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Calcitriol

A Review of its Use in the Treatment of Postmenopausal Osteoporosis and its Potential in Corticosteroid-Induced Osteoporosis

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Abstract

Synopsis

A synthetic form of calcitriol (1,25-dihydroxycholecalciferol; 1,25-dihydroxyvitamin D3), the most physiologically active metabolite of vitamin D, has shown efficacy in the treatment of postmenopausal osteoporosis and promise in corticosteroid-induced osteoporosis. Although results of small studies investigating calcitriol in the treatment of postmenopausal osteoporosis have been conflicting, a clinical trial in 622 women with postmenopausal osteoporosis demonstrated that patients with mild to moderate disease who received calcitriol (0.25μg twice daily) had a significant 3-fold lower rate of new vertebral fractures after 3 years of treatment, compared with patients receiving elemental calcium 1000 mg/day. In patients commencing long term treatment with prednisone or prednisolone, calcitriol 0.5 to 1.0μg/day plus calcium 1000 mg/day, administered with or without intranasal calcitonin 400 IU/day, prevented steroid-induced bone loss.

Overall, calcitriol is well tolerated. As shown in clinical studies, at recommended dosages hypercalcaemia is infrequent and mild, generally responding to reductions in calcium intake and/or calcitriol dosage. The narrow ‘therapeutic window’ of calcitriol requires that its use be adequately supervised, with periodic monitoring of serum calcium and creatinine levels. However, significant renal toxicity has not been seen in patients with osteoporosis treated with calcitriol in high dosages for several years in comparative and noncomparative trials.

In conclusion, as with other drugs currently used in the management of patients with osteoporosis, questions remain to be answered regarding the efficacy of calcitriol relative to other agents, and its tolerability in such patients during the very long term. Nonetheless, at this stage, calcitriol should be considered a useful treatment option in patients with mild to moderate postmenopausal osteoporosis.

Pharmacological Properties

Calcitriol (1,25-dihydroxycholecalciferol; 1,25-dihydroxyvitamin D3) is one of the hormones responsible for calcium homeostasis and mineralisation of the skeleton. As a primary cause of postmenopausal osteoporosis is believed to be impairment of calcium absorption, one of the premises for the use of a synthetic form of calcitriol in this disease is to stimulate the intestinal absorption of calcium, reduce parathyroid hormone secretion and thus prevent the breakdown of bone.

Orally administered calcitriol increases calcium absorption by about 25 to 55% in women with postmenopausal osteoporosis. This effect may be a result of increased circulating calcitriol levels and a local action of calcitriol in the intestine. Recent evidence suggests that calcitriol levels in bone are also reduced in the aged and in patients with osteoporosis.

Calcitriol influences bone remodelling: it stimulates resorption of bone by osteoclasts through receptor-mediated activity on osteoblasts, as demonstrated in rat osteoblastic cells in vitro, and may also have a weak effect on bone formation. In osteoblastic cells, calcitriol has been shown to stimulate production of the bone-specific protein osteocalcin, which is important for bone mineralisation.

Calcitriol administration prevented the loss of bone mass in lumbar vertebrae of oophorectomised adult beagles compared with untreated controls. In castrated female beagles with established bone loss, calcitriol at dosages ≥0.015 μg/kg/day reversed changes in bone density. In women with established postmenopausal osteoporosis, calcitriol therapy (>0.6 μg/day) for 2 years halted bone loss, compared with a 4% decrease in bone density in placebo recipients.

The pharmacokinetic properties of calcitriol in humans are not well described in the published literature. Peak serum calcitriol concentrations occur 3 to 6 hours after oral doses of 0.25 to 0μg. The serum elimination half-life is 3 to 6 hours. Calcitriol is excreted mainly in the faeces.

