John A Kanis, University of Sheffield, UK
Published online: January 2003
DOI: 10.1038/npg.els.0002108
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 D‐resistant states are treated with its hydroxylated derivatives.
Keywords: rickets; osteomalacia; secondary hyperparathyroidism; calcitriol; calcidiol
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Figure 1.
Steps in the metabolism of vitamin D. |
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Figure 2.
Bowing of the femora and genu valgum in an adolescent with osteomalacia. |
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Figure 3.
A Looser zone on the femoral neck of an adult with osteomalacia. |
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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