Pediatrics in Review
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(Pediatrics in Review. 2000;21:286. doi:10.1542/10.1542/pir.21-8-286)
© 2000 American Academy of Pediatrics
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Planning the Treatment of a Patient Who Has Rickets



Only a growing child, prior to fusion of the epiphyses, can develop rickets, which is characterized by poor mineralization of epiphyseal cartilage and consequent growth retardation. Several circumstances result in clinical rickets, including inadequate dietary intake of vitamin D, inadequate exposure to ultraviolet rays in sunlight to form endogenous vitamin D, acquired or inherited disorders of vitamin D metabolism, inherited renal tubular defects that produce hypophosphatemia or acidosis, hereditary resistance to the final metabolite of vitamin D (dihydroxycholecalciferol), and chronic administration of anticonvulsants.

Appropriate levels of both calcium and phosphorous are essential for optimal bone mineralization. Although calcium homeostasis is controlled in the intestines, phosphate homeostasis is regulated in the kidneys. Vitamin D is generated initially either by ingestion in the diet or by endogenous production in the skin following ultraviolet irradiation. It is transported to the liver where it is hydroxylated to 25(OH)D or hydroxycholecalciferol, which in turn circulates to the kidneys and undergoes further hydroxylation to 1,25(OH)2D . . . [Full Text of this Article]


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