![]() | Only 14 pages are availabe for public view |
Abstract The major physiologic control of bone mineralization in infancy involves calciwn and phosphorus. Calcitropic hormones (parathyroid honnone, calcitonin and 1, 25 dihydroxyvitamin D) modulate the response of major end organs - intestine, kidney and bone - to balance the need to maintain a relatively stable extracellular biochemical environment with the need for adequate mineralization of the bone. Clinical bone demineralization occurs primarily in extremely premature infants (Koo a11d Tsa11g, 1984). Parathyroid honnone is a polypeptide secreted by the parathyroid glands to defend against hypocalcemia by controlling the level of ionized calcium in extracellular fluid through its direct actions on mineral transport in bone and kidney and its secondary actions on mineral transport in intestine (mediated by l, 25 (OH), D) and it serves as a principal regulator of process of mineralization rather than calcitonin (Aurbach et aL, 1992). The principal matemal adjustrnent of calcium homeostasis during pregnancy is through an increase in parathyroid honnone secretion which maintains the serum cakium concentrations in the face of placental calcium transfer. The placenta transports calcium ions actively, making the fetus hypercalcemic relative to its mother, which in tum stimulates calcitonin release and perhaps suppresses parathyroid hormone secretion by the fetus (Pitkill, 1985). |