Medsafe Logo
<% Dim q q = request.form("q") If len(q) > 0 Then Response.redirect "/searchResults.asp?q=" & q End if %>
Hide menus
Show menus

Publications

Published: February 2002
ADR update

Low dose oral steroids can increase fracture risk

Prescriber Update 23(1): 6–7
February 2002

Marius Rademaker, Hon Associate Professor and Specialist Dermatologist, Hamilton 
and the Medsafe Editorial Team

Corticosteroids can reduce bone density and increase the risk of fractures.  This occurs quite quickly and even with low doses.  It is estimated that up to 50% of patients using oral corticosteroids will develop bone fractures.  Upon cessation of the steroid, fracture risk decreases.  Preventative measures include using the lowest possible corticosteroid dose and regularly reviewing the need for continuation.  Also address factors such as smoking, calcium intake and abnormal vitamin D levels.  Bisphosphonates and sex hormones can be used to treat reduced bone density.

Risk factors include age and concurrent inflammatory disease

The incidence of fractures in patients taking corticosteroids ranges from 11%1 to 50%.2  The risk of developing steroid-induced osteoporosis is increased in persons older than 50 or younger than 15 years of age, those with a slim build and in women who are post-menopausal.1  Corticosteroid users with medical conditions such as rheumatoid arthritis,2 chronic obstructive pulmonary disease, amenorrhoea and inflammatory bowel disease are also at increased risk.3  Bone density during steroid use is related to duration of steroid treatment and average dose, as well as factors that influence pre-treatment bone density such as weight and age.1

Loss of bone mineral density occurs rapidly but can be reversed

Bone loss appears to be greatest in the first two to three months of corticosteroid use.1,4,5  Fracture risk returns to baseline when steroid treatment is discontinued, with the risk reduction occurring mostly within the first year of stopping.5  As a general guide, the period required for the restoration of bone density is approximately equal to the period of treatment.6

Even doses as low as 5mg daily can increase bone fracture risk

While the minimum dose for steroid-induced bone loss is unknown, reduced bone density and fractures have occurred with doses as low as 5mg of prednisone per day.1  A study5 of over 200,000 oral corticosteroid users found that the risk of fracture was augmented with increasing dose.  Even at daily doses of prednisone equivalent to 2.5-7.5mg, there was an increased risk of hip and vertebral fractures, compared to the control group on no corticosteroids.5  It is unknown whether bone density is affected by short, tapered courses of steroids such as those prescribed for asthma exacerbations.4

Consider prophylaxis to minimise risk of osteoporosis

Preventative measures may be beneficial and include using the minimum effective corticosteroid dose, and regularly reviewing it.7  Alternate-day therapy does not reduce the risk of bone loss, but may help minimise hypothalamic-pituitary-adrenal suppression.8  Where practical, address factors such as high alcohol intake,3 smoking and low body weight, and prescribe calcium supplements.9  Also encourage patients to undertake regular weight-bearing exercise.7  Check serum 25-hydroxyvitamin D levels and normalise with calciferol if necessary.9  Bone density monitoring is recommended in patients taking corticosteroids long term.10

Pharmacological intervention includes bisphosphonates and sex hormones

If bone density is reduced, the first treatment of choice is bisphosphonates such as cyclical etidronate plus calcium, or alendronate.9  Hormone replacement therapy (HRT) may also be beneficial in post-menopausal women,9 however the risks and contraindications of HRT need to be considered.  Testosterone therapy may be indicated in men with androgen deficiency.10  Intervention should also be offered to patients with a past history of fracture after minimal trauma, as this indicates the skeleton is less able to cope with the usual strains of daily living.10

Competing interests (authors): none declared.

Correspondence to Dr Marius Rademaker, Dermatology Department, Waikato Hospital, Private Bag 3200, Hamilton. E-mail: Rademakm@hwl.co.nz

References
  1. Jenkinson T, Bhalla AK. A reappraisal of steroid-induced osteoporosis. Br J Hosp Med 1993;50(8):472-476.
  2. Adachi JD. Corticosteroid-induced osteoporosis. Am J Med Sci 1997;313(1):41-49.
  3. Picado C, Luengo M. Corticosteroid-induced bone loss: Prevention and Management. Drug Saf 1996;15(5):347-359.
  4. McKenzie R, Reynolds JC, O'Fallon A, et al. Decreased bone mineral density during low dose glucocorticoid administration in a randomized placebo controlled trial. J Rheumatol 2000;27(9):2222-2226.
  5. Van Staa TP, Leufkens HGM, Abenhaim L, et al. Use of oral corticosteroids and risk of fractures. J Bone Miner Res 2000;15(6):993-1000.
  6. Laan RFJM, Vanriel PLCM, Vandeputte LBA, et al. Low-dose prednisone induces rapid reversible axial bone loss in patients with rheumatoid arthritis - a randomized, controlled study. Ann Intern Med 1993;119:963-968.
  7. Eastell R, Reid DM, Compston J, et al. A UK Consensus Group on management of glucocorticoid-induced osteoporosis: an update. J Intern Med 1998;244:271-292.
  8. Corticosteroids. In Parfitt K (Ed) Martindale 32nd Edn. 1999: Massachusetts, p.1011.
  9. Reid IR. Time to end steroid-induced fractures. Arch Dermatol 2001;137:493-494.
  10. PreMeC. Prevention and treatment of glucorticoid-induced osteoporosis. Premec Medicines Information Bulletin 1999; No.79 (May). http://www.premec.org.nz/bulletins/79.htm

 

0 1 2 4 5 6 7 9 [ /