TY - JOUR
T1 - The role of magnesium in neonatal calcium homeostasis
T2 - Effects of magnesium infusion on calciotropic hormones and calcium
AU - Shaul, P. W.
AU - Mimouni, F.
AU - Tsang, R. C.
AU - Specker, B. L.
PY - 1987
Y1 - 1987
N2 - Magnesium (Mg) deficiency is a possible etiologic factor contributing to neonatal hypocalcemia. In adults, parathyroid hormone (PTH) secretion is negatively feedback regulated by acute changes in serum Mg concentration, but paradoxically Mg deficiency may lead to functional hypoparathyroidism and hypocalcemia. We hypothesized that in neonates, Mg administration will cause changes in PTH secretion and serum Ca concentration that will be inversely related to serum Mg status. We also hypothesized that Mg administration will result in increased calcitonin (CT) secretion. Thirty-nine newborn infants with birth weights > 1500 g were studied on day 3 of life. Ten received placebo, and 29 intravenous magnesium sulfate (MgSO4), 6 mg elemental Mg/kg body weight, over 1 h. Serum Mg, Ca, PTH, and CT were measured at time 0 (baseline, preinfusion) and 1, 2, 6, 12, 24, and 48 h postinfusion. In both groups combined, baseline PTH correlated with baseline Mg (r = 0.72, p < 0.005), and with baseline Ca (r = 0.68, p < 0.005). In the control group there was no change in serum Mg, Ca, PTH, and CT during the study period. In magnesium sulfate-infused infants: 1) serum Mg concentration rose from 1.80 ± 0.06 to 2.82 ± 0.07 mg/dl (mean ± SEM, p < 0.001); 2) the change from baseline in serum PTH at 1, 6, and 12 h postinfusion correlated inversely with baseline Mg (p < 0.05); 3) the change from baseline in serum Ca at 1, 2, and 24 h postinfusion correlated inversely with baseline Mg (p < 0.005); 4) serum CT remained unchanged. We conclude that Mg plays an important role in neonatal calcium metabolism. PTH and Ca responses to magnesium sulfate infusion were inversely related to neonatal serum Mg concentrations, consistent with the hypothesis tested. Mg infusion, however, did not affect neonatal serum CT concentrations.
AB - Magnesium (Mg) deficiency is a possible etiologic factor contributing to neonatal hypocalcemia. In adults, parathyroid hormone (PTH) secretion is negatively feedback regulated by acute changes in serum Mg concentration, but paradoxically Mg deficiency may lead to functional hypoparathyroidism and hypocalcemia. We hypothesized that in neonates, Mg administration will cause changes in PTH secretion and serum Ca concentration that will be inversely related to serum Mg status. We also hypothesized that Mg administration will result in increased calcitonin (CT) secretion. Thirty-nine newborn infants with birth weights > 1500 g were studied on day 3 of life. Ten received placebo, and 29 intravenous magnesium sulfate (MgSO4), 6 mg elemental Mg/kg body weight, over 1 h. Serum Mg, Ca, PTH, and CT were measured at time 0 (baseline, preinfusion) and 1, 2, 6, 12, 24, and 48 h postinfusion. In both groups combined, baseline PTH correlated with baseline Mg (r = 0.72, p < 0.005), and with baseline Ca (r = 0.68, p < 0.005). In the control group there was no change in serum Mg, Ca, PTH, and CT during the study period. In magnesium sulfate-infused infants: 1) serum Mg concentration rose from 1.80 ± 0.06 to 2.82 ± 0.07 mg/dl (mean ± SEM, p < 0.001); 2) the change from baseline in serum PTH at 1, 6, and 12 h postinfusion correlated inversely with baseline Mg (p < 0.05); 3) the change from baseline in serum Ca at 1, 2, and 24 h postinfusion correlated inversely with baseline Mg (p < 0.005); 4) serum CT remained unchanged. We conclude that Mg plays an important role in neonatal calcium metabolism. PTH and Ca responses to magnesium sulfate infusion were inversely related to neonatal serum Mg concentrations, consistent with the hypothesis tested. Mg infusion, however, did not affect neonatal serum CT concentrations.
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U2 - 10.1203/00006450-198709000-00016
DO - 10.1203/00006450-198709000-00016
M3 - Article
C2 - 3658552
AN - SCOPUS:0023617106
SN - 0031-3998
VL - 22
SP - 319
EP - 323
JO - Pediatric Research
JF - Pediatric Research
IS - 3
ER -