Brandi L, Daugaard H, Tvedegaard E, Storm T, Olgaard K
Medical Department P, Rigshospitalet, Copenhagen, Denmark.
Nephron. 1989;53(3):194-200. doi: 10.1159/000185744.
The effect of intravenous 1 alpha(OH)D3 on circulating intact parathyroid hormone (PTH) and COOH-terminal immunoreactive PTH was examined in 21 patients on chronic hemodialysis. The patients were treated for 3 months with increasing doses of 1 alpha(OH)D3 under careful control of serum Ca2+. 1 alpha(OH)D3 was given intravenously at doses of up to 4 micrograms three times a week, and blood samples were obtained every week, including 1 week before treatment (basal control). No patients were treated with oral vitamin D metabolites. At the end of the study intact PTH levels were reduced by an average of 67 +/- 6%, and COOH-terminal immunoreactive PTH levels were reduced by 35 +/- 6%. Serum Ca2+ was kept within normal levels, but showed a slight increase from 1.17 to 1.30 mmol/l. An effect of calcium on PTH secretion could not be excluded, but an effect of 1 alpha(OH)D3, independent of serum Ca2+ was also found. This effect may be mediated by 1,25(OH)2D3, assuming a large capacity of the 25-hydroxylase in the liver to convert 1 alpha(OH)D3 to 1,25(OH)2D3. Also, the parathyroid glands may possess receptors for 1 alpha(OH)D3 with an effect similar to that established for the 1,25(OH)2D3 receptors. Thus, although the exact mechanisms of the action of 1 alpha(OH)D3 have not yet been completely clarified, it is concluded that intravenous administration of 1 alpha(OH)D3 may be of benefit in the treatment of secondary hyperparathyroidism of uremia.
在21例慢性血液透析患者中，研究了静脉注射1α(OH)D3对循环中完整甲状旁腺激素（PTH）和羧基末端免疫反应性PTH的影响。在血清Ca2+的仔细监测下，患者接受了3个月递增剂量的1α(OH)D3治疗。1α(OH)D3静脉注射剂量高达每周三次，每次4微克，每周采集血样，包括治疗前1周（基础对照）。所有患者均未接受口服维生素D代谢物治疗。研究结束时，完整PTH水平平均降低67±6%，羧基末端免疫反应性PTH水平降低35±6%。血清Ca2+维持在正常水平，但从1.17 mmol/l略有升高至1.30 mmol/l。不能排除钙对PTH分泌的影响，但也发现了1α(OH)D3独立于血清Ca2+的作用。假设肝脏中的25-羟化酶有很大能力将1α(OH)D3转化为1,25(OH)2D3，这种作用可能由1,25(OH)2D3介导。此外，甲状旁腺可能具有1α(OH)D3受体，其作用类似于已确定的1,25(OH)2D3受体。因此，尽管1α(OH)D3的确切作用机制尚未完全阐明，但得出结论，静脉注射1α(OH)D3可能有助于治疗尿毒症继发性甲状旁腺功能亢进。
