» Articles » PMID: 18515308

Intravenous Calcitriol Therapy in an Early Stage Prevents Parathyroid Gland Growth

Overview
Date 2008 Jun 3
PMID 18515308
Citations 2
Authors
Affiliations
Soon will be listed here.
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.

Citing Articles

Comparison of oral and intravenous alfacalcidol in chronic hemodialysis patients.

Lessard M, Ouimet D, LeBlanc M, Nadeau-Fredette A, Bell R, Lafrance J BMC Nephrol. 2014; 15:27.

PMID: 24495277 PMC: 3915223. DOI: 10.1186/1471-2369-15-27.


Vitamin D effects on pregnancy and the placenta.

Shin J, Choi M, Longtine M, Nelson D Placenta. 2010; 31(12):1027-34.

PMID: 20863562 PMC: 2993775. DOI: 10.1016/j.placenta.2010.08.015.

References
1.
Halstead L, Scott M, Rifas L, Avioli L . Characterization of osteoblast-like cells from normal adult rat femoral trabecular bone. Calcif Tissue Int. 1992; 50(1):93-5. DOI: 10.1007/BF00297304. View

2.
Liou H, Chiang S, Huang T, Shieh S, Akmal M . Comparative effect of oral or intravenous calcitriol on secondary hyperparathyroidism in chronic hemodialysis patients. Miner Electrolyte Metab. 1994; 20(3):97-102. View

3.
Canaff L, Hendy G . Human calcium-sensing receptor gene. Vitamin D response elements in promoters P1 and P2 confer transcriptional responsiveness to 1,25-dihydroxyvitamin D. J Biol Chem. 2002; 277(33):30337-50. DOI: 10.1074/jbc.M201804200. View

4.
Akiba T, Kurihara S, Yamada T, Ogasawara M, Yoneshima H, Marumo F . Intravenous calcitriol can increase bone mass in hemodialysis patients with osteitis fibrosa. Miner Electrolyte Metab. 1995; 21(1-3):109-13. View

5.
Tominaga Y, Takagi H . Molecular genetics of hyperparathyroid disease. Curr Opin Nephrol Hypertens. 1996; 5(4):336-41. DOI: 10.1097/00041552-199607000-00008. View