Abstract
The physiology and regulation of bone minerals in the fetus and the newborn is significantly different from children and adults. The bone minerals calcium, phosphate and magnesium are all maintained at higher concentrations in utero to achieve adequate bone accretion. This is an integral component of normal fetal development which facilitates safe neonatal transition to post-natal life. When deciphering the cause of bone mineral disorders in newborns, the potential differential diagnosis list is broad and complex, including several extremely rare conditions. Also, significant discoveries including new embryological molecular genetic transcription factors, the role of active placental mineral transport, and hormone regulation factors have changed the understanding of calcium and phosphate homeostasis in the fetus and the newborn. This article will guide clinicians through an updated review of calcium and phosphate physiology, then review specific conditions pertinent to successful neonatal care. Furthermore, with the advancement of increasingly rapid molecular genetic testing, genomics will continue to play a greater role in this area of fetal diagnostics and prognostication.
Highlights
Over the past 35 years there have been significant advances in the understanding of materno-fetal mineral homeostatic mechanisms
Parathyroid hormone related peptide (PTHrP) was first described in 1985 as a new compound with parathyroid hormone (PTH)-like bioactivity that accounted for the discrepancy between human umbilical cord and maternal PTH levels [1]
Passive and active transport of bone-minerals occurs across the placenta to achieve higher fetal concentration of calcium, phosphate, and magnesium compared to maternal levels
Summary
Over the past 35 years there have been significant advances in the understanding of materno-fetal mineral homeostatic mechanisms. Parathyroid hormone related peptide (PTHrP) was first described in 1985 as a new compound with parathyroid hormone (PTH)-like bioactivity that accounted for the discrepancy between human umbilical cord and maternal PTH levels [1]. This discovery provided new insight as to why fetal PTH levels were so low, yet fetal calcium levels were maintained higher than and independent of maternal calcium concentrations. Magnesium and vitamin D homeostasis will be briefly discussed
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