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1.  Pre- and Postoperative Studies of Plasma Calcitonin in Primary Hyperparathyroidism 
Journal of Clinical Investigation  1979;63(4):602-608.
The importance of calcitonin in the homeostatic response to the chronic hypercalcemia of primary hyperparathyroidism is uncertain. To clarify this issue, we have used a new, sensitive radioimmunoassay for human calcitonin to measure basal plasma calcitonin concentrations in 50 patients with primary hyperparathyroidism (32 female, 18 male). We assayed calcium-stimulated calcitonin concentrations preoperatively in 22 of the patients (16 female, 6 male) and postoperatively in 6. Finally, we assayed pentagastrin-stimulated calcitonin concentrations preoperatively in eight of the patients (three female, five male). Plasma calcitonin values after an overnight fast were indistinguishable from those in normal subjects (mean±SE, males, 48±3 normal and 46±5 pg/ml hyperparathyroid, females, 31±2 normal and 37±3 pg/ml hyperparathyroid.) Among hyperparathyroid patients of both sexes, increases of calcitonin during Ca infusion (15 mg Ca/kg in 4 h) were within normal limits. However, the mean maximal increase of calcitonin was significantly lower in hyperparathyroid than in normal subjects (P < 0.05). In six patients normocalcemic 5-15 mo after parathyroid surgery, fasting plasma calcitonin values were not significantly different, but responses to Ca infusion were greater than preoperatively (Δ calcitonin ±SE: 13±4 preoperatively and 53±35 pg/ml postoperatively). The mean maximal increase of calcitonin after pentagastrin (0.5 μg/kg i.v.) was slightly lower than normal in the patients (mean±SE, males, 45±8 normal and 38±10 pg/ml hyperparathyroid, females, 6±2 normal and 0 pg/ml hyperparathyroid). Thus, primary hyperparathyroidism is accompanied by normal steady-state concentrations of circulating calcitonin, and normal-to-blunted C-cell responses to pentagastrin or induced hypercalcemia, the response to calcium generally increasing after successful parathyroid surgery. These results clearly show that primary hyperparathyroidism is not characterized by hypercalcitoninemia. The seemingly paradoxical absence of elevated steady-state calcitonin concentrations may be accounted for partly by decreased secretory reserve. However, primary hyperparathyroidism may also be accompanied by an increase in the threshold of sensitivity for calcium stimulation of calcitonin secretion.
PMCID: PMC371994  PMID: 438324
2.  Plasma Calcitonin in Normal Man 
Journal of Clinical Investigation  1977;60(5):1135-1140.
We measured plasma calcitonin concentrations in healthy volunteers (20 men, ages 23-45 yr, mean, 30 yr; 25 women, ages 21-46 yr, mean, 30 yr) with a radioimmunoassay capable of detecting 5 pg of calcitonin/500 μl incubation volume, or 25 pg/ml of unextracted plasma. All subjects had 4-h calcium infusion (15 mg Ca/kg), and 24 subjects had intravenous pentagastrin injection (0.5 μg/kg) on separate days. Men had higher basal plasma immunoreactive calcitonin concentrations than women (P < 0.001): mean, 49 pg/ml (range, <25-73) and 31 pg/ml (range, <25-51), respectively. 18 of the 20 men (90%) responded to induced hypercalcemia with increases in plasma immunoreactive calcitonin; only 14 of the 25 women (56%) responded. In men, the mean increase of plasma immunoreactive calcitonin±SE was 58±9 pg/ml, but for women was only 25±6 pg/ml. 8 of 10 men (80%) responded to pentagastrin with an increase of plasma immunoreactive calcitonin >30 pg/ml, compared with such a response in only 1 of 14 women (7%). These differences of plasma immunoreactive calcitonin responses between the sexes were statistically significant (calcium infusion, P < 0.02; pentagastrin, P < 0.001). The physiologic importance of these observations is unknown, but we speculate that a lifelong, relative deficiency of calcitonin in some women could play a role in age- and sex-related bone loss, particularly during the estrogen-deficient postmenopausal years.
PMCID: PMC372466  PMID: 908756
3.  Etiology of Hyperparathyroidism and Bone Disease during Chronic Hemodialysis. III. EVALUATION OF PARATHYROID SUPPRESSIBILITY 
Journal of Clinical Investigation  1973;52(1):173-180.
Parathyroid function was assessed by calcium infusions (4-8 h) in 16 patients with chronic renal insufficiency being treated by long-term hemodialysis. The concentrations of two immunoreactive species of parathyroid hormone in plasma (iPTH-9, mol wt 9500; iPTH-7, mol wt 7000) were estimated by radioimmunoassays utilizing two relatively specific antisera. Control values of the smaller species, iPTH-7, were uniformly high, whereas values of iPTH-9 were normal in 12 of 19 studies. Response of iPTH-7 to calcium infusions was variable, with significant decreases occurring only five times in 27 infusions. Concentrations of iPTH-9, however, decreased during every calcium infusion. In contrast to these acute responses, five of six patients studied during periods of dialysis against both low (< 6 mg/100 ml) and high (7-8 mg/100 ml) calcium concentrations in the dialyzate showed a decrease in values of iPTH-7 during the period of dialysis against the higher calcium concentration. It is concluded that plasma concentrations of iPTH-9 reflect primarily the moment-to-moment secretory status of the parathyroid glands, while concentrations of iPTH-7 reflect more closely chronic parathyroid functional status. It is further concluded that the failure of iPTH-7 to decrease during induced hypercalcemia should not be equated with autonomy of parathyroid gland function.
PMCID: PMC302239  PMID: 4734166

Results 1-3 (3)