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Published on: November 20, 2015
Intrapartum magnesium sulfate exposure attenuates neutrophil function in preterm neonates
1Department of Pediatrics, Division of Neonatal Medicine, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, New Brunswick, NJ 08903, USA. mehtara@umdnj.edu
Background:
Prenatal exposure to magnesium sulfate, a drug that is frequently used for attempted tocolysis in preterm labor, could alter neutrophil functional activity in infants born preterm.
Objectives:
To determine the association between maternal tocolysis with magnesium sulfate and the cord blood neutrophil functional activity of preterm neonates.
Methods:
The chemotaxis, random motility, and chemiluminescence of neutrophils were compared in the cord blood of 10 preterm neonates born to mothers tocolysed with magnesium sulfate, 10 preterm infants whose mothers had not received any tocolysis, and 10 term infants. Data regarding the maternal and neonatal magnesium and calcium levels were collected and analyzed in association with the cord blood neutrophil functional activity of the preterm infants.
Results:
Neutrophil functional activity in the cord blood of the preterm neonates was significantly lower than in term neonates. However, the alteration of neutrophil chemotaxis, random motility and chemiluminescence was more noticeable in neonates with intrapartum exposure to magnesium sulfate as compared to preterm infants whose mothers received no tocolysis (30.9 +/- 2.3 vs. 36.7 +/- 2.7 microm, p < 0.01; 26.6 +/- 1.9 vs. 33.1 +/- 3.1 microm, p < 0.01; and 74.3 +/- 6.5 vs. 89.9 +/- 6.25 x 10(3) counts per min (cpm), p < 0.01, respectively). Furthermore, the reduction in neutrophil functional activity of preterm infants with intrapartum exposure to magnesium was directly correlated with the maternal serum magnesium levels (r = -0.90 to -0.85, p < 0.01).
Conclusion:
In infants born preterm, intrapartum exposure to magnesium sulfate is a risk factor contributing to the alteration in neutrophil motility and post-phagocytic bactericidal capacity.