Therapeutic Efficacy

Results of randomised controlled clinical trials evaluating the effects of calcitriol treatment on the vertebral fracture rate in postmenopausal women have been conflicting, owing in part to their widely varying methodologies. However, a recent long term study involving 622 women with established postmenopausal osteoporosis reported a significant 3-fold lower vertebral fracture rate in the third year of treatment in women who received calcitriol 0.25μg twice daily compared with those randomised to calcium gluconate supplementation (equivalent to 1000 mg/day of elemental calcium). This decrease was evident in patients with mild to moderate osteoporosis (≤5 vertebral fractures at entry) but not in those with more severe disease.

Preliminary evidence suggests that calcitriol may also have a role in the prevention of corticosteroid-induced osteoporosis. In 92 evaluable patients commencing long term therapy with either prednisone or prednisolone, treatment with calcitriol 0.5 to 1 μg/day plus calcium 1000 mg/day, administered prophylactically with or without intranasal salmon calcitonin 400 IU/day for 12 months, attenuated corticosteroid-induced bone loss in the lumbar spine. It remains to be shown whether this decrease in bone loss will translate into a reduced incidence of corticosteroid-induced vertebral fractures.

Tolerability

Calcitriol has been well tolerated in uncontrolled and controlled clinical studies performed for at least 2 years in patients with postmenopausal osteoporosis and for 1 year in those with corticosteroid-induced osteoporosis. In the majority of patients who developed mild hypercalcaemia and hypercalciuria, these symptoms resolved following decreases in calcium intake and/or in calcitriol dosage. The incidence of adverse effects (primarily gastrointestinal and neurological) leading to withdrawal during the 3-year treatment period in the largest clinical trial was 8.6% in women receiving calcitriol vs 6.5% in calcium recipients. Significant renal toxicity has not been a feature of calcitriol use. Rare instances of decreased creatinine clearance and nephrolithiasis have been reported during calcitriol therapy, although this latter effect has also been documented with placebo. Possible causality to treatment cannot be ascertained because of a lack of baseline evaluations.

Dosage and Administration

The recommended dosage of calcitriol in the treatment of postmenopausal osteoporosis is 0.25μg twice daily. Serum creatinine and calcium levels should be monitored at 4 weeks, 3 months and 6 months after initiating therapy, and at regular intervals (every 6 months) thereafter. Calcium supplementation is not generally required in patients receiving calcitriol and daily calcium intake should not exceed 600 to 800mg. In the event of hypercalcaemia, calcitriol should be discontinued until serum calcium levels normalise. Therapy may then be reinstituted at a dosage 0.25 μg/day lower than previously, and the dosage may be increased 1 month later to 0.25μg twice daily if serum calcium levels remain normal.

Concomitant use of calcitriol with digitalis may increase the risk of cardiac arrhythmias. To avoid the risk of hypermagnesaemia, calcitriol should not be used with products containing magnesium. The efficacy of calcitriol may be impaired by coadministration with cholestyramine.

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References

  1. Brommage R, DeLuca HF. Evidence that 1, 25-dihydroxyvitamin D3 is the physiologically active metabolite of vitamin D3. Endocr Rev 1985; 6: 491–511

    Article  PubMed  CAS  Google Scholar 

  2. Holick MF, Krane SM, Potts JG IT. Calcium, phosphorus and bone metabolism: calcium-regulating hormones. In: Wilson JD et al., editors. Harrison’s Principles of Internal Medicine, 12th ed. New York: McGraw-Hill, 1991: 1888–901

    Google Scholar 

  3. DeLuca HF. Osteoporosis and the metabolites of vitamin D. Metabolism 1990; 39 Suppl. 1: 3–9

    Article  PubMed  CAS  Google Scholar 

  4. Silver J, Naveh-Many T, Mayer H, et al. Regulation by vitamin D metabolites of parathyroid hormone gene transcription in vivo in the rat. J Clin Invest 1986; 78: 1296–301

