CONTROL OF SECRETION OF PARATHYROID HORMONE IN SECONDARY HYPERPARATHYROIDISM

The response of the parathyroids to an infusion of calcium has been studied in patients with secondary hyperparathyroidism due to either vitamin D deficiency or to chronic renal failure. Two specific homologous immunoradiometric assays for human parathyroid hormone (PTH) have been used to assess the response, one specific for the amino-terminus (N-PTH), the other specific for the carboxy-terminus (C-PTH) of the molecule.
In both the vitamin D deficient and the uraemic patients, in response to a 4 mg/kg/h infusion of calcium generally for 4 h, suppression of N-PTH was similar, falling to around 20–30% of the initial value. In the uraemic subjects, the degree of suppression was inversely related to the initial plasma calcium ( r = 0·9, P < 0·001). Measured with the C-PTH assay, the response was generally less, particularly in the uraemic subjects in whom it was often preceded by an initial rise in C-PTH.
In both groups of subjects, suppression of N-PTH began as soon as the plasma calcium began to rise and before hypercalcaemia was produced. At the end of the infusion the concentration of N-PTH rose quickly, although the plasma calcium was still high. In four uraemic subjects the rate of infusion of calcium was reduced after 1–1·5 h to limit the rise in plasma calcium. As the calcium approached a plateau, the concentration of N-PTH was found to rise again.
These results indicate the importance of using PTH assays of well defined specificity to evaluate autonomy, and show that the degree of suppression achieved is dependent both on renal function and basal plasma calcium. In addition, these observations suggest that the direction and rate of change of plasma calcium are important in the control of secretion of parathyroid hormone.