Latency of late preterm steroid administration to delivery and risk of neonatal hypoglycemia.

BACKGROUND: Late preterm antenatal corticosteroid administration has been associated with an increased risk of neonatal hypoglycemia. The mechanism is thought to be secondary to transient fetal hyperinsulinemia, which may be more likely if delivery occurs during peak antenatal corticosteroid levels. OBJECTIVE: This study aimed to investigate whether there is a latency interval between antenatal corticosteroid administration and delivery that places neonates at the greatest risk of hypoglycemia. STUDY DESIGN: This was a retrospective matched cohort study of pregnant women who received antenatal corticosteroid vs unexposed women between 34 0/7 and 36 6/7 weeks of gestation from 2016 to 2019. Unexposed women were those who did not receive antenatal corticosteroid matched according to gestational age at delivery, diabetes mellitus status, and maternal body mass index from 2010 to 2015. Latency periods from initial steroid administration to delivery were defined in grouped intervals until ≥72 hours. The primary outcome was neonatal hypoglycemia, defined as a neonatal glucose level of <40 mg/dL within 24 hours of life. Poisson regression was used to generate an adjusted relative risk of hypoglycemia for each latency period adjusting for confounders. RESULTS: A total of 812 women were included in the analysis (406 exposed and 406 unexposed). Women who received antenatal corticosteroids were more likely to be nulliparous (P=.009); moreover, the women were well matched on pregnancy complications and baseline demographics. Neonatal hypoglycemia was more frequently identified in women receiving antenatal corticosteroids than in women not receiving antenatal corticosteroids (42% vs 26%; P<.001). Severe hypoglycemia, defined as a glucose level of <20 mg/dL, was significantly more common in patients receiving antenatal corticosteroids than in patients not receiving antenatal corticosteroids (8.4% vs 2.7%; P<.001). Latency time intervals of 12 to 71 hours from antenatal corticosteroid administration were significantly associated with neonatal hypoglycemia in exposed women compared with unexposed women after adjustment; within this time frame, the highest risk was 24 to 47 hours after antenatal corticosteroid administration (adjusted relative risk, 2.09; 95% confidence interval, 1.29-3.38). CONCLUSION: In the late preterm period, the risk of neonatal hypoglycemia is the greatest in the latency period of 12 to 71 hours between steroid administration and delivery. Neonates exposed to antenatal corticosteroids were more likely to experience severe hypoglycemia within 24 hours of life than unexposed neonates.

Dexamethasone Alters Tracheal Aspirate T-Cell Cytokine Production in Ventilated Preterm Infants.

Postnatal corticosteroids improve respiratory status and facilitate respiratory support weaning in preterm infants with bronchopulmonary dysplasia (BPD). Older literature describes characteristic cytokine profiles in tracheal aspirates (TA) of BPD patients which are altered with corticosteroids. Corticosteroids also influence peripheral blood T-cell presence. However, little is known regarding TA T-cell phenotype and cytokine production before or after exogenous corticosteroids. We hypothesized that postnatal dexamethasone alters the TA T-cell cytokine profiles of preterm infants. TA samples were collected from 14 infants born from 23 0/7 to 28 6/7 weeks who were mechanically ventilated for at least 14 days. Samples were collected up to 72 h before a ten-day dexamethasone course and again 1 to 3 calendar days after dexamethasone initiation. The primary outcome was change in T cell populations present in TA and their intracellular cytokine profile after dexamethasone treatment, ascertained via flow cytometry. Following dexamethasone treatment, there were significant decreases in respiratory severity score (RSS), percent CD4+IL-6+ cells, CD8+IL-6+ cells, CXCR3+IL-6+ cells, and CXCR3+IL-2+ cells and total intracellular IFN-γ in TA. RSS significantly correlated with TA percent CD4+IL-6+ cells. To our knowledge, this is the first study demonstrating that dexamethasone reduced T-cell IL-6 and this reduction was associated with improved RSS in pre-term infants with evolving BPD.