TY - JOUR
T1 - Management of secondary hyperparathyroidism of dialysis patients
AU - Akizawa, Tadao
AU - Kamimura, Motohiro
AU - Mizobuchi, Masahide
AU - Shiizaki, Kazuhiro
AU - Sumikado, Shinji
AU - Sakaguchi, Toshibumi
AU - Negi, Shigeo
AU - Ogata, Hiroaki
AU - Kinugasa, Eriko
N1 - Copyright:
Copyright 2008 Elsevier B.V., All rights reserved.
PY - 2003/10
Y1 - 2003/10
N2 - 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.
AB - 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.
KW - Calcimimetics
KW - Maxacalcitol
KW - Percutaneous intervention therapy
KW - Phosphorus binder
KW - Secondary hyperparathyroidism
KW - Vitamin D
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U2 - 10.1046/j.1440-1797.8.s.9.x
DO - 10.1046/j.1440-1797.8.s.9.x
M3 - Article
C2 - 15012693
AN - SCOPUS:0348224186
SN - 1320-5358
VL - 8
SP - S53-S57
JO - Nephrology
JF - Nephrology
IS - SUPPL.
ER -