Effect of 22-oxacalcitriol on hyperparathyroidism of dialysis patients: results of a preliminary study.

نویسندگان

  • K Kurokawa
  • T Akizawa
  • M Suzuki
  • T Akiba
  • E Ogata
  • E Slatopolsky
چکیده

Intermittent high dose administration of calcitriol or alfacalcidol is effective in suppressing secondary hyperparathyroidism in chronic dialysis patients, however calcaemic action of these vitamin D derivatives is a major obstacle. 22-Oxacalcitriol (OCT) has been reported to have less calcaemic action than calcitriol, while preserving a comparable suppressive effect on parathyroid hormone (PTH) secretion. This preliminary study was conducted to examine the effects of OCT on secondary hyperparathyroidism in chronic dialysis patients. OCT was administrated intravenously immediately after every haemodialysis session three times a week for 12 weeks to three haemodialysis patients with secondary hyperparathyroidism. An initial dose of OCT of 5.5 micrograms/haemodialysis session was increased stepwise by 5.5 micrograms/haemodialysis up to 22 micrograms/haemodialysis according to the suppression of PTH and calcaemic action. OCT was discontinued for at least a week when serum calcium adjusted to albumin concentration measured just before haemodialysis exceeded 11.5 mg/dl. Marked reduction in plasma PTH, alkaline phosphatase and tartrate-resistant acid phosphatase was observed in all three patients. Although the dose of OCT was increased to 22 micrograms/haemodialysis in one patient, the final dose of OCT remained 5.5 micrograms/haemodialysis in the other two patients because of hypercalcaemia. It is concluded that OCT is highly effective in suppressing PTH in dialysis patients with secondary hyperparathyroidism. Hypercalcaemia may be a major factor which limits the use of OCT, though it may occur with higher doses of OCT than those of calcitriol usually given to suppress PTH hypersecretion.

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عنوان ژورنال:
  • Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association

دوره 11 Suppl 3  شماره 

صفحات  -

تاریخ انتشار 1996