»HYPOPARATHYROIDISM«, HYPEROSTOSIS, NORMOPHOSPHATAEMIA AND THYROCALCITONIN. A POSSIBLE CASE OF HYPERTHYROCALCITONINISM

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Abstract
A patient with idiopathic hypoparathyroidism, diffuse hyperostosis, hypocalcaemia and normophosphataemia is reported. The normal renal response to an injection of parathyroid extract rules out a resistance of the kidney to the parathyroid hormone (PTH). A normal phosphate excretion and a decreased tubular phosphate reabsorption have not been observed in the absence of PTH. They are probably the result of a normal or increased PTH secretion. A calcium infusion test produces a significantly smaller decrease in the phosphate excretion as compared to normal controls and this can be interpreted as a moderate inhibition of the PTH secretion in the presence of an excess of thyrocalcitonin (TCT). The main signs in our patient, i. e. the hyperostosis, the decreased area of bone resorption, the absence of osteoclasts, and the hypocalcaemia can be demonstrated in the rat treated with TCT. We conclude that our patient probably has an increased TCT secretion in the presence of a normal or increased PTH secretion. The diffuse hyperostosis has been reported in a third of the patients with idiopathic hypoparathyroidism and pseudohypoparathyroidism. We are tempted to believe that a long standing increased secretion of TCT has a marked effect on calcium uptake in bone, in addition to its inhibitory effect on bone resorption. In contrast, PTH primarily increases bone resorption with only a small effect on bone formation.