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Treatment of Vitamin D-Resistant Hypoparathyroidism With 25-Hydroxycholecalciferol
Charles Y. C. Pak, MD;
Hector F. DeLuca, PhD;
Jose M. Chavez de los Rios, MD;
Tatsua Suda, DDS;
Belle Ruskin, MA;
Catherine S. Delea
Arch Intern Med. 1970;126(2):239-247.
Abstract
Twenty-five-hydroxycholecalciferol (25-HCC) is believed to be the biologically active metabolite of vitamin D3 circulating in the blood. Its clinical usefulness was determined in four patients with hypoparathyroidism, three of whom were resistant to vitamin D. Two patients with Vitamin D resistance responded to 25-HCC (5,000 units or less per day) with a significant increase in serum calcium concentration and in urinary calcium excretion. A similar response was shown in a patient with idiopathic hypoparathyroidism who was probably not vitamin D-resistant. In all three patients, 25-HCC significantly increased the gastrointestinal absorption of calcium. In one patient, it increased the urinary excretion of hydroxyproline. In a fourth patient, who had shown resistance to dihydrotachysterol and cholecalciferol, 25-HCC did not significantly affect serum calcium concentration. This patient, unlike the rest, had a degree of moderate renal failure.
Author Affiliations
Bethesda, Md; Madison, Wis; Bethesda, Md; Madison, Wis; Bethesda, Md
From the Endocrinology Branch, National Heart and Lung Institute, Bethesda, Md, and the Department of Biochemistry, University of Wisconsin, Madison.
Footnotes
Received for publication March 2, 1970; accepted April 10.
Read in part at the general session of the American Federation of Clinical Research, Atlantic City, NJ, May 4,1969.
Reprint requests to 8N214 Bldg 10, National Institutes of Health, Bethesda, Md 20014 (Dr. Pak).
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