title: Differential effects of very high doses of doxercalciferol and paricalcitol on serum phosphorus in hemodialysis patients.
abstract: BACKGROUND
  Treatment of secondary hyperparathyroidism (SHPT) includes use of calcitriol (1,25D(3)) to suppress parathyroid hormone (PTH), but dosing of 1,25D(3) is limited by the development of hypercalcemia and a high calcium x phosphorus (Ca x P) product due to gut absorption of calcium and phosphorus as well as enhanced bone resorption. The vitamin D analog 19-Nor-1,25(OH)2-vitamin D2 (paricalcitol) and the prohormone 1alpha-OH-vitamin D2 (doxercalciferol) have been proposed as alternatives which may cause less hypercalcemia and elevated Ca x P, while still suppressing PTH.
  
  
  METHODS
  We performed a prospective study to assess the acute bone mobilization effects of very high doses of paricalcitol and doxercalciferol. 13 hemodialysis patients received 160 mcg of paricalcitol and 120 mcg of doxercalciferol on 2 separate occasions in a research center while on a low calcium, low phosphorus diet, and sevelamer alone as a phosphorus binder. Changes in Ca, PO4, and PTH were measured over 36 h.
  
  
  RESULTS
  Serum phosphorus rose faster, and peaked significantly higher at 36 h following doxercalciferol (2.12 +/- 0.11 mmol/l) than paricalcitol (1.85 +/- 0.07 mmol/l; p = 0.025). Ca x P product also rose more following doxercalciferol than paricalcitol, and peaked higher at 36 h (5.02 +/- 0.26 vs. 4.54 +/- 0.21 mmol/l; p = 0.061). In contrast, suppression of PTH at 36 h was comparable (63% after paricalcitol and 65% with doxercalciferol).
  
  
  CONCLUSIONS
  Consistent with animal studies, paricalcitol provides profound PTH suppression, while stimulating bone resorption and/or intestinal absorption less than doxercalciferol, resulting in less elevation of serum phosphorus and Ca x P.
authors.affiliation: Renal Division, Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
authors.forename: H E
authors.initials: HE
authors.lastname: Joist
authors.forename: S N
authors.initials: SN
authors.lastname: Ahya
authors.forename: K
authors.initials: K
authors.lastname: Giles
authors.forename: K
authors.initials: K
authors.lastname: Norwood
authors.forename: E
authors.initials: E
authors.lastname: Slatopolsky
authors.forename: D W
authors.initials: DW
authors.lastname: Coyne
mesh_terms: D000328:Adult; D000368:Aged; D050071:Bone Density Conservation Agents / Q000008:administration & dosage; D002118:Calcium / Q000097:blood; D004872:Ergocalciferols / Q000008:administration & dosage*; D005260:Female; D006801:Humans; D006962:Hyperparathyroidism, Secondary / Q000097:blood / Q000188:drug therapy / Q000209:etiology; D007676:Kidney Failure, Chronic / Q000097:blood / Q000150:complications / Q000628:therapy; D008297:Male; D008875:Middle Aged; D010758:Phosphorus / Q000097:blood*; D011446:Prospective Studies; D006435:Renal Dialysis
chemical_list: D050071:Bone Density Conservation Agents; D004872:Ergocalciferols; D010758:Phosphorus; C042533:1 alpha-hydroxyergocalciferol; C084656:paricalcitol; D002118:Calcium