透過您的圖書館登入
IP:3.147.66.149
  • 期刊
  • OpenAccess

Effects of Intravenous Administration of Calcitriol on Serum Calcitonin Levels in Hemodialysis Patients with Secondary Hyperparathyroidism

靜脈注射活性維生素D對血液透析合併次發性副甲狀腺功能患者血清抑鈣激素之作用

摘要


Calcitonin (CT) secretion may be regulated by calcitriol and parathyroid hormone (PTH) on account of the presence of calcitriol receptors on C cells of thyroid gland and direct stimulation of PTH. The effects of the partial suppression of hyperparathyroidism by intravenous administration of calcitriol on serum CT levels were studied in twenty uremic patients with secondary parathyroidism (2° HPT). All received intravenous calcitriol 1μg at the end of hemodialysis thrice weekly for 4 weeks. Serum calcitriol, CT, intact parathyroid hormone (I-PTH), total calcium (TCa), ionized calcium (ICa) were determined simultaneously before and after 4 weeks of therapy. After 4 weeks of calcitriol treatment, five of twenty uremic patients were calcitriol unresponsive, defined as a fall of less than 10% of initial circulating I-PTH, and fifteen were calcitriol responsive. In calcitriol responders, there was a significant decrement in serum I-PTH (439.1 ± 43.6 vs 241.8 ± 30.1 pg/ml, p<0.001) associated with a significant increment in serum ICa (1.16 ± 0.03 vs 1.27 ± 0.03 mmol/l, p<0.001), a significant increment of serum calcitriol (8.37 ± 0.46 vs 14.74 ± 0.63 pg/ml, p<0.001) and CT levels (57.6 ± 7.6 vs 79.3 ± 7.7 pg/ml, p<0.05). In calcitriol nonresponders, there was also a significant increment of serum calcitriol (10.26 ± 0.68 vs 16.18 ± 1.11 pg/ml, p<0.01) in parallel with a significant increase in serum ICa (1.14 ± 0.03 vs 1.26 ± 0.03 mmol/l, p<0.01) and CT levels (49.6 ± 9.2 vs 74.6 ± 8.7 pg/ml, p<0.05). Since chronic hypercalcemia does not stimulate CT secretion, we conclude that calcitriol supplement enhances the CT secretion in uremic patients with 20 HPT probably via its stimulatory action on calcitriol receptors on the C-cells.

並列摘要


Calcitonin (CT) secretion may be regulated by calcitriol and parathyroid hormone (PTH) on account of the presence of calcitriol receptors on C cells of thyroid gland and direct stimulation of PTH. The effects of the partial suppression of hyperparathyroidism by intravenous administration of calcitriol on serum CT levels were studied in twenty uremic patients with secondary parathyroidism (2° HPT). All received intravenous calcitriol 1μg at the end of hemodialysis thrice weekly for 4 weeks. Serum calcitriol, CT, intact parathyroid hormone (I-PTH), total calcium (TCa), ionized calcium (ICa) were determined simultaneously before and after 4 weeks of therapy. After 4 weeks of calcitriol treatment, five of twenty uremic patients were calcitriol unresponsive, defined as a fall of less than 10% of initial circulating I-PTH, and fifteen were calcitriol responsive. In calcitriol responders, there was a significant decrement in serum I-PTH (439.1 ± 43.6 vs 241.8 ± 30.1 pg/ml, p<0.001) associated with a significant increment in serum ICa (1.16 ± 0.03 vs 1.27 ± 0.03 mmol/l, p<0.001), a significant increment of serum calcitriol (8.37 ± 0.46 vs 14.74 ± 0.63 pg/ml, p<0.001) and CT levels (57.6 ± 7.6 vs 79.3 ± 7.7 pg/ml, p<0.05). In calcitriol nonresponders, there was also a significant increment of serum calcitriol (10.26 ± 0.68 vs 16.18 ± 1.11 pg/ml, p<0.01) in parallel with a significant increase in serum ICa (1.14 ± 0.03 vs 1.26 ± 0.03 mmol/l, p<0.01) and CT levels (49.6 ± 9.2 vs 74.6 ± 8.7 pg/ml, p<0.05). Since chronic hypercalcemia does not stimulate CT secretion, we conclude that calcitriol supplement enhances the CT secretion in uremic patients with 20 HPT probably via its stimulatory action on calcitriol receptors on the C-cells.

延伸閱讀