Download Vitamin D and Rickets (Endocrine Development, Vol. 6) by Z. Hochberg, P.-E. Mullis PDF

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By Z. Hochberg, P.-E. Mullis

Centuries in the past, throughout the business revolution, rickets, often known as 'the English disease', unfold quickly between city-dwelling bad childrens and have become endemic because of diet D deficiency and inadequate entry to daylight. these days apparently to be endemic back because the raise of diet D deficiency is paralleling the primacy of breast-feeding in Western societies. Breastfeeding, dietary prestige and darkish epidermis are the most possibility components for rickets or 'rachitis' as is the proper clinical time period. Rickets is a formative years disease and the foundation for knowing the illness is rooted within the idea of mineral metabolism and its keep watch over mechanisms within the growing to be fetus, boy or girl and baby. because it is now understood that rickets is not just as a result of diet D deficiency, it needs to be stored in brain that diet D and calcium deficiency is universal in constructing international locations in addition to in prosperous societies, the place childrens and their moms usually are not uncovered to as a lot sun as they wish.

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Extra resources for Vitamin D and Rickets (Endocrine Development, Vol. 6)

Sample text

Accumulating evidence indicates that alterations in vitamin D metabolism during pregnancy is the major maternal adaptive mechanism, although increased resorption from the maternal skeleton may also play a part. The main characteristic of vitamin D metabolism during pregnancy is the 2- to 3-fold rise in maternal serum free and total 1,25(OH)2D levels [3–7] (fig. 1). This increase starts as early as at 10–12 weeks of gestation and continues throughout the entire pregnancy. The rise in serum 1,25(OH)2D concentration apparently causes increased intestinal expression of the vitamin Ddependent calcium binding protein, calbindin 9 k/D and, subsequently, a 2-fold increase in calcium absorption in the gut [4].

In the neonatal period and during lactation, the newborn must quickly adjust to the loss of placental calcium supply while continuing to undergo rapid skeletal growth and the mother must continue to supply the daily calcium needs of the growing infant throughout the lactation period. These adjustments in calcium metabolism take place with minimal long-term consequences to the maternal skeleton. This is a review of the present understanding of human calcium metabolism and the vitamin D endocrine system during normal pregnancy, the neonatal period and lactation.

The situation in humans is not known. There are indications, however, that the passive non-vitamin D dependent absorption of calcium is important, at least in preterm babies [76]. Nonetheless, vitamin D supplementation of preterm infants increased the absorption of calcium by 2–4 weeks after birth [77]. Furthermore, neonates with hypocalcemia responded to treatment with 1-␣-hydroxyvitamin D or with 1,25(OH)2D by increasing their calcium levels [78, 79]. These observations indicate the integrity of the 1,25(OH)2D receptor-effector system in the newborn intestine.

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