Vitamin D Deficiency

Abstract

Vitamin D is a secosteroid that must be metabolized before exerting biological effects. Vitamin D deficiency states may arise from inadequate supplies, defective metabolism or target tissue resistance. Privational vitamin D deficiency is treated with vitamin D, whereas vitamin DÔÇÉresistant states are treated with its hydroxylated derivatives.

Keywords: rickets; osteomalacia; secondary hyperparathyroidism; calcitriol; calcidiol

Figure 1.

Steps in the metabolism of vitamin D.

Figure 2.

Bowing of the femora and genu valgum in an adolescent with osteomalacia.

Figure 3.

A Looser zone on the femoral neck of an adult with osteomalacia.

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References

Compston JE (1998) Vitamin D deficiency: time of action. British Medical Journal 317: 1466–1467.

Haussler MR, Haussler CA, Jurutka PW et al. (1997) The vitamin D hormone and its nuclear receptor: molecular actions and disease states. Journal of Endocrinology 154: S57–73.

Norman AW (1998) Receptors for 1α,25(OH)2D3: past, present and future. Journal of Bone and Mineral Research 13: 1360–1369.

Smith R (1996) Disorders of the skeleton. In: Weatherall DJ, Ledingham JGG and Warrell DA (eds) Oxford Textbook of Medicine, 3rd edn, pp. 3055–3097. Oxford: Oxford Medical Publications

Further Reading

Favus M (ed.) (1996) American Society for Bone and Mineral Research. Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, 3rd edn. Philadelphia: Lippincott‐Raven.

Holick MF (1994) Vitamin D: new horizons for the 21st century. American Journal of Clinical Nutrition 60: 619–630.

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How to Cite close
Kanis, John A(Jan 2003) Vitamin D Deficiency. In: eLS. John Wiley & Sons Ltd, Chichester. http://www.els.net [doi: 10.1038/npg.els.0002108]