Comparison of oral falecalcitriol and intravenous calcitriol in hemodialysis patients with secondary hyperparathyroidism: a randomized, crossover trial.
BACKGROUND
Falecalcitriol is a novel vitamin D analog, which has a greater potential to suppress parathyroid hormone (PTH) and a longer half-life. There are few studies to compare clinical effects of oral falecalcitriol treatment with those of intravenous calcitriol treatment.


METHODS
Twenty-one patients with moderate to severe SHPT were included in a random 2 x 2 crossover trial with the two vitamin D analogs (12 weeks for each treatment). The primary endpoint measure was a decrease in serum intact PTH (iPTH) level, and the secondary outcome measures included changes in serum calcium (Ca), phosphate (P), and metabolic bone marker levels.


RESULTS
Both treatments decreased iPTH and whole PTH (wPTH) levels by similar degrees (iPTH, -200.1 +/- 107.0 with falecalcitriol vs. -200.8 +/- 114.9 pg/ml with calcitriol, p = 0.9895; wPTH, -137.1 +/- 73.1 with falecalcitriol vs. -120.4 +/- 81.1 pg/ml with calcitriol, p = 0.5603). Serum Ca, P, and Ca x P product levels at the end of each treatment were comparable and the frequencies of hypercalcemia and hyperphosphatemia were also similar during each treatment period. Although intravenous calcitriol treatment significantly changed intact osteocalcin and cross-linked N-telopeptide of type I collagen after 12 weeks, oral falecalcitriol treatment did not change any bone metabolic marker level.


CONCLUSIONS
The present study showed that oral falecalcitriol treatment is effective for PTH suppression, and Ca and P metabolism in hemodialysis patients with moderate to severe SHPT, as well as intravenous calcitriol administration.
Ito
H
H
Department of Internal Medicine, Showa University Northern Yokohama Hospital, Yokohama, Japan.
Ogata
H
H
Yamamoto
M
M
Takahashi
K
K
Shishido
K
K
Takahashi
J
J
Taguchi
S
S
Kinugasa
E
E
D000284:Administration, Oral; D000469:Alkaline Phosphatase / Q000097:blood; D015415:Biomarkers / Q000097:blood; D050071:Bone Density Conservation Agents / Q000008:administration & dosage*; D001842:Bone and Bones / Q000187:drug effects / Q000378:metabolism; D002117:Calcitriol / Q000008:administration & dosage* / Q000031:analogs & derivatives*; D002118:Calcium / Q000097:blood; D024042:Collagen Type I / Q000097:blood / Q000187:drug effects; D018592:Cross-Over Studies; D005260:Female; D006801:Humans; D006962:Hyperparathyroidism, Secondary / Q000188:drug therapy* / Q000209:etiology; D007275:Injections, Intravenous; D007676:Kidney Failure, Chronic / Q000628:therapy; D008297:Male; D008875:Middle Aged; D015675:Osteocalcin / Q000097:blood / Q000187:drug effects; D010281:Parathyroid Hormone / Q000097:blood; D010455:Peptides / Q000097:blood / Q000187:drug effects; D010758:Phosphorus / Q000097:blood; D006435:Renal Dialysis / Q000009:adverse effects; D016896:Treatment Outcome; D005466:Fluorocarbons
D000469:Alkaline Phosphatase; D015415:Biomarkers; D050071:Bone Density Conservation Agents; D002117:Calcitriol; D002118:Calcium; D024042:Collagen Type I; D015675:Osteocalcin; D010281:Parathyroid Hormone; D010455:Peptides; D010758:Phosphorus; C052929:collagen type I trimeric cross-linked peptide; C040488:26,26,26,27,27,27-hexafluoro-1,25-dihydroxyvitamin D3; D005466:Fluorocarbons