The effects of
calcium injection (3 mg/Kg/10 min) or oral
calcium administration (
calcium lactate 7.7 g) on plasma iPTH and Nephrogenous
cyclic AMP (NcAMP) were studied in 6 normal controls and 13 patients with
primary hyperparathyroidism. In the control subjects, plasma iPTH determined by a predominantly carboxyl-terminal antiserum was less than 0.3 ng/ml before and after both
calcium loads, whereas 41 approximately 98% (mean 67%) of NcAMP was rapidly and uniformly suppressed to a level lower than the normal value. In 2 patients with
primary hyperparathyroidism, iPTH was clearly reduced from 8.0 to 4.6 ng/ml and 1.6 to 0.96 ng/ml, respectively, by the
calcium load. However, in the other 7 patients with
primary hyperparathyroidism who showed only a slight elevation of iPTH: less than 0.3 approximately 0.9 ng/ml, the reductions in iPTH were not detected after the
calcium load: less than 0.3 approximately 0.7 ng/ml. In contrast, 30 approximately 54% (1.02 approximately 3.85 nmol/dl GF) of NcAMP, which was greater than the diurnal variation, was suppressed after
calcium injection in 5 patients with
primary hyperparathyroidism (2 of 4 patients with urological, and 3 of 5 patients with chemical
hyperparathyroidism). But NcAMP was not suppressed in all 4 patients with skeletal
hyperparathyroidism including one with
proximal renal tubular dysfunction whose basal iPTH was elevated markedly but reduced clearly by the
calcium load. In general, suppression of NcAMP was followed by a decrease of
phosphate excretion. On the other hand, even in a patient with
primary hyperparathyroidism whose NcAMP was not suppressed at all after the
calcium injection,
calcium infusion (15 mg/Kg/3h) resulted in some (23%) decrease in NcAMP. Oral
calcium administration resulted in responses which were almost the same as those produced by
calcium injection. These results suggest that NcAMP provides a useful index in the parathyroid suppression test in patients with
primary hyperparathyroidism, especially those who display a rather mild elevation of iPTH. This is not the case, however, in a few patients who show a marked elevation of iPTH and/or
proximal renal tubular dysfunction.