title: Prevention of corticosteroid osteoporosis. A comparison of calcium, calcitriol, and calcitonin.
abstract: BACKGROUND
  Prolonged corticosteroid therapy increases the risk of osteoporosis and fracture. We studied whether corticosteroid-induced osteoporosis could be prevented by treatment with calcium, calcitriol (1,25-dihydroxyvitamin D3), and calcitonin.
  
  
  METHODS
  One hundred three patients starting long-term corticosteroid therapy were randomly assigned to receive 1000 mg of calcium per day orally and either calcitriol (0.5 to 1.0 microgram per day orally) plus salmon calcitonin (400 IU per day intranasally), calcitriol plus a placebo nasal spray, or double placebo for one year. Data on treatment efficacy were available for 92 of these patients. Bone density was measured every four months for two years by photon absorptiometry. There were no significant differences between groups with respect to age, underlying disease, initial bone density, or corticosteroid dose during the first year.
  
  
  RESULTS
  Calcitriol (mean dose, 0.6 microgram per day), with or without calcitonin, prevented more bone loss from the lumbar spine (mean rates of change, -0.2 and -1.3 percent per year, respectively) than calcium alone (-4.3 percent per year, P = 0.0035). Bone loss at the femoral neck and distal radius was not significantly affected by any treatment. In the second year, lumbar bone loss did not occur in the group previously treated with calcitonin plus calcitriol (+0.7 percent per year), but it did occur in the group given calcium alone (-2.3 percent per year). The calcitriol group also lost lumbar bone (-3.6 percent per year) but received more corticosteroid in the second year than the other two groups.
  
  
  CONCLUSIONS
  Calcitriol and calcium, used prophylactically with or without calcitonin, prevent corticosteroid-induced bone loss in the lumbar spine.
authors.affiliation: Bone and Mineral Research Division, Garvan Institute of Medical Research, St. Vincent's Hospital, Darlinghurst, N.S.W., Australia.
authors.forename: P
authors.initials: P
authors.lastname: Sambrook
authors.forename: J
authors.initials: J
authors.lastname: Birmingham
authors.forename: P
authors.initials: P
authors.lastname: Kelly
authors.forename: S
authors.initials: S
authors.lastname: Kempler
authors.forename: T
authors.initials: T
authors.lastname: Nguyen
authors.forename: N
authors.initials: N
authors.lastname: Pocock
authors.forename: J
authors.initials: J
authors.lastname: Eisman
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D015519:Bone Density; D002116:Calcitonin / Q000097:blood / Q000627:therapeutic use*; D002117:Calcitriol / Q000097:blood / Q000627:therapeutic use*; D002118:Calcium / Q000097:blood / Q000627:therapeutic use*; D004311:Double-Blind Method; D005260:Female; D005938:Glucocorticoids / Q000009:adverse effects*; D006801:Humans; D007154:Immune System Diseases / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology; D008171:Lung Diseases / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D010024:Osteoporosis / Q000139:chemically induced / Q000378:metabolism / Q000517:prevention & control*; D012216:Rheumatic Diseases / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology
chemical_list: D005938:Glucocorticoids; D002116:Calcitonin; D002117:Calcitriol; D002118:Calcium