Background: Neonatal hypoglycemia is a significant clinical concern, particularly in infants born to mothers with gestational diabetes mellitus (GDM). Betamethasone, administered antenatally to enhance fetal lung maturity in late preterm pregnancies, induces transient maternal hyperglycemia, potentially exacerbating the neonatal insulin response and subsequent risk of hypoglycemia. Corticosteroids increase maternal blood glucose levels by increasing hepatic gluconeogenesis, inhibiting glucose uptake in adipose tissue, and antagonizing insulin synthesis (Schäcke et al., Pharmacology 95% CI: 1.06–3.14; p = 0.0303). This significant result may relate to timing, with 43% delivering the same day as randomization and 96% delivering within one day, corresponding closely with peak maternal hyperglycemia post-betamethasone (Itoh et al. Endocrine Journal 2016). Multiple logistic regression analyses showed the adjusted odds ratio (aOR) for neonatal hypoglycemia among infants born to mothers with GDM randomized to two doses was 1.132 (95% CI: 0.75–1.68). Among infants whose mothers received a single dose, the aOR was 1.540 but was not statistically significant (95% CI: 0.83–2.79). A larger trial may be needed to detect a true effect. Conversely, mothers who received both doses had similar odds for neonatal hypoglycemia (aOR 0.8658; 95% CI: 0.48–1.50). Conclusion: Among women receiving antenatal corticosteroids in the late preterm period, maternal GDM was not associated with an increased risk for neonatal hypoglycemia compared with euglycemic patients. These results support the practice of administering antenatal steroids in late preterm pregnancies complicated by GDM. A large randomized clinical trial is warranted to determine whether GDM patients receiving antenatal late preterm steroids are at increased risk for neonatal hypoglycemia.
Gaspar et al. (Sun,) studied this question.
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