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WILLIAM H. BERGSTROM, MD

Am J Dis Child. 1975;129(10):1137-1138.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Rickets has become so uncommon that many experienced pediatricians have never been personally responsible for its diagnosis or management. Of the few cases still seen, the majority in Europe and North America are due to hereditary metabolic aberrations. Nevertheless, some children still suffer from deformity and growth retardation as a result of calciferol deficiency. In their behalf the following outline presents predisposing factors that define high-risk groups.

A complex and fascinating sequence has been defined by recent research in calciferol metabolism.¹ As a result of this work, the term "vitamin D," though persistent, is obsolete, and calciferol is clearly recognized as a member of the family of steroid hormones. The family resemblance has always been striking; only close inspection distinguishes cholecalciferol from its relatives, estradiol, cortisol, aldosterone, and testosterone.

Vertebrates synthesize 7-dehydrocholesterol in the liver and intestinal mucosa by slight modification of the cholesterol framework common to all steroid . . . [Full Text PDF of this Article]

Author Affiliations
Department of Pediatrics Upstate Medical Center 750 E Adams St Syracuse, NY 13210

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