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題 名 | 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 |
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作 者 | 蔡建松; 鄒順生; 洪永祥; 陳金順; 林石化; | 書刊名 | 醫學研究 |
卷 期 | 20:1 1999.08[民88.08] |
頁 次 | 頁21-28 |
分類號 | 415.9 |
關鍵詞 | 抑鈣激素; 副甲狀腺激素; 活性維生素D; 尿毒; Calcitonin; Calcitriol; Secondary hyperparathyroidism; Uremia; |
語 文 | 英文(English) |
中文摘要 | 甲狀腺 C 細胞上有活性維生素 D 接受器,可受活性維生素 D 及副甲狀腺激素之刺激而分泌抑鈣激素。 本研究藉著靜脈注射活性維生素 D 來抑制副甲狀腺機能,對 20 位尿毒患者合併次發性副胛狀腺功能亢進者,進行評估血清抑鈣激素之作用。全部這些病人接受每週三次血液透析,為期四週,在血液透析結束前給予靜脈注射一微克活性維生素D。在治療四週前後測量血清活性維生素D、抑鈣激素、副甲狀腺激素、游離鈣離子。在活性維生素D治療前,尿毒患者合併次發性副甲狀腺亢進與正常健康人比較,呈現血清抑鈣激素增加,血清活性維生素D較低。在四週治療後,有5位是活性維生素D無反應者(定義為血清副甲狀腺素下降少於10%),其他15位為活性維生素D反應者。在活性維生素D反應者血清副甲狀腺素有明顯下降(439.1 ± 43.6 vs 241.8 ± 30.1 pg/ml, p<0.05),及血清游離鈣離子上升(1.16 ± 0.03 vs 1.27 ± 0.03 mmol/l, p<0.001),活性維生素D上升(8.37 ± 0.46 vs 14.74 ± 0.63 pg/ml, p<0.001),及抑鈣激素有意義上升(57.6 ± 7.6 us 79.3 ± 7.7 pg/ml, p<0.05)。在活性維生素D無反應者,雖然副甲狀腺素無有意義上升,但血清游離鈣離子仍然上升(1.14 ± 0.03 vs 1.26 ± 0.03 mmol/l, p<0.01), 活性維生素D(10.26 ± 0.68 vs 16.18 ± 1.11 pg/ml, p<0.01)及抑鈣激素上升(49.6 ± 9.2 vs 74.6 ± 8.7 pg/ml, p<0.05)。因為慢性血鈣上升不會刺激抑鈣激素之分泌,我們結論為尿毒患者合併次發性副甲狀腺功能亢進,補充活性維生素D可增加抑鈣激素之分泌,可能經由刺激於C細胞上的活性維生素D接受器之作用。 |
英文摘要 | 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(2oHPT). All received intravenous calcitriol 1£gg 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¢H of initial circulating I-PTH, and fifteen were calcitriol responsive. In calcitriol responders, there was a significant decrement in serum I-PTH(439.1¡Ó43.6 vs 241.8¡Ó30.1 pg/ml, p¡Õ0.001) associated with a significant increment in serum ICa(1.16¡Ó0.03 vs 1.27¡Ó0.03 mmol/l, p¡Õ0.001), a significant increment of serum calcitriol(8.37¡Ó0.46 vs 14.74¡Ó0.63 pg/ml, p¡Õ0.001) and CT levels(57.6¡Ó7.6 vs 79.3¡Ó7.7 pg/ml, p¡Õ0.05). In calcitriol nonresponders, there was also a significant increment of serum calcitriol(10.26¡Ó0.68 vs 16.18¡Ó1.11 pg/ml, p¡Õ0.01)in parallel with a significant increase in serum ICa(1.14¡Ó0.03 vs 1.26¡Ó0.03 mmol/l, p¡Õ0.01) and CT levels(49.6¡Ó9.2 vs 74.6¡Ó8.7 pg/ml, p¡Õ0.05). Since chronic hypercalcemia does not stimulate CT secretion, we conclude that calcitriol supplement enhances the CT secretion in uremic patients with 2oHPT probably via its stimulatory action on calcitrion receptors on the C-cells. |
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