Thomas A K, McVie R, Levine S N
Department of Medicine, Louisiana State University Medical Center, Shreveport 71130, USA.
Am J Perinatol. 1999;16(10):515-20. doi: 10.1055/s-1999-7280.
Normal fetal and neonatal calcium homeostasis is dependent upon an adequate supply of calcium from maternal sources. Both maternal hypercalcemia and hypocalcemia can cause metabolic bone disease or disorders of calcium homeostasis in neonates. Maternal hypercalcemia can suppress fetal parathyroid function and cause neonatal hypocalcemia. Conversely, maternal hypocalcemia can stimulate fetal parathyroid tissue causing bone demineralization. We report two asymptomatic women, one with previously unrecognized hypoparathyroidism and the other with unrecognized familial benign hypercalcemia, who were diagnosed when their newborn infants presented with abnormalities of calcium metabolism. J.B. was born at 34 weeks' gestation with transient hyperbilirubinemia and thrombocytopenia. At 1 month of age he had severe bone demineralization, cortical irregularities, widening and cupping of the metaphyses, and lucent bands in the scapulae. The total serum calcium and phosphorus 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 all increased. P.B., mother of J.B., had no symptoms of hypocalcemia either prior to, or during this pregnancy. She had severe hypocalcemia and hyperphosphatemia, laboratory values typical of hypoparathyroidism. J.N. presented at 6 weeks of age with new onset of seizures and tetany secondary to severe 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/24 hr, with a low fractional excretion of calcium ranging from 0.0064 to 0.0073. P.N. has a brother who previously had parathyroid surgery. Both J.N. and P.N. meet the diagnostic criteria for familial benign hypercalcemia. These cases illustrate the important relationships between maternal serum calcium levels and neonatal calcium homeostasis. They emphasize the need to assess maternal calcium levels when infants are born with abnormal serum calcium levels or metabolic bone disease.
正常胎儿和新生儿的钙稳态依赖于母体来源充足的钙供应。母体高钙血症和低钙血症均可导致新生儿代谢性骨病或钙稳态紊乱。母体高钙血症可抑制胎儿甲状旁腺功能并导致新生儿低钙血症。相反，母体低钙血症可刺激胎儿甲状旁腺组织，导致骨质脱矿。我们报告了两名无症状女性，一名患有先前未被识别的甲状旁腺功能减退症，另一名患有未被识别的家族性良性高钙血症，她们在其新生儿出现钙代谢异常时被诊断出来。J.B.在妊娠34周时出生，患有短暂性高胆红素血症和血小板减少症。1个月大时，他出现严重的骨质脱矿、皮质不规则、干骺端增宽和杯口状改变以及肩胛骨透亮带。血清总钙和磷正常，离子钙为5.4mg/dL（4.6 - 5.4）。他的碱性磷酸酶、甲状旁腺激素和1,25 - 二羟维生素D水平均升高。J.B.的母亲P.B.在此次妊娠之前或期间均无低钙血症症状。她患有严重的低钙血症和高磷血症，这些实验室值是甲状旁腺功能减退症的典型表现。J.N.在6周龄时因严重低钙血症出现新发癫痫和手足搐搦。血清磷、肌酐、碱性磷酸酶和甲状旁腺激素水平正常。15周龄时，他的钙略有升高，钙排泄分数较低。J.N.的母亲P.N.在此次妊娠之前或期间均无高钙血症症状。她的血清钙为12.7mg/dL，尿钙为66.5mg/24小时，钙排泄分数较低，范围为0.0064至0.0073。P.N.有一个先前接受过甲状旁腺手术的兄弟。J.N.和P.N.均符合家族性良性高钙血症的诊断标准。这些病例说明了母体血清钙水平与新生儿钙稳态之间的重要关系。它们强调了在婴儿出生时血清钙水平异常或患有代谢性骨病时评估母体钙水平的必要性。
