses could be reduced by reactive oxygen species–mediated injury at birth. Furthermore, antenatal glucocorticoid treatment may accelerate the development of lungs via the two types of NOS.

Association of antenatal and postnatal dexamethasone exposure with outcomes in extremely low birth weight neonates.

Recent studies of preterm neonates have indicated that antenatal dexamethasone (ADX) may have adverse effects on cranial ultrasound findings at the time of hospital discharge, including periventricular leukomalacia. Furthermore, both ADX and postnatal dexamethasone (PDX) may have adverse effects on subsequent neurodevelopmental outcome. 1) To assess the effects of ADX exposure on cranial ultrasound findings at the time of hospital discharge and 2) to evaluate the individual effects of ADX and/or PDX exposure on subsequent neurodevelopmental outcome in extremely low birth weight (ELBW) neonates in whom confounding risk factors known to influence outcome were controlled. One hundred seventy-three ELBW (< or =1000 g) neonates were studied using a prospectively collected database and hospital and clinic records. Study patients were assigned to 1 of 4 groups according to dexamethasone exposure: group I, no dexamethasone exposure; group II, ADX exposure to hasten fetal lung maturity; group III, PDX exposure for chronic lung disease; group IV, both ADX and PDX exposure. The 4 groups were compared using multinomial logistic regression or analysis of covariance to control for confounding variables. Primary outcome variables were cranial ultrasound findings at hospital discharge and results of developmental testing at 18 to 22 months' corrected age (Bayley Scales of Infant Development). Cranial ultrasound results as well as Bayley Scales of Infant Development scores were similar in groups I and II and in groups III and IV. The likelihood of abnormal cranial ultrasound studies and lower scores on neurodevelopmental testing was greater in groups III and IV versus groups I and II. In this study, ADX did not seem to increase the risk of periventricular leukomalacia. ADX exposure is not associated with an increase in abnormal cranial ultrasound findings in ELBW neonates. PDX exposure, but not ADX exposure, is associated with worse neurodevelopmental outcome in this population. These results are supportive of the recent statement by the American Academy of Pediatrics (Committee on Fetus and Newborn) and the Canadian Paediatric Society (Fetus and Newborn Committee) and emphasize that PDX should be used with caution in ELBW neonates.

Effect of antenatal dexamethasone on the expression of endothelial nitric oxide synthase in the lungs of postnatal pups

Activities of endothelial nitric oxide synthase (eNOS) are developmentally regulated and its presence at birth may play a role in the transition of cardiopulmonary circulation. Antenatal dexamethasone (Dex) therapy accelerates fetal lung maturation. We speculate that Dex therapy may enhance pulmonary eNOS protein expression in the newborn. This article examines whether antenatal Dex therapy affected the expression of eNOS in the lungs of rat pups in the postnatal period. Time-dated pregnant Wistar rats were subjected to 2 doses of Dex (0.8 mg/kg, intramuscularly, daily) or equivalent volume of normal saline at the 18th and 19th gestational day and delivered naturally. The newborn pups were randomly assigned to 4 groups by age: days 1, 3, 5, and 7. After homogenization, abundance of eNOS protein in lungs was determined by Western blot analysis. There were 7 dams in each group. Mean body weights of the pups in the Dex group were lighter than those in the control at birth and remained stunted up to day 7 (5.68+/-0.47 g v 6.34+/-0.47 g, P <.01). However, there were no differences in wet lung weights and lung/body weight ratios between both groups in the study period. Abundance of eNOS protein expression decreased in both the control and Dex groups (P < .01). Pups that received antenatal Dex had 39% more in abundance of eNOS protein expression in lungs when compared to the control on day 1 (P < .05) but there were no differences between both groups from day 3 to 7. We conclude that antenatal Dex therapy enhances the abundance of eNOS protein expression in the lung at birth and could be a factor in improving respiratory functions in infants who received antenatal steroid therapy.

Effect of Antenatal Dexamethasone (Dex) on the Expression of Nitrix Oxide Synthase (NOS) in the Developmental Lungs of Postnatal Pups

Effect of Antenatal Dexamethasone (Dex) on the Expression of Nitrix Oxide Synthase (NOS) in the Developmental Lungs of Postnatal Pups

The effect of antenatal dexamethasone on maternal and fetal retinol-binding protein

Sixteen rhesus monkeys received 0.1 to 15 mg/kg of antenatal dexamethasone at 132 days' gestation; seven control animals received placebo. At 135 days' gestation they underwent cesarean section, and maternal and fetal serum was assayed for retinol-binding protein. Fetal and maternal concentrations of retinol-binding protein increased after dexamethasone (p < 0.05) and there was a trend for fetal levels of retinol-binding protein to increase with increasing dosage (p < 0.01). Whether the elevation of retinol-binding protein in response to antenatal dexamethasone is a desirable side effect is not clear at this time.