title: Efficacy of calcitriol in treating glucocorticoidinduced osteoporosis in patients with nephrotic syndrome: an open-label, randomized controlled study.
abstract: OBJECTIVE
  To evaluate the efficacy and safety of calcitriol in the prevention and treatment of glucocorticoid-induced osteoporosis.
  
  
  METHODS
  66 patients treated with glucocorticoids (GC) for primary nephrotic syndrome (NS) were randomly assigned to 3 groups. Groups were designated as follows: calcitriol alone (n = 22), calcitriol plus calcium carbonate (n = 23), or calcium carbonate alone (n = 21). Serum markers of bone metabolism and bone mineral density (BMD) were tested at 3 different time points: the initiation of GC treatment (baseline), 12 weeks, and 24 weeks after the initiation of treatment.
  
  
  RESULTS
  Levels of serum 25-hydroxy vitamin D, serum osteocalcin, and total serum collagen type N-terminal extension of the peptide were significantly decreased following GC therapy (p < 0.05). β-collagen serum-specific sequences were significantly increased following GC therapy. The above-mentioned changes were less dramatic in patients treated with calcitriol, although the differences were significant (p < 0.05). Changes in serum levels of calcium, phosphorus, alkaline phosphatase, and parathyroid hormone (PTH) were not significant. 24 weeks after the initiation of treatment, BMD of the lumbar spine and femoral bone significantly decreased in all of 3 groups. However, patients who received calcitriol had significantly higher BMD of the lumbar spine than patients who received calcium carbonate alone (calcitriol plus calcium carbonate vs. calcium carbonate alone: 0.82 ± 0.19 g/cm2 vs. 0.62 ± 0.23 g/cm2 p < 0.05; calcitriol vs. calcium carbonate alone 0.805 ± 0.203 g/cm2 vs. 0.615 ± 0.225 g/cm2 p < 0.05), respectively. No serious adverse events were observed.
  
  
  CONCLUSIONS
  Calcitriol may be more effective than calcium carbonate in preventing and treating GC-induced osteoporosis in patients with NS.
authors.forename: Yi
authors.initials: Y
authors.lastname: Chen
authors.forename: Jian-Xin
authors.initials: JX
authors.lastname: Wan
authors.forename: De-Wen
authors.initials: DW
authors.lastname: Jiang
authors.forename: Bin-Bin
authors.initials: BB
authors.lastname: Fu
authors.forename: Jiong
authors.initials: J
authors.lastname: Cui
authors.forename: Gui-Fen
authors.initials: GF
authors.lastname: Li
authors.forename: Cai-Ming
authors.initials: CM
authors.lastname: Chen
mesh_terms: D000328:Adult; D000469:Alkaline Phosphatase / Q000097:blood; D015519:Bone Density / Q000187:drug effects; D002117:Calcitriol / Q000009:adverse effects / Q000627:therapeutic use*; D002119:Calcium Carbonate / Q000627:therapeutic use; D005260:Female; D005938:Glucocorticoids / Q000009:adverse effects*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009404:Nephrotic Syndrome / Q000188:drug therapy*; D015675:Osteocalcin / Q000097:blood; D010024:Osteoporosis / Q000139:chemically induced / Q000188:drug therapy*; D010281:Parathyroid Hormone / Q000097:blood; D014807:Vitamin D / Q000031:analogs & derivatives / Q000097:blood
chemical_list: D005938:Glucocorticoids; D010281:Parathyroid Hormone; D015675:Osteocalcin; D014807:Vitamin D; C104450:25-hydroxyvitamin D; D000469:Alkaline Phosphatase; D002117:Calcitriol; D002119:Calcium Carbonate