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16 - Disorders of mineral, vitamin D and bone homeostasis

Published online by Cambridge University Press:  10 December 2009

Patti J. Thureen
By
Oussama Itani  and
Reginald Tsang
Edited by
William W. Hay
Patti J. Thureen
Affiliation:
University of Colorado at Denver and Health Sciences Center
Oussama Itani
Affiliation:
Michigan State University and Kalamazoo Center for Medical Studies, and Borgess Medical Center, Kalamazoo, MI
Reginald Tsang
Affiliation:
Department of Pediatrics, Children’s Hospital Medical Center, Cincinnati, OH
William W. Hay
Affiliation:
University of Colorado at Denver and Health Sciences Center
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Summary

Disorders of mineral homeostasis

Fetal mineral homeostasis is closely linked to that of the mother. In the pregnant woman and the fetus there is an intimate and delicate relationship amongst the calciotropic hormones, growth factors, and the minerals Ca, P, and Mg. Any perturbation of maternal or placental homeostatic mineral balance may affect that of the fetus and may have metabolic sequelae in the fetus manifesting in the neonatal period and infancy.

Disorders of calcium homeostasis

A wide variety of factors can cause significant disturbances in calcium and bone homeostasis in the fetus and neonate.

Maternal hypocalcemia

Maternal hypocalcemia results in fetal hypocalcemia, which stimulates the fetal parathyroid glands to synthesize and secrete more parathyroid hormone (PTH to achieve normocalcemia. PTH does not appear to cross the placenta in either direction. Causes of maternal hypocalcemia are listed in Table 16.1. Impaired secretion of PTH because of hypoparathyroidism or magnesium depletion and resistance to PTH because of mutant receptors, as in pseudohypoparathyroidism, result in maternal hypocalcemia. Hypocalcemia may also be a manifesting feature of abnormal vitamin D deficiency; in particular, maternal vitamin D deficiency may be caused by insufficient sunlight exposure, inadequate dietary intake, or malabsorption. Maternal liver disease may be associated with defective 25-hydroxylase activity resulting in low serum 25-hydroxyvitamin D (25-OHD) concentration, hypocalcemia, and rickets.

Defective 1 alpha-hydroxylase activity may be caused by renal or parathyroid gland diseases.

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Neonatal Nutrition and Metabolism , pp. 229 - 272
Publisher: Cambridge University Press
Print publication year: 2006

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  • Disorders of mineral, vitamin D and bone homeostasis
    • By Oussama Itani, Michigan State University and Kalamazoo Center for Medical Studies, and Borgess Medical Center, Kalamazoo, MI, Reginald Tsang, Department of Pediatrics, Children’s Hospital Medical Center, Cincinnati, OH
  • Patti J. Thureen, University of Colorado at Denver and Health Sciences Center
  • Edited by William W. Hay, University of Colorado at Denver and Health Sciences Center
  • Book: Neonatal Nutrition and Metabolism
  • Online publication: 10 December 2009
  • Chapter DOI: https://doi.org/10.1017/CBO9780511544712.017
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  • Disorders of mineral, vitamin D and bone homeostasis
    • By Oussama Itani, Michigan State University and Kalamazoo Center for Medical Studies, and Borgess Medical Center, Kalamazoo, MI, Reginald Tsang, Department of Pediatrics, Children’s Hospital Medical Center, Cincinnati, OH
  • Patti J. Thureen, University of Colorado at Denver and Health Sciences Center
  • Edited by William W. Hay, University of Colorado at Denver and Health Sciences Center
  • Book: Neonatal Nutrition and Metabolism
  • Online publication: 10 December 2009
  • Chapter DOI: https://doi.org/10.1017/CBO9780511544712.017
Available formats
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  • Disorders of mineral, vitamin D and bone homeostasis
    • By Oussama Itani, Michigan State University and Kalamazoo Center for Medical Studies, and Borgess Medical Center, Kalamazoo, MI, Reginald Tsang, Department of Pediatrics, Children’s Hospital Medical Center, Cincinnati, OH
  • Patti J. Thureen, University of Colorado at Denver and Health Sciences Center
  • Edited by William W. Hay, University of Colorado at Denver and Health Sciences Center
  • Book: Neonatal Nutrition and Metabolism
  • Online publication: 10 December 2009
  • Chapter DOI: https://doi.org/10.1017/CBO9780511544712.017
Available formats
×