Abstract
Nutritional rickets remains a global public health problem, despite effective and inexpensive methods to prevent and treat the disease. It is most prevalent in the infant/toddler age groups and the adolescent, but vitamin D deficiency is also prevalent in women of child-bearing age, resulting in babies being born with low vitamin D stores and the mothers having inadequate vitamin D in breast milk, thus exacerbating the risk for rickets in these infants. In the very-low-birth-weight infant, low dietary phosphorus intake also plays a role in the development of the metabolic bone disease of prematurity. In a number of subtropical developing countries, rickets appears to be due to low dietary calcium intakes (approximately 200mg/day) rather than vitamin D deficiency. Biochemically, these children are differentiated from those with vitamin D deficiency by having markedly elevated serum 1,25(OH)2D concentrations and high fractional intestinal calcium absorption. Nutritional rickets represents the outcome of a spectrum of causes, ranging from vitamin D deficiency on one hand to dietary calcium deficiency on the other, while in between low dietary intakes and vitamin D insufficiency act synergistically to increase the risk of developing the disease.
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