医学
继发性甲状旁腺功能亢进
帕利骨化醇
骨化三醇
高磷血症
维生素D与神经学
甲状旁腺功能亢进
内分泌学
内科学
维生素D缺乏
钙
骨化三醇受体
甲状旁腺激素
塞维莱默
作者
Tadao Akizawa,Motohiro Kamimura,Masahide Mizobuchi,Kazuhiro Shiizaki,Shinji Sumikado,Toshibumi Sakaguchi,Shigeo Negi,Etsuro Ogata,Eriko Kinugasa
出处
期刊:Nephrology
[Wiley]
日期:2003-10-01
卷期号:8 (s2)
被引量:11
标识
DOI:10.1046/j.1440-1797.8.s.9.x
摘要
SUMMARY: Hyperphosphatemia, vitamin D deficiency, and resulted hypocalcemia have been regarded as classical pathogeneses of secondary hyperparathyroidism. These factors have been treated by the administration of phosphorus binder and vitamin D derivatives. However, these therapies have not brought about a successful result for the prevention and treatment of secondary hyperparathyroidism. The reason could be mainly attributed to the hypercalcemia that results from the administration of calcium salts as a phosphorus binder and the calcemic action of vitamin D. To prevent hypercalcemia, non‐calcium containing phosphorus binder (sevelamer hydrochloride) and vitamin D analogues, which suppress PTH secretion with minimum calcemic action, have been developed. These new vitamin D analogues include 19‐nor‐1‐alpha, 25‐dihydroxyvitamin D2 (paricalcitol), 1‐alpha‐hydroxyvitamin D2 (doxercalciferol), 22oxa‐calcitriol (maxacalcitol) and F6‐calcitriol (falecalcitriol). Furthermore, calcimimetics that stimulate calcium‐sensing receptor of parathyroid cells as calcium and suppress PTH secretion are now under clinical trial. Percutaneous direct injection therapy of vitamin D, vitamin D analogue or calcimimetics into parathyroid gland has also been reported. The combination of these new strategies is expected to effectively and safely suppresses secondary hyperparathyroidism that has been resistant to conventional medical treatments.
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