Abstract
In the patient described clinical and chemical signs of osteomalacia developed as a result of phosphorus depletion caused by ingestion of excessive amounts of aluminum hydroxide. Symptoms disappeared and serum calcium and phosphorus levels were restored to normal by discontinuing these medications. Four years later hyperparathyroidism due to an autonomously functioning adenoma (“tertiary” hyperparathyroidism) developed. It is postulated that osteomalacia, with low serum calcium and phosphate concentrations, served as the stimulus for the development of secondary parathyroid hyperplasia and, in turn, to an autonomously functioning parathyroid adenoma.
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