TY - JOUR
T1 - Calcium-sensing by parathyroid glands in secondary hyperparathyroidism
AU - Goodman, William G.
AU - Veldhuis, Johannes D.
AU - Belin, Thomas R.
AU - Van Herle, Andre J.
AU - Juppner, Harald
AU - Salusky, Isidro B.
N1 - Copyright:
Copyright 2007 Elsevier B.V., All rights reserved.
PY - 1998
Y1 - 1998
N2 - Calcium-sensing by the parathyroids is abnormal in familial benign hypocalciuric hypercalcemia and in primary hyperparathyroidism (1°HPT), but the role of a calcium-sensing defect in uremic secondary hyperparathyroidism (2°HPT) remains controversial. To study the regulation of PTH release by calcium, set point estimates were obtained using the four parameter model during in vivo dynamic tests of parathyroid gland function in 31 patients with 2°HPT, 8 patients with advanced 2°HPT studied shortly before undergoing parathyroidectomy (Pre-PTX), 3 patients with 1°HPT, and 20 subjects with normal renal function (NL); the response to 2-h iv calcium infusions was also evaluated. Neither blood ionized calcium (iCa+2) levels nor the set point for calcium-regulated PTH release differed between 2°HPT and NL; iCa+2 levels and set point values were moderately elevated in Pre- PTX and markedly elevated in 1°HPT. Compared with values obtained in NL, the lowest serum PTH levels achieved during calcium infusions, expressed as a percentage of preinfusion values, were incrementally greater in 2°HPT, Pre- PTX, and 1°HPT, whereas the slope of the relationship between iCa+2 and PTH, expressed as the natural logarithm (In) of percent preinfusion values, decreased incrementally in 2°HPT, Pre-PTX, and 1°HPT. The inhibitory effect of calcium on PTH release is blunted both in 2°HPT and 1°HPT because of increases in parathyroid gland mass, but a calcium-sensing defect is a late; rather than early, consequence of renal 2°HPT.
AB - Calcium-sensing by the parathyroids is abnormal in familial benign hypocalciuric hypercalcemia and in primary hyperparathyroidism (1°HPT), but the role of a calcium-sensing defect in uremic secondary hyperparathyroidism (2°HPT) remains controversial. To study the regulation of PTH release by calcium, set point estimates were obtained using the four parameter model during in vivo dynamic tests of parathyroid gland function in 31 patients with 2°HPT, 8 patients with advanced 2°HPT studied shortly before undergoing parathyroidectomy (Pre-PTX), 3 patients with 1°HPT, and 20 subjects with normal renal function (NL); the response to 2-h iv calcium infusions was also evaluated. Neither blood ionized calcium (iCa+2) levels nor the set point for calcium-regulated PTH release differed between 2°HPT and NL; iCa+2 levels and set point values were moderately elevated in Pre- PTX and markedly elevated in 1°HPT. Compared with values obtained in NL, the lowest serum PTH levels achieved during calcium infusions, expressed as a percentage of preinfusion values, were incrementally greater in 2°HPT, Pre- PTX, and 1°HPT, whereas the slope of the relationship between iCa+2 and PTH, expressed as the natural logarithm (In) of percent preinfusion values, decreased incrementally in 2°HPT, Pre-PTX, and 1°HPT. The inhibitory effect of calcium on PTH release is blunted both in 2°HPT and 1°HPT because of increases in parathyroid gland mass, but a calcium-sensing defect is a late; rather than early, consequence of renal 2°HPT.
UR - http://www.scopus.com/inward/record.url?scp=0031727116&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0031727116&partnerID=8YFLogxK
U2 - 10.1210/jc.83.8.2765
DO - 10.1210/jc.83.8.2765
M3 - Article
C2 - 9709944
AN - SCOPUS:0031727116
SN - 0021-972X
VL - 83
SP - 2765
EP - 2772
JO - Journal of Clinical Endocrinology and Metabolism
JF - Journal of Clinical Endocrinology and Metabolism
IS - 8
ER -