    Article  PubMed  CAS  Google Scholar 

  5. Nordin BE, Morris HA. The calcium deficiency model for osteoporosis. Nutr Rev 1989; 47: 65–72

    Article  PubMed  CAS  Google Scholar 

  6. Riggs BL, Melton III LJ. The prevention and treatment of osteoporosis. N Engl J Med 1992; 327: 620–7

    Article  PubMed  CAS  Google Scholar 

  7. Parfitt AM. Bone remodelling: relationship to the amount and structure of bone, and the pathogenesis and prevention of fractures. In: Riggs BL & Melton LJ III, editors. Osteoporosis: etiology, diagnosis and management. New York: Raven Press, 1988: 45–93

    Google Scholar 

  8. Parfitt AM, Mathews CHE, Villanueva AR, et al. Relationships between surface, volume, and thickness of iliac trabecular bone in aging and in osteoporosis. Implications for the microanatomic and cellular mechanisms of bone loss. J Clin Invest 1983; 72: 1396–409

    Article  PubMed  CAS  Google Scholar 

  9. Bullamore JR, Gallagher JC, Wilkinson R, et al. Effect of age on calcium absorption. Lancet 1970; 2: 535–7

    Article  PubMed  CAS  Google Scholar 

  10. Gallagher JC, Riggs BL, Eisman J, et al. Intestinal calcium absorption and serum vitamin D metabolites in normal subjects and osteoporotic patients. J Clin Invest 1979; 64: 729–36

    Article  PubMed  CAS  Google Scholar 

  11. Compston JE, Silver AC, Croucher PI, et al. Elevated serum intact parathyroid hormone levels in elderly patients with hip fracture. Clin Endocrinol 1989; 31: 667–72

    Article  CAS  Google Scholar 

  12. Eastell R, Yergey AL, Vieira NE, et al. Interrelationship among vitamin D metabolism, true calcium absorption, parathyroid function, and age in women: evidence of an age-related intestinal resistance to 1,25-dihydroxyvitamin D action. J Bone Min Res 1991; 6: 125–32

    Article  CAS  Google Scholar 

  13. Endres DB, Morgan CH, Garry PJ, et al. Age-related changes in serum immunoreactive parathyroid hormone and its biological action in healthy men and women. J Clin Endocrinol Metab 1987; 65: 724–31

    Article  PubMed  CAS  Google Scholar 

  14. Gallagher JC, Riggs BL, Jerpbak CM, et al. The effect of age on serum immunoreactive parathyroid hormone in normal and osteoporotic women. J Lab Clin Med 1980; 95: 373–85

    PubMed  CAS  Google Scholar 

  15. Wiske PS, Epstein S, Bell NH, et al. Increases in immunoreactive parathyroid hormone with age. N Engl J Med 1979; 300: 1419–21

    Article  PubMed  CAS  Google Scholar 

  16. Tsai K-S, Heath III H, Kumar R, et al. Impaired vitamin D metabolism with aging in women. J Clin Invest 1984; 73: 1668–72

    Article  PubMed  CAS  Google Scholar 

  17. Caniggia A, Gennari C, Bianchi V, et al. Intestinal absorption of Ca in senile osteoporosis. Acta Med Scand 1963; 173: 613–7

    Article  PubMed  CAS  Google Scholar 

  18. Lund Bj, Sorensen OH, Lund Bi, et al. Serum 1, 25-dihydroxyvitamin D in normal subjects and in patients with postmenopausal osteopenia. Influence of age, renal function and oestrogen therapy. Horm Metab Res 1982; 14: 271–4

    Article  PubMed  CAS  Google Scholar 

  19. Riggs BL, Nelson KL. Effect of long term treatment with calcitriol on calcium absorption and mineral metabolism in postmenopausal osteoporosis. J Clin Endocrinol Metab 1985; 61: 457–61

    Article  PubMed  CAS  Google Scholar 

  20. Christiansen C, Rødbro P. Serum vitamin D metabolites in younger and elderly postmenopausal women. Calcif Tissue Int 1984; 36: 19–24

    Article  PubMed  CAS  Google Scholar 

  21. Morris HA, Need AG, Horowitz M, et al. Calcium absorption in normal and osteoporotic women. Calcif Tissue Int 1991; 49: 240–3

