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Thorax 1998;53:331-332 doi:10.1136/thx.53.5.331
  • Editorial

Bisphosphonates and glucocorticoid-induced osteoporosis: implications for patients with respiratory diseases

  1. SIMONE COWAN
  1. Respiratory Epidemiology Unit
  2. Department of Epidemiology and Biostatistics
  3. McGill University
  4. Montreal
  5. Quebec H3A 1A3
  6. Canada
  7. Department of Medicine
  8. McGill University Health Centre
  9. Montreal
  10. Quebec H3G 1A4
  11. Canada
  12. Division of Respiratory Medicine
  13. McGill University Health Centre
  14. Montreal
  15. Quebec H3G 1A4
  16. Canada
    1. SUZANNE MORIN
    1. Respiratory Epidemiology Unit
    2. Department of Epidemiology and Biostatistics
    3. McGill University
    4. Montreal
    5. Quebec H3A 1A3
    6. Canada
    7. Department of Medicine
    8. McGill University Health Centre
    9. Montreal
    10. Quebec H3G 1A4
    11. Canada
    12. Division of Respiratory Medicine
    13. McGill University Health Centre
    14. Montreal
    15. Quebec H3G 1A4
    16. Canada
      1. PIERRE ERNST
      1. Respiratory Epidemiology Unit
      2. Department of Epidemiology and Biostatistics
      3. McGill University
      4. Montreal
      5. Quebec H3A 1A3
      6. Canada
      7. Department of Medicine
      8. McGill University Health Centre
      9. Montreal
      10. Quebec H3G 1A4
      11. Canada
      12. Division of Respiratory Medicine
      13. McGill University Health Centre
      14. Montreal
      15. Quebec H3G 1A4
      16. Canada

          Osteoporosis is a well known consequence of glucocorticoid treatment that can result in significant morbidity and mortality.1-4 Glucocorticoid-induced bone loss occurs early, usually within 6–12 months of starting therapy. During this time the rate of bone loss is rapid before decreasing or reaching a plateau.1 2 4 Clinically this decrease in bone mineral density puts patients at an increased risk of fracture.1 2 4 5 Specifically, with a decline in bone mass of one standard deviation below the mean for young adults, the risk of fracture doubles.5 Characteristically, glucocorticoid-induced osteopenia and osteoporosis occur at a faster rate in trabecular bone; consequently, the ribs and vertebrae are common sites of fracture, although hip fractures have also been reported.6 7 As long term treatment with oral glucocorticoids is a common practice in the management of patients with chronic respiratory diseases, strategies to decrease the burden of glucocorticoid-induced osteoporosis are needed.

          Glucocorticoid-induced bone loss results from a decrease in bone formation due to reduced intestinal calcium absorption, increased urinary calcium excretion, and reduced osteoblast formation and function.1 2 4 8 The bisphosphonates, a class of drugs structurally similar to pyrophosphate, alter the bone remodelling process. By binding to hydroxyapatite these agents structurally inhibit osteoclastic activity and prevent bone resorption.9 This significantly increases bone mineral density in the lumbar spine and femur and decreases the rate of fracture at these sites.10-13 For this reason, bisphosphonates such as etidronate and alendronate have received official approval for the treatment and prevention of postmenopausal osteoporosis in many countries. The bisphosphonates have also been studied in the prevention and treatment of glucocorticoid-induced osteoporosis.

          In this issue of Thorax Pitt et al shed further light on the …

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