Intrauterine Hyperparathyroidism: A Complication of Untreated Maternal Hypoparathyroidism1

Aceto, Thomas; Batt, Ronald E.; Bruck, Erika; Schultz, Robert B.; Pérez, Yohana; Jablonski, Ernest

doi:10.1210/jcem-26-5-487

Cited by 56 publications

(18 citation statements)

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“…Interestingly, the impaired reproductive capacity observed in the Pth Ϫ/Ϫ mice has also been described in women with untreated hypoparathyroidism (17). Although successful pregnancies are reported in patients receiving vitamin D and calcium replacement in this setting, lack of therapy (17) or inadequate therapy (calcium concentration Յ 7 mg/dl) (18) places the pregnancy at considerable risk.…”

Section: Discussionmentioning

confidence: 98%

Skeletal Abnormalities in Pth-Null Mice Are Influenced by Dietary Calcium

Miao

Lanske³

et al. 2004

Endocrinology

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We have examined the role of PTH in the postnatal state in a mouse model of PTH deficiency generated by targeting the Pth gene in embryonic stem cells. Mice homozygous for the ablated allele, when maintained on a normal calcium intake, developed hypocalcemia, hyperphosphatemia, and low circulating 1,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)] levels consistent with primary hypoparathyroidism. Bone turnover was reduced, leading to increased trabecular and cortical bone volume in PTH-deficient mice. When mutant mice were placed on a low-calcium diet, renal 25-hydroxyvitamin D 1 alpha-hydroxylase expression increased despite the absence of PTH, leading to a rise in circulating 1,25(OH)(2)D(3) levels, marked osteoclastogenesis, and profound bone resorption. These studies demonstrate the dependence of the skeletal phenotype in animals with genetically depleted PTH on the external environment as well as on internal hormonal and ionic circulatory factors. They also show that, although PTH action is the first defense against hypocalcemia, 1,25(OH)(2)D(3) can be mobilized, even in the absence of PTH, to guard against extreme calcium deficiency.

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Section: Discussionmentioning

confidence: 98%

Skeletal Abnormalities in Pth-Null Mice Are Influenced by Dietary Calcium

Miao

Lanske³

et al. 2004

Endocrinology

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“…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. XII, C and D).…”

Section: Pthmentioning

confidence: 99%

“…When maternal hypocalcemia during pregnancy has been prolonged and severe, fetal hyperparathyroidism has developed, in turn causing a severely demineralized skeleton, and fractures in utero or during birth (11,76,389,586,652). Spontaneous abortion, stillbirth, and neonatal death have also occurred (25,170,302).…”

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

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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“…If maternal hypocalcemia is prolonged and severe, then fetal hyperparathyroidism can cause a severely demineralized skeleton, and fractures in utero or during birth. [229][230][231][232][233] Spontaneous abortion, stillbirth, and neonatal death have also occurred. [234][235][236] The fetal parathyroids are enlarged and hyperplastic, and the cord blood calcium may be normal, low, or even increased.…”

Section: Hypoparathyroidism In the Mothermentioning

confidence: 99%

Parathyroid Function and Disease during Pregnancy, Lactation, and Fetal/Neonatal Development

Kovacs

2015

The Parathyroids

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Intrauterine Hyperparathyroidism: A Complication of Untreated Maternal Hypoparathyroidism1

Cited by 56 publications

References 1 publication

Skeletal Abnormalities in Pth-Null Mice Are Influenced by Dietary Calcium

Skeletal Abnormalities in Pth-Null Mice Are Influenced by Dietary Calcium

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

Parathyroid Function and Disease during Pregnancy, Lactation, and Fetal/Neonatal Development

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