    Article  PubMed  CAS  Google Scholar 

  22. Ebeling PR, Sandgren ME, DiMagno EP, et al. Evidence of an age-related decrease in intestinal responsiveness to vitamin D: relationship between serum 1, 25-dihydroxyvitamin D3 and intestinal vitamin D receptors concentrations in normal women. J Clin Endocrinol Metab 1992; 75: 176–82

    Article  PubMed  CAS  Google Scholar 

  23. Lidor C, Sagiv P, Amdur B, et al. Decrease in bone levels of 1, 25-dihydroxy vitamin D3 in women with subcapital fracture of the femur. Proceedings of the Fourth International Symposium on Osteoporosis and Consensus Development Conference; 1993 Mar 27-Apr 2; Hong Kong: 11–2

    Google Scholar 

  24. Sagiv P, Lidor C, Hallel T, et al. Decrease in bone level of 1,25-dihydroxy vitamin D in women over 45 years old. Calcif Tissue Int 1992; 51: 24–6

    Article  PubMed  CAS  Google Scholar 

  25. Slovik DM, Adams JS, Neer RM, et al. Deficient production of 1,25-dihydroxy vitamin D in elderly osteoporotic patients. N Engl J Med 1981; 305: 372–4

    Article  PubMed  CAS  Google Scholar 

  26. Riggs BL, Melton III LJ. Involutional osteoporosis. N Engl J Med 1986; 314: 1676–86

    Article  PubMed  CAS  Google Scholar 

  27. Richelson LS, Wahner HW, Melton III LJ, et al. Relative contributions of ageing and estrogen deficiency to postmenopausal bone loss. N Engl J Med 1984; 311: 1273–5

    Article  PubMed  CAS  Google Scholar 

  28. Silverberg SJ, Shane E, de la Cruz L, et al. Abnormalities in parathyroid hormone secretion and 1,25-dihydroxyvitamin D3 formation in women with osteoporosis. N Engl J Med 1989; 320: 277–81

    Article  PubMed  CAS  Google Scholar 

  29. Koren R, Ravid A, Liberman UA, et al. Responsiveness to 1,25 dihydroxyvitamin D3 is reduced in lymphocytes from osteoporotic women. J Bone Miner Res 1992; 7: 1057–61

    Article  PubMed  CAS  Google Scholar 

  30. Joseph JC. Corticosteroid-induced osteoporosis. Am J Hosp Pharm 1994; 51: 188–97

    PubMed  CAS  Google Scholar 

  31. Egsmose C, Lund B, McNair P, et al. Low serum levels of 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D in institutionalized old people: influence of solar exposure and vitamin D supplementation. Age Ageing 1987; 16: 35–40

    Article  PubMed  CAS  Google Scholar 

  32. Gallagher JC. Vitamin D metabolism and therapy in elderly subjects. South Med J 1992; 85 Suppl. 2: 43–7

    Google Scholar 

  33. Lips P, van Ginkel FC, Netelenbos C, et al. Lower mobility and markers of bone resorption in the elderly. Bone Miner 1990; 9: 49–57

    Article  PubMed  CAS  Google Scholar 

  34. Bauer DC, Browner WS, Cauley JA, et al. Factors associated with appendicular bone mass in older women. The Study of Osteoporotic Fractures Research Group. Ann Intern Med 1993; 118: 657–65

    PubMed  CAS  Google Scholar 

  35. Williams AR, Weiss NS, Ure CL, et al. Effect of weight, smoking, and estrogen use on the risk of hip and forearm fractures in postmenopausal women. Obstet Gynecol 1982; 60: 695–9

