Neonatal Parathyroid Secretion and Renal Receptor Maturation in Premature Infants

Mallet, E.; Basuyau, Jean-Paul; Brunelle, P; Devaux, A M; Fessard, C

doi:10.1159/000241088

Cited by 24 publications

(13 citation statements)

References 5 publications

(6 reference statements)

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“…The possibility that refractoriness to parathy roid hormone plays a pathogenetic role is worthy o f consideration. The finding of re duced phosphaturic and renal cyclic A M P responses to parathyroid extract in premature infants during the first few days of life is con sistent with this thesis [28,29]. However, in contrast to the impaired renal response, a sig nificant calcemic response to parathyroid ex tract in premature infants has been reported [28,29].…”

Section: Early Neonatal Hypocalcemiamentioning

confidence: 69%

“…The finding of re duced phosphaturic and renal cyclic A M P responses to parathyroid extract in premature infants during the first few days of life is con sistent with this thesis [28,29]. However, in contrast to the impaired renal response, a sig nificant calcemic response to parathyroid ex tract in premature infants has been reported [28,29]. Thus refractoriness to parathyroid hormone is not likely to play a role in the pathogenesis of neonatal hypocalcemia.…”

Section: Early Neonatal Hypocalcemiamentioning

confidence: 78%

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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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Section: Early Neonatal Hypocalcemiamentioning

confidence: 69%

Section: Early Neonatal Hypocalcemiamentioning

confidence: 78%

Human Neonatal Hypocalcemia

Sallé

Delvin²,

Glorieux³

et al. 1990

Neonatology

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“…This likely reflects not only the increasing level of PTH in the circulation, but (as in the rodent) a developmental increase in renal responsiveness to PTH that has been demonstrated in term and preterm infants (378,406).…”

Section: Human Datamentioning

confidence: 86%

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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“…The apparent resistance of the kidney to the action of exogenous PTH on the uri nary excretion of cAMP has been demon strated in human neonates born at term [16] and in premature neonates [17], This appar ent renal resistance to PTH in the 24-hourold suckling neonate is not due to immatur ity of the receptor, as the response to PTH is very marked in the fetus at day 16.5, i.e. 6 days earlier.…”

Section: Discussionmentioning

confidence: 99%

Sensitivity of the Renal Adenylate Cyclase Receptor System to Parathormone during the Last Third of Pregnancy in the Rat

Gügi¹,

Mallet²

1989

Neonatology

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During the last third of pregnancy, the rat phospho-calcic metabolism is clearly modified. Sensitivity of the renal receptor to parathormone (PTH) was investigated over this period in the fetuses and their mothers. As early as day 16.5 of pregnancy, the fetal kidney is sensitive to bovine PTH (1–34) on the basis of cAMP production. Sensitivity declines on the last day of pregnancy. The newborn kidney showed a higher response to PTH 3 h after birth than after 24 h. The basal adenylate cyclase activity in renal membranes of maternal kidney does not change. The sensitivity to PTH and to fluoride both decreased on day 18.5. A desensitization process of the PTH receptor A-C system has to be studied in order to explain these results.

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Neonatal Parathyroid Secretion and Renal Receptor Maturation in Premature Infants

Cited by 24 publications

References 5 publications

Human Neonatal Hypocalcemia

Human Neonatal Hypocalcemia

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

Sensitivity of the Renal Adenylate Cyclase Receptor System to Parathormone during the Last Third of Pregnancy in the Rat

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