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The results of surgical exploration in 267 patients with primary hyperparathyroidism are the basis for this slender volume. The author postulates that primary hyperparathyroidism results from a combination of some hypocalcemic stimulus and an abnormality in growth regulation of parathyroid cells, impaired feedback mechanism of parathyroid hormonal secretion, or impaired capacity for parathyroid involution after hypocalcemia. The suggested pathogenesis of parathyroid tumors in the face of a chronic or intermittent stimulus is normal gland, then hypertrophy and hyperplasia, followed by nodular hyperplasia, adenoma(s), and, rarely, carcinoma. He views primary hyperplasia as a forerunner of the solitary adenoma and attributes the
Surgical Treatment of Hyperparathyroidism. With an Analysis of 267 Cases.. Ann Intern Med. 1972;77:491. doi: https://doi.org/10.7326/0003-4819-77-3-491_2
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Published: Ann Intern Med. 1972;77(3):491.
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Print ISSN: 0003-4819 | Online ISSN: 1539-3704
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