Etiology of Primary Hyperparathyroidism

About 80% of patients with primary hyperparathyroidism have a single adenoma, 15% have hyperplasia of all four glands, and 5% have double adenomas.2 The cause of parathyroid adenoma or hyperplasia is not known. Head and neck irradiation increases the risk of primary hyperparathyroidism by 11% per centigray.3-4 Ten percent of parathyroid adenomas have a PRAD-1 oncogene (cyclin D gene activated by PTH promoter). Mutations in the calcium sensor protein appear not to be an important cause of primary hyperparathyroidism,5 although decreased calcium receptor has been described in parathyroid adenomas and in hyperplastic parathyroid glands in patients with chronic renal failure.

Retinoblastoma tumor suppressor gene is found to be frequently mutated in parathyroid cancers,6 whereas p53 mutations are rare.7 Two thirds of apparently sporadic parathyroid cancers have mutations in the HRPT2 gene, the gene responsible for the hyperparathyroidism-jaw tumor syndrome.8

Patients with multiple endocrine neoplasia (MEN) types 1 and 2A are more likely to have hyperparathyroidism, as are family members of patients with familial hyperparathyroidism. In the mouse, deletion of the MEN 1 tumor suppressor gene in the parathyroid gland results in parathyroid neoplasia and hypercalcemic hyperparathyroidism.9 Patients with Cowden's disease10 (breast cancer, thyroid neoplasm, and gastrointestinal polyps) and McCune-Albright syndrome11 (caused by activating mutations of the stimulating guanosine triphosphate-binding protein) are also at higher risk for developing primary hyperparathyroidism.

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