Prior to 1925, the occasional autopsy findings of enlargement of the parathyroid glands in patients with generalized bone disease were thought to be the result of a compensatory hypertrophy of the glands. In 1925 Felix Mandl treated a patient with generalized osteitis fibrosa with injections of parathyroid extract and attempts at parathyroid transplants. Since the patient did not improve, a neck exploration was done, and an adenomatous enlargement of one of the parathyroids was found and removed. The patient steadily improved.1
The demonstration that a serious metabolic disorder of bone could be surgically corrected stimulated a widespread interest in the early diagnosis of primary hyperparathyroidism which has continued to the present. Metabolic bone disease of the osteitis fibrosa variety, nephrolithiasis or nephrocalcinosis, or a combination of these manifestations, have been the clinical hallmarks of primary hyperparathyroidism.
In 1957 St. Goar called attention to the frequency with which gastrointestinal symptoms
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