Failure to heal D-deficiency rickets and suppress secondary hyperparathyroidism with conventional doses of 1,25-dihydroxy vitamin D3.

The actions of 1,25-dihydroxy vitamin D, (1,25(OH)2D,) are thought to account for most of the known effects of vitamin D, and defective production and low plasma concentrations of 1,25(OH)XD, are frequently associated with osteomalacia and secondary hyperparathyroidism.1 Exogenous 1,25(OH)XD , (or its synthetic analogue la-hydroxy vitamin D,) has been given successfully in doses close to its physiological rate of production -0 3-1 0 ug daily-to treat patients who have osteomalacia and hyperparathyroidism accompanied by dietary vitamin D deficiency, chronic liver disease, treatment with anticonvulsant drugs, chronic renal failure, and vitamin D-dependent rickets (type I).2 -7 Despite the association of defective mineralisation of bone and hyperparathyroidism with low concentrations of 1,25(OH),D,, and the ability of 1,25(OH),D, to reverse these abnormalities, it is not clear whether these effects of 1,25(OH),D, are due to direct actions on bone or the parathyroid glands or whether they are mediated indirectly by changes induced in extracellular calcium and phosphorus concentrations or in other vitamin D metabolites. We report on a patient with severe osteomalacia and secondary hyperparathyroidism whose response to treatment with 1,25(OH)2D, was critically dependent on the calcium in his diet.