• D P Cruikshank, R M Pitkin, W A Reynolds, G A Williams, and G K Hargis.
• Am. J. Obstet. Gynecol. 1979 Jun 1;134(3):243-9.

AbstractSerial maternal and cord blood determinations of the ions and hormones involved in calcium homeostasis were made in pre-eclamptic women treated with intravenous magnesium sulfate. A 4 gm loading dose followed by 1 to 2 gm/hr caused maternal serum magnesium concentrations to rise 150%, to levels of 3.3 to 4.5 mEq/L, and ionized calcium levels to fall 16%, to 1.89 mEq/L. The hypocalcemia etly altering calcitonin. Changes in total calcium paralleled those of ionized calcium; phosphorus levels were not affected by magnesium infusion. At the time of delivery the offspring of these women were hypermagnesemic and relatively hypocalcemic, although less so than their mothers. Fetal ionized calcium levels, although lower with magnesium treatment than in control subjects, were within the lower limits of the normal range, which perhaps explains why the fetus did not respond with increased PTH or decreased calcitonin output. These results indicate that the principal maternal response to magnesium-induced hypocalcemia involves increased parathyroid hormone secretion which tends to preserve maternal calcium homeostasis, while the fetus is partially protected from hypermagnesemia and hypocalcemia by the placenta.

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