Endocrine Abstracts

The main source of vitamin D is by the conversion of 7-dehydrocholesterol in the skin to cholecalceferol upon exposure to sun’s ultraviolet B radiation. Vitamin D in diet may be supplied as cholecalceferol or as ergocalciferol, which is derived from plant sources. Vitamin D is metabolised in the liver to 25-hydroxyvitamin D (25OHD; measure of an individual’s vitamin D status) and by kidneys to 1,25-dihydroxyvitamin D, which is responsible for calcium & phosphorous homeostasis and skeletal mineralisation. Maternal 25OHD crosses the placenta and vitamin D stores of maternal origin are depleted in the infant by eight weeks of age.

There are anecdotal reports of congenital rickets among newborn infants of mothers with severe vitamin D deficiency. Maternal vitamin D deficiency during pregnancy is also associated with craniotabes, seizures secondary to neonatal hypocalcaemia, impaired fetal skeletal mineralisation and dental enamel hypoplasia. Infants born to vitamin D deficient mothers and who are fed on breast milk (contains ∼40 IU vitamin D per litre) without vitamin D supplementation are at risk of developing rickets and heart failure secondary to dilated cardiomyopathy. Javaid et al have recently shown that reduced maternal concentration of 25OHD during late pregnancy was associated with significantly lower whole body and lumbar spine bone mineral content, in the children at age 9 years (Lancet 2006; 367(9504):36–43). Therefore, maternal vitamin D deficiency might contribute to the burden of osteoporotic fractures, through inadequate acquisition of peak bone mass in the growing skeleton.

In the UK there is confusion regarding vitamin D supplementation in pregnancy; the Department of Health recommends that all pregnant and lactating mothers should receive 400 IU of vitamin D daily, whereas the National Institute for Clinical Excellence guideline on routine antenatal care does not recommend routine vitamin D supplementation.