Primary hyperparathyroidism, pregnancy, and neonatal hypocalcemia.
Primary hyperparathyroidism in the mother during pregnancy is known to result in a high rate of fetal complications; spontaneous abortions, still births, and neonatal tetany occur in excessive incidence. To understand the pathophysiology of neonatal hypocalcemia that accompanies this disorder, transplacental calcium dynamics were studied in female sheep during the last trimester of pregnancy and in their fetal lambs after hysterotomy. Calcium ion was shown to move rapidly across the placenta. However, this organ blocked the passage of both parathyroid hormone and calcitonin from the maternal and to the fetal circulations. Our studies support the hypothesis that in primary hyperparathyroidism maternal hypercalcemia results in fetal hypercalcemia, which leads to suppression of fetal parathyroid gland function. In such a situation, neonatal hypocalcemia would occur after birth when maternal calcium flow is interrupted. Parathyroidectomy performed in the mother, especially during the second trimester of pregnancy when operation is safest, would break this cycle and permit normal serum calcium homeostasis in the fetus.
D000818:Animals; D002116:Calcitonin / Q000378:metabolism; D002118:Calcium / Q000378:metabolism / Q000494:pharmacology; D005260:Female; D006801:Humans; D006961:Hyperparathyroidism / Q000378:metabolism* / Q000601:surgery; D006996:Hypocalcemia / Q000151:congenital* / Q000378:metabolism; D008431:Maternal-Fetal Exchange; D010280:Parathyroid Glands / Q000601:surgery; D010281:Parathyroid Hormone / Q000378:metabolism; D011247:Pregnancy; D011248:Pregnancy Complications / Q000378:metabolism* / Q000601:surgery; D012756:Sheep
D010281:Parathyroid Hormone; D002116:Calcitonin; D002118:Calcium