New strategies for the treatment of secondary hyperparathyroidism

Classic pathogeneses of secondary hyperparathyroidism (2HPT), hyperphosphatemia, vitamin D deficiency, and hypocalcemia, have been treated by the administration of phosphorus binders and vitamin D derivatives. However, these therapies have not brought about a successful result. The main reason could...

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Veröffentlicht in:American journal of kidney diseases 2003-03, Vol.41 (3), p.S100-S103
Hauptverfasser: Akizawa, Tadao, Shiizaki, Kazuhiro, Hatamura, Ikuji, Kamimura, Motohiro, Mizobuchi, Masahide, Narukawa, Nobuhiko, Sumikado, Shinji, Sakaguchi, Toshibumi, Negi, Shigeo, Ogata, Hiroaki, Kinugasa, Eriko
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Sprache:eng
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Zusammenfassung:Classic pathogeneses of secondary hyperparathyroidism (2HPT), hyperphosphatemia, vitamin D deficiency, and hypocalcemia, have been treated by the administration of phosphorus binders and vitamin D derivatives. However, these therapies have not brought about a successful result. The main reason could be attributed to hypercalcemia resulting from the administration of calcium salts as a phosphorus binder and the calcemic action of vitamin D. To prevent hypercalcemia, non-calcium-containing phosphorus binders and vitamin D analogues, which suppress parathyroid hormone (PTH) secretion with minimum calcemic action, have been developed. Furthermore, calcimimetics that stimulate the calcium-sensing receptor of parathyroid cells and suppress PTH secretion are now under clinical trial. Direct injection therapy of vitamin D analogues or calcimimetics into the parathyroid gland also has been reported. These new strategies are expected to effectively and safely suppress 2HPT, which has been resistant to conventional medical treatments. Am J Kidney Dis 41(S1):S100-S103. © 2003 by the National Kidney Foundation, Inc.
ISSN:0272-6386
1523-6838
DOI:10.1053/ajkd.2003.50095