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.
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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. | |
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Norman AW
(1998)
Receptors for 1,25(OH) | |
| book 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 | |
| book 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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