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NDT Advance Access published online on May 30, 2008

Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfn264
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© The Author [2008].
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions@oxfordjournals.org



Intravenous calcitriol therapy in an early stage prevents parathyroid gland growth

Masatomo Taniguchi1, Masanori Tokumoto1, Kazuhiko Tsuruya1,2, Hideki Hirakata3 and Mitsuo Iida1

1 Department of Medicine and Clinical Science 2 Department of Integrated Therapy for Chronic Kidney Disease, Graduate School of Medical Sciences, Kyushu University 3 Department of Nephrology, Fukuoka Red Cross Hospital, Fukuoka, Japan

Correspondence and offprint requests to: Masatomo Taniguchi, Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Maidashi 3-1-1, Higashi-Ku, Fukuoka 812-8582, Japan. Tel: +81-92-642-5843; Fax: +81-92-642-5846; E-mail: masatomo{at}kcu.med.kyushu-u.ac.jp



  Abstract

Background. Both the phenotypic alterations of parathyroid (PT) cells, e.g. down-regulation of the calcium-sensing receptor, and the increase of the PT cell number in nodular hyperplasia are the main causes of refractory secondary hyperparathyroidism. It is of great importance to prevent PT growth in an early stage.

Methods. To examine a more effective method of calcitriol therapy for the prevention of PT hyperplasia, we randomized haemodialysis patients with mild hyperparathyroidism to receive either daily orally administered calcitriol (n = 33) or intravenous calcitriol (n = 27) over a 12-month study period. Calcitriol was modulated so as to keep the serum intact PTH level between 100 and 150 pg/ml.

Results. Both groups showed similar reductions of the serum PTH level and similar increases in serum calcium. In both groups, there were no significant changes in the serum phosphate level. Long-term daily oral calcitriol therapy failed to prevent the increase of both maximum PT volume and total volume, as assessed by ultrasonography; however, intravenous calcitriol therapy successfully suppressed this progression. In the daily, oral group, both the bone-specific alkaline phosphatase (BAP) and the N-telopeptide cross-linked of type I collagen (NTX) significantly decreased, which was probably due to the PTH suppression. However, these bone metabolism markers remained stable in the intravenous group. The total dosage of calcitriol during the study was comparable in both groups.

Conclusions. These data indicate that intravenous calcitriol therapy in an early stage of secondary hyperparathyroidism is necessary to prevent PT growth and to keep a good condition of bone metabolism.

Keywords: calcium; calcitriol; growth; parathyroid; phosphate

Received for publication: 13. 2.08
Accepted in revised form: 17. 4.08


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[Abstract] [Full Text] [PDF]



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