Hypervitaminosis was produced in young growing rats and the effect of daily injections of cortisone acetate (CA) was studied on growth, metastatic calcification, urinary phosphorus excretion and bone ash.
Cortisone treatment did not ameliorate the weight loss, clinical appearance, histological lesions or the increased urinary phosphorus. excretion of the hypervitaminotic rats. Control rats, treated with CA alone, showed no untoward effects at the dose levels employed.
It is concluded that cortisone does not act as a direct antimetabolite towards vitamin D. The antagonistic effect of the hormone observed in man may be due to reversal of the toxic action of vitamin D by an indirect mechanism, affecting the metabolic sites, such as intestinal tissue, kidney tubules and/or skeletal tissue, on which both vitamin D and cortisone appear to act.