Parathyroid Hormone Secretion in Primary Hyperparathyroidism

The serum levels of parathyroid hormone (PTH) were measured in normal subjects and in hyperparathyroid patients, using an anti-PTH antiserum which reacts with the COOH-terminal half of PTH. The basal PTH concentrations permitted a complete discrimination between normal subjects (264 ± 18 pg/ml, mean ± SEM, n = 15) and patients with either a solitary parathyroid adenoma (737 ± 42 pg/ml, n = 27) or parathyroid hyperplasia (1198 ± 103 pg/ml, n = 6) After EDTA infusion (50 mg/kg/2 h), the absolute rise in serum PTH level was higher in patients with parathyroid hyperplasia (+403 pg/ml) than in patients with solitary tumor (+170 pg/ml) or than in normal subjects (+239 pg/ml). Preoperative discrimination between both diseases, however, was impossible due to a wide variation of the individual degree of autonomy of PTH secretion. Oral phosphorus loading did not increase serum PTH levels in normal subjects but was a significant stimulus in primary hyperparathyroidism. A calcium infusion in 6 hyperparathyroid patients suppressed the PTH secretion, inferred from the serum PTH level and its half-life, from 0 to 100% The changes in serum PTH induced by hypercalcemia or hypocalcemia were significantly correlated. This implies that a tumor secreting much PTH during EDTA infusion reacts similarly during phosphorus stimulation and suppresses its secretion during infusion of calcium, whereas other tumors are largely autonomous during all tests. From these PTH measurements with a COOHterminal antiserum we conclude: 1) Basal rather thanstimulated PTH concentrations are diagnostically helpful; 2) Parathyroid tumors have an individual degree of autonomy of their secretion in response to changes in serum calcium and this autonomy is largely independent from the histologic appearance of the tumor.