    PubMed  CAS  Google Scholar 

  36. Hopper JL, Seeman E. The bone density of female twins discordant for tobacco use. N Engl J Med 1994; 330: 387–92

    Article  PubMed  CAS  Google Scholar 

  37. Bikle DD, Genant HK, Cann C, et al. Bone disease in alcohol abuse. Ann Intern Med 1985; 103: 42–8

    PubMed  CAS  Google Scholar 

  38. Calvo MS. Dietary phosphorus, calcium metabolism and bone. J Nutr 1993; 123: 1627–33

    PubMed  CAS  Google Scholar 

  39. DeLuca HF. Applications of new vitamin D compounds to disease. Drug News Perspect 1992; 5: 87–92

    Google Scholar 

  40. Sandgren M, Danforth L, Plasse TF, et al. 1,25-Dihy-droxyvitamin D3 receptors in human carcinomas: a pilot study. Cancer Res 1991; 51: 2021–4

    PubMed  CAS  Google Scholar 

  41. Frampton RJ, Suva LJ, Eisman JA, et al. Presence of 1, 25-dihydroxyvitamin D3 receptors in established human cancer cell lines in culture. Cancer Res 1982; 42: 1116–9

    PubMed  CAS  Google Scholar 

  42. Marie PJ, Travers R. Continuous infusion of 1,25 dihydroxyvitamin D3 stimulates bone turnover in the normal young mouse. Calcif Tissue Int 1983; 35: 418–25

    Article  PubMed  CAS  Google Scholar 

  43. Raisz LG, Trummel CL, Holick MF, et al. 1,25-Dihy-droxycholecalciferol: a potent stimulator of bone resorption in tissue culture. Science 1972; 175: 768–9

    Article  PubMed  CAS  Google Scholar 

  44. Reynolds JJ, Holick MF, DeLuca HF. The role of vitamin D metabolites in bone resorption. Calcif Tissue Res 1973; 12: 295–301

    Article  PubMed  CAS  Google Scholar 

  45. McSheehy PMJ, Chambers TJ. 1,25-Dihydroxyvitamin D3 stimulates rat osteoblastic cells to release a soluble factor that increases osteoclastic bone resorption. J Clin Invest 1987; 80: 425–9

    Article  PubMed  CAS  Google Scholar 

  46. Medhora MM, Teitelbaum S, Chappel J, et al. 1-α,25-Dihydroxyvitamin D3 up-regulates expression of the osteoclast integrin αvβ3. J Biol Chem 1993; 268: 1456–61

    PubMed  CAS  Google Scholar 

  47. Zarrabeitia MT, Riancho JA, Amado JA, et al. Effect of calcitriol on the secretion of prostaglandin E2, interleukin 1, and tumor necrosis factor a by human monocytes. Bone 1992; 13: 185–9

    Article  PubMed  CAS  Google Scholar 

  48. Stein GS, Lian JB, Uskovic M, et al. Effects of 1,25(OH)2D3 and vitamin-D analogs on developmental control of cell growth and tissue-specific expression during osteoblast differentiation. Bioorg Med Chem Lett 1993; 3: 1885–90

    Article  CAS  Google Scholar 

  49. Marie PJ, Connes D, Hott M, Miravet. Comparative effects of a novel vitamin D analogue MC-903 and 1,25-dihydroxyvitamin D3 on alkaline phosphatase activity, osteocalcin and DNA synthesis by human osteoblastic cells in culture. Bone 1990; 11: 171–9

    Article  PubMed  CAS  Google Scholar 

  50. Pols HAP, Schilte HP, Herrmann-Erlee NMP, et al. The effects of 1,25 dihydroxyvitamin D3 on growth, alkaline phosphatase and adenylate cyclase of rat osteoblast-like cells. Bone Miner 1986; 1: 397–405

    PubMed  CAS  Google Scholar 

  51. Lomri A, Marie PJ, Tran PV, et al. Characterization of endosteal osteoblastic cells isolated from mouse caudal vertebrae. Bone 1988; 9: 165–75

    Article  PubMed  CAS  Google Scholar 

  52. Kanatani M, Sugimoto T, Fukase M, et al. Effect of 1,25 dihydroxyvitamin D3 on the proliferation of osteoblastic MC3T3-E1 cells by modulating the release of local regulators from monocytes. Biochem Biophys Res Commun 1993; 190: 529–35

