It is well known that when parathyroid extract, the active principle of the parathyroid gland, is injected into an organism, hypercalcemia is produced. If these injections are continued a negative calcium balance results, with ultimate decalcification. This is followed by the formation of fibrous bone lesions, as Jaffe, Bodansky and Blair1 have recently shown. That a condition similar to this experimental hyperparathyroidism could exist clinically was not clearly recognized until Mandl2 in 1926 removed a parathyroid tumor in a case of generalized osteitis fibrosa cystica and thereby effected a prompt and apparently permanent clinical improvement. This suggested that the causative factor of osteitis fibrosa cystica was a hyperactive parathyroid. The correctness of this conclusion has been fairly well established by a series of other cases reviewed by Barr and Bulger,3 and correlated under the term "clinical hyperparathyroidism." In this paper we are presenting another case of osteitis
QUICK AJ, HUNSBERGER A. HYPERPARATHYROIDISM: THE CLINICAL PICTURE IN THE FAR ADVANCED STAGE. JAMA. 1931;96(10):745–751. doi:10.1001/jama.1931.02720360015004
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