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

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... hyroidism 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. Case report A 19-year-old Pakistani man, who had lived in England for four years, presented with a one-year history of bone pain in the rib cage and legs and proximal muscle weakness. He and his family ate a traditional diet including bread made from chapatti flour, but there was no family history of bone disease. His daily calcium intake was estimated to be 10 mmol (400 mg) and vitamin D intake 1 Fkg (UK recommended daily intake: 12 5-15 mmol (500-600 mg) and 2 5 stg respectively8).