Effects of antenatal magnesium sulfate administration on parathyroid hormone secretion in preterm infants

Antenatal magnesium sulfate (MgSO₄) administration has raised concerns regarding its potential impact on calcium metabolism in preterm infants. However, its effects on parathyroid hormone (PTH) secretion in infants remain unclear. This study aimed to evaluate the influence of antenatal MgSO₄ on parathyroid function in preterm infants.

Preterm infants born at 28-33 weeks of gestation were divided into two groups: the Mg group (infants who received antenatal MgSO₄, n = 41) and the non-Mg group (infants who did not receive antenatal MgSO₄, n = 24). Neonatal blood samples, collected within 0.5-3 h after birth, were analyzed for serum calcium, phosphorus, magnesium, alkaline phosphatase, and whole PTH levels. Biochemical data were compared between the groups, and multivariate analysis was performed to assess antenatal MgSO₄ as an independent factor associated with lower whole PTH levels. The relationships between serum calcium and serum whole PTH levels were also analyzed in each group to evaluate MgSO₄'s suppressive effect on parathyroid function during hypocalcemia.

Serum whole PTH levels were significantly lower in the Mg group (24.7 ± 20.1 pg/mL) than in the non-Mg group (56.2 ± 47.1 pg/mL, p = 0.002). Serum phosphorus, magnesium, and alkaline phosphatase levels were significantly elevated in the Mg group (p < 0.001 for all). Multivariate analysis confirmed that antenatal MgSO₄ was an independent factor associated with lower whole PTH levels, even after adjusting for gestational age, sex, and serum calcium levels (β = -0.44, p < 0.001). A significant inverse correlation between serum whole PTH and serum calcium levels was observed in the non-Mg group (ρ = -0.77, p < 0.001), but not in the Mg group.

Antenatal MgSO₄ administration reduces PTH levels and suppresses the parathyroid response to hypocalcemia in preterm infants. Postnatal calcium homeostasis should be closely monitored in these infants.