Cytochemical bioassay of parathyroid hormone in maternal and cord blood.

Allgrove, Jeremy; Adami, Silvano; Manning, R. M.; O’Riordan, J. L. H.

doi:10.1136/adc.60.2.110

Cited by 82 publications

(31 citation statements)

References 36 publications

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“…This is in line with the study of Bowyer et al 41 Seki et al 42 found a significantly lower PTH level in cord blood compared with maternal blood at birth, and this was in accordance with the results of Allgrove et al 43 who found low PTH levels in cord blood. They supported the contention that PTH secretion is suppressed by hypercalcemia in late fetal life, and thus Seki et al 42 suggest that stimulation of the placental calcium pump by PTHrP may be operative in humans, leading to low cord blood PTH at birth.…”

Section: Maternal and Infant Vitamin D Status S Vij Streym Et Alsupporting

confidence: 82%

Maternal and infant vitamin D status during the first 9 months of infant life—a cohort study

et al. 2013

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BACKGROUND/OBJECTIVES: The objective of this study was to assess vitamin D status and possible consequences of low plasma 25-hydroxyvitamin D (25OHD) levels in a population of healthy mothers and their infants. SUBJECTS/METHODS: A total of 107 women aged 24-41 years gave birth to 108 infants. They were followed up three times during 9 months. RESULTS: Cord blood 25OHD level (43.3 ± 20.4 nmol/l) on average was 62 ± 16% of maternal levels (73.3 ± 30.7 nmol/l), measured 1-2 weeks postpartum. Cord blood 25OHD correlated positively with maternal 25OHD levels (r ¼ 0.83, Po0.001). At birth, 23% of mothers and 61% of infants had 25OHD o50 nmol/l. Vitamin D deficiency (25OHDo25 nmol/l) was present in 66% of the children born by mothers with 25OHD levels below 50 nmol/l (Po0.01), whereas only one child was born with deficiency among mothers with 25OHD 450 nmol/l. During follow-up, most of the children (485%) had 25OHD levels 450 nmol/l, which most likely was attributable to the use of supplements, as more than 95% of the children were given daily vitamin D supplements of 10 mg of vitamin D. Cord blood parathyroid hormone levels were very low (median 0.21; interquartile range 0.11-0.33 pmol/l), with increasing levels (Po0.01) reaching 3.08 (2.67-3.92 pmol/l) at the last visit. Vitamin D levels were not associated with anthropometric indices of the newborn infant or their growth during follow-up. CONCLUSIONS: Vitamin D deficiency is widespread in newborn. Maternal 25OHD levels above 50 nmol/l are needed to prevent vitamin D deficiency among newborn.

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Section: Maternal and Infant Vitamin D Status S Vij Streym Et Alsupporting

confidence: 82%

Maternal and infant vitamin D status during the first 9 months of infant life—a cohort study

et al. 2013

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“…Cytochemical assays have revealed that fetal blood contains high PTH-like bioactivity, which cannot be accounted for by the low immunoreactive levels of PTH (3,20,67). Following the discovery of PTHrP and the development of specific radioimmunoassays for it, studies in fetal pigs (7) and sheep (94,396) determined that high immunoreactive levels of PTHrP correlated closely with, and likely accounted for, the high PTH-like bioactivity in fetal blood.…”

Section: Pthrpmentioning

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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“…6 It has been suggested that this may be driven by parathyroid hormone (PTH); 7 however, more recent studies have shown a signi¢cant decrease in PTH during pregnancy and have suggested the possible involvement of parathyroid hormone -related protein (PTHrP). 8,9 Bone histology suggests an increase in resorption at this time, 10 and this is supported by recent studies of biochemical markers of bone turnover.…”

Section: Introductionmentioning

confidence: 99%