Direct in vivo comparison of calcium-regulated parathyroid hormone secretion in normal volunteers and patients with secondary hyperparathyroidism
JA Ramirez, WG Goodman, J Gornbein, C Menezes, L Moulton, GV Segre and IB Salusky
Department of Pediatrics, University of California School of Medicine, Los Angeles 90024.
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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