Disorders of maternal calcium metabolism implicated by abnormal calcium metabolism in the neonate

Normal fetal and neonatal calcium homeostasis is dependent upon an adequate supply of calcium from maternal sources. Both maternal hypercalcemia and h ypocalcemia can cause metabolic bone disease or disorders of calcium homeos tasis in neonates. Maternal hypercalcemia can suppress fetal parathyroid fu nction and cause neonatal hypocalcemia. Conversely, maternal hypocalcemia c an stimulate fetal parathyroid tissue causing bone demineralization. We rep ort two asymptomatic women, one with previously unrecognized hypoparathyroi dism and the other with unrecognized familial benign hypercalcemia, who wer e diagnosed when their newborn infants presented with abnormalities of calc ium metabolism. J.B. was born at 34 weeks' gestation with transient hyperbi lirubinemia and thrombocytopenia. At 1 month of age he had severe bone demi neralization, cortical irregularities, widening and cupping of the metaphys es, and lucent bands in the scapulae. The total serum calcium and phosphoru s were normal with an ionized calcium of 5.4 mg/dL (4.6-5.4). His alkaline phosphatase, parathyroid hormone, and 1,25-dihydroxyvitamin D levels were a ll increased. P.B., mother of J.B., had no symptoms of hypocalcemia either prior to, or during this pregnancy. She had severe hypocalcemia and hyperph osphatemia, laboratory values typical of hypoparathyroidism. J.N. presented at 6 weeks of age with new onset of seizures and tetany secondary to sever e hypocalcemia. The serum phosphorus, creatinine, alkaline phosphatase, and parathyroid hormone levels were normal. At 15 weeks of age his calcium was slightly elevated with a low fractional excretion of calcium. P.N., mother of J.N., had no symptoms of hypercalcemia either prior to, or during this pregnancy. Her serum calcium was 12.7 mg/dL and urine calcium was 66.5 mg/2 4 hr, with a low fractional excretion of calcium ranging from 0.0064 to 0.0 073, P.N. has a brother who previously had parathyroid surgery. Both J.N. a nd P.N. meet the diagnostic criteria for familial benign hypercalcemia. The se cases illustrate the important relationships between maternal serum calc ium levels and neonatal calcium homeostasis. They emphasize the need to ass ess maternal calcium levels when infants are born with abnormal serum calci um levels or metabolic bone disease.