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JAMA. 1970;213(9):1480-1481.

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A therapeutic problem not infrequently encountered in the management of patients with hypoparathyroidism is the development of vitamin D resistance. Three types of resistance have been reported: a complete resistance in which the patient fails to respond to all commercial forms of vitamin D, a partial resistance where the patient is resistant to some but not all of the vitamin D preparations, and an intermittent type in which the resistance to the same form of vitamin D appears only some of the time in the same patient.

The basis for this resistance may be the defective synthesis in vivo of 25-hydroxycholecalciferol (25-HCC). Recent studies suggest that 25-HCC may be the biologically active metabolite of vitamin D₃.^1,2 This compound, and not vitamin D₃, is believed to be responsible for virtually all the biological effects attributed to the vitamin. Normally, 25-HCC is formed in the liver by hydroxylation of . . . [Full Text PDF of this Article]

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