Intravenous calcitriol therapy in an early stage prevents parathyroid gland growth.
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.
Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Higashi-Ku, Fukuoka 812-8582, Japan. masatomo@kcu.med.kyushu-u.ac.jp
Masatomo
M
Taniguchi
Masanori
M
Tokumoto
Kazuhiko
K
Tsuruya
Hideki
H
Hirakata
Mitsuo
M
Iida
D000284:Administration, Oral; D000368:Aged; D001842:Bone and Bones / Q000378:metabolism; D002117:Calcitriol / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D002118:Calcium / Q000097:blood; D024042:Collagen Type I / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D005260:Female; D006801:Humans; D006962:Hyperparathyroidism, Secondary / Q000209:etiology / Q000473:pathology / Q000517:prevention & control*; D006965:Hyperplasia / Q000517:prevention & control; D007275:Injections, Intravenous; D008137:Longitudinal Studies; D008297:Male; D008875:Middle Aged; D010280:Parathyroid Glands / Q000000981:diagnostic imaging / Q000187:drug effects / Q000473:pathology*; D010281:Parathyroid Hormone / Q000097:blood; D010455:Peptides / Q000378:metabolism; D010758:Phosphorus / Q000097:blood; D006435:Renal Dialysis; D051437:Renal Insufficiency / Q000150:complications* / Q000628:therapy; D014463:Ultrasonography; D014807:Vitamin D / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*
D024042:Collagen Type I; D010281:Parathyroid Hormone; D010455:Peptides; C052929:collagen type I trimeric cross-linked peptide; D014807:Vitamin D; D010758:Phosphorus; D002117:Calcitriol; D002118:Calcium