Abstract. Experimental studies have suggested that in primary hyperparathyroidism (HPT) the cells of the hyperfunctioning parathyroid tissue retain some capacity for stimulation and that an increase in secretion of parathyroid hormone (PTH) can occur when the extracellular calcium concentration is lowered within the hypercalcaemic range.
We have tested this hypothesis in 23 patients with HPT, 10 patients with hypercalcaemia of other origin (7 of whom had disseminated malignant disease) and 17 normal subjects.
In all three groups a single injection of 100 MRC units of salmon calcitonin caused a reduction in serum calcium of approximately 3 to 5%. In the hypercalcaemic patients this reduction was correlated to the basal calcium level (r = −0.57, P < 0.01). In the patients with HPT, although they all remained hypercalcaemic, the decrease in serum calcium was associated with a mean increase in serum PTH of 10%. Only in 2 patients did such an increase fail to occur despite an adequate decrease in serum calcium. These 2 patients had high basal PTH levels and the lack of response might have been due to a high degree of autonomous parathyroid function. Calcitonin also reduced serum calcium and increased serum PTH in normal subjects.
None of the patients with hypercalcaemia of other origin than primary HPT displayed a secretory PTH response to serum calcium reduction.
Thus, this test could be of practical clinical value, particularly in patients with borderline PTH values. A calcitonin-induced rise in PTH while serum calcium is lowered within the hypercalcaemic range strongly suggests primary HPT.