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  • Title: Direct in vivo comparison of calcium-regulated parathyroid hormone secretion in normal volunteers and patients with secondary hyperparathyroidism.
    Author: Ramirez JA, Goodman WG, Gornbein J, Menezes C, Moulton L, Segre GV, Salusky IB.
    Journal: J Clin Endocrinol Metab; 1993 Jun; 76(6):1489-94. PubMed ID: 8501155.
    Abstract:
    The regulation of PTH secretion by calcium is altered in patients with primary hyperparathyroidism. A similar disturbance may occur in secondary hyperparathyroidism, but direct in vivo comparisons of PTH secretion in normal subjects and those with secondary hyperparathyroidism have not been made. Thus, 13 patients with end-stage renal failure and secondary hyperparathyroidism and 20 healthy volunteers underwent dynamic tests of PTH secretion. Changes in ionized calcium were induced by 2-h iv infusions of calcium gluconate or sodium citrate on consecutive days, and the sigmoidal relationship between serum ionized calcium and PTH levels was examined. During sodium citrate infusions, serum ionized calcium levels decreased by 0.21 +/- 0.04 and 0.20 +/- 0.05 mmol/L, respectively (mean +/- SD), in normal volunteers and dialyzed patients (P = NS). Serum PTH levels rose from 27 +/- 7 to 107 +/- 33 pg/mL in controls and from 480 +/- 238 to 859 +/- 412 pg/mL in dialyzed subjects; thus, maximum PTH levels were 396% of preinfusion values in normal subjects, but only 79% greater than baseline values in dialyzed patients (P < 0.001). During the first 30 min of calcium infusions, the increase in serum ionized calcium did not differ between groups, but PTH levels fell more rapidly in normal volunteers; values were 24% of preinfusion levels in controls, but only 56% of the baseline in dialyzed patients (P < 0.01) after 30 min. Minimum PTH levels were attained after 50 min of calcium infusion in normal volunteers and after 70 min in dialyzed patients. The derived values for set-point were 1.21 +/- 0.04 and 1.24 +/- 0.06 mmol/L, respectively, in control and dialyzed subjects (P = NS). These results do not support the contention that the set-point for calcium-regulated PTH secretion is greater than normal in patients with secondary hyperparathyroidism due to end-stage renal disease.
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