Comparison of the efficacy of an oral calcitriol pulse or intravenous 22-oxacalcitriol therapies in chronic hemodialysis patients.
BACKGROUND
1,25-dihydroxy-22-ovavitamin D(3) (22-oxacalcitriol, OCT) was recently introduced commercially as an analogue of 1,25 (OH)(2) vitamin D(3), but one which has less pronounced calcemic activity.


METHODS
To examine the efficacy and tolerability of OCT, 46 hemodialysis patients with secondary hyperparathyroidism were randomly assigned to receive either intravenous OCT or oral calcitriol pulse therapies. The patients were monitored for serum calcium, phosphate, intact parathyroid hormone (PTH), and bone alkaline phosphatase (BAP) for 24 weeks. The efficacy of intravenous OCT was also examined in 24 additional patients who were refractory to oral calcitriol pulse therapy.


RESULTS
In the randomized trial, intact PTH levels were significantly suppressed within 4 weeks after the initiation of each therapy, and this effect was well maintained thereafter in both treatment groups. While intact PTH was significantly lower at 4 weeks in the calcitriol pulse group than in the OCT group (P = 0.02), no statistical differences were observed during later treatment periods. BAP was reduced equally by each treatment. At 4 weeks (P = 0.02) and thereafter (P = 0.06), serum calcium was higher among calcitriol-treated patients than among those who received OCT treatment. Eight of 24 patients who were refractory to oral calcitriol pulse therapy responded to intravenous OCT. The patients who responded tended to have lower serum intact PTH and phosphorus levels and smaller parathyroid glands at the start of OCT treatment than nonresponders.


CONCLUSIONS
OCT is as effective as oral calcitriol pulse therapy in suppressing intact PTH and BAP in chronic hemodialysis patients. It was confirmed that OCT exhibits less calcemic activity than calcitriol. Moreover, under certain conditions, switching to OCT may help in the treatment of hyperparathyroidism, which is refractory to conventional oral calcitriol pulse therapy.
Tamura
Shigeo
S
Department of Medicine and Clinical Science, Gunma University Graduate School of Medicine, 3-39-15 Showa-machi, Maebashi, Gunma, 371-8511, Japan. kueki@showa.gunma-u.ac.jp
Ueki
Kazue
K
Mashimo
Keiichi
K
Tsukada
Yoshito
Y
Naitoh
Miyuki
M
Abe
Yukiko
Y
Kawai
Hironobu
H
Tsuchida
Akiyasu
A
Wakamatsu
Ryoji
R
Nojima
Yoshihisa
Y
D000284:Administration, Oral; D000368:Aged; D000469:Alkaline Phosphatase / Q000097:blood; D001842:Bone and Bones / Q000201:enzymology; D002117:Calcitriol / Q000008:administration & dosage* / Q000009:adverse effects / Q000031:analogs & derivatives*; D002118:Calcium / Q000097:blood; D005260:Female; D006801:Humans; D006934:Hypercalcemia / Q000139:chemically induced; D006962:Hyperparathyroidism, Secondary / Q000188:drug therapy / Q000517:prevention & control*; D007275:Injections, Intravenous; D008297:Male; D008875:Middle Aged; D010281:Parathyroid Hormone / Q000097:blood; D020551:Pulse Therapy, Drug; D006435:Renal Dialysis / Q000009:adverse effects
D010281:Parathyroid Hormone; D000469:Alkaline Phosphatase; D002117:Calcitriol; C051883:maxacalcitol; D002118:Calcium