[Convulsions and neonatal hypoparathyroidism revealing maternal hyperparathyroidism]

Arch Pediatr. 1994 Mar;1(3):255-9.
[Article in French]

Abstract

Background: Severe prolonged hypocalcemia may occur in neonates whose parathyroid hormone production has been blocked by maternal hyperparathyroidism. This report describes such a case.

Case report: A 7 day-old girl was admitted suffering from dyspnea and repeated convulsions that had continued for 2 days. Her birthweight was 3,500 g and her height 50 cm. Her mother had been given an iron preparation and calcium during pregnancy. Clinical examination of the newborn at birth revealed a cleft palate and micrognathia. The baby had been given milk-formula plus ergocalciferol, 1,200 IU/day. At admission, the baby was hypotonic. Her serum total calcium was 1.27 mmol/l; total proteins 61 g/l; ionized calcium 1.1 mmol/l; phosphorus 2.14 mmol/l; intact PTH 21 pg/ml (N = 10-65) and 25(OH)D 8 ng/ml (N = 8-30). She was given intravenous calcium gluconate (1 g/m2/d), diazepam (0.5 mg/kg) rectally, intravenous phenobarbital (20 mg/kg) but intravenous phenytoin was needed to stop clinical and electrical seizures. Her blood calcium was normalized 5 days later. Her mother, who was clinically normal, had: total serum calcium: 2.72 and 2.77 mmol/l; total proteins: 71 g/l; phosphorus: 0.85 mmol/l; intact PTH: 73 pg/ml; 25(OH)D: 6 ng/ml; Ultrasonography showed an adenoma of the right parathyroid. Further studies on the baby showed no signs of Di George syndrome.

Conclusion: Neonatal hypocalcemia always requires investigation of both the infant and mother. Measurements of vitamin D metabolites and intact PTH are required to recognize maternal hyperparathyroidism.

Publication types

  • Case Reports
  • English Abstract

MeSH terms

  • Female
  • Humans
  • Hyperparathyroidism / complications*
  • Hypocalcemia / etiology
  • Hypoparathyroidism / etiology*
  • Infant, Newborn
  • Maternal-Fetal Exchange
  • Pregnancy
  • Seizures / etiology*