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Transcutaneous Microcirculatory Imaging in Preterm Neonates
Published on: December 31, 2015
Transient hypercalcemia followed by hypocalcemia in a preterm infant after maternal magnesium sulfate therapy
Takahiro Tominaga1, Kazushige Ikeda1, Midori Awazu2
1Division of Neonatology, Departments of Pediatrics, Saitama City Hospital, Saitama, Japan.
Maternal use of magnesium sulfate has been associated with neonatal hypocalcemia and bone changes. We report the case of a preterm male infant who presented hypercalcemia before developing hypocalcemia after maternal magnesium sulfate therapy. Magnesium sulfate was used for premature rupture of membranes for 32 days, and the patient was delivered at 33 weeks gestation. The cord blood showed ionized calcium 1.54 mmol/L. His serum calcium and magnesium were 11.4 mg/dL and 3.5 mg/dL after birth and fell to 6.6 mg/dL and 2.7 mg/dL at 6 hours, respectively. The intact parathyroid hormone level was 18 pg/mL at 6 h. Radiography showed transverse radiolucent metaphyseal bands of the proximal humerus bone, suggesting disturbance in normal ossification. Transient hypercalcemia before the development of hypocalcemia after maternal magnesium sulfate therapy has not been previously reported. We speculate that maternal long-term magnesium sulfate therapy led to defective ossification and transient hypercalcemia in the offspring. Subsequent hypocalcemia was thought to be due to the inhibition of parathyroid hormone secretion by hypercalcemia and hypermagnesemia.
Maternal use of magnesium sulfate has been associated with neonatal hypocalcemia and bone changes. We report the case of a preterm male infant who presented hypercalcemia before developing hypocalcemia after maternal magnesium sulfate therapy. Magnesium sulfate was used for premature rupture of membranes for 32 days, and the patient was delivered at 33 weeks gestation. The cord blood showed ionized calcium 1.54 mmol/L. His serum calcium and magnesium were 11.4 mg/dL and 3.5 mg/dL after birth and fell to 6.6 mg/dL and 2.7 mg/dL at 6 hours, respectively. The intact parathyroid hormone level was 18 pg/mL at 6 h. Radiography showed transverse radiolucent metaphyseal bands of the proximal humerus bone, suggesting disturbance in normal ossification. Transient hypercalcemia before the development of hypocalcemia after maternal magnesium sulfate therapy has not been previously reported. We speculate that maternal long-term magnesium sulfate therapy led to defective ossification and transient hypercalcemia in the offspring. Subsequent hypocalcemia was thought to be due to the inhibition of parathyroid hormone secretion by hypercalcemia and hypermagnesemia.
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