Hyperparathyroidism in Relation to Pregnancy

Ludwig, George D.

doi:10.1056/nejm196209272671302

Cited by 83 publications

(29 citation statements)

References 35 publications

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“…XII, A, B, and G). These findings have been observed in babies born of mothers whose hypercalcemia during pregnancy was caused by primary hyperparathyroidism (79,149,304,393,609,718), inactivating mutations of Casr (529), or hypercalcemia of malignancy (9,131,278,454,529,673,674,700). Conversely, maternal hypocalcemia caused by hypoparathyroidism (11,76,389,586,652,710) or pseudohypoparathyroidism (226,710) has been associated with fetal parathyroid gland hyperplasia, normal cord blood calcium, increased PTH, and effects on the fetal skeleton that include increased resorption, demineralization, and fractures occurring in utero or during delivery (see sect.…”

Section: Pthmentioning

confidence: 82%

“…However, there are indirect indications that placental calcium transport may be altered when maternal serum calcium is significantly increased or decreased. Maternal hypercalcemia due to primary hyperparathyroidism or familial hypocalciuric hyercalcemia causes suppression of the fetal parathyroid glands that can last for months after birth or be permanent (54,79,393,417,493,529,609,674). Maternal hypercalcemia likely increases the flow of calcium across the placenta, thereby suppressing the fetal parathyroids.…”

Section: Maternal Regulation Of Placental Mineral Transportmentioning

confidence: 99%

“…Failure of the neonate's parathyroids to upregulate promptly after birth may precipitate hypocalcemia and tetany. In several case series 50% of neonates had tetany or other complications of maternal hypercalcemia, while 25-30% of them died (149,304,393,718). Hypoparathyroidism normally resolves by 3-5 mo after birth (609), but permanent hypoparathyroidism has also occurred (79,393,609).…”

Section: Human Datamentioning

confidence: 99%

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

Kovacs

2014

Physiological Reviews

211

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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Section: Pthmentioning

confidence: 82%

Section: Maternal Regulation Of Placental Mineral Transportmentioning

confidence: 99%

Section: Human Datamentioning

confidence: 99%

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

Kovacs

2014

Physiological Reviews

211

188

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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

383

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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“…Postpartum neonatal tetany and hypoparathyroidism can happen in severe cases (2). Although hypoparathyroidism in the infant is typically transient, there have been rare case reports of permanent hypoparathyroidism in the child due to suppression of the fetal parathyroid glands in utero (6)(7)(8). It is therefore very important to diagnose the condition early and to treat promptly.…”

Section: Discussionmentioning

confidence: 99%

Primary Hyperparathyroidism In A First-Trimester Woman With Hyperemesis Gravidarum And Pancreatitis

Burks

Harary

Solórzano

et al. 2017

AACE Clinical Case Reports

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Objective: Primary hyperparathyroidism during pregnancy is rare and is most often due to a solitary parathyroid adenoma. It is usually asymptomatic, but symptoms of hypercalcemia may be difficult to diagnosis, as they are often similar to those of pregnancy, such as fatigue and vomiting. If untreated, there is a high risk of both fetal and maternal complications. Early recognition and treatment are crucial to preventing long-term or lethal consequences. We present a case of severe primary hyperparathyroidism due to a parathyroid adenoma in a 31-year-old G3P2 female which required urgent parathyroidectomy.Methods: Case identified is described. Results:The patient was admitted at 11 weeks of gestation for refractory nausea and vomiting. Laboratory results were diagnostic for primary hyperparathyroidism and showed an elevated calcium of 12.6 mg/dL, elevated parathyroid hormone of 103 pg/mL, and low phosphorus of 1.6 mg/dL. Albumin level was normal. 25-Hydroxyvitamin D was low/normal at 25 ng/mL and 1,25-dihydroxyvitamin D level was elevated at 129 pg/mL. Amylase and lipase levels were elevated, demonstrating concomitant pancreatitis. Thyroid/neck ultrasound showed a 1.0 × 0.6 × 0.4 cm right, lower parathyroid adenoma. She was treated for pancreatitis, and a parathyroidectomy was planned for the second trimester. She returned days later with persistent nausea and vomiting and worsening hypercalcemia to a level of 14.1 mg/dL. Urgent parathyroidectomy was performed with a good outcome.Conclusion: Primary hyperparathyroidism in pregnancy is rare but must be recognized and treated to reduce maternal and fetal complications. (AACE Clinical Case Rep. 2017;3:e31-e34)

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Hyperparathyroidism in Relation to Pregnancy

Cited by 83 publications

References 35 publications

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

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

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

Primary Hyperparathyroidism In A First-Trimester Woman With Hyperemesis Gravidarum And Pancreatitis

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