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AFTER the radioimmunoassay for parathyroid hormone (PTH) was introduced by Berson et al. in 1963,1 initial enthusiasm for its clinical application was tempered because widely differing results were reported from several laboratories.2 3 4 5 The overlap of serum levels of immunoreactive PTH (iPTH) between normal subjects and patients with hyperparathyroidism ranged from 0 to 50 per cent. In addition, whereas Reiss and Canterbury3 reported that serum levels of iPTH were not reduced by calcium infusion in patients with parathyroid adenomas, Potts and his coworkers4 found marked suppression of serum iPTH levels in response to induced hypercalcemia in a similar group of patients. . . .
Martin et al. (Thu,) studied this question.