Journal of Clinical Investigation · 1989 · 260 citations · 30 references
MedicineEndocrinologyPharmacologyCalcium HomeostasisMineral MetabolismRenal PathophysiologyCalcium EndocrinologyCalcium MetabolismParathyroid DisordersParathyroid Gland PhysiologyParathyroid Hormone PhysiologyParathyroid Hormone RegulationParathyroid Cell FunctionParathyroid Gland FunctionParathyroid Hormone BiologyParathyroid Hormone BiosynthesisParathyroid Hormone KineticsParathyroid Hormone ResponseProtocol ISerum 25-Hydroxyvitamin D Status
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 less than 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 less than 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.
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Timothy A. Reinhardt, Ronald L. Horst, John W. Orf et al. · The Journal of Clinical Endocrinology & Metabolism · 1984 · 805 citations