Hypocalcemic tetany in the newborn as a manifestation of unrecognized maternal primary hyperparathyroidism

Pieringer, Herwig; Hatzl-Griesenhofer, M; Shebl, Omar; Wiesinger-Eidenberger, G; Maschek, W; Biesenbach, Georg

doi:10.1007/s00508-006-0748-1

Cited by 23 publications

(12 citation statements)

References 20 publications

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“…But even in modern cases fetal death still occurs, such as in 30/62 medically managed cases that ended in a late spontaneous abortion (the risk correlated with the level of maternal serum calcium), whereas no complications were seen in 15 cases operated upon during the second trimester (667). Neonatal hypocalcemia and tetany still occur after supposed mild primary hyperparathyroidism in the mothers (716) and the hypoparathyroidism can be prolonged and permanent (125,576,824). A twin pregnancy illustrated the variability of responses to maternal primary hyperparathyroidism, with one neonate having hypocalcemic seizures and the other staying normocalcemic (616).…”

Section: Mineral Metabolism During Pregnancy and Lactationmentioning

confidence: 99%

Maternal Mineral and Bone Metabolism During Pregnancy, Lactation, and Post-Weaning Recovery

Kovacs

2016

Physiological Reviews

359

524

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During pregnancy and lactation, female physiology adapts to meet the added nutritional demands of fetuses and neonates. An average full-term fetus contains ϳ30 g calcium, 20 g phosphorus, and 0.8 g magnesium. About 80% of mineral is accreted during the third trimester; calcium transfers at 300-350 mg/day during the final 6 wk. The neonate requires 200 mg calcium daily from milk during the first 6 mo, and 120 mg calcium from milk during the second 6 mo (additional calcium comes from solid foods). Calcium transfers can be more than double and triple these values, respectively, in women who nurse twins and triplets. About 25% of dietary calcium is normally absorbed in healthy adults. Average maternal calcium intakes in American and Canadian women are insufficient to meet the fetal and neonatal calcium requirements if normal efficiency of intestinal calcium absorption is relied upon. However, several adaptations are invoked to meet the fetal and neonatal demands for mineral without requiring increased intakes by the mother. During pregnancy the efficiency of intestinal calcium absorption doubles, whereas during lactation the maternal skeleton is resorbed to provide calcium for milk. This review addresses our current knowledge regarding maternal adaptations in mineral and skeletal homeostasis that occur during pregnancy, lactation, and post-weaning recovery. Also considered are the impacts that these adaptations have on biochemical and hormonal parameters of mineral homeostasis, the consequences for long-term skeletal health, and the presentation and management of disorders of mineral and bone metabolism.

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Section: Mineral Metabolism During Pregnancy and Lactationmentioning

confidence: 99%

Maternal Mineral and Bone Metabolism During Pregnancy, Lactation, and Post-Weaning Recovery

Kovacs

2016

Physiological Reviews

359

524

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“…However, neonatal hypocalcemia and tetany have occurred after seemingly mild cases of primary hyperparathyroidism (522). A twin pregnancy complicated by maternal hypercalcemia provides a seminal example of the variability: one neonate remained normocalcemic while the other had hypocalcemic seizures (431).…”

Section: Human Datamentioning

confidence: 99%

Bone Development and Mineral Homeostasis in the Fetus and Neonate: Roles of the Calciotropic and Phosphotropic Hormones

Kovacs

2014

Physiological Reviews

207

188

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Mineral and bone metabolism are regulated differently in utero compared with the adult. The fetal kidneys, intestines, and skeleton are not dominant sources of mineral supply for the fetus. Instead, the placenta meets the fetal need for mineral by actively transporting calcium, phosphorus, and magnesium from the maternal circulation. These minerals are maintained in the fetal circulation at higher concentrations than in the mother and normal adult, and such high levels appear necessary for the developing skeleton to accrete a normal amount of mineral by term. Parathyroid hormone (PTH) and calcitriol circulate at low concentrations in the fetal circulation. Fetal bone development and the regulation of serum minerals are critically dependent on PTH and PTH-related protein, but not vitamin D/calcitriol, fibroblast growth factor-23, calcitonin, or the sex steroids. After birth, the serum calcium falls and phosphorus rises before gradually reaching adult values over the subsequent 24 -48 h. The intestines are the main source of mineral for the neonate, while the kidneys reabsorb mineral, and bone turnover contributes mineral to the circulation. This switch in the regulation of mineral homeostasis is triggered by loss of the placenta and a postnatal fall in serum calcium, and is followed in sequence by a rise in PTH and then an increase in calcitriol. Intestinal calcium absorption is initially a passive process facilitated by lactose, but later becomes active and calcitriol-dependent. However, calcitriol's role can be bypassed by increasing the calcium content of the diet, or by parenteral administration of calcium.

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“…As a consequence, transient neonatal hypoparathyroidism can occur in an infant born to a mother with untreated hyperparathyroidism. Transient neonatal hypoparathyroidism due to maternal hypercalcemic hyperparathyroidism is not uncommon [1,3,8,9,12,14]. In contrast, maternal normocalcemic hyperparathyroidism causing neonatal hypoparathyroidism is extremely rare [5] and not easily recognized.…”

Section: Introductionmentioning

confidence: 99%

Transient neonatal hypoparathyroidism in two siblings unmasking maternal normocalcemic hyperparathyroidism

2007

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Hypoparathyroidism is one of the recognized causes of late-onset neonatal hypocalcemia. Maternal hypercalcemic hyperparathyroidism has been shown to suppress fetal parathyroid glands, causing transient neonatal hypoparathyroidism. We report two siblings (6 years apart) with transient hypoparathyroidism presented with hypocalcemic seizures during the first 2 weeks of life. Subsequent investigation revealed an unrecognized normocalcemic hyperparathyroidism with nephrocalcinosis in the mother. Maternal hyperparathyroidism was caused by two parathyroid adenomas. In conclusion, our report highlights the importance of careful evaluation of neonatal hypoparathyroidism in uncovering an unrecognized, asymptomatic hyperparathyroidism in the mother.

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Hypocalcemic tetany in the newborn as a manifestation of unrecognized maternal primary hyperparathyroidism

Cited by 23 publications

References 20 publications

Maternal Mineral and Bone Metabolism During Pregnancy, Lactation, and Post-Weaning Recovery

Maternal Mineral and Bone Metabolism During Pregnancy, Lactation, and Post-Weaning Recovery

Bone Development and Mineral Homeostasis in the Fetus and Neonate: Roles of the Calciotropic and Phosphotropic Hormones

Transient neonatal hypoparathyroidism in two siblings unmasking maternal normocalcemic hyperparathyroidism

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