Plasma human calcitonin (hCT) levels in normal and pathologic conditions, and their responses to short calcium or tetragastrin infusion.

Pre- and Postoperative Studies of Plasma Calcitonin in Primary Hyperparathyroidism

“…The studies described here further characterize C-cell function in 10HPT, and suggest that hypercalcitoninemia is not the usual homeostasic response in this disorder. With regard to the basal iCT values, our results show no significant difference between the 60 control and 50 surgically-proven 10HPT patients and are in accord with those of several other laboratories (9)(10)(11)(12). These findings suggest that CT does not circulate in supranormal concentrations in patients with 1°HPT, whether mild or severe (Fig.…”

Enhanced calcitonin secretion in the rat after parathyroidectomy and during chronic calcium deprivation

“…Accordingly, the storage and secretion of CT by parafollicular cells in the hypocalcaemic rat is influenced by plasma calcium in a manner similar to that demonstrated in patients with untreated hypoparathyroidism [6]. They responded to calcium and pentagastrin infusion with a higher serum CT increase than normals [7]. Similar secretory patterns have been found in pigs made hypocalcaemic with EDTA infusions.…”

“…It has been well established that the secretion of calcitonin (CT) by the C-cells of the thyroid is controlled by blood calcium [I] and that acute hypercalcaemia stimulates the release of this hormone. During chronic hypercalcaemic states in rats [2] and humans [3][4][5], the CT response to acute calcium stimulation and the CT content of the thyroid are diminished, whereas in patients with chronic hypocalcaemia, such as hypoparathyroidism, calcium infusions result in a greater increase in serum CT than in controls [6,7]. Gittes et al [8], Peng and Garner [9], and Vanderwiel et al [ hypocalcaemia.…”

Effect of Plasma Calcium Concentration on the Metabolic Clearance Rate of Calcitonin in the Dog

“…However, there is controversy as to whether or not plasma iCT levels are elevated in chronic hypercalcemic states (not involving malignancy) in man. Although three groups have reported elevated basal iCT levels in the chronic hypercalcemia of primary hyperparathyroidism (Heynen and Franchimont 1974;Silva, Snider and Becker 1974;Parthemore and Deftos 1979), the majority of studies have demonstrated normal or low iCT levels (Tashjian, Howland, Melvin and Hill 1970;Deftos, Bury, Habener, Singer and Potts 1971;Adachi, Abe, Tanaka, Yamaguchi, Miyakawa, Hirakawa and Tanaka 1976;Goldsmith, Sizemore, Chen, Zalme and Altemeier l976;Rojanasathit andHaddad 1977;Morita, Fukunaga, Yamamoto, Mori and Torizuka 1975;Lambert, Heath and Sizemore 1979;Becker, Silva, Wisneski, Cyrus, Snider, Moore and Higgins 1980;Ericsson, Berg, Ingemansson, Jernby and Jarhult 1981). However, decreased thyroidal CT content (Tashjian and Voelkel 1967;Aliapoulios and Watts 1966;Broulik, Hradec and Pacovsky 1978) and C-cell hyperplasia (Kracht, Hachmeister and Christ 1970;Ljungberg and Dymling 1972;LiVolsi, Feind, LoGerfo and Tashjian 1973) as well as a diminished CT response to challenge with calcium (Lambert, Heath and Sizemore 1979;Becker et al 1980) have been reported in patients with primary hyperparathyroidism.…”