    Article  PubMed  CAS  Google Scholar 

  53. Beresford JN, Gallagher JA, Poser JW, et al. Production of osteocalcin by human bone cells in vitro. Effects of 1,25(OH)2D3, 24,25(OH)2D3, parathyroid hormone and glucocorticoids. Metab Bone Dis Rel Res 1984; 5: 229–34

    Article  CAS  Google Scholar 

  54. Price PA, Baukol SA. 1,25-Dihydroxy vitamin D3 increases serum levels of the vitamin K-dependent bone protein. Biochem Biophys Res Commun 1981; 99: 928–35

    Article  PubMed  CAS  Google Scholar 

  55. Morrison NA, Cheng Qi J, Tokita A, et al. Prediction of bone density from vitamin D receptor alleles. Nature 1994; 367: 284–7

    Article  PubMed  CAS  Google Scholar 

  56. Drezner MK, Nesbitt T. Role of calcitriol in prevention of osteoporosis: part I. Metabolism 1990; 39 Suppl. 1: 18–23

    Article  PubMed  CAS  Google Scholar 

  57. Malluche HH, Faugere M-C. Role of calcitriol in the management of osteoporosis. Metabolism 1990; 39 Suppl. 1: 24–6

    Article  PubMed  CAS  Google Scholar 

  58. Aloia JF, Vaswani A, Yeh JK, et al. Calcitriol in the treatment of postmenopausal osteoporosis. Am J Med 1988; 84: 401–8

    Article  PubMed  CAS  Google Scholar 

  59. Gallagher JC, Goldgar D. Treatment of postmenopausal osteoporosis with high doses of synthetic calcitriol. Ann Intern Med 1990; 113: 649–55

    PubMed  CAS  Google Scholar 

  60. Ott SM, Chesnut III CH. Calcitriol treatment is not effective in postmenopausal osteoporosis. Ann Intern Med 1989; 110: 267–74

    PubMed  CAS  Google Scholar 

  61. Ott SM, Chesnut III CH. Tolerance to doses of calcitriol is associated with improved bone density in women with postmenopausal osteoporosis [abstract no. 449]. J Bone Miner Res 1990; 5 Suppl. 2: 186

    Google Scholar 

  62. Roche Laboratories. Treatment of postmenopausal osteoporosis. Hoffmann-LaRoche Inc., data on file. NDA-18-044, May 5, 1994

  63. Caniggia A, Nuti R, Lore F, et al. Long-term treatment with calcitriol in postmenopausal osteoporosis. Metabolism 1990; 39 Suppl. 1:43–9

    Article  CAS  Google Scholar 

  64. Francis RM, Peacock M. Local action of oral 1,25-dihydroxycholecalciferol on calcium absorption in osteoporosis. Am J Clin Nutr 1987; 46: 315–8

    PubMed  CAS  Google Scholar 

  65. Sakhaee K, Zisman A, Poindexter JR, et al. Metabolic effects of thiazide and 1,25-(OH)2 vitamin D in postmenopaual osteoporosis. Osteoporos Int 1993; 3: 209–14

    Article  PubMed  CAS  Google Scholar 

  66. Roche Laboratories. Calcitriol prescribing information, Nutley, New Jersey, 1993

  67. Blumenthal HP, Bryce GF, Mallon JP, et al. Serum concentrations of 1,25 (OH)2 — vitamin D3 following 0.25μg and 0.5μg of Rocaltrol or no drug. Hoffmann-La Roche Inc., New Jersey, data on file. N-34279 (ref. 801); Oct 10, 1980

    Google Scholar 

  68. Papapoulos SE, Clemens TL, Sandler LM, et al. The effect of renal function on changes in circulating concentrations of 1,25-dihydroxycholecalciferol after an oral dose. Clin Sci 1982; 62: 427–9

    PubMed  CAS  Google Scholar 

  69. Bryce GF, Mallon JP, Miller ON. Further studies on the pharmacokinetics and turnover of calcitriol in normal man. Hoffmann-LaRoche Inc., New Jersey, data on file. N-32179 (ref. 803); Jun 20, 1980

