Osteoporosis International

, Volume 17, Issue 1, pp 105–108 | Cite as

High-dose glucocorticoid treatment induces rapid loss of trabecular bone mineral density and lean body mass

  • Koshi Natsui
  • Kiyoshi Tanaka
  • Michio Suda
  • Akihiro Yasoda
  • Yoko Sakuma
  • Ami Ozasa
  • Shoichi Ozaki
  • Kazuwa Nakao
Original Article

Abstract

A recent large-scale study revealed that glucocorticoid treatment increased fracture risk, which occurred at a far smaller dose and by a shorter duration than previously thought. To study the underlying mechanism for the increased risk of fracture, we studied the early changes in bone mineral density (BMD) and body composition by dual energy X-ray absorptiometry (DXA) after initiating high-dose glucocorticoid treatment. High-dose glucocorticoid treatment was arbitrarily defined as daily doses of ≥40 mg of a predonisolone equivalent. The 33 patients enrolled in this study had not received glucocorticoid treatment before. Only 2 months of treatment resulted in substantial BMD loss, most markedly in the lumbar spine, followed by the femoral neck and total body, which suggests the preferential trabecular bone loss. Body composition was also greatly affected. Thus, 2-month treatment with glucocorticoid significantly reduced bone mineral content (BMC), lean body mass (LBM) and increased fat mass (FAT). Our results are likely to have some clinical relevance. First, BMD loss occurs quite rapidly after starting glucocorticoid treatment, and patients receiving glucocorticoid treatment should be more carefully monitored for their BMD. Second, LBM, which mainly represents muscle volume, decreases rapidly after initiating glucocorticoid treatment. Decreased LBM might be also responsible for the increased risk of fracture, since falling is a well-known risk factor for fracture, and patients receiving glucocorticoid treatment should also be evaluated for their body composition.

Keywords

Body composition Dual energy X-ray absorptiometery Glucocorticoid-induced osteoporosis Lean body mass Steroid myopathy 

References

  1. 1.
    Saag KG, Koehnke R, Caldwell JR, Brasington R, Burmeister LF, Zimmerman B, Kohler JA, Furst DE (1994) Low dose long-term corticosteroid therapy in rheumatoid arthritis: an analysis of serious adverse events. Am J Med 96:115–123CrossRefPubMedGoogle Scholar
  2. 2.
    van Staa TP, Leufkens HGM, Abenhaim L, Zhang B, Cooper C (2000) Use of oral corticosteroid and risk of fractures. J Bone Miner Res 15:993–1000PubMedCrossRefADSGoogle Scholar
  3. 3.
    van Staa TP, Leufkens HG, Cooper C (2002) The epidemiology of corticosteroid-induced osteoporosis: a meta-analysis. Osteoporos Int 13:777–787CrossRefPubMedADSGoogle Scholar
  4. 4.
    Wallach S, Cohen S, Reid DM, Hughes RA, Hosking DJ, Laan RF, Doherty SM, Maricic M, Rosen C, Brown J, Barton I, Chines AA (2000) Effects of risedronate treatment on bone density and vertebral fracture in patients on corticosteroid therapy. Calcif Tissue Int 67:277–285CrossRefPubMedMathSciNetGoogle Scholar
  5. 5.
    Kanda F, Okuda S, Matsushita T, Takatani K, Kimura KI, Chihara K (2001) Steroid myopathy: pathogenesis and effects of growth hormone and insulin-like growth factor-I administration. Horm Res 56:S24–S28CrossRefGoogle Scholar
  6. 6.
    American College of Rheumatology Task Force on Osteoporosis Guidelines (1996) Recommendations for the prevention and treatment of glucocorticoid-induced osteoporosis. Arth Rheum 39:1791–1801Google Scholar
  7. 7.
    Pearson D, Miller CG (eds) (2002) Clinical trials in osteoporosis. Springer, Heidelberg Germany New YorkGoogle Scholar
  8. 8.
    Bonnick SL, Lewis LA (2002) Bone densitometry for technologists. Humana Press, Totowa, NJGoogle Scholar
  9. 9.
    Canalis E, Giustina A (2001) Glucocorticoid-induced osteoporosis: summary of a workshop. J Clin Endocrinol Metab 86:5681–5685CrossRefPubMedGoogle Scholar
  10. 10.
    Canalis E, Delany AM (2002). Mechanism of glucocorticoid action in bone. Ann NY Acad Sci 966:73–81PubMedCrossRefGoogle Scholar
  11. 11.
    Luengo M, Picado C, Del Rio L, Guanabens N, Monsterrat JM, Setoain J (1991) Vertebral fractures in steroid dependent asthma and involutional osteoporosis. Thorax 46:803–806PubMedCrossRefGoogle Scholar
  12. 12.
    Selby PL, Halsey JP, Adams KRH, Klimiuk P, Knight SM, Pal B, Stewart IM, Swinson DR (2000) Corticosteroids do not alter the threshold for vertebral fracture. J Bone Miner Res 15:952–956PubMedCrossRefGoogle Scholar
  13. 13.
    Houtkooper LB, Going SB, Sproul J, Blew RM, Lohman TG (2000) Comparison of methods for assessing body-composition changes over 1 year in postmenopausal women. Am J Clin Nutr 72:401–406PubMedGoogle Scholar
  14. 14.
    Vestergaard P, Olsen ML, Paaske Johnsen S, Rejnmark L, Toft Sorensen H, Mosekilde L. (2003) J Intern Med 254:486–493CrossRefPubMedGoogle Scholar
  15. 15.
    Bone and Tooth Society, National Osteoporosis Society, Royal College of Physicians. (2002) Glucocorticoid-induced osteoporosis: guidelines for prevention and treatment. Royal College of Physicians, LondonGoogle Scholar

Copyright information

© International Osteoporosis Foundation and National Osteoporosis Foundation 2005

Authors and Affiliations

  • Koshi Natsui
    • 1
  • Kiyoshi Tanaka
    • 2
  • Michio Suda
    • 3
  • Akihiro Yasoda
    • 4
  • Yoko Sakuma
    • 4
  • Ami Ozasa
    • 4
  • Shoichi Ozaki
    • 5
  • Kazuwa Nakao
    • 4
  1. 1.Department of MedicineFukui Red Cross HospitalFukuiJapan
  2. 2.Department of Food and NutritionKyoto Women’s UniversityKyotoJapan
  3. 3.Department of EndocrinologyKyoto City HospitalKyotoJapan
  4. 4.Department of Endocrinology and MetabolismKyoto University HospitalKyotoJapan
  5. 5.Division of Rheumatology and AllergySt. Marianna University School of MedicineKawasakiJapan

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