Endogenous calcitonin does not protect against hyperparathyroid bone disease in renal failure.

The paper challenges the widely held notion that calcitonin antagonizes effects of the parathyroid hormone (PTH) on bone and inhibits the development of hyperparathyroid bone disease in uremic patients. This was done by studying 16 patients on chronic maintenance dialysis with various levels of PTH and endogenous calcitonin. In addition, 2 patients with normal kidney function and high calcitonin levels due to medullary carcinoma of the thyroid were evaluated, one of them with an excessive, the other with a low-normal PTH level. Undecalcified bone histology was done in all patients and quantitative static and dynamic parameters of bone structure, bone formation, mineralization and resorption were correlated with serum calcitonin and PTH levels using Dunn's multiple comparison procedure. Covariables such as bone aluminum accumulation, immobilization or other diseases were taken into consideration or avoided. In contrast to the literature, no correlations were found between calcitonin and PTH or between calcitonin and bone histology, whereas PTH correlated with parameters of bone resorption and formation. One uremic patient with no circulating calcitonin and high PTH did not show excessive signs of PTH activity on bone. In addition, bone histology in the nonuremic patient with high PTH and high calcitonin did reveal signs of a PTH overactivity on bone which were not seen in the other nonuremic patient with high calcitonin only. These findings indicate that endogenous calcitonin is not protective against hyperparathyroid bone disease.

Effects of calcitonin on basal and thyrotropin-releasing hormone-stimulated prolactin secretion in man.

Plasma PRL fell in nine healthy subjects and four patients with hyperprolactinemia after iv administration of salmon calcitonin (CT). The maximum fall was observed 30--60 min after the infusion. There was no change in the plasma concentrations of the other anterior pituitary hormones tested (GH, FSH, LH, and TSH). In five healthy subjects, TRH was injected 60 min after the CT infusion. This protocol was repeated in the same subjects at 3-day intervals, except CT was not administered. Plasma PRL before TRH injection was clearly lower when CT had been administered. Plasma concentrations of the other anterior pituitary hormones did not change. PRL and TSH responses to TRH were markedly inhibited when CT had been previously infused. These observations are in agreement with preceeding studies showing a similar effect of CT on the plasma concentration of various other polypeptide hormones. This general effect of CT could be attributed to a change in intracellular calcium of the secreting cells.

Effect of parathyroid hormone on plasma prolactin in man.

The iv infusion of parathyroid extract or the synthetic fragments of 1-34 bovine or human parathyroid hormone produced a rapid and marked increase of plasma PRL in normal subjects. The stimulation of the release of endogenous parathyroid hormone by administration of disodium EDTA also resulted in a parallel increase of plasma PRL. Parathyroid hormone did not act via plasma cAMP, as the plasma level reached by this nucleotide was too small to produce PRL release. The ingestion of L-dopa 2 h before parathyroid hormone infusion suppressed the PRL response, suggesting that dopamine and parathyroid hormone interact at a common site. As it has been recently shown that PRL stimulates the renal synthesis of 1,25-dihydroxycholecalciferol, the present data suggest that the effect of parathyroid hormone on this synthesis may be due to the increase in plasma PRL.