    Google Scholar 

  70. Gallagher JC. The pathogenesis of osteoporosis. Bone Miner 1990; 9: 215–27

    Article  PubMed  CAS  Google Scholar 

  71. Riggs BL, Melton III LJ. Evidence for two distinct syndromes of involutional osteoporosis. Am J Med 1983; 75: 899–901

    Article  PubMed  CAS  Google Scholar 

  72. Krane SM, Holick NF. Metabolic bone disease: osteoporosis. In: Wilson JD et al., editors. Harrison’s Principles of Internal Medicine, 12th ed. New York: McGraw-Hill, 1991: 1921–6

    Google Scholar 

  73. Gallagher JC, Riggs BL, Recker RR, et al. The effect of calcitriol on patients with postmenopausal osteoporosis with special reference to fracture frequency. Proc Soc Exp Biol Med 1989; 191:287–92

    PubMed  CAS  Google Scholar 

  74. Tilyard MW, Spears GFS, Thomson J, et al. Treatment of postmenopausal osteoporosis with calcitriol or calcium. N Engl J Med 1992; 326: 357–62

    Article  PubMed  CAS  Google Scholar 

  75. Recker RR. Final study report: effects of Rocaltrol® (calcitriol) on senile osteoporosis — protocol no. 860. Hoffmann-LaRoche Inc., New Jersey, data on file. N-122915 (ref. 860); Jan 20, 1984

    Google Scholar 

  76. Riggs BL. Final study report: effects of 1,25 (OH)2D3 (Rocaltrol®) on senile osteoporosis. Hoffmann-LaRoche Inc., New Jersey, data on file. N-122913, Jan 20, 1984

    Google Scholar 

  77. Sambrook P, Birmingham J, Kelly P, et al. Prevention of corticosteroid osteoporosis. A comparison of calcium, calcitriol, and calcitonin. N Engl J Med 1993; 328: 1747–52

    Article  PubMed  CAS  Google Scholar 

  78. Tilyard MW. Calcitriol compared with calcium in the treatment of established postmenopausal osteoporosis. Proceedings of the Fourth International Symposium on Osteoporosis and Consensus Development Conference; 1993 Mar 27-Apr 2; Hong Kong: 15–7

    Google Scholar 

  79. Cooper C, Aihie A. Osteoporosis: recent advances in pathogenesis and treatment. Q J Med 1994; 87: 203–9

    PubMed  CAS  Google Scholar 

  80. Arnaud CD, Kolb FO. The calciotropic hormones and metabolic bone disease. In: Greenspan FS, editor. Basic and clinical endocrinology. Norwalk: Appleton & Lange, 1991: 247–322

    Google Scholar 

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    Kerry L. Dechant & Karen L. Goa

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Various sections of the manuscript reviewed by: H.E DeLuca, Department of Biochemistry, University of Wisconsin-Madison, Madison, Wisconsin, USA; S. Edelstein, Biochemistry Department, Weizmann Institute of Science, Rehovot, Israel; J.C. Gallagher, Bone Metabolism Unit, Creighton University, Omaha, Nebraska, USA; S. Giannini, Istituto de Medicina Interna, Universita di Padova, Padova, Italy; S.I. Girgis, Royal Postgraduate Medical School, Hammersmith Hospital, London, England; U. Lindgren, Department of Orthopaedic Surgery, Huddinge University Hospital, Huddinge, Sweden; D.E. Meier, Department of Geriatrics, The Mount Sinai Medical Center, New York, New York, USA; P.J. Marie, Unite de Recherche 349, Centre Viggo Petersen, INSERM, Paris, France; P. Sambrook, The Garvan Institute of Medical Research, S1. Vincent’s Hospital, Sydney, New South Wales, Australia; M. W. Tilyard, Department of General Practice, Otago Medical School, Dunedin, New Zealand.

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Dechant, K.L., Goa, K.L. Calcitriol. Drugs & Aging 5, 300–317 (1994). https://doi.org/10.2165/00002512-199405040-00006

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