By Z. Hochberg, P.-E. Mullis
Centuries in the past, throughout the commercial revolution, rickets, often known as 'the English disease', unfold swiftly between city-dwelling terrible kids and have become endemic as a result of diet D deficiency and inadequate entry to daylight. these days it sounds as if to be endemic back because the raise of nutrition D deficiency is paralleling the primacy of breast-feeding in Western societies. Breastfeeding, dietary prestige and darkish dermis are the most probability elements for rickets or 'rachitis' as is the proper clinical time period. Rickets is a formative years affliction and the foundation for figuring out the affliction is rooted within the thought of mineral metabolism and its keep watch over mechanisms within the turning out to be fetus, toddler and baby. because it is now understood that rickets isn't just brought on by nutrition D deficiency, it needs to be stored in brain that diet D and calcium deficiency is general in constructing nations in addition to in prosperous societies, the place young children and their moms are usually not uncovered to as a lot solar as they want.
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Extra resources for Vitamin D and Rickets (Endocrine Development, Vol. 6)
Example text
Therefore, while there is now widespread agreement that inadequate calcium and phosphorus and not vitamin D nutritional status or metabolism is the major cause of rickets in preterm infants, the need for vitamin D supplementation should be taken into consideration. It has been recommended by the American Academy of Pediatrics that preterm infants receive Ն400 IU vitamin D per day. The European Society of Pediatric Maternal, Fetal and Neonatal Vitamin D and Calcium Metabolism 43 Gastroenterology recommended a dose of 1,000 IU vitamin D per day to breast-fed preterm infants [84, 85].
To date, however, there is no proof that vitamin D plays a major role in human placental calcium transport. Furthermore, 25-hydroxyvitamin D 1␣-hydroxylase activity in the placenta and decidua is significantly higher in the first and second trimesters than in the third trimester of pregnancy, while calcium transport is much higher in the third trimester [45]. The authors of that study suggested that 1,25(OH)2D production by the placenta and decidua has an autocrine/paracrine immunomodulatory function and a role in the implantation/placentation processes during early pregnancy.
A more important factor may be the residence time of the calcium in the segments of the intestine. The intestinal calcium absorption occurs by two processes, a saturable, active transfer in the upper and mid section of the small intestine and a nonsaturable, diffusional transfer. The latter, along the entire small intestine, is independent of the vitamin D status. In preterm infants, as calcium intake increases, so does the intestinal absorption of calcium. Human milk fed and formula fed infants supplemented with vitamin D exhibit significantly greater absorption of calcium compared with their unsupplemented counterparts.
