Calcitonin levels in chronic renal disease.

High levels of serum calcitonin were found in patients with chronic renal failure. Serum calcitonin correlated directly with the phosphate to total calcium ratio; calcitonin levels correlated inversely with serum calcium in those patients on dialysis and directly with serum calcium in nondialysis patients. All patients had elevated serum gastrin. The high levels of serum calcitonin usually decreased following successful kidney transplantation. The pathophysiology of this hypercalcitonemia and its relationship to renal osteodystrophy and the disordered calcium metabolism of uremia remains to be elucidated.

In vitro studies of calcitonin release in man.

The influence of various agents on calcitonin release from human thyroid was studied in vitro. Under the condition of this investigation, calcium, magnesium and phosphate did not stimulate calcitonin release from short-term incubated slices of human thyroid. However, pentagastrin and USP glucagon were potent stimulators of calcitonin release. Theophylline and dibutyryl cyclic AMP were also potent stimuli. A highly purified preparation of pancreatic glucagon was without an effect. Those agents which stimulated calcitonin release were associated with augmented cyclic AMP accumulation. Although maximal discharge of calcitonin required the presence of calcium, out in vitro experiments raise the question as to whether a gastrointestinal hormone, rather than calcium, might not be the principal agent affecting calcitonin release.

Paradoxical effect of salmon calcitonin on serum calcium: studies in intact and thyroparathyroidectomized men and dogs.

Total serum calcium of normal men, a hypoparathyroid man, two thyroparathyroidectomized men, and intact and thyroparathyroidectomized dogs were studied at multiple intervals following the acute administration of synthetic salmon calcitonin. Calcitonin produced marked fluctuations in serum calcium in one normal man and a biphasic hypocalcaemic response in another. In four of five intact dogs, calcitonin caused absolute or relative hypercalcaemia. In contrast, administration of calcitonin to thyroparathyroidectomized dogs caused a hypocalcaemia with less fluctuations and with no periods of hypercalcaemia. It is possible that some of the paradoxical responses of serum calcium induced by exogenous calcitonin are due to overcompensation by parathyroid hormone. However, other mechanisms may be involved. Our findings indicate that when the disturbing influence is sufficiently great, the control of serum calcium is not as well modulated as previously suspected. In addition, our findings of paradoxically hypercalcaemic responses to calcitonin indicates that the pathophysiologic interpretation of serum calcium at any single moment in time following the administration of this hormone to either intact or thyroparathyroidectomized men or dogs is a precarious endeavour.