In primary hyperparathyroidism, hypercalcaemia is due to inappropriate hypersecretion of parathormone (PTH). Yet, the intestinal or osseous origin of the excess in plasma calcium and the symptoms of the disease are largely conditioned by vitamin D reserve and metabolism. In cases with sufficient vitamin D reserve and normal metabolism, the primary disorder is hyperabsorption of calcium by the intestine, and there is a risk of renal stone formation. In patients with vitamin D deficiency, there is a significant increase of bone resorption accompanied by osteoarticular symptoms. In addition, other factors, as yet unidentified, seem to intervene in the reabsorption of calcium by the renal tubule, which commands the degree of hypercalcaemia. Hypersecretion of parathormone may be due either to a reduced sensitivity of parathyroid cells to calcium (as in adenomas) or to an increase of the PTH-secreting thyroid mass (as in hyperplasia and some adenomas).