This Article  • References  • Full text PDF  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Contact me when this article is cited  Related Content  • Similar articles in JAMA  Social Bookmarking   What's this?

Jack W. Coburn, MD
Veterans Administration Wadsworth Hospital Center UCLA School of Medicine Los Angeles

Anthony W. Norman, PhD
University of California at Riverside Riverside

JAMA. 1976;236(4):347.

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

To the Editor.—

The reader who is not highly familiar with the recent developments concerning vitamin D and its various active forms may be misled by certain comments made (235: 164, 1976) by Teitelbaum and associates.

First, the major reason for the interest in the treatment of renal osteodystrophy with 1,25-dihydroxycholecalciferol (1,25-dihydroxy-vitamin D₃ [1,25 {OH}₂D₃]) and 1-hydroxycholecalciferol (1-hydroxy-vitamin D₃ [1 {OH} D₃]) arises not because of "antirachitic properties of vitamin D in uremia," but because of discoveries that these compounds bypass the necessity for 1-hydroxylation in the kidney.^1,2 Thus, the kidney is the only known organ capable of converting 25(OH)D₃ to 1,25(OH)₂D₃, the most active, naturally occurring form of vitamin D; also, 1,25(OH)₂D₃ may account for all biologic actions heretofore ascribed to vitamin D itself. Moreover, a characteristic of renal osteodystrophy is a resistance to treatment . . . [Full Text PDF of this Article]

CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter     What's this?