In hypoparathyroidism and pseudohypoparathyroidism, pharmacologic doses of vitamin D correct hypocalcemia, but the mechanism is unknown. In two children with hypoparathyroidism and one with pseudohypoparathyroidism we tested the hypothesis that in these conditions there is a defect in synthesis of 1 alpha,25-dihydroxyvitamin D3, the principal active metabolite of vitamin D. In both conditions, minute doses of the metabolite (0.04 to 0.08 mug per kilogram of body weight per day) quickly corrected hypocalcemia and increased intestinal calcium absorption. On the other hand, the effective dose of 25-hydroxyvitamin D3 to maintain normocalcemia was 3 to 4 mug per kilogram per day in the two conditions. Thus, the dosage ratio of 25-hydroxyvitamin D3 to 1 alpha,25-dihydroxyvitamin D3 approximated 100:1. By contrast this ratio was approximately 3:1 in two infants with vitamin D deficiency, a condition in which optimal metabolism of vitamin D would be expected. These findings suggest an impaired conversion of 25-hydroxyvitamin D to 1 alpha,25-dihydroxyvitamin D in both hypoparathyroidism and pseudohypoparathyroidism.

Treatment of hypoparathyroidism and pseudohypoparathyroidism with metabolites of vitamin D: evidence for impaired conversion of 25-hydroxyvitamin D to 1 alpha,25-dihydroxyvitamin D.

lα,25-dihydroxyvitamin D3 receptor: competitive binding of vitamin D analogs

Magnesium-induced reversal of vitamin-D resistance in hypoparathyroidism.

https://www.amjmed.com/article/0002-9343(74)90765-7/pdf

The therapeutic approach to hypoparathyroidism.

The clinical physiology of calcium homeostasis, parathyroid hormone, and calcitonin. I.

Twenty-five-hydroxycholecalciferol (25-HCC) is believed to be the biologically active metabolite of vitamin D3circulating 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.

Treatment of Vitamin D-Resistant Hypoparathyroidism With 25-Hydroxycholecalciferol

Twenty-five-hydroxycholecalciferol (25-HCC) is believed to be the biologically active metabolite of vitamin D 3 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.

Treatment of vitamin D-resistant hypopara-thyroidism with 25-hydroxycholecalciferol.

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Treatment of Vitamin D-Resistant Hypoparathyroidism With 25-Hydroxycholecalciferol

Treatment of vitamin D-resistant hypopara-thyroidism with 25-hydroxycholecalciferol.