Observations on the Effects of Vitamin D in Man, Including the Relation to Cortisone

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Abstract
In order to study the effects of vitamin D in man, metabolic balance studies were performed in 6 normal Bantu subjects, 5 patients with various types of rickets, 2 patients with secondary hypoparathyroidism, and 4 patients with sarcoidosis. Attempts were also made to provide evidence concerning the theory that cortisone and its analogues are antagonists of vitamin D in man. An increase in the intestinal absorption of calcium due to administration of vitamin D was observed only in cases of rickets; it was not found when vitamin D was given to normal subjects or to the other patients, except occasionally as a late and possibly secondary phenomenon. Vitamin D exerted the primary actions of increasing both serum and urinary calcium, largely independently of each other. This indicates withdrawal of calcium from bone. A further independent action was the raising of the serum phosphorus level. This led to an elevated urinary excretion of phosphorus which could not have been produced by changes in renal tubular reabsorption. Only in severe cases of “resistant rickets” did vitamin D in large doses increase the tubular reabsorption of phosphorus. Only in one case (apart from hypoparathyroid subjects) was there any evidence that vitamin D decreased the tubular reabsorption of phosphate. Thus, in general, no “parathyroid-like” effect was observed. Some cases of sarcoidosis showed hypersensitivity to administered vitamin D. This is in keeping with the idea that the natural hypercalcemia in this state is the result of hypersensitivity to normal amounts of this vitamin. Cortisone and its analogues did not appear to be complete vitamin D antagonists. They did not prevent the various metabolic effects of vitamin D, but they may have reduced hypersensitivity to it.