Fetus, Neonate and Infant

Kovacs, Christopher S.

doi:10.1016/b978-0-12-381978-9.10035-6

Cited by 26 publications

(11 citation statements)

References 200 publications

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“…The unique physiological environment during pregnancy, determined by cardinal transient factors such as the presence of the placenta (which is equipped with an endocrine machinery) and the demand for building blocks for the development of fetal organs and tissues (including bone), challenge adaptations in mineral metabolism. First, we must call attention to prominent differences in the consequences of vitamin D and PTH deficiencies in pregnant woman and the fetus (138,139). Physiological adaptations during pregnancy and lactation affect the management of maternal hypoparathyroidism.…”

Section: How Should Hypoparathyroidism Be Managed During Pregnancy Anmentioning

confidence: 99%

Diagnosis and treatment of hypoparathyroidism: a position statement from the Brazilian Society of Endocrinology and Metabolism

Maeda¹,

Moreira²,

Borba³

et al. 2018

Archives of Endocrinology and Metabolism

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Objective To present an update on the diagnosis and treatment of hypoparathyroidism based on the most recent scientific evidence. Materials and methods The Department of Bone and Mineral Metabolism of the Sociedade Brasileira de Endocrinologia e Metabologia (SBEM; Brazilian Society of Endocrinology and Metabolism) was invited to prepare a document following the rules set by the Guidelines Program of the Associação Médica Brasileira (AMB; Brazilian Medical Association). Relevant papers were retrieved from the databases MEDLINE/PubMed, LILACS, and SciELO, and the evidence derived from each article was classified into recommendation levels according to scientific strength and study type. Conclusion An update on the recent scientific literature addressing hypoparathyroidism is presented to serve as a basis for the diagnosis and treatment of this condition in Brazil.

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Section: How Should Hypoparathyroidism Be Managed During Pregnancy Anmentioning

confidence: 99%

Diagnosis and treatment of hypoparathyroidism: a position statement from the Brazilian Society of Endocrinology and Metabolism

Maeda¹,

Moreira²,

Borba³

et al. 2018

Archives of Endocrinology and Metabolism

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“…As explained earlier, intestinal calcium absorption is largely passive at birth but becomes calcitriol dependent as the baby matures (330,332,335); this is why vitamin D-dependent rickets usually develops after calcitriol becomes required to maintain the supply of calcium for the developing skeleton. Vitamin D-deficiency rickets also needs to be distinguished from rickets of prematurity, which is the result of the preterm skeleton having a much higher demand for calcium than what the preterm intestines can absorb from a normal intake of milk or formula (see sect.…”

Section: Observational Studies and Case Reportsmentioning

confidence: 99%

“…Epidemiological data show that hypocalcemia and rickets due to vitamin D deficiency are not usually diagnosed until weeks to months after birth; the peak incidence is between 6 and 18 mo, even in regions where vitamin D deficiency is endemic (17,49,332,510). Clinically recognized cases within the first few weeks after birth are rare and the subject of individual case reports.…”

Section: Observational Studies and Case Reportsmentioning

confidence: 99%

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

Kovacs

2014

Physiological Reviews

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207

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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“…This is due to the fact that in the neonate intestinal calcium absorption is largely passive, nonsaturable and not dependent on 1,25(OH) 2 D. As postnatal age increases, enterocytes express higher levels of the vitamin D receptor and intestinal calcium absorption changes from a nonsaturable, passive process to an active, saturable, 1,25(OH) 2 D-dependent process. 46 Initially thought to be limited to the nephron it is now established that CYP27B1 is also expressed in skeletal and non-skeletal tissues. It has been detected in chondrocytes, osteoblasts, keratinocytes, macrophages, monocytes, placenta decidual cells, vasculature endothelial cells, enterocytes and pancreas islets.…”

Section: Pseudo-vitamin D Deficiency Ricketsmentioning

confidence: 99%

Vitamin D/dietary calcium deficiency rickets and pseudo-vitamin D deficiency rickets

Glorieux

Pettifor

2014

BoneKEy Reports

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This review describes the pathogenesis, clinical presentation and biochemical perturbations found in privational (nutritional) rickets and pseudo-vitamin D deficiency rickets (PDDR), an autosomal recessive condition with loss of function mutations in CYP27B1. It may seem strange to combine a discussion on privational rickets and PDDR as a single topic, but privational rickets and PDDR present with similar clinical signs and symptoms and with similar perturbations in bone and mineral metabolism. Of interest is the characteristic lack of features of rickets at birth in infants with PDDR, a finding which has also been reported in infants born to vitamin D-deficient mothers. This highlights the independence of the fetus and neonate from the need for vitamin D to maintain calcium homeostasis during this period. The variable roles of vitamin D deficiency and dietary calcium deficiency in the pathogenesis of privational rickets are discussed and the associated alterations in vitamin D metabolism highlighted. Although PDDR is a rare autosomal recessive disorder, results of long-term follow-up are now available on the effect of treatment with calcitriol, and these are discussed. Areas of uncertainty, such as should affected mothers breastfeed their infants, are emphasized.

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Fetus, Neonate and Infant

Cited by 26 publications

References 200 publications

Diagnosis and treatment of hypoparathyroidism: a position statement from the Brazilian Society of Endocrinology and Metabolism

Diagnosis and treatment of hypoparathyroidism: a position statement from the Brazilian Society of Endocrinology and Metabolism

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

Vitamin D/dietary calcium deficiency rickets and pseudo-vitamin D deficiency rickets

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