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Update On Corticosteroid-Induced Osteoporosis

Posted on: 08/28/2008
Osteoporosis (brittle bones) can be a devastating disease leading to vertebral compression and hip fractures. Postmenopausal women are affected most often. But a second group is also at increased risk. Anyone who takes corticosteroids over a long period of time for chronic conditions is at risk for corticosteroid-induced osteoporosis.

Corticosteroid therapy is a common treatment for asthma, inflammatory bowel disease, and autoimmune disorders. These drugs have adverse side effects that lead to osteoporosis. For example, corticosteroids decrease the amount of calcium available in the bloodstream and decrease the amount of bone formation. They also cause an increased amount of bone to be resorbed by the body.

Early measures to prevent osteoporosis in this group of patients are advised. The physician must assess each patient's individual risk of fracture. They do this by first looking at the total daily dose of steroids in use. Any amount of steroid used daily is a risk factor for osteoporosis and fractures. But high-doses (over 10 milligrams per day) increase the risk of fracture even more.

How soon do these effects occur? Some studies show that fractures can occur early on when taking corticosteroids. Bone changes occur quickly. Others have found the risk to increase after 90 days of corticosteroid use. Taking daily doses of steroids has a greater impact on fracture risk than intermittent use. But there is a cumulative effect no matter how much or how often these drugs are used.

Some tips for prevention of corticosteroid-induced osteoporosis include:

  • Patients should be given the lowest dose possible that is still effective for the problem.
  • Taking the drug every other day does not decrease the risk of osteoporosis caused by steroids.
  • When corticosteroid therapy is necessary, practice prevention strategies such as calcium and vitamin D supplementation. All patients on oral corticosteroids should be using supplementation.
  • Consider the use of medications such as bisphosphonates, calcitonin, or parathyroid hormone whenever appropriate.
  • Encourage lifestyle changes such as quitting smoking, getting the right kind of exercise, and reducing alcohol intake.
  • Anyone taking more than 7.5 mg of oral prednisone (or an equivalent amount of other steroid) for more than three months should be tested for bone mineral density and started on preventive medication.

    Exercise should include both weight-bearing and resistance training. Preventive steps should be taken if the T-score is more than -1. This score is found when doing bone mineral density testing. It's a different cut off point for patients taking steroids than the score used to diagnose postmenopausal osteoporosis (less than -2.5).

    That's because the risk of fracture goes up faster with corticosteroid use compared with menopause-induced osteoporosis. Even a small amount of bone loss puts patients who are taking corticosteroids at risk of fracture. In other words, their fracture risk is already greater at the lower T-score level.

    Medications such as bisphosphonates (prevent bone resorption) are recommended when there has been a previous history of bone fracture, suspected vertebral fracture, or family history of osteoporosis.

    Other risk factors that should be taken into consideration when decided to use bisphosphonates include low body weight and men over the age of 50. Anyone who is immobilized due to other health problems is also considered a good candidate for prevention of osteoporosis using bisphosphonates.

    All the preventive steps are turned into treatment when the T-scores are less than -2.5. This means osteoporosis has already developed. Prevention is not an option. Treatment is required. At that point, more rigorous measures are needed combining lifestyle modifications with drug treatment.

  • References:
    Kathryn M. Ruf, BS, et al. Risk Factors, Prevention, and Treatment of Corticosteroid-Induced Osteoporosis in Adults. In Orthopedics. August 2008. Vol. 31. No. 8. Pp. 768-772.

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