Thallium-Technetium Subtraction Scintigraphy of Enlarged Parathyroid Glands after Calcitonin Stimulation of Parathyroid Hormone Secretion

1992 ◽  
Vol 33 (4) ◽  
pp. 319-322 ◽  
Author(s):  
A. Bergenfelz ◽  
J. Tennvall ◽  
B. Ahrén
Keyword(s):  
Parathyroid Hormone ◽  
Primary Hyperparathyroidism ◽  
Plasma Levels ◽  
Hormone Secretion ◽  
Serum Levels ◽  
Parathyroid Glands ◽  
Preoperative Localization ◽  
Intact Parathyroid Hormone ◽  
Stimulation Of ◽  
Subtraction Scintigraphy

To improve the sensitivity of thallium-technetium subtraction scintigraphy for preoperative localization procedure of enlarged parathyroid glands in primary hyperparathyroidism, we administered calcitonin intramuscularly 4 hours before the scintigraphy in 14 consecutive patients. Injection of calcitonin reduced plasma levels of ionized calcium from 1.47 ± 0.10 mmol/l to 1.41 ± 0.09 mmol/l (p < 0.01). Concomitantly, serum levels of intact parathyroid hormone increased from 6.4 ± 2.5 pmol/l to 7.9 ± 2.6 pmol/l (p < 0.001). The scintigram after calcitonin injection visualized 11 adenomas (sensitivity 78%) compared to only 9 (sensitivity 64%) in conventional scintigrams. In addition, 5 of the adenomas were more distinctly imaged in the scintigram after calcitonin injection, whereas in only one patient was the conventional scintigram better. Thus, the calcitonin injection improved the scintigram in 7 cases and was inferior in only one case (p = 0.031). We conclude that stimulation of parathyroid hormone secretion with calcitonin results in a better preoperative localization of enlarged parathyroid glands in primary hyperparathyroidism.

scholarly journals Relationship between parathyroid calcium-sensing receptor expression and potency of the calcimimetic, cinacalcet, in suppressing parathyroid hormone secretion in an in vivo murine model of primary hyperparathyroidism

2005 ◽  
Vol 153 (4) ◽  
pp. 587-594 ◽  
Author(s):  
Takehisa Kawata ◽  
Yasuo Imanishi ◽  
Keisuke Kobayashi ◽  
Takao Kenko ◽  
Michihito Wada ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Primary Hyperparathyroidism ◽  
Secondary Hyperparathyroidism ◽  
Murine Model ◽  
Hormone Secretion ◽  
Suppressive Effect ◽  
Receptor Expression ◽  
Parathyroid Glands ◽  
Calcium Sensing Receptor ◽  
Calcium Sensing

Cinacalcet HCl, an allosteric modulator of the calcium-sensing receptor (CaR), has recently been approved for the treatment of secondary hyperparathyroidism in patients with chronic kidney disease on dialysis, due to its suppressive effect on parathyroid hormone (PTH) secretion. Although cinacalcet’s effects in patients with primary and secondary hyperparathyroidism have been reported, the crucial relationship between the effect of calcimimetics and CaR expression on the parathyroid glands requires better understanding. To investigate its suppressive effect on PTH secretion in primary hyperparathyroidism, in which hypercalcemia may already have stimulated considerable CaR activity, we investigated the effect of cinacalcet HCl on PTH-cyclin D1 transgenic mice (PC2 mice), a model of primary hyperparathyroidism with hypo-expression of CaR on their parathyroid glands. A single administration of 30 mg/kg body weight (BW) of cinacalcet HCl significantly suppressed serum calcium (Ca) levels 2 h after administration in 65- to 85-week-old PC2 mice with chronic biochemical hyperparathyroidism. The percentage reduction in serum PTH was significantly correlated with CaR hypo-expression in the parathyroid glands. In older PC2 mice (93–99 weeks old) with advanced hyperparathyroidism, serum Ca and PTH levels were not suppressed by 30 mg cinacalcet HCl/kg. However, serum Ca and PTH levels were significantly suppressed by 100 mg/kg of cinacalcet HCl, suggesting that higher doses of this compound could overcome severe hyperparathyroidism. To conclude, cinacalcet HCl demonstrated potency in a murine model of primary hyperparathyroidism in spite of any presumed endogenous CaR activation by hypercalcemia and hypo-expression of CaR in the parathyroid glands.

Measurement of intact parathyroid hormone in the diagnosis of hyperparathyroidism

1991 ◽  
Vol 125 (6) ◽  
pp. 668-674 ◽  
Author(s):  
Anders Bergenfelz ◽  
Stig Valdermarsson ◽  
Bo Ahrén
Keyword(s):  
Parathyroid Hormone ◽  
Plasma Level ◽  
Primary Hyperparathyroidism ◽  
Plasma Levels ◽  
Diagnostic Information ◽  
Intact Parathyroid Hormone ◽  
Infusion Test ◽  
Intact Pth ◽  
Baseline Plasma Level ◽  
Edta Infusion

Abstract. Plasma levels of parathyroid hormone were determined pre-operatively in 27 consecutive patients with clinical and biochemical signs of primary hyperparathyroidism, by the use of one assay recognizing the intact PTH molecule and one assay recognizing the mid-portion of PTH. Plasma levels of mid-molecule PTH were normal in 5 of the patients with primary hyperparathyroidism. In 4 of these patients, plasma levels of intact PTH were raised. Conversely, in 6 patients with primary hyperparathyroidism, intact PTH were normal pre-operatively. In 5 of these cases, plasma levels of mid-molecule PTH were raised. The EDTA infusion test was performed in 6 patients with normal baseline plasma level of intact PTH pre-operatively. The test correctly predicted all the patients in this group who were found to have primary hyperparathyroidism, as well as a patient with normal parathyroid glands found at operation. We conclude that some patients with primary hyperparathyroidism have normal baseline plasma levels of intact PTH. In these patients, plasma levels of mid-molecule PTH and an EDTA infusion test provide further diagnostic information.

Stimulation of parathyroid hormone secretion by EDTA infusion – a test for the differential diagnosis of hypercalcaemia

1986 ◽  
Vol 111 (4) ◽  
pp. 498-506 ◽  
Author(s):  
Lars Benson ◽  
Jonas Rastad ◽  
Leif Wide ◽  
Göran Åkerström ◽  
Sverker Ljunghall
Keyword(s):  
Parathyroid Hormone ◽  
Healthy Subjects ◽  
Calcium Concentration ◽  
Reference Range ◽  
Hormone Secretion ◽  
Serum Levels ◽  
Ionized Calcium ◽  
Healthy Control ◽  
Edta Infusion ◽  
Stimulation Of

Abstract. A constant EDTA infusion of 24 mg/kg/h during 60–120 min was given to 26 patients with primary hyperparathyroidism (HPT), 8 patients with hypercalcaemia of other origin and 10 healthy control subjects. PTH and ionized calcium concentrations were measured at 5–10 min intervals. In all three groups the infusion caused a linear decrease in plasma ionized calcium. In both the HPT patients and the healthy subjects there was a prompt increase in the serum levels of parathyroid hormone (PTH) until a plateau was reached. The PTH response of the HPT patients appeared already within the hypercalcaemic range and the plateau value was attained at higher levels of PTH and ionized calcium than in the healthy subjects. The enhanced response distinguished half of the HPT patients with basal PTH values within the reference range from the healthy controls. The patients with nonhyperparathyroid hypercalcaemia displayed no increase in PTH values until the ionized calcium concentration was reduced far into or below the reference range. Thus the EDTA infusion permitted a complete differentiation between HPT and other causes of hypercalcaemia. In most cases an infusion over 30 min was sufficient for this purpose.

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