3 results
Factors affecting newborn bone mineral content: in utero effects on newborn bone mineralization
- Ran Namgung, Reginald C. Tsang
-
- Journal:
- Proceedings of the Nutrition Society / Volume 59 / Issue 1 / February 2000
- Published online by Cambridge University Press:
- 28 February 2007, pp. 55-63
-
- Article
-
- You have access Access
- Export citation
-
Several factors have been found recently to have a significant impact on newborn bone mineral content (BMC) and developing fetal bone. Recently we showed that maternal vitamin D deficiency may affect fetal bone mineralization. Korean winter-born newborn infants had extremely low serum 25-hydroxyvitamin D (25-OHD), high serum cross-linked carboxy-terminal telopeptide of type I collagen (ICTP; a bone resorption marker), and markedly lower (8 %) total body BMC than summer-born newborn infants. Infant total body BMC was positively correlated with cord serum 25-OHD and inversely correlated with ICTP, which was also negatively correlated with vitamin D status. In three separate studies on North American neonates we found markedly lower (8–12 %) BMC in summer newborn infants compared with winter newborn infants, the opposite of the findings for Korean neonates. The major reason for the conflicting BMC results might be the markedly different maternal vitamin D status of the North American and Korean subjects. Recently, we found evidence of decreased bone formation rates in infants who were small-for-gestational age (SGA) compared with infants who were appropriate-for-gestational age; we reported reduced BMC, cord serum osteocalcin (a marker of bone formation) and 1,25-dihydroxyvitamin D (the active metabolite of vitamin D), but no alterations in indices of fetal bone collagen metabolism. In theory, reduced utero-placental blood flow in SGA infants may result in reduced transplacental mineral supply and reduced fetal bone formation. Infants of diabetic mothers (IDM) have low BMC at birth, and infant BMC correlated inversely with poor control of diabetes in the mother, specifically first trimester maternal mean capillary blood glucose concentration, implying that factors early in pregnancy might have an effect on fetal BMC. The low BMC in IDM may be related to the decreased transplacental mineral transfer. Cord serum ICTP concentrations were higher in IDM than in control subjects, implying increased intrauterine bone resorption. BMC is consistently increased with increasing body weight and length in infants. Race and gender differences in BMC appear in early life, but not at birth. Ethanol consumption and smoking by the mother during pregnancy affect fetal skeletal development.
16 - 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
- Published online:
- 10 December 2009
- Print publication:
- 04 May 2006, pp 229-272
-
- Chapter
- Export citation
-
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.
15 - Normal bone and mineral physiology and metabolism
-
- 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
- Published online:
- 10 December 2009
- Print publication:
- 04 May 2006, pp 185-228
-
- Chapter
- Export citation
-
Summary
Introduction
Perinatal calcium (Ca), phosphorus (P), and magnesium (Mg) metabolism involves an intricate and complex biological system of interrelated hormones and growth factors that regulate the concentrations of these minerals in the tissues of the mother, fetus, and neonate. Mineral metabolism depends on the availability of mineral substrates and interactions with hormones and growth factors including parathyroid hormone (PTH), calcitonin (CT), 1,25 dihydroxyvitamin D (1,25(OH)2D), insulin-like growth factors (IGFs) and possibly leptins. Understanding of the perinatal physiology of these minerals is important in the prevention and management of mineral disorders in the neonate.
In this chapter we review the perinatal physiology of Ca, P, and Mg metabolism in the fetus and neonate and offer a practical approach to the pathophysiology and management of Ca, P, and Mg disorders. We also review the current nutritional requirements of these minerals for enteral as well as parenteral nutrition. Finally, we review normal bone physiology, and discuss the pathophysiology, prevention, and management of metabolic bone disease or rickets/ osteopenia of prematurity.
Mineral, vitamin D and bone physiology
Body mineral content
Calcium is the fifth most abundant inorganic element in the human body. The adult human body contains about 1200 g of calcium (19 g of Ca per kg body weight). The total body Ca content in a full-term newborn is approximately 28 g, almost all of which (99%) resides in bone (8 g of Ca per kg body weight) where it serves structural and metabolic functions.