MARKED SUPPRESSION OF SECONDARY HYPERPARATHYROIDISM BY INTRAVENOUS ADMINISTRATION OF 1,25-DIHYDROXYCHOLECALCIFEROL IN UREMIC PATIENTS
MARKED SUPPRESSION OF SECONDARY HYPERPARATHYROIDISM BY INTRAVENOUS ADMINISTRATION OF 1,25-DIHYDROXYCHOLECALCIFEROL IN UREMIC PATIENTS
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DOI：
10.1172/jci111639
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发表时间：
1984-01-01
影响因子：
15.9
通讯作者：
MARTIN, KJ
中科院分区：
文献类型：
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作者：
SLATOPOLSKY, E;WEERTS, C;MARTIN, KJ
目前的证据表明，对慢性肾功能不全患者给予1,25(OH)2D3[1,25-二羟基胆钙化醇]，只有在发生高钙血症时才会抑制继发性甲状旁腺功能亢进。由于甲状旁腺具有1,25(OH)2D3和钙结合蛋白的特异性受体，因此人们对1,25(OH)2D3对甲状旁腺激素（PTH）分泌的可能的直接影响非常感兴趣，而不依赖于血清钙的变化。最近的发现表明，1,25(OH)2D3在肠道中大量降解，因此，有可能口服维生素D代谢物增加肠道钙吸收，1,25(OH)2D3向外周靶器官的递送可能受到限制。比较口服和静脉注射1,25(OH)2D3对血浆1,25(OH)2D3水平的影响及两种治疗方式对甲状旁腺激素分泌的影响。然而，口服125 (OH)2D3剂量足以维持血清钙在正常上限，并没有改变甲状旁腺激素水平，显著抑制（70.1 .+-）。在所有给予静脉注射1,25(OH)2D3的20例患者中，PTH水平升高3.2%。时间研究显示20.1 .+-。注射1,25(OH)2D3后，甲状旁腺激素降低5.2%，血清钙含量无明显变化。5例患者口服碳酸钙后血清钙升高，血清i-甲状旁腺激素仅下降25 +-。6.65%与73.5 .+-。给药1,25(OH)2D3获得5.08% （P < 0.001）。因此，通过静脉注射125 (OH)2D3而不是碳酸钙获得的类似血清钙对甲状旁腺激素释放的抑制作用更大。1,25(OH)2D3静脉注射比口服可能导致更多的维生素D代谢物递送到外周目标组织而不是肠道，并允许在外周组织中更好地表达1,25(OH)2D3的生物效应。因此，使用i.v. 1,25(OH)2D3为抑制透析患者继发性甲状旁腺功能亢进提供了一种简单而极其有效的方法。
Current evidence suggests that administration of 1,25(OH)2D3 [1,25-dihydroxycholecalciferol] to patients with chronic renal insufficiency results in suppression of secondary hyperparathyroidism only if hypercalcemia occurs. Since the parathyroid glands possess specific receptors for 1,25(OH)2D3 and a Ca binding protein, there is considerable interest in a possible direct effect of 1,25(OH)2D3 on parathyroid hormone (PTH) secretion independent of changes in serum Ca. Recent findngs indicate substantial degradation of 1,25(OH)2D3 in the intestine, therefore, it is possible that while oral administration of the vitamin D metabolite increases intestinal Ca absorption, the delivery of 1,25(OH)2D3 to peripheral target organs may be limited. The effects of orally or i.v. 1,25(OH)2D3 on the plasma levels of 1,25(OH)2D3 and the effects of these 2 modes of treatment on PTH secretion were compared. Whereas oral administration of 1,25(OH)2D3 in doses adequate to maintain serum Ca at the upper limits of normal did not alter PTH levels, a marked suppression (70.1 .+-. 3.2%) of PTH levels was seen in all 20 patients given i.v. 1,25(OH)2D3. Temporal studies suggested a 20.1 .+-. 5.2% decrease in PTH without a significant change in serum Ca with i.v. 1,25(OH)2D3. In 5 patients the serum Ca was increased by the oral administration of calcium carbonate, the decrement in serum i-PTH was only 25 .+-. 6.65% when compared with 73.5 .+-. 5.08% (P < 0.001) obtained by the administration of i.v. 1,25(OH)2D3. Thus, a similar serum Ca achieved by i.v. 1,25(OH)2D3 rather than calcum carbonate has a greater suppressive effect in the release of PTH. 1,25(OH)2D3 administered i.v. rather than orally may result in a greater delivery of the vitamin D metabolite to peripheral target tissues other than the intestine and allow a greater expression of biological effects of 1,25(OH)2D3 in peripheral tissues. The use of i.v. 1,25(OH)2D3 thus provides a simple and extremely effective way to suppress secondary hyperparathyroidism in dialysis patients.