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Concepts of the mechanisms and the manifestations of hyperparathyroidism are still in the process of evolution. This situation is not surprising, for only thirty years have elapsed since the first successful removal of a parathyroid adenoma by Mandl from a patient with osteitis fibrosa cystica. The subsequent demonstration by Albright, Bauer, Ropes and Aub (1) that the parathyroid hormone causes increased urinary excretion of calcium and phosphate led to the recognition of nephrolithiasis as a more common clinical complication of hyperparathyroidism. Furthermore, it has since been shown that chemical hyperparathyroidism can exist without apparent osseous or renal involvement (2).
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Chambers et al. (1956) studied this question.
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