Parathyroid function in infants of diabetic mothers

Tsang, Reginald C.; Chen, I‐Wen; Friedman, Mary Anne; Gigger, Mardi; Steichen, Jean J.; Koffler, Herbert; Fenton, Lawrence J.; Brown, David R.; Pramanik, Arun K.; Keenan, William; Strub, Robert; Joyce, T. H.

doi:10.1016/s0022-3476(75)80970-x

Cited by 76 publications

(20 citation statements)

References 14 publications

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“…The five IDM studied at birth displayed a trend toward lower plasma magnesium concentrations than either the term or preterm nondiabetic infants. Hypomagnesemia and early neonatal hypocalcemia in IDM have been associated with depressed parathyroid function (53,54).…”

Section: Discussionmentioning

confidence: 99%

Circulating Levels of Biologically Active and Immunoreactive Intact Parathyroid Hormone in Human Newborns

et al. 1991

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ABSTRACT. We evaluated circulating levels of biologically active and immunoreactive intact parathyroid hormone in 47 newborns at birth and eight hypocalcemic preterm infants during the first 10 d of life. Use of two sensitive detection systems, the cytochemical bioassay and an immunoradiometric assay specific for intact parathyroid hormone, enabled us to compare plasma concentrations of PTH-like bioactivity (bioPTH) and iPTH-(1-84). Mean umbilical venous plasma bioPTH was elevated in nondiabetic term and preterm newborns [22.5 + 3.1 (fSEM) and 15.8 f 2.5 ng-equiv/L, respectively] compared with normal adult subjects (9.8 2 2.6 ng-equiv/ L; p < 0.01). Umbilical bioPTH was suppressed in five term infants of diabetic mothers (2.6 f 0.4 ng-equiv/L). In contrast, iPTH-(1-84) was low in term and preterm nondiabetic infants' and term infants of diabetic mothers' umbilical samples (5.4 f 1.5, 4.3 ' . 1.5, and 2.4 + 1.0 ng/ L, respectively). Umbilical venous bioPTH was highly correlated with the magnitude of the transplacental calcium gradient (r = 0.90; p < 0.05). In eight preterm infants studied longitudinally, by 24-36 h of life, declining plasma total and ionized calcium (1.71 f 0.04 and 0.78 f 0.03 mmol/L, respectively) were accompanied by a significant rise in both bioPTH (41.2 f 6.3 ng-equiv/L) and iPTH-(1-84) (56.3 f 11.6 ng/L). These data indicate that the 3rd trimester fetoplacental circulation contains levels of bioPTH several-fold higher than those of immunoreactive intact hormone. We also conclude that even hypocalcemic preterm newborn infants can significantly elevate circulating levels of FTH. (Pediatr Res 29: 201-207,1991) Abbreviations PTH, parathyroid hormone iPTH-(1-84), immunoreactive intact parathyroid hormone bioPTH, parathyroid hormone-like biologic activity IDM, infant of a diabetic mother Can total calcium concentration Ca,, ionized calcium concentration CBA, cytochemical bioassay G6PD, glucose 6-phosphate dehydrogenase DCT, distal convoluted tubule PTHrP, parathyroid hormone-related peptide Received June 14, 1990; accepted October 2, 1990. In humans and other mammals, the extracellular total and ionized calcium concentrations change dynamically during the transition from fetal to extrauterine life. The fetal circulation of mammals in the 3rd trimester is hypercalcemic relative to that of the mother. In humans, cessation of transplacental flow of calcium at birth is associated with decrements in CaT and Ca, concentrations. Blood calcium stabilizes I to 2 d after birth, then rises progressively to levels observed in older children and adults. An exaggeration of this sequence of events, early neonatal hypocalcemia (CaT < 1.75 mmol/L; <7.0 mg/dL), occurs in at least 35 to 50% of preterm newborn infants ( l , 2 ) and more than 90% of extremely preterm infants (3).Inference from other hypercalcemic states has suggested that the chronic hypercalcemia of late fetal existence might suppress fetal PTH secretion (4) and that neonatal parathyroid suppression might persist for several days postpartum, ...

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Section: Discussionmentioning

confidence: 99%

Circulating Levels of Biologically Active and Immunoreactive Intact Parathyroid Hormone in Human Newborns

et al. 1991

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“…The mechanism for this is unknown. One case series found high ionized and total serum calcium levels in cord blood of infants of diabetic mothers (684), which could account for suppression of the fetal parathyroids. But why maternal diabetes should cause fetal hypercalcemia is unclear, unless some aspect of the maternal diabetic state leads to increased maternal-fetal flow of calcium.…”

Section: Maternal Diabetes Causing Fetal and Neonatal Hypoparathyrmentioning

confidence: 99%

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

Kovacs

2014

Physiological Reviews

208

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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“…Hypocalcemia of infants of diabetic mothers (IDM ) has been the subject of a number o f studies and several pathogenetic factors have been suggested in this metabolic disorder including hypoparathyroidism, hy perphosphatemia, hypomagnesemia, and hypercalcitoninemia [34][35][36][37][38]. Hypocalcemia of ID M shares some similarities with EN H .…”

Section: Hypocalcemia Of Infants Of Diabetic Mothersmentioning

confidence: 99%

Human Neonatal Hypocalcemia

Sallé

Delvin²,

Glorieux³

et al. 1990

Neonatology

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Hypocalcemia is commonly observed in the neonatal period and is usually transient from a few days to a few weeks. On only rare occasions is neonatal hypocalcemia permanent and secondary to congenital hypoparathyroidism caused by either isolated absence of parathyroid glands or in association with other malformations. Most cases of neonatal hypocalcemia fall into one of two clinical categories. Namely early neonatal hypocalcemia occurs in 24–48 h of life and it is usually observed in premature infants or infants of diabetic mothers. Late neonatal hypocalcemia is observed at the end of the first week of life. In addition of these two major categories, neonatal hypocalcemia may occur in association with hypomagnesemia.

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Parathyroid function in infants of diabetic mothers

Cited by 76 publications

References 14 publications

Circulating Levels of Biologically Active and Immunoreactive Intact Parathyroid Hormone in Human Newborns

Circulating Levels of Biologically Active and Immunoreactive Intact Parathyroid Hormone in Human Newborns

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

Human Neonatal Hypocalcemia

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