Adult Hypoparathyroidism: Treatment With Calcifediol

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Abstract
Patients [21] with hypoparathyroidism were given calcifediol for 1-28 mo. (mean 11 mo.), for a total of 19 patient-years. The dosages required to maintain normocalcemia ranged 50-300 .mu.g daily (mean 150 .mu.g). The rate of increase in plasma Ca level was about 0.15 mg/dl per day and varied 0.05-0.4 mg/dl per day. Normocalcemia was attained in most patients in 3-4 wk. The rate of decrease in plasma Ca level after cessation of treatment was about 0.1 mg/dl per day so that after mild overtreatment, normocalcemia is regained in about 3 wk. Both the rates of onset and offset are more rapid than for ergocalciferol, but less rapid than for dihydrotachysterol, so that calcifediol is less satisfactory than dihydrotachysterol for the treatment of acute postsurgical hypoparathyroidism. Except in 1 patient, there was no change in plasma phosphate within 4 wk of starting or stopping calcifediol. In 5 patients the maximum effect of a constant daily dose took longer than 3 mo. to attain and, in 1 patient, longer than 6 mo. In several patients, determination of the optimum dose has taken longer than 1 yr. With 1 exception, the mean plasma Ca level in patients whose conditions were well stabilized was between 8.9 and 10.0 mg/dl. The SD of plasma Ca ranged from 0.22-0.51 mg/dl with a mean of 0.35. This is at least as good and possibly superior to the precision attainable with pharmaceutically adequate preparations of ergocalciferol or dihydrotachysterol. As presently formulated, calcifediol is superior to any preparation of ergocalciferol currently available in the USA, but this advantage is pharmaceutical rather than biologic. Whether calcifediol is superior to dihydrotachysterol either in general or in specific patients is much less certain. In patients whose conditions are stabilized with ergocalciferol or cholecalciferol, only 5-10% of the administered dosage can be subjected to 25-hydroxylation and 90-95% must be excreted or metabolized by some other route(s), since calcifediol is about 15 times more potent than the parent vitamin. Similarly, in patients whose conditions are stabilized with calcifediol, less than 1% of the administered dosage (and possibly none at all) can be subjected to 1-hydroxylation, since 1,25(OH)2D3 [1,25-dihydroxy vitamin D3] is at least 100 times more potent than calcifediol. Since calcifediol has about 100 times the antirachitic potency of dihydrotachysterol but only about 5 times the hypercalcemic potency, the antirachitic effect of calcifediol cannot depend solely on raising the plasma Ca level.

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