Calcitriol oral therapy for the prevention of secondary hyperparathyroidism in patients with predialytic renal failure.
Calcitriol oral therapy for the prevention of secondary hyperparathyroidism in patients with predialytic renal failure.
复制标题
骨化三醇口服疗法用于预防透析前肾衰竭患者继发性甲状旁腺功能亢进症。
DOI：
10.1007/s40278-016-23775-4
复制
发表时间：
1998
影响因子：
1.1
通讯作者：
R. Palla
中科院分区：
文献类型：
--
作者：
V. Panichi;B. Andreini;S. De Pietro;M. Migliori;D. Taccola;L. Giovannini;M. Ferdeghini;R. Palla
继发性甲状旁腺功能亢进是慢性肾功能衰竭的共同特征，维生素D缺乏在这种异常的发展中起着重要作用。几种治疗骨化三醇方案已用于治疗尿毒症甲状旁腺功能亢进，但最近已提出口服丸剂更有效。在这项研究中，我们比较了三种不同的口服骨化三醇方案在抑制透析前慢性肾衰竭中iPTH分泌的功效。16例患者（平均年龄51 +/- 16岁；肌酐清除率22.9 +/- 9.8 ml；范围8-32 ml/min）采用交叉随机设计，每日口服骨化三醇0.5微克/例（治疗a），每周口服3次骨化三醇2微克（治疗B），每周口服1次骨化三醇2微克（治疗C）。所有治疗期持续三个月，然后是一个月的洗脱期。每两周检测血清iPTH （Allegro Nichols）、1-25维生素D （IRMA-MAB）、总钙和离子钙（Nova 8 Pabish）、血清磷酸盐、碱性磷酸酶和肌酐清除率。对照组15例患者（平均年龄47 +/-12岁，肌酐清除率21 +/-12 ml/min）在没有骨化三醇治疗的情况下观察3个月，同时测定血清iPTH。每日口服0.5微克骨化三醇可防止iPTH升高而不引起高钙血症，但只有口服剂量（B和C）可降低iPTH：从270 +/- 169 pg/ml降至135 +/- 76 pg/ml （p < 0.01； B）和165 +/- 121 pg/ml （p < 0.05； C）。血清iPTH由293 +/- 121升高至323 +/- 129 pg/ml （p = ns）。在不同的研究期间，肾功能没有明显的差异。我们的研究结果证实了多次骨化三醇口服丸剂的良好疗效，但也首次建议每周一次丸剂作为治疗透析前肾功能衰竭继发性甲状旁腺功能亢进的可靠方法。
Secondary hyperparathyroidism is a common feature of chronic renal failure and vitamin D deficiency plays an important role in the development of this abnormality. Several therapeutical calcitriol schedules have been used in treating uremic hyperparathyroidism but recently oral boluses have been proposed as more effective. In this study we compare the efficacy of three different oral calcitriol regimens in suppressing iPTH secretion in predialytic chronic renal failure. Sixteen (16) patients (mean age 51 +/- 16 years; creatinine clearance 22.9 +/- 9.8 ml; range 8-32 ml/min) were treated in a cross-over randomized design with oral daily calcitriol 0.5 micrograms/die (Treatment A), three oral boluses of 2 micrograms of calcitriol a week (Treatment B) and a single oral bolus of 2 micrograms of calcitriol a week (Treatment C). All treatment periods lasted three months and were followed by a wash-out period of one month. Serum iPTH (Allegro Nichols), 1-25 vitamin D (IRMA-MAB), total and ionized calcium (Nova 8 Pabish), serum phosphate, alkaline phosphatase and creatinine clearance were measured every two weeks. Serum iPTH was also determined in a control group of fifteen (15) patients (mean age 47 +/- 12 years, creatinine clearances of 21 +/-12 ml/min) observed for three months without calcitriol treatment. Daily oral intake of 0.5 micrograms of calcitriol prevents an increase of iPTH without causing hypercalcemia, but only oral boluses (B and C) decreased iPTH: from 270 +/- 169 pg/ml to 135 +/- 76 pg/ml (p < 0.01; B) and to 165 +/- 121 pg/ml (p < 0.05; C). Serum iPTH increased from 293 +/- 121 to 323 +/- 129 pg/ml (p = n.s.). No significant differences in renal function were observed during the different study periods. Our results confirm the good efficacy of multiple calcitriol oral boluses but also suggest for the first time a single weekly bolus as a reliable approach to the treatment of secondary hyperparathyroidism in pre-dialytic renal failure.