TY - JOUR
T1 - Parathyroid hormone suppression by intravenous 1,25-dihydroxyvitamin D. A role for increased sensitivity to calcium
AU - Delmez, J. A.
AU - Tindira, C.
AU - Grooms, P.
AU - Dusso, A.
AU - Windus, D. W.
AU - Slatopolsky, E.
PY - 1989
Y1 - 1989
N2 - Numerous in vitro studies in experimental animals have demonstrated a direct suppressive effect of 1,25-dihydroxyvitamin D (1,25(OH)2D) on parathyroid hormone (PTH) synthesis. We therefore sought to determine whether such an effect could be demonstrated in uremic patients undergoing maneuvers designed to avoid changes in serum calcium concentrations. In addition, the response of the parathyroid gland in patients undergoing hypercalcemic suppression (protocol I) and hypocalcemic stimulation (protocol II) before and after 2 wk of intravenous 1,25(OH)2D was evaluated. In those enlisted in protocol I, PTH values fell from 375 ± 66 to 294 ± 50 pg (P < 0.01) after 1,25(OH)2D administration. During hypercalcemic suppression, the 'set point' (PTH max + PTH min/2) for PTH suppression by calcium fell from 5.24 ± 0.14 to 5.06 ± 0.15 mg/dl (P < 0.05) with 1,25(OH)2D. A similar decline in PTH levels after giving intravenous 1,25(OH)2D was noted in protocol II patients. During hypocalcemic stimulation, the parathyroid response was attenuated by 1,25(OH)2D. We conclude that intravenous 1,25(OH)2D directly suppresses PTH secretion in uremic patients. This suppression, in part, appears to be due to increased sensitivity of the gland to ambient calcium levels.
AB - Numerous in vitro studies in experimental animals have demonstrated a direct suppressive effect of 1,25-dihydroxyvitamin D (1,25(OH)2D) on parathyroid hormone (PTH) synthesis. We therefore sought to determine whether such an effect could be demonstrated in uremic patients undergoing maneuvers designed to avoid changes in serum calcium concentrations. In addition, the response of the parathyroid gland in patients undergoing hypercalcemic suppression (protocol I) and hypocalcemic stimulation (protocol II) before and after 2 wk of intravenous 1,25(OH)2D was evaluated. In those enlisted in protocol I, PTH values fell from 375 ± 66 to 294 ± 50 pg (P < 0.01) after 1,25(OH)2D administration. During hypercalcemic suppression, the 'set point' (PTH max + PTH min/2) for PTH suppression by calcium fell from 5.24 ± 0.14 to 5.06 ± 0.15 mg/dl (P < 0.05) with 1,25(OH)2D. A similar decline in PTH levels after giving intravenous 1,25(OH)2D was noted in protocol II patients. During hypocalcemic stimulation, the parathyroid response was attenuated by 1,25(OH)2D. We conclude that intravenous 1,25(OH)2D directly suppresses PTH secretion in uremic patients. This suppression, in part, appears to be due to increased sensitivity of the gland to ambient calcium levels.
UR - http://www.scopus.com/inward/record.url?scp=0024563652&partnerID=8YFLogxK
U2 - 10.1172/JCI114022
DO - 10.1172/JCI114022
M3 - Article
C2 - 2703535
AN - SCOPUS:0024563652
SN - 0021-9738
VL - 83
SP - 1349
EP - 1355
JO - Journal of Clinical Investigation
JF - Journal of Clinical Investigation
IS - 4
ER -