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Vitamin D Deficiency

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Endocrinology and Diabetes

Abstract

Vitamin D is derived from skin production through exposure to ultraviolet light and from oral intake of natural foods, fortified foods and supplements. While the principal source of vitamin D is skin production, oral intake has primacy over sunlight exposure in both the correction and prevention of privational vitamin D deficiency. Vitamin D deficiency is associated causally with rickets in childhood and osteomalacia in adulthood, but the evidence is inconsistent and inconclusive for a causal association with cancer, infections, autoimmune diseases and cardiovascular disease.

Measurement of serum 25-hydroxyvitamin D (25OHD) is the best marker of vitamin D supply. It is not a clinical outcome, but is a measure of risk of skeletal disease. Adequate supply corresponds to a 25OHD level ranging from 30–50 nmol/L (12–20 ng/ml). A value below 30 nmol/L (12 ng/ml) constitutes an increase in risk of skeletal disease. In those at risk, the clinician must decide whether it is necessary to advise empirically about ensuring adequate intake according to the dietary reference intakes of the 2011 Institute of Medicine (IOM) Report, or to proceed with initial biochemical tests such as serum calcium, phosphorus, total alkaline phosphatase and parathyroid hormone (PTH). Additional tests include bone turnover markers, bone densitometry, bone imaging and rarely dynamic bone histomorphometry. Patients who are diagnosed with vitamin D deficiency should be divided into those who are sun-deprived (privational vitamin deficiency) and those who are disease-related such as those with intestinal, liver or kidney disorders. The principal differential diagnosis for vitamin D-related bone disease is hypophosphataemic bone disease, especially that mediated by excessive fibroblast growth factor 23 (FGF23).

Regarding treatment, those with privational vitamin D deficiency should be managed according to IOM recommendations with respect to vitamin D and calcium requirements. Patients with disease-specific causes may require higher intakes of calcium and vitamin D. High dose vitamin D therapy should be avoided; instead, 1α,25-dihydroxyvitamin D is preferable in refractory cases with close metabolic supervision. Patients with severe hyperparathyroidism secondary to chronic malabsorption may need parathyroid surgery.

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Correspondence to Malachi J. McKenna M.D., F.R.C.P.I., F.A.C.P. .

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McKenna, M.J., Murray, B. (2014). Vitamin D Deficiency. In: Bandeira, F., Gharib, H., Golbert, A., Griz, L., Faria, M. (eds) Endocrinology and Diabetes. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-8684-8_23

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  • DOI: https://doi.org/10.1007/978-1-4614-8684-8_23

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