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
REINFRANK RF. Primary Hyperparathyroidism with Depression. Arch Intern Med. 1961;108(4):606–610. doi:10.1001/archinte.1961.03620100098014
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