TY - JOUR
T1 - New strategies for the treatment of secondary hyperparathyroidism
AU - Akizawa, Tadao
AU - Shiizaki, Kazuhiro
AU - Hatamura, Ikuji
AU - Kamimura, Motohiro
AU - Mizobuchi, Masahide
AU - Narukawa, Nobuhiko
AU - Sumikado, Shinji
AU - Sakaguchi, Toshibumi
AU - Negi, Shigeo
AU - Ogata, Hiroaki
AU - Kinugasa, Eriko
N1 - Funding Information:
We acknowledge the Commemorative Association for the Japan World Exposition (1970), Japanese Association of Dialysis Physicians, Osaka Pharmaceutical Manufacturers Association, and the Pharmaceutical Manufacturers Association of Tokyo for financial support to publish this supplement.
Copyright:
Copyright 2018 Elsevier B.V., All rights reserved.
PY - 2003/3/1
Y1 - 2003/3/1
N2 - 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.
AB - 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.
KW - Calcimimetics
KW - Chronic renal failure (CRF)
KW - Maxacalcitol
KW - Percutaneous calcitriol analogue injection
KW - Phosphorus binder
KW - Secondary hyperparathyroidism (2HPT)
KW - Vitamin D analogue
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U2 - 10.1053/ajkd.2003.50095
DO - 10.1053/ajkd.2003.50095
M3 - Article
C2 - 12612963
AN - SCOPUS:0037374519
SN - 0272-6386
VL - 41
SP - S100-S103
JO - American Journal of Kidney Diseases
JF - American Journal of Kidney Diseases
IS - 3 SUPPL. 